PREDICTING CONTRAST INDUCED NEPHROPATHY IN POST

PERCUTANEOUS CORONARY INTERVENTION PATIENTS – A

PROSPECTIVE OBSERVATIONAL COHORT STUDY

Submitted to
Nizam’s Institute of Medical Sciences, Hyderabad
In Partial Fulfillment of Rules and Regulations for the Award
of
D.M. degree in Cardiology to be held in July 2021.

By

Dr. SHAHOOD AJAZ KAKROO

DEPARTMENT OF CARDIOLOGY
Nizam’s Institute of Medical Sciences, Hyderabad.

Under the guidance of

DR. N. RAMA KUMARI, M.D, D.M

ADDITIONAL PROFESSOR
DEPARTMENT OF CARDIOLOGY

NIZAM’S INSTITUTE OF MEDICAL SCIENCES

PUNJAGUTTA, HYDERABAD
 ACKNOWLEDGMENT

At the outset, I express my deep sense of gratitude and sincere regards to Dr. N. RAMA
KUMARI, my guide and Additional Professor, Department of Cardiology, NIMS,
Hyderabad for her constant guidance, supervision and encouragement in accomplishing this
research.
I am highly grateful to my Professor & Head of department, Cardiology, DR. O SAI
SATISH for his valuable guidance, suggestions and encouragement during the preparation of
this dissertation. I am thankful to him for allowing me to undertake this study and utilize the
hospital records for the same.
My sincere respect and regards to Professor Dr. M. Jyotsna, Additional Professor Dr. B
Srinivas, Associate Professors Dr. N. Lalita, Dr. V.S. Bharathi Lakshmi and Dr. Sreekanth,
Assistant professors Dr. Jeethender Kumar Kala, Dr. M. Naveen Kumar, Dr. Parameshwar
Reddy and Dr. Goutami for their constructive criticisms and valuable suggestions.
My sincere thanks to my colleagues Dr. A. Goutham, Dr. S. Sri Krishna, Dr. S.V.V.
Mani Krishna, Dr. B.Vijay Kumar, Dr. Sudhanshu Garg, Dr. Kalyan Chakravarthi, Dr.
Daya Vaswani, Dr. Ankur Sabherwal, Dr. Kapil Karthikeya Reddy, Dr. R. Archana, Dr. Ravi
Kumar, Dr. Harish, Dr. Ashwin, Dr. Shashidar, Dr. Sagar, Dr. Sajad, Dr. Srikiran, Dr.
Sreekar, Dr. Shailaish, Dr. Rajshekhar, Dr Abhinay, Dr. Pradeep and Dr. Srikanth who
helped me a lot during my study.
My sincere thanks and regards to Dr. Inaam ul haq, who helped me with the statistics of the
study.
I take this opportunity to thank my grandparents, parents, wife, father and mother in law,
brother and sister for their prayers, patience and sacrifice to help me complete this study.
Above all, my sincere belief, gratitude and thanks to the Almighty God, without whose
blessings this research would not have been possible.
I acknowledge my gratitude to the Director, Dean and Medical Superintendent for permitting
me to undertake this study in the institute.
Lastly, it would be a great injustice if I fail to offer my deepest sense of gratitude towards my
patients and paramedical staff of cardiology department without whose co-operation I would
not have been able to perform this study.
Dr. Shahood Ajaz Kakroo
Resident in Cardiology,
Nizam’s Institute of Medical Sciences,
Hyderabad
 ABBREVIATION

ACE Angiotensin converting enzyme

ACS Acute coronary syndrome

AKI Acute kidney injury

AKI-D Acute kidney injury requiring dialysis

AMI Acute myocardial infarction

ARF Acute renal failure

BUN Blood urea nitrogen

CAG Coronary angiography

CHF Congestive heart

failure

CIN Contrast induced nephropathy

CKD Chronic kidney disease

CM Contrast media

CS- CIN Clinically significant contrast induced

nephropathy e- GFR Estimated glomerular filtration rate

LVEF Left ventricular ejection fraction

MRS Mehran risk score

NSTEMI Non ST segment elevation myocardial infarction

PCI Percutaneous coronary intervention

STEMI ST segment elevation myocardial infarction

S No CONTENTS Page No

1 INTRODUCTION 1

2 AIMS AND OBJECTIVES 13

3 REVIEW OF LITERATURE 14

4 MATERIAL AND METHODS 38

5 RESULTS 41

6 DISCUSSION 63

7 SUMMARY OF THE STUDY 76

8 LIMITATIONS OF THE STUDY 79

9 CONCLUSION 80

10 BIBLIOGRAPHY 81

11 ANNEXURE-I - ETHICAL COMMITTEE

CLEARANCE CERTIFICATE AND CONSENT FORM
93

11 ANNEXURE-II - STUDY PROFORMA

99

12 ANNEXURE-III – MASTER CHART 100

 1

Introduction

Coronary artery disease is one of the leading causes of death worldwide and remains a

substantial contributor to morbidity, mortality and healthcare expenditure. One of the modalities

of treatment is revascularization using percutaneous coronary intervention (PCI). Advances in

PCI technology have resulted in increasing numbers of patients undergoing coronary

revascularization via this approach.1 The use of radiocontrast media has increased greatly from

the past decades for diagnostic radiography and interventional procedures and it is estimated that

in approximately 60 million people in the world radiocontrast media is used each year.2

However, the use of such contrast media might result in acute events and injuries after the

procedure. Contrast-induced acute kidney injury (CI-AKI) is prevalent but underdiagnosed

complication of PCI that is associated with increased in-hospital morbidity and mortality. 3-6

Patients undergoing percutaneous coronary interventions are at risk of several complications, one

of the most common of which is contrast-induced nephropathy (CIN).

Definition:

Acute kidney injury (AKI) is characterized by the sudden impairment of kidney function

resulting in the retention of nitrogenous and other waste products. AKI represents a

heterogeneous group of conditions that share common diagnostic features including an increase

in the plasma or serum creatinine concentration and/or an increase in the blood urea nitrogen

(BUN) concentration often associated with a reduction in urine volume. 7 It is a complex disorder

of renal function that occurs in a variety of settings with clinical manifestations ranging from a

minimal elevation of serum creatinine to renal failure. Acute kidney injury (AKI) in the setting

after contrast media (CM) administration derives from many causes including ischemia,

atheroembolism, or nephrotoxicity of the contrast media itself. The latter is referred to as contrast
 2

induced nephropathy (CIN).8 Contrast induced nephropathy is generally defined as an increase in

serum creatinine concentration of > 0.5 mg/dl (>44 μmol/ L) or 25% above baseline within 48

hours after contrast administration.9 Most recently, the acute kidney injury network has defined

contrast- induced acute kidney injury(CI-AKI) as a rise in the serum creatinine level > 0.3 mg/ dl

or an increase in the serum creatinine level of >50% or more from baseline that occurred within

48 hour after contrast administration.10 It occurs within 24-48 hours of exposure, with creatinine

level typically peaking 3-5 days after procedure and returning to baseline or near baseline value

in 1-3 weeks.11 Functionally, CIN is considered an intrinsic acute kidney injury (AKI), usually

with conserved diuresis, but in severe cases acute tubular necrosis and even end-stage renal

disease may develop.12

As acute renal failure is associated with disabling morbidity and mortality, prevention

and early detection of CIN are of utmost clinical relevance. Direct measurement of glomerular

filtration rate (GFR) before and after the administration of contrast agent is the most accurate

method to determine the renal function. Serum creatinine, an end product of muscle metabolism,

is the most commonly used measurement to estimate the renal function.

GFR was calculated according to the Modification of Diet in Renal Disease (MDRD) formula.13

GFR = 175 x standardized serum creatinine) (-1.154) x age (-0.203) x 1.212 (if black) x

0.742 (if female).

Serum creatinine in mg/dl, age in years

Incidence of CIN occurrence can vary between 2% in low-risk populations to more than

50% in high risk patients14, with up to 15% in patients identified with mild renal impairment.

The figure is higher when CIN follows PCI.15 Contrast induced nephropathy occurs in 2 - 25% of

patients undergoing coronary intervention.16 In the retrospective analysis of the Mayo Clinic PCI
 3

registry comprising of 7586 patients. However, incidence of CIN rises up to 20% or more in

selected patient subsets, especially in patients with underlying cardiovascular disease. 17 CIN is

generally transient and reversible form of acute kidney injury. Among all the procedures that

uses radio contrast materials for the purpose of diagnosis and therapeutics, coronary angiography

and percutaneous coronary interventions (PCI) are associated with higher risk of CIN. 18 CIN is

associated with several adverse outcomes, the most noteworthy of which are an increased need

for hemodialysis, persistent decline in renal function, and increased mortality. Contrast induced

nephropathy is also strongly associated with an extended inpatient care period, and increased

cost of care.19,20 In those patients needing hospital care after acquiring CIN, the mortality rate is

34%.21 Underlying risk profiles have a major role for adverse events, particularly CIN following

coronary angiography or angioplasty.22 Several factors increase the patient’s risk of CIN,

including but not limited to chronic kidney disease (CKD), volume and type of contrast media

used, and pre-existing patient conditions. 23 Diabetes, congestive heart failure (CHF), increased

age, anemia, and a decreased circulating blood volume are just some of the conditions that

increase a patient’s risk of CIN.24,25

Contrast Media

Contrast Media have been traditionally classified according to their osmolality: high-

osmolar contrast media (HOCM), >1500 mOsm/kg (5-8 times plasma osmolality); low-osmolar

contrast media (LOCM), 550-850 mOsm/kg (2-3 times plasma osmolality); and iso-osmolar

contrast media (IOCM), 290 mOsm/kg (i.e. isotonic to plasma osmolality). 26 Products containing

different concentrations of iodine may change their osmolality and viscosity, which are

important properties for the development of CIN. A summary of important properties of various

contrast media commonly used in radiological practice is presented in Table 1.

 4

Table 1. Characteristics of some commonly used contrast media.

Viscosity
Osmolality Viscosity
Iodine
Type Generic name cPs
cPs
(mg/ml) (mOsm/kg)
(at 20-250C) (at 370C)

HOCM

1. Ionic Monomer Diatrizoate 300-370 1500-2000 3.3-16.4 1.4-19.5

2. Ionic Monomer Metrizoate 280-370 2100 5-9 2.8-5

3. Ionic Monomer Iothalamate 141-325 600-1843 2-9 1.5-5

LOCM

1. Ionic Dimer Ioxaglate 280-320 600 12-15.7 6-7.5

2. Non-ionic Iohexol 140-350 322-844 2.3-20.4 1.5-10.4

Monomer

3. Non-ionic
Loxilan 300-350 610-721 9.4-16.3 5.1-8.1
Monomer

4. Non-ionic
Ioversol 240-350 502-792 4.6-14.3 3.0-9.0
Monomer

5. Non-ionic

Monomer Iomeprol 150-400 301-726 1.9-27.5 1.3-12.6

 5

6. Non-ionic

Monomer
Iopentol 150-350 310-810 2.7-26.6 1.7-12.0

7. Non-ionic

Monomer
Iopromide 150-370 328-774 2.3-22 1.5-10
8. Non-ionic

Monomer

Iopamidol 150-370 342-796 2.3-20.9 1.5-9.4

IOCM

1. Non-ionic Dimer Iodixanol 270-320 290 12-26.6 6.3-11.8

2. Non-ionic Dimer Iotrolan 240-300 270-320 6.8-16.4 3.9-8.1

3. Non-ionic Dimer Isominol 280 273 10.9 6.3

HOCM; High osmolar contrast media, LOCM; Low osmolar contrast media, IOCM; Iso-

osmolar contrast media.

Pathogenesis:

Although the pathogenesis of CIN is not well understood, there is increasing evidence

that it occurs as a combination of direct toxicity to the renal tubular epithelium, oxidative stress,

ischemic injury, and renal tubular obstruction.27-29 Also, increased intratubular pressure

secondary to contrast-induced diuresis and increased perivascular hydrostatic pressure may lead
 6

to medullary hypoxia through lower medullary blood flow. 30 Renal ischemia may be the result of

an imbalance between vasoactive substances (Adenosine and Endothelin) and vasodilators

(Nitric oxide and Prostaglandins). Reduction in renal perfusion and toxic effects on the tubular

cells caused by the direct and indirect effects of contrast media on the kidneys are generally

recognized as important mechanisms for the development of CIN. Furthermore, contrast

exposure causes a certain degree of imbalance between increased renal vasoconstriction and

decreased vasodilatation; this leads to a decrease in renal blood flow and contraction of the

afferent glomerular arteriole, as well as renal ischemia and cell necrosis. 31 Oxygen radicals

released by the ischemia–reperfusion contribute to not only renal damage but also the apoptosis

of the renal tubular epithelial cells.

Risk factors and risk assessment for CIN

Several factors are associated with the development of AKI. Sepsis is the most common

cause, followed by cardiac surgery.32-34 Critical illness, burns, trauma, and exposure to radio

contrast material are other frequently described causes. 35-37 However, the individual patient´s

susceptibility determines whether an exposure will lead to AKI. Dehydration, congestive heart

failure, advanced age, chronic kidney disease (CKD), anemia and diabetes mellitus are examples

of potential predisposing factors. (Table 2)

Despite advances in preventive measures, CIN is the third leading cause of AKI and is

associated with higher rates of morbidity and mortality in hospitalized patients, with a more

complicated and longer in-hospital stay.38,39 It is of great concern because of its adverse effects

on patients’ clinical outcomes, including prolonged hospitalization and increased morbidity and

mortality.40
 7

Table 2: Risk factors for development of Contrast-induced Nephropathy

Patient-related factors:

Nonmodifiable Modifiable

 Age  Volume depletion

 Diabetes mellitus with CKD  Anemia, PCI related blood loss

 Preexisting renal failure  Nephrotoxic drug use

 Congestive heart failure  Low serum albumin

 Hemodynamic instability

 Nephrotic syndrome

 Renal transplant

CKD; Chronic kidney disease, PCI ;Percutaneous Coronary intervention

Procedure-related factors

Nonmodifiable Modifiable

 IABP  Volume of contrast media

 Multiple administration of CM within 72

 Emergent/primary PCI
hours

 Intraarterial CM administration  Osmolality and ionicity of CM

IABP; Intraaortic balloon counterpulsation, PCI; Percutaneous coronary intervention, CM;

Contrast media.
 8

Pre-Existent CKD is probably the most important pre-procedural risk factor for CIN. The

European Society of Urogenital Radiology Consensus Working Panel 41 in 1999 stated that CIN

risk becomes clinically significant when baseline serum creatinine concentration is ≥1.3 mg/dL

(≥115 mmol/L) in men and ≥1.0 mg/dL (≥88.4 mmol/L) in women. These figures approximate to

an eGFR <60 mL/min/1.73 m2, which defines CKD stages 3–5 and which is now generally

recognised as the threshold for CIN risk.42 This simple biochemical assessment is the most

widely adopted screening tool; however, it is important to recognise that serum creatinine is an

insensitive measure of renal function and that other risk factors are highly contributory to CIN,

which can occur in patients without pre-existent CKD.

Based on clinical experience, dehydration is a major risk factor for CIN; however, as it is largely

a clinical diagnosis and is challenging to quantify, it has never been formally investigated in

clinical trials. Hypotension, defined as a systolic blood pressure of <80 mm Hg for more than 60

min, is a recognised risk factor for CIN, attributable to intravascular volume depletion (eg,

severe dehydration, haemorrhage or sepsis), cardiogenic shock (eg, acute myocardial infarction)

or excessive vasodilation (eg, anaphylaxis) which results in renal hypoperfusion and thus

increased sensitivity to CM-induced renal ischaemia. According to Mehran et al, 43 the presence

of congestive cardiac failure classified according to New York Heart Failure Association III or

IV, a recent history of pulmonary oedema or acute myocardial infarction 44 was an independent

risk factor for development of CIN. Rehal et al found that left ventricular ejection fraction of less

than 45% was associated with development of CIN. 45,46 Diabetes mellitus is also an independent

CIN risk factor as demonstrated in a number of clinical trials, especially so when coexistent with

CKD.47 Advanced age, usually quantified as over 75 years, is also associated with CIN. Anaemia

is another important risk factor, usually defined as a haematocrit (HCT) of less than 0.39 in

males or 0.36 in females.48 The coadministration of nephrotoxic agents are thought to increase
 9

the risk of CIN, although this is not well documented in clinical studies. 49 There is conflicting

evidence regarding the risk of concurrent treatment with ACE inhibitors and angiotensin receptor

blocker’s (ARB’s), however if part of established therapy, continuation is considered safer than

the risk of withdrawal.

According to Maioli et al50 procedural factors such as the total volume of contrast media (>350

mL or >4 mL/kg) and previous contrast medium exposure within 72 h are directly related to the

development of CIN. A specific method for quantifying the maximum safe volume of contrast

has been proposed by Laskey et al who demonstrated that a ratio of the volume of contrast media

to creatinine clearance (V/CrCl) greater than 3.7:1 correlates strongly with the risk of developing

CIN in patients with moderate CKD undergoing coronary angioplasty. In addition, the presence

of periprocedural haemodynamic instability requiring the use of inotropic agents or intra-arterial

balloon pump therapy is particularly high-risk feature. A number of these risk factors have been

integrated into a well-known post-procedure risk scoring system and validated in a large cohort

study by Mehran et al (table 3)

Table 3: The Mehran Risk Score for prediction of CIN.

 1

A similar scoring system has also been proposed by Tziakas et al 51 who found that pre-existing

renal disease, metformin use, history of previous PCI, peripheral arterial disease and ≥300 mL of

contrast volume were also independent predictors of CIN.

A limitation of these scoring systems is that calculation is only possible after contrast media has

been administered. However, it is clinically desirable to be able to predict the risk of CIN before

the patient is exposed to contrast media allowing appropriate precautionary measures to be taken.

Such a pre-procedural CIN risk score has been proposed by Maioli et al, following validation in

a prospective cohort study (table 4).

Table 4: A pre procedural risk score for CIN (adopted from Maioli et al)51
 1

Another risk model, Canada acute coronary syndrome (C-ACS) risk score was developed to

predict development of CIN in acute coronary syndrome patients with STEMI before undergoing

Primary Percutaneous Coronary Interventions. It is based on readily available clinical

information and includes four categorical variables including heart rate > 100 beat/min, systolic

blood pressure < 100 mmHg, age > 75 years and killip class >1. It is quick, useful and simple

risk score to predict development of CIN, short and long term outcomes. A number of other

novel CIN risk factors have been identified, including pre-procedure glucose levels 52,53 and low-

density lipoprotein cholesterol;54 however, these have yet to be integrated into risk scoring

systems. It may be possible to use commonly used cardiovascular risk scoring methods to

approximate CIN risk, for example, a Global Registry of Acute Coronary Events score of >140

in patients with AMI having normal baseline renal function has been shown to predict risk of

CIN in a small cohort study.55 A novel fluid status assessment method using Bio-Impedance

Vector Analysis has also been demonstrated to independently predict CIN 56 in a small clinical

trial; however, it has not yet been translated into a CIN risk scoring system or guided volume

repletion strategy.
 1

Prevention of CIN

Preventive strategies for Contrast Induced Nephropathy traditionally include pre- procedural

hydration with isotonic saline, the usage of isoosmolar non-ionic contrast media, pre-medicating

with Nacetyl cysteine, and the withdrawal of nephrotoxic drugs.57-59 Despite the best of

precautions, around 20–30% of patients with underlying risk factors for CIN undergoing

percutaneous coronary intervention (PCI) go on to develop CIN.60

The Mehran CIN-Risk score (MRS) was developed and initially validated for prediction of CIN

after percutaneous coronary interventions. This score includes 8 clinical and procedural

variables: age >75 years, hypotension, congestive heart failure, intra-aortic balloon pump, serum

creatinine, diabetes, anemia, and volume of contrast. In such cases a risk score of <6, 6 to 11, 11

to 16, and >16 indicates a CIN risk of 7.5%, 14%, 26%, and 57%, respectively.61 It has been

proved that the risk of CIN has a direct association with the volume of contrast media

delivered.62

We also tried to identify if the Mehran Risk Score (MRS) could be used to accurately predict the

incidence of CIN in patients belonging to the respective risk groups in an Indian population. It

should be noted that the well validated MRS was formulated in a western population where the

incidence of CIN was found to be 13.1%. The population in the Indian subcontinent has higher

atherogenic burden with a higher incidence of risk factors for CIN.

 1

Aims and objectives

1. To study the incidence of Contrast Induced Nephropathy (CIN) in patients who

underwent percutaneous coronary intervention.

2. To study the predictors of contrast induced nephropathy in these patients.

3. Applicability of Mehran risk score (MRS) in predicting the contrast induced nephropathy.
 1

REVIEW OF LITERATURE

Rihal CS et al. (2002)45 identified all patients who had coronary interventional

procedures from January 1996 through May 2000 in their retrospective analysis of the Mayo

Clinic PCI registry and determined the incidence of, risk factors for, and prognostic implications

of acute renal failure (defined as an increase in serum creatinine > 0.5 mg/dl from baseline) after

percutaneous coronary intervention (PCI). Of 7586 patients, 254 (3.3%) experienced acute renal

failure (ARF). Among patients with baseline creatinine <2.0, the risk of acute renal failure was

higher among diabetic than nondiabetic patients, whereas among those with a baseline creatinine

>2.0 mg/dl, all had a significant risk of acute renal failure. In multivariate analysis, acute renal

failure was associated with baseline serum creatinine, acute myocardial infarction, shock, and

volume of contrast medium administered. Twenty-two percent of patients with acute renal failure

died during the index hospitalization compared with only 1.4% of patients without acute renal

failure (P<0.0001). After adjustment, acute renal failure remained strongly associated with death.

Among hospital survivors with acute renal failure, 1- and 5-year estimated mortality rates were

12.1% and 44.6%, respectively, much greater than the 3.7% and 14.5% mortality rates in patients

without ARF (P<0.0001). They concluded that the overall incidence of ARF after PCI is low.

Diabetic patients with baseline Cr values <2.0 mg/dL are at higher risk than nondiabetic patients,

whereas all patients with a serum Cr >2.0 are at high risk for ARF. ARF was highly correlated

with death during the index hospitalization and after dismissal.

Mehran et al (2004)43 conducted a study of 8,357 patients to develop a simple risk score

for development of contrast induced nephropathy. The baseline clinical and procedural

characteristics of the 5,571 patients in the development dataset were considered as candidate

univariate predictors of CIN (increase ≥25% and/or ≥0.5 mg/dl in serum creatinine at 48 h after
 1

PCI vs. baseline). Multivariate logistic regression was then used to identify independent

predictors of CIN with a p value <0.0001. Based on the odds ratio, eight identified variables

(hypotension, intra-aortic balloon pump, congestive heart failure, chronic kidney

disease, diabetes, age >75 years, anemia, and volume of contrast) were assigned a weighted

integer; the sum of the integers was a total risk score for each patient. The overall occurrence of

CIN in the development set was 13.1% (range 7.5% to 57.3% for a low [≤5] and high [≥16] risk

score, respectively); the rate of CIN increased exponentially with increasing risk score (Cochran

Armitage chi-square, p < 0.0001). In the 2,786 patients of the validation dataset, the model

demonstrated good discriminative power (cstatistic = 0.67); the increasing risk score was again

strongly associated with CIN (range 8.4% to 55.9% for a low and high risk score, respectively).

Rudnick M, Feldman H (2008)63 in their study Contrast-Induced Nephropathy: What

Are the True Clinical Consequences conducted a literature review focusing on observational

studies that assessed factors associated with mortality in patients with CIN. The deaths of some

patients with CIN are complicated by factors that cannot be directly related to CIN, such as liver

disease, sepsis, respiratory failure, bleeding, etc. However, it is plausible that CIN contributes to

cardiovascular causes of death in patients with CIN. They concluded that CIN is a marker for

increased mortality at the very least.

Shoukat S et al. (2010)64 in their study to examine the pathophysiology, risk factors, and

clinical course of CIN, as well as its prevention and potential therapeutic interventions,

especially during PCI concluded that CIN is an iatrogenic disorder with high morbidity and

mortality and a high incidence in elderly, diabetics, and patients with preexisting renal failure.

Despite uncertainty regarding the degree of nephrotoxicity produced by various contrast agents,

nonionic low-osmolar or iso-osmolar contrast media remains the preferred choice. Limiting the
 1

volume of contrast as much as possible is recommended. Best way to prevent CIN is to identify

patients at high risk and provide adequate volume administration. However, use of sodium

bicarbonate or N-Acetylcysteine in its prevention remains inconclusive in light of available

evidence. Although the role of various drugs in prevention remains controversial, nephrotoxic

drugs should be avoided before and after the procedure. Also, there still is no conclusive

evidence to recommend gadolinium as a better alternative to iodinated contrast media in order to

prevent CIN.

Alam ABMM et al. (2012)65 conducted a prospective study among the patients who

underwent coronary angiography and percutaneous coronary intervention in the Department of

Cardiology, Dhaka Medical College Hospital during January 2010 to December 2010. A total of

111 patients age range from 25 to 75 years were included in the study. Serum creatinine level at

baseline and at the end of 48 hours was done in all these patients. Study population was divided

into two groups according to development of acute kidney injury (AKI). Group-I = AKI, Group

II = Not developed AKI. AKI developed 11.7% of the study patient. DM and Preexisting renal

insufficiency were significantly higher in group I patients. HTN was (61.5% Vs 44.9%) higher in

group I but not significantly. History of ACE inhibitor/ARB, NSAID intake and LVEF <40%

were significantly higher in group I patients. The mean±SD volume of CM (Contrast Media)

were 156.9±44.8 ml and 115.4±30.0 ml in group I and group II respectively, which was

significant. The mean±SD of serum creatinine after 48-72 hours of CAG/PCI was 1.4±0.37

mg/dl and 1.1±0.2 mg/dl in group I and group II respectively. The serum creatinine level

increased significantly (p<0.05) after 48-72 hours of CAG/PCI in group I. In group II, S.

creatinine level increased but not significant (p>0.05). Impaired renal function was found 76.9%

and 2.0% in group I and group II respectively. DM, HTN, preexisting renal insufficiency, ACE
 1

inhibitor/ARB, NSAIDs, contrast volume (>150 ml), eGFR (<60 ml/min/1.73m2) and LVEF

(<40%) are significantly (p0.05) associated for CIN development. They concluded that CIN is an

iatrogenic but preventable disorder results from the administration of contract media. Although

rare in the general population, CIN occurs frequently in patients with underlying renal

dysfunction and diabetes. In patients with pre angiographic normal renal function, the prevalence

is low but in pre-existing renal impairment it may pose a serious threat. Thus risk factors are

synergistic in their ability to predispose to the development of CIN.

Fei He et al. (2012)66 did a retrospective case control study done in 325 patients who

underwent intracoronary stent implantation from January 2010 to March 2011 at the Drum

Tower Hospital of Nanjing University School of Medicine. Of the 325 patients, 51(15.7%)

developed AKI. Hospital day and in-hospital mortality were increased significantly in the AKI-

group. Univariate analysis showed that age, pre-operative parameters (left ventricular

insufficiency, peripheral angiopathy, creatinine, urea nitrogen, estimated glomerular filtration

rate, hyperuricemia, proteinuria, hydration), emergency operation, intraoperative parameters

(operative time, hypotension) and postoperative hypotension were significantly different.

However, multivariate logistic regression analysis revealed that increased age (OR=0.253, 95%

CI=0.088–0.727), pre-operative proteinuria (OR=5.351, 95% CI=2.128–13.459), pre-operative

left ventricular insufficiency (OR=8.704, 95% CI=3.170–23.898), eGFR"60 ml/min/1.73 m2

(OR=6.677, 95% CI=1.167–38.193), prolonged operative time, intraoperative hypotension

(OR=25.245, 95%CI=1.001–1.034) were independent risk factors of AKI. They concluded that

AKI is a common complication and associated with ominous outcome following intracoronary

stent implantation. Increased age, pre-operative proteinuria, pre-operative left ventricular

 1

insufficiency, pre-operative low estimated glomerular filtration rate, prolonged operative time,

intraoperative hypotension were the significant risk factors of AKI.

Perrin T, Descombes E, Cook S (2012)67 in their review study Contrast-induced

nephropathy in invasive cardiology done to assess incidence, pathophysiology, diagnosis,

prevention and prognosis of CIN concluded that even in patients with risk factors such as CKD

or diabetes, the risk of dialysis-dependent end-stage renal disease due to CIN remains low

(<1%). Although gadolinium has been proposed as CM for angiography in high-risk patients for

CIN, its use is grieved with the risk of development of nephrogenic systemic fibrosis (NSF) in

CKD patients, especially those with eGFR ≤30 ml/min or dialysis-dependent. As no treatment

specifically targets CIN once it develops, the main goal for clinicians remains prevention. They

can use several scores to carefully estimate the risk of CIN before referring a patient for elective

PCI, particularly for high-risk patients and/or procedures. Once decision for CM-injection is

made, clinicians have only 2 proven ways to reduce the incidence of CIN: (1.) optimal hydration

with some data favouring the use of sodium bicarbonate over normal saline and (2.) the use of

lowest amount of CM.

Salvatore Evola (2012)68 conducted a study to assess risk factors for contrast

induced nephropathy among Italian patients. This study aimed to make a profile of patients at

highest risk of developing contrast induced nephropathy (CIN) in order to take appropriate

prevention measures. 591 patients undergoing coronary procedures were divided into two

groups: patients with (CIN-group) and without (no-CIN) an increase in creatinine level equal or

more than 25% from baseline values within 24–48 h after the coronary procedure. All patients

underwent an accurate anamnesis, objective exam, hematochemical measurements, and

diagnostic exams. The results of this study while confirming that, average age (p = 0.01),
 1

diabetes mellitus (p < 0.0001), base line renal insufficiency (p = 0.0001), diuretic therapy

(p = 0.002), higher contrast doses (p = 0.01), are associated with a higher risk of contrast-

induced nephropathy, also demonstrated that both clinical (p = 0.01) and subclinical (p < 0.0001)

atherosclerosis, and higher preprocedural high sensitive C-reactive protien levels (hs- CRP)

(p = 0.02) are risk factors for CIN.

Nough H et al (2013)69 in their study of Incidence and Main Determinants of

Contrast-Induced Nephropathy following Coronary Angiography or Subsequent Balloon

Angioplasty first determined the incidence of contrast-induced nephropathy (CIN) in a sample of

Iranian patients who candidated for coronary angiography and/or angioplasty, and then assessed

major risk factors predicting the appearance of CIN following these procedures. Two hundred

and fifty consecutive, eligible patients scheduled for coronary angiography and/ or angioplasty at

the Afshar Hospital in Yazd between January 2009 and August 2010 were considered for

enrollment. Renal function was measured at baseline and 48 h after the intervention, and CIN

was defined by an increase in creatinine of >0.5 mg/dl or 25% of the initial value. The predictive

role of potential risk factors was determined in a multivariate model adjusted for comorbidities,

preexisting renal impairment, and angiographic data. They found that CIN following coronary

angiography or angioplasty appeared in 12.8% of the cases. A myocardial infarction before the

procedure (OR = 2.121, p = 0.036) and a prior history of hypertension (OR = 2.789, p = 0.025)

predicted the appearance of acute renal failure following angiography or subsequent angioplasty.

A low estimated glomerular filtration rate at baseline slightly predicted CIN after these

interventions. They concluded that transient acute renal dysfunction occurred in 12.8% of the

patients within 48 h after angiography or subsequent angioplasty and could be predicted by a

myocardial infarction before the procedure or by a prior history of systolic hypertension.

 2

Neyra JA et al (2013)70 conducted a retrospective observational cohort study to

analyze in-hospital and long-term outcomes of CIAKI following coronary angiography in

patients with or without CKD (eGFR ≥ 60 mL/min/1.73 m2) from January 2008 through

December 2009. CI-AKI was defined as serum creatinine either ≥ 25% or ≥ 0.5 mg/dl from

baseline within 72 h after contrast exposure. A total of 1160 patients were included in the study.

CI-AKI occurred in 19% of CKD patients and in 18% of non-CKD patients. In CKD and non-

CKD patients, CI-AKI was more frequent in patients requiring mechanical ventilation or

inotropes or in those given furosemide, and it was associated with adverse in-hospital (prolonged

hospitalization, acute dialysis and mortality) and long-term (increased creatinine, initiation of

dialysis and mortality) outcomes. In multivariable analysis, CKD patients had greater in-hospital

mortality if they developed CI-AKI (P = 0.005), and non-CKD patients had greater long-term

mortality if they developed CI-AKI (P = 0.016). they concluded that CI-AKI following coronary

angiography was associated with adverse in-hospital and long-term outcomes in both CKD and

non-CKD patients.

Islam N et al. (2013)71 in their Prospective, observational study of Impact of Blood

Glucose Levels on Contrast Induced Nephropathy after Percutaneous Coronary Intervention in

Patients not known to be Diabetic with Acute Coronary Syndrome done in the department of

Cardiology, National Institute of Cardiovascular Diseases (NICVD), Dhaka found that the

incidence of CIN was 24% in high blood glucose group and 4% in normal blood glucose group

(p=0.004). It was also observed that gradual incremental increase in risk of CIN associated with

higher admission blood glucose level. There was positive correlation between serum creatinine

and admission blood glucose but it showed negative correlation between serum creatinine and

admission blood glucose after PCI in ACS patients not known to be diabetic. The present study
 2

revealed that index admission high blood glucose in acute coronary syndrome patients not

known to be diabetic is associated with increased incidence of contrast induced nephropathy

after percutaneous coronary intervention.

Tehrani S et al. (2013)72 in their article to review the definition, pathogenesis and

management of CI-AKI and highlight potential therapeutic options for preventing CI-AKI in

post-PCI patients found that CI-AKI is an important but underdiagnosed complication of PCI

that is associated with increased in-hospital morbidity and mortality. Patients with pre-existing

renal impairment and diabetes are particularly susceptible to this complication post-PCI.

Optimization of the patients’ circulating volume remains the mainstay for preventing CI-AKI,

although the best strategy for achieving this is still controversial.

Kashif W et al. (2013)73 conducted a descriptive study to evaluate the frequency and risk

factors associated with clinically significant contrast-induced nephropathy (CIN) in patients

undergoing non-emergent coronary angiography. Case records of patients who underwent

coronary angiography with a serum creatinine of ³ 1.5 mg/dl at the time of procedure were

evaluated. 116 patients met the inclusion criteria. Mean age was 64.0 ± 11.5 years, 72% were

males. Overall prevalence of CIN was 17% (rise of serum creatinine by ³ 0.5 mg/dl) while that of

clinically significant CIN (CSCIN) was 9.5% (11 patients). Patients with CSCIN had

significantly lower left ventricular ejection fraction (p = 0.03) and higher prevalence of

cerebrovascular disease (p < 0.001). Mean baseline serum creatinine was significantly higher, 3.0

± 1.5 vs. 2.0 ± 1.1 mg/dl (p = 0.03, OR: 1.47) whereas mean GFR estimated by Cockcroft-Gault

formula was significantly lower at 25 ± 7.4 vs. 41.0 ± 14.6 ml/minute (p = 0.001) at the time of

procedure in patients with CSCIN. Mean length of hospital stay was significantly higher in this

group compared to those without CIN, 9.0 ± 5.1 vs. 3.0 ± 3.2 days (p = 0.001). Multivariate
 2

analysis revealed low GFR (p = 0.001) and low ejection fraction (p = 0.03) to be independent

factors associated with CSCIN. No significant differences were noted between the two groups in

patients with hypertension, diabetes and heart failure. They concluded that CSCIN is a

significant concern in high risk groups despite prophylaxis. Patients with lower EF,

cerebrovascular disease and low GFR at the time of procedure are more likely to have CIN.

Suma M Victor et al (2014)74 did a prospective single center study of 1200 consecutive

patients who underwent PCI from 2008 to 2011 to evaluate the collective probability of CIN in

Indian population by developing a scoring system of several identified risk factors in patients

undergoing PCI. Patients were randomized in 3:1 ratio into development (n = 900) and

validation (n = 300) groups. Seven independent predictors of CIN were identified using logistic

regression analysis - amount of contrast, diabetes with microangiopathy, hypotension, peripheral

vascular disease, albuminuria, glomerular filtration rate (GFR) and anemia. The mean (±SD) age

was 57.3 (±10.2) years. 83.6% were males. The total incidence of CIN was 9.7% in the

development group. The total risk of renal replacement therapy in the study group is 1.1%.

Mortality is 0.5%. The risk scoring model correlated well in the validation group (incidence of

CIN was 8.7%, sensitivity 92.3%, specificity 82.1%, c statistic 0.95). They concluded that a

simple risk scoring equation can be employed to predict the probability of CIN following PCI,

applying it to each individual. More vigilant preventive measures can be applied to the high risk

candidates.

Narula A et al (2014)75 conducted a study on contrast-induced acute kidney injury after

primary percutaneous coronary intervention: results from the HORIZONS-AMI substudy to

examine the short- and long-term outcomes of patients who developed contrast-induced acute

kidney injury (CI-AKI; defined as an increase in serum creatinine of ≥0.5 mg/dl or a 25%
 2

relative rise within 48 h after contrast exposure) from the large-scale HORIZONS-AMI trial.

Multivariable analyses were used to identify predictors of CI-AKI, as well predictors of the

primary and secondary endpoints. The incidence of CI-AKI in this cohort of ST-segment

elevation myocardial infarction (STEMI) patients was 16.1% (479/2968). Predictors of CI-AKI

were contrast volume, white blood cell count, left anterior descending infarct-related artery, age,

anaemia, creatinine clearance ,60 mL/min, and history of congestive heart failure. Patients with

CI-AKI had higher rates of net adverse clinical events [NACE; a combination of major bleeding

or composite major adverse cardiac events (MACE; consisting of death, reinfarction, target

vessel revascularization for ischaemia, or stroke)] at 30 days (22.0 vs. 9.3%; P 0.0001) and 3

years (40.3 vs. 24.6%; P 0.0001). They also had higher rates of mortality at 30 days (8.0 vs.

0.9%; P 0.0001) and 3 years (16.2 vs. 4.5%; P 0.0001). Multivariable analysis confirmed CI-AKI

as an independent predictor of NACE[hazard ratio ([HR), 1.53;95%confidence interval (CI),

1.23–1.90; P ¼ 0.0001],MACE(HR, 1.56;95%CI, 1.23–1.98; P ¼ 0.0002), non-coronary artery

bypass grafting major bleeding (HR, 2.07; 95% CI, 1.57–2.73; P 0.0001), and mortality (HR,

1.80; 95% CI, 1.19–2.73; P ¼ 0.005) at 3-year follow-up. They concluded that Contrast-induced

acute kidney injury is associated with poor short- and long-term outcomes after primary

percutaneous coronary intervention in STEMI.

Sharma SK et al (2014)76 undertook an observational descriptive study to find the

incidence of contrast induced nephropathy and to identify risk factors for the development of

contrast induced nephropathy in patients undergoing coronary angiography and angioplasty in a

tertiary care hospital. 540 patients undergoing coronary intervention from 2011 to 2013 were

enrolled by convenient sampling technique. 210 patients were excluded from the study.

Therefore, a total of 330 patients were studied and analyzed. Contrast induced nephropathy was
 2

defined as an increase of >25% or >0.5 mg/dl in pre-catheterization serum creatinine at or after

48 h after percutaneous coronary intervention. 27 (8.18%) patients experienced contrast induced

nephropathy. The incidence of contrast induced nephropathy in patients with baseline creatinine

clearance <60 ml/min was 45.9%. Contrast induced nephropathy developed in 10% of anemic

and 12.5% diabetic patients. The amount of the contrast agent administered was similar for both

groups of patients (138.20±91.34ml vs. 175.56±118.86ml; p =0.254). No correlation was found

between the amount of contrast agent administered and the change of serum creatinine

concentration. Multivariate logistic regression analysis found that baseline e-GFR and baseline

hemoglobin were independent predictors for Contrast induced nephropathy. They concluded that

the overall incidence of Contrast induced nephropathy after coronary intervention in this study is

high. Patients with both preexisting renal insufficiency and anemia were at high risk of Contrast

induced nephropathy.

Thomas T Tsai et al (2014)77 developed risk models for predicting acute kidney injury

(AKI) and AKI requiring dialysis (AKI-D) after percutaneous coronary intervention (PCI) to

support quality assessment and the use of preventative strategies. AKI was defined as an absolute

increase of ≥0.3 mg/dL or a relative increase of 50% in serum creatinine (AKIN Stage 1 or

greater) and AKI-D was a new requirement for dialysis following PCI. Data from 947 012

consecutive PCI patients and 1253 sites participating in the NCDR Cath/PCI registry between

6/09 and 7/11 were used to develop the model, with 70% randomly assigned to a derivation

cohort and 30% for validation. AKI occurred in 7.33% of the derivation and validation cohorts.

Eleven variables were associated with AKI: older age, baseline renal impairment (categorized as

mild, moderate, and severe), prior cerebrovascular disease, prior heart failure, prior PCI,

presentation (non-ACS versus NSTEMI versus STEMI), diabetes, chronic lung disease,
 2

hypertension, cardiac arrest, anemia, heart failure on presentation, balloon pump use, and

cardiogenic shock. STEMI presentation, cardiogenic shock, and severe baseline CKD were the

strongest predictors for AKI. The full model showed good discrimination in the derivation and

validation cohorts (c-statistic of 0.72 and 0.71, respectively) and identical calibration (slope of

calibration line=1.01). The AKI-D model had even better discrimination (c-statistic=0.89) and

good calibration (slope of calibration line=0.99). They concluded that the NCDR AKI prediction

models can successfully risk-stratify patients undergoing PCI. The potential for this tool to aid

clinicians in counseling patients regarding the risk of PCI, identify patients for preventative

strategies, and support local quality improvement efforts should be prospectively tested.

Hamdy Shams-Eddin Taher (2014)78 conducted a study to assess the incidence and

predictors of contrast induced nephropathy (CIN) in unselected patients undergoing coronary

intervention either coronary angiography (CA) or percutaneous coronary interventions (PCI), at

Assiut university hospitals. It was an observational prospective cohort study. Two hundred

consecutive patients between December 2011 and August 2012 underwent CA and PCI were

enrolled in the study. Blood samples were collected at baseline and 3 days after interventions.

All patients were followed up for 2 weeks for major adverse events. CIN was observed in 23

(11.5%) patients. According to Mehran risk score, 84.5% of our patients had low risk for CIN,

15.5% had moderate risk for CIN, and no one had high risk score. Multivariate logistic

regression analysis of predictors for CIN, showed that the use of high osmolar contrast media

(CM) (Telebrix) was associated with 4 times higher incidence of CIN than the use of low

osmolar CM (Ultravest) (OR = 4.07; 95% CI = 1.1–15.1). None of their patients had clinical

signs or symptoms of acute renal failure, or required haemodialysis at 2 weeks of follow up.
 2

Rather FA et al. (2015)79 conducted a prospective study over a period of two years from

December 2009 to November 2011 to determine the incidence, etiology, risk factors and

outcome of acute kidney injury (AKI) after open heart surgery. A total of 62 patients who

underwent open heart surgery were included in the study. Post-operative AKI was considered

when the post-operative serum creatinine was >1.5 mg/dL or there was doubling of serum

creatinine above the baseline (pre-operative) with a prior normal renal function. The incidence of

AKI in the post- operative period in our study was 17.7%. The common etiological factors for

AKI in our study were sepsis, hypotension, prolonged need for ventilator and inotropic support

and drugs given in the post-operative period. The important risk factors for the development of

AKI in the post-operative period were hypertension, diabetes mellitus, gout, prolonged total

bypass time and prolonged aortic cross–clamp time. The overall mortality in our study subjects

was 11.3% (7 of 62 died) and the mortality in the patients who developed post-operative AKI

was 71.4%.

Taher HSE et al (2015)80 conducted an observational prospective cohort study with the

purpose to assess the incidence and predictors of contrast induced nephropathy (CIN) in

unselected patients undergoing coronary intervention either coronary angiography (CA) or

percutaneous coronary interventions (PCI), at Assiut university hospitals. Two hundred

consecutive patients between December 2011 and August 2012 who underwent CA and PCI

were enrolled in the study. Blood samples were collected at baseline and 3 days after

interventions. All patients were followed up for 2 weeks for major adverse events. CIN was

observed in 23 (11.5%) patients. According to Mehran risk score, 84.5% of our patients had low

risk for CIN, 15.5% had moderate risk for CIN, and no one had high risk score. Multivariate

logistic regression analysis of predictors for CIN, showed that the use of high osmolar contrast
 2

media(CM) (Telebrix) was associated with 4 times higher incidence of CIN than the use of low

osmolar CM (Ultravest) (OR = 4.07; 95% CI= 1.1–15.1). None of the patients had clinical signs

or symptoms of acute renal failure, or required haemodialysis at 2 weeks of follow up. They

concluded that although most of their study population was at low risk, the incidence of CIN was

relatively high due to the use of high osmolar CM.

Dutta PK, Mannan MM (2015)81 conducted a cross sectional observational study in a

Tertiary hospital of Bangladesh to assess the proportion of CI-AKI with their risk factors over a

period of six months.50 patients were included in the study. 24 had hypertension (HTN) and 14

had diabetes mellitus (DM). Among 14 diabetic patients 7(50.0%) developed CI-AKI, among 24

hypertensive patients 6(25.0%) developed CI-AKI, among 14 patients with baseline serum

creatinine level ≥ 1.2 mg/dl 10(71.4%) developed CI-AKI. Statistical analysis showed base line

serum creatinine ≥ 1.2 mg/dl (p<0.000) and DM (p<0.05) are the important predictor for the

development of CI-AKI. Though CI-AKI was more in the hypertensive, male and age >50 years,

but there was no statistical significance (p>0.05). Diabetic patients and patients with serum

creatinine ≥ 1.2 mg/dl had 2.5 times and 6.4 times higher risk of developing CI-AKI

respectively. They concluded that diabetes and even mild degree of renal insufficiency were

found to be risk factors predicting CI-AKI following coronary angiogram.

Shacham Y et al. (2015)82 performed a retrospective study of acute cardio-renal

Syndrome as a cause for renal deterioration among Myocardial Infarction patients treated with

Primary Percutaneous Intervention in which they analyzed 1656 consecutive patients admitted

with the diagnosis of STEMI between January 2008 to December 2014, and treated with primary

PCI. AKI occurred in 168(10%) of patients. Patients with AKI were older, of female sex, with

more comorbidities, had longer time of reperfusion, and were more likely to have hemodynamic
 2

impairment including critical state, congestive heart failure, life threatening arrhythmias, and

worse left ventricular function (p<0.001 for all). They concluded that among STEMI patients,

who underwent primary PCI, AKI should not be assumed to be solely contrast induced

nephropathy and hemodynamic abnormalities should be also considered.

Assarch A et al (2016)83 did a cross-sectional and prospective study and the aim of study

was evaluation of CIN in diabetic and nondiabetic patients with normal renal function

undergoing coronary angiography. This study was conducted on patients with normal renal

function candidate for diagnostic coronary angiography at Imam hospital, Ahvaz, Iran from

October 2010 to February 2011. A standardized questionnaire was used to collect demographics,

clinical and laboratory data. A total of 254 patients (140 males and 114 females with mean age of

56.6 ± 11.9 years) were included in the study. Of them, 60 patients (23.6%) had congestive heart

failure (CHF) and 57 patients (22.4%) had diabetes mellitus (DM). The mean serum creatinine

levels before contrast administration in men and women were 1.05 ± 0.22 and 0.93 ± 0.17 mg/dL

respectively. In overall CIN occurred in 27 patients (10.6%) with no difference between males

and females (P = 0.386) and in patients with or without CHF (P = 0.766). There was a significant

association between CIN and DM (P = 0.001) and mean volume of contrast administration (P =

0.001). They concluded that although CIN is a common problem in patients with diabetic

nephropathy undergoing coronary angiography, diabetic patients without diabetic nephropathy

and also patients without DM who had normal renal function are also at risk of contrast

nephropathy.

Farhan S et al (2016)84 conducted a study of contrast induced acute kidney injury in

acute coronary syndrome patients: A single centre experience. The aim of the study was to

investigate predictors of contrast induced acute kidney injury, in-hospital and long-term
 2

mortality in patients with acute coronary syndrome treated by percutaneous coronary

intervention. They investigated 536 consecutive patients with acute coronary syndrome who

underwent percutaneous coronary intervention. Contrast induced acute kidney injury was

classified according to risk, injury, failure, loss of kidney function and end-stage kidney

disease/acute kidney injury network (RIFLE/AKIN) criteria into those with normal kidney

function, risk, RIFLE stage I and those with stage ⩾II. They investigated in-hospital, all-cause

mortality during index hospitalization and long-term all-cause mortality during the follow-up

period of 94 months (interquartile 81.6–108.9 months) in adjustment with parameters of the

Global Risk of Acute Coronary Events score. Patients with contrast induced acute kidney injury

had worse baseline clinical characteristics and displayed more co-morbidities than patients with

normal kidney function. In multivariate logistic regression analysis intra-aortic balloon pump

use, congestive heart failure, age >75 years and admission serum creatinine >1.5mg/dl were

independent predictors of contrast induced acute kidney injury development. Contrast induced

acute kidney injury RIFLE stage ⩾II was an independent predictor of in-hospital mortality (odds

ratio 33.16, confidence interval 1.426–770.79, p=0.029) and long-term mortality (hazard ratio

4.713, confidence interval 1.53–14.51, p=0.007) even after adjustment for confounders (variables

of Global Risk of Acute Coronary Events score). They concluded that contrast induced acute

kidney injury is a common complication of acute coronary syndrome patients treated by

percutaneous coronary intervention. Advanced deterioration in renal function after percutaneous

coronary intervention is an independent predictor for in-hospital and long-term mortality.

Pérez-Topete SE et al (2016)85 did their study of contrast-induced nephropathy in

patients undergoing percutaneous coronary intervention with objectives to calculate incidence of

CIN and to describe the clinical and periprocedural risk factors for patients receiving contrast
 3

media. Secondary objective was to compare mortality between group 1 and group 2. In this

retrospective, observational, descriptive cohort study, patients who were admitted to the hospital

for diagnostic and/or therapeutic coronary angiography between January 2014 to September

2015, the serum creatinine and glomerular filtration rate (GFR) prior to angiography and 72

hours later was measured. 70 patients were included, of which 14.2% developed CIN. The

leading risk factors for developing AKI were: age > 65 years (OR 12.6, p = 0.03); the presence

of anemia (OR 7.5,p = 0.006); and procedural time more than 90 minutes (OR 16, p = 0.001).

Higher mortality was observed in the NIC group (30% vs. 1.6%, p = 0.004). They concluded that

the leading associated risk factors were age > 65, anemia and procedural time > 90 minutes and

the development of CIN carries a higher mortality.

Amin AP et al (2017)86 did a study of Association of Variation in Contrast Volume With

Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Intervention. In this cross-

sectional study involving more than 1.3 million patients who underwent percutaneous coronary

intervention, a large variation in acute kidney injury incidence and contrast use was observed

among physicians who performed the procedures. The objective was to examine the national

variation in AKI incidence and contrast use among US physicians and the variation’s association

with patients’ risk of developing AKI after PCI. This cross-sectional study used the American

College of Cardiology National Cardiovascular Data Registry (NCDR) CathPCI Registry to

identify in-hospital care for PCI in the United States. Participants included 1 349 612 patients

who underwent PCI performed by 5973 physicians in 1338 hospitals between June 1, 2009, and

June 30, 2012. Data analysis was performed from July 1, 2014, to August 31, 2016. The primary

outcome was AKI, defined according to the Acute Kidney Injury Network criteria as an absolute

increase of 0.3 mg/dL or more or a relative increase of 50% or more from preprocedural to peak
 3

creatinine. A secondary outcome was the mean contrast volume as reported in the NCDR

CathPCI Registry. Of the 1 349 612 patients who underwent PCI, the mean (SD) age was 64.9

(12.2) years, 908 318 (67.3%) were men, and 441 294 (32.7%) were women. Acute kidney

injury occurred in 94 584 patients (7%). A large variation in AKI rates was observed among

individual physicians ranging from 0% to 30% (unadjusted), with a mean adjusted 43% excess

likelihood of AKI (median odds ratio, 1.43; 95% CI, 1.41-1.44) for statistically identical patients

presenting to 2 random physicians. A large variation in physicians’ mean contrast volume,

ranging from 79 mL to 487 mL with an intraclass correlation coefficient of 0.23 (interquartile

range, 0.21-0.25), was also observed, implying a 23% variation in contrast volume among

physicians after adjustment. There was minimal correlation between contrast use and patients’

AKI risk (r = −0.054). Sensitivity analysis after excluding complex cases showed that the

physician variation in AKI remained unchanged. They concluded that acute kidney injury rates

vary greatly among physicians, who also vary markedly in their use of contrast and do not use

substantially less contrast in patients with higher risk for AKI. These findings suggest an

important opportunity to reduce AKI by reducing the variation in contrast volumes across

physicians and lowering its use in higher-risk patients.

Singhala G, Pathak V, Kumar M (2017) 87 conducted a study of Incidence of contrast

induced acute kidney injury in patients undergoing percutaneous coronary intervention in North

Indian population The aim of the study was to assess the incidence, clinical predictors and

outcome of Contrast induced nephropathy (CIN) after percutaneous coronary interventions (PCI)

in coronary artery disease patients in overburdened north india tertiary care center. In 300

consecutive coronary artery diseased patients treated with coronary angioplasty in our

catheterization laboratory they measured serum creatinine and GFR at baseline and serum
 3

creatnine at 48 h and at 7th day. CIN was defined as a rise in serum creatinine level more than 0.5

mg/dl or 25% of baseline at 48 h. CIN developed in 32 patients (10.66%). In univariate analysis,

10 factors were significant for development of CIN. In multivariate analysis contrast dose (odds

ratio 1.048,95% CI), number of stents, reduced ejection fraction, diabetes mellitus and use of

ACE inhibitors were significantly associated with CIN. They concluded that in the era of PCI for

CAD patients, CIN is a frequent complication, even in patients with normal renal function, and is

associated with a more complicated in-hospital course. In overburdened Indian hospitals, CIN is

frequently underreported because of day care procedures and early discharge. They found a new

factor for development of CIN. CIN was associated with ≥3 number of stents deployment,

contrast volume more than 250 ml, EF ≤30% and in diabetic patients. There was no effect of iso-

osmolar contrast from low osmolar contrast.

Tan CS et al (2017)88 did a retrospective observational study of incidence and

epidemiology of contrast induced acute kidney injury following percutaneous coronary

angiogram - single centre experiences to determine the incidence of CI-AKI post PCI in a

cardiac centre of Northern Malaysia. The records of all patients underwent PCI between 1

January 2011 to 31 March 2011 were reviewed. KDIGO AKI definition was used to identify CI-

AKI. Renal function was obtained on admission as baseline and 48 h after the intervention.

Patients on Renal Replacement Therapy (RRT) were excluded. Data were collected from the

electronic medical record system. Statistical analysis was performed using SPSS version 23.0. A

total of 199 patients underwent PCI during the study period. 11 patients were excluded, 8

because they were already on RRT prior to the PCI and another 3 did not have repeat serum

creatinine. The mean age was 62.1±11.45, 22.3% aged > 70 years and 70.7% were male. 42%

were diabetes and 67% had hypertension. 78.2% of the cohort were Malay, 14.4% Chinese, 5.9%
 3

Indian and others made up the remaining 7.5%. The mean serum creatinine was 119.11± 56.65

umol/L, (51 – 585 umol/L), 46.8% had chronic kidney disease stage III and above (MDRD

formula). 5.3% experienced cardiogenic shock. Of these 188 patients, 18 patients (9.6%)

developed CI-AKI post PCI. None of the patients required transient haemodialysis support. They

concluded that the overall incidence of CI-AKI in patients who underwent PCI in their centre

was 9.6%.

Yuan Y et al (2017)89 in their study of risk Factors of Contrast-induced Acute Kidney

Injury in Patients Undergoing Emergency Percutaneous Coronary Intervention enrolled a total of

1061 consecutive patients undergoing emergency PCI during January 2013 and June 2015 were

and divided into CI-AKI and non-CI-AKI group. Univariable and multivariable analyses were

used to identify the risk factors of CI-AKI in emergency PCI patients. The incidence of CI-AKI

in patients undergoing emergency PCI was 22.7% (241/1061). Logistic multivariable analysis

showed that body surface area (BSA) (odds ratio [OR] 0.213, 95% confidence interval [CI]:

0.075–0.607, P = 0.004), history of myocardial infarction (MI) (OR 1.642, P = 0.021), left

ventricular ejection fraction (LVEF) (OR 0.969, P = 0.015), hemoglobin (Hb) (OR 0.988, P =

0.045), estimated glomerular filtration rate (OR 1.027, P < 0.001), left anterior descending

(LAD) stented (OR 1.464, P = 0.050), aspirin (OR 0.097, P = 0.049), and diuretics use (OR

1.850, P = 0.003) were independent predictors of CI-AKI in patients undergoing emergency PCI.

They concluded that history of MI, low BSA, LVEF and Hb level, LAD stented, and diuretics

use are associated with increased risk of CI-AKI in patients undergoing emergency PCI.

Oren Caspi, MD, PhD (2017)90 aimed to determine the causal association of contrast

material exposure and the incidence of AKI following primary PCI using a control group of

propensity score–matched patients with ST-segment– elevation myocardial infarction who were
 3

not exposed to contrast material. They studied 2025 patients with ST-segment–elevation

myocardial infarction who underwent primary PCI and 1025 patients receiving fibrinolysis or no

reperfusion who were not exposed to contrast material during the first 72 hours of hospital stay

(control group). The development of AKI in patients with ST-segment–elevation myocardial

infarction undergoing primary PCI was mainly related to older age, baseline estimated

glomerular filtration rate, heart failure, and hemodynamic instability. Risk for AKI was similar

among ST-segment–elevation myocardial infarction patients with and without contrast material

exposure.

Sandeep Kumar (2017)91 studied the incidence of CIN and its risk factors in patients

undergoing CAG. In this prospective study, they included all patients with normal renal

parameters undergoing CAG with nonionic radiocontrast media. They excluded patients with

known chronic kidney disease, baseline creatinine more than 1.5 mg/dL, significant hypotension,

anemia, and patients with acute myocardial infarction undergoing emergency PCI. Serum

creatinine was done at baseline and serially for seven days after the procedure. Appropriate

statistical tests were used to analyze the results and P <0.05 was considered statistically

significant. The study population (n = 500, 348 males and 152 females) had a mean age of 56.6 ±

12.5 years. Twelve patients (2.4%) developed CIN and were equally distributed irrespective of

the age, diabetes, or PCI procedure. CIN was observed to be more common in patients with

hypertension than in those without hypertension (P = 0.0158). The total volume of contrast

administered to CIN group (175 ± 59.3) was not significant as compared to that of non-CIN

(159.1 ± 56) group (P = 0.334). None of the patients in our study required renal replacement

therapy, and there was no mortality. CIN is observed in 2.4% of patients undergoing CAG and

had a self-limiting course. Hypertension is the only observed risk factor, and further large-scale
 3

studies are necessary to delineate the novel risk factors for CIN in the general population with

normal kidney function.

Sanjai Pattu Valappil et al (2018) 92 conducted a prospective observational study where

patients with an estimated glomerular filtration rate (eGFR) between 30 and 60 ml/mt underwent

elective percutaneous coronary intervention (PCI) over a period of 15 months and were

evaluated for the development of CIN. The patients who developed CIN were then analysed for

the presence of specific risk factors. The patients were categorized into the 4 risk groups based

on the MRS. Among the 100 high risk patients who underwent PCI during the study period, the

incidence of CIN was 29%. On multivariate analysis, the presence of anemia (p = 0.007),

increased contrast volume usage (as defined by >5* B.Wt/S.cr) (p = 0.012) and usage of loop

diuretics (p = 0.033) were independently found to confer a significant risk of CIN. In patients

belonging to the high Mehran risk group (MRS10- 15) and very high risk group (MRS >15) the

risk of CIN was 3 fold (OR: 3.055, 95% CI: 1.18–7.94, p = 0.022) and 24 fold (OR: 24, 95% CI:

2.53–228.28, p = 0.006) higher respectively when compared to intermediate and low risk patients

(MRS <10). The incidence of CIN in high risk patients undergoing PCI is substantially higher in

south indian population compared to similar studies in the west. The MRS risk prediction is

pertinent even in an Indian population.

Amrendra Mandal et al (2018)93 conducted an observational prospective study to study

the incidence of CIN in Nepalese populations and compare the outcome to international reprinted

values with coronary artery disease (CAD) undergoing PCI. All consecutive patients with CAD

undergoing PCI between February 2010 and July 2010 were enrolled in the study. One hundred

fifty-two patients were enrolled in the study during six months period. Twenty (13.20%) patients

developed CIN following PCI. Out of them 70% were diabetics and 30% were non-diabetics.
 3

Mean age of patients was 58.5 ± 23 years; male:female ratio was 2.7:1. Mean contrast volume

injected was 160.3 ± 78.3 ml. Diabetic patients 21.8% (14/64) had significant CIN compared to

non-diabetic patients 6.8% (6/88) following PCI (<0.01).

Kazumasa Kurogi et al (2019)94 enrolled 952 consecutive patients who underwent

primary percutaneous coronary intervention for acute myocardial infarction. CIN was defined as

an increase in serum creatinine levels ≥0.5 mg/dL or ≥25% from baseline within 72 hours after

percutaneous coronary intervention. Persistent renal dysfunction was defined as residual

impairment of renal function over 2 weeks, and transient renal dysfunction was defined as

recovery of renal function within 2 weeks, after CIN. The overall incidence of CIN was 8.8%

and that of persistent CIN was 3.1%. A receiver-operator characteristic curve showed that the

optimal cutoff value of the contrast volume/baseline estimated glomerular filtration rate ratio for

persistent CIN was 3.45. In multivariable logistic analysis, a contrast volume/baseline estimated

glomerular filtration rate >3.45 was an independent correlate of persistent renal dysfunction. At 3

years, the incidence of death was significantly higher in patients with persistent renal dysfunction

than in those with transient renal dysfunction (P=0.001) and in those without CIN (P<0.001).

Cox regression analysis showed that persistent renal dysfunction (hazard ratio, 4.99; 95% CI,

2.30–10.8; P<0.001) was a significant risk factor for mortality. A similar trend was observed for

the combined end points, which included mortality, hemodialysis, stroke, and acute myocardial

infarction.

Dileep Kumar et al (2020)95 conducted an observational study in which they included

282 patients who presented with STEMI and underwent primary PCI at the National Institute of

Cardiovascular Disease, Karachi, Pakistan, from October 2017 to April 2018. The serum

creatinine (mg/dl) levels were obtained at baseline and 48 to 72 hours after the primary PCI
 3

procedure, and patients with a 25% increase or ≥ 0.5 mg/dl rise in post-procedure creatinine level

(after 48 to 72 hour) were categorized for CIN. Out of a total sample of 282 patients, 68.4%

(193) were males, and the mean age was 56.4 ± 9.1 years. A majority of the patients, 78.7%

(222), were hypertensive and 34% (96) were diabetic. The CIN was observed in 13.1% (37) of

the patients, and increased risk of CIN was found to be associated with the presence of diabetes

mellitus and increased (>200 ml) use of contrast during the procedure, with odds ratios of 2.3

(1.14-4.63) and 3.12 (1.36-7.17), respectively.

 3

Materials and methods

Study setting: Nizam’s Institute of Medical Sciences, Hyderabad

Study Design: Prospective Observational Cohort Study

Study Period: March 2019 to March 2020.

Recruitment and method: This study was done after explaining the study details in a language

understandable to the patient. The patient was provided with information sheet and consent form.

Informed consent was taken from the patients who were willing to get enrolled in the study.

A total number of 432 patients were enrolled in the study.

Inclusion Criteria

1. Patients (age ≥ 18 years) with diagnosis of acute coronary syndrome (ACS) who

underwent percutaneous coronary intervention.

2. Patients with known coronary artery disease (CAD) who were admitted to undergo

percutaneous coronary intervention (PCI), between March 2019 and March 2020.

Acute Coronary Syndrome (ACS) diagnosis was based on fourth universal

definition of myocardial infarction defined by standard criteria of elevation of cardiac troponin

levels with presence of atleast one of the following - chest pain, ischemic changes in ECG,

imaging evidence of new regional wall motion abnormality or identification of coronary

thrombus by angiography.
 3

Exclusion criteria

1. Pregnancy

2. Contrast media (CM) allergy

3. End stage kidney disease and on regular dialysis

4. Cardiogenic shock

5. unwillingness to give consent.

Baseline characteristics Demographic data (age, sex), risk factors and indication for

intervention were collected. Cardiac catheterization and PCI was performed in accordance with

established clinical practice using standard diagnostic and guide catheters, wires, balloon

catheters, and stents via the femoral/radial approach. The amount of contrast media administered

was decided by the interventional cardiologist.

Risk stratification for development of CIN was calculated for all patients using the

Mehran risk score. The risk score included hypotension (5 points, if systolic blood pressure <80

mm Hg for at least 1 h requiring inotropic support), use of intra-aortic balloon pump (5 points),

congestive heart failure (5 points, if class III/IV by New York Heart association classification or

history of pulmonary edema), age (4 points, if >75 years), anemia (3 points, if hematocrit <39%

for men and <36% for women), diabetes mellitus (3 points), contrast media volume (1 point per

100 mL), estimated glomerular filtration rate (GFR; GFR in mL/min per 1.73 m2 ; 2 points, if

GFR 60–40; 4 points, if GFR 40–20; 6 points, if GFR < 20). A risk score of <5, 6–10, 11–15,

and >16 indicates a risk for CIN of 7.5%, 14%, 26%, and 57%, respectively.

Serum creatinine concentrations and GFR were determined at hospital admission

(prior to the procedure), and at 24 hours and 48 hours after the procedure. The changes of serum
 4

creatinine level were analyzed. The eGFR was calculated according to the Modification of Diet

in Renal Disease (MDRD) formula. CIN was defined as an increase in the serum creatinine level

of more than 0.5 mg/dl or more than 25% from baseline within 48 hours after procedure without

any other identifiable cause of acute kidney injury.

Outcomes

Number of patients who developed CIN post percutaneous coronary intervention (incidence of

CIN) was measured by changes in serum creatinine concentration.

Statistical Analysis

Data was entered in a Microsoft Excel spreadsheet and analysed using STATA 15. Continuous

variables were summarized as mean + standard deviation. Categorical variables were

summarized as percentage. Incidence of CIN was reported in percentage along with its 95%

confidence interval. Unadjusted Odds Ratio was reported for each individual risk factor. Chi-

square test for independence was used to test the relationship between two categorical variables.

A multivariate binary logistic regression model was used to assess the independent effect of

potential risk factors on CIN. Adjusted odds ratio was reported along with their 95% confidence

intervals. Two sided p values were reported and a p value <0.05 was considered as statistically

significant.
 4

Results

Baseline characteristics

In our study, 432 patients who were enrolled for the study underwent percutaneous coronary

intervention and were followed for the development of CIN. 132 patients who underwent optical

coherence tomography (OCT) guided percutaneous coronary intervention were also included in

the study. Mean age of the study population was 57.2 + 10.43 years with around 21 patients (4.9

%) more than 75 years of age. Among the study population, males were 348 (80.6%) and

females 84 (19.4%). Hypertension was present in 257 patients (59.5%), diabetes in 208 patients

(48.1 %), smoking in 208 (48.1 %), anemia in 104 patients (24.1 %), heart failure in 95 patients

(22 %), Mean Mehran risk score of 5.44 + 4.78, Mean eGFR of 88.4 + 30.65 ml/min/1.73 m2

and mean contrast volume usage of 122.8 + 41.9 ml. (Table 5)

Table 5: Baseline characteristics and risk factors for CIN.

Variable Percentage/Mean

Age (years) 57.2 + 10.43

Males (%) 80.6

Hypertension (%) 59.5

Diabetes (%) 48.1

Smoking (%) 48.1

Anemia (%) 24.1

Heart failure (%) 22

eGFR (ml/min/1.73 m2) 88.4 + 30.65

 4

Contrast volume (ml) 122.8 + 41.9

Mehran risk score 5.44 + 4.78

eGFR Estimated glomerular filtration rate.

Patients were categorized into four groups based on Mehran risk score (MRS) into low risk

(MRS < 5), intermediate risk (MRS 6-10), high risk (MRS 11-15) and very high risk groups

(MRS > 16). (Table 6)

Table 6: Categorization of patients based on Mehran Risk score (Table 6)

MRS Risk category N Percentage Predicted risk of CIN from

(%) Mehran et al

<5 Low 265 61.3 7.5 %

6-10 Intermediate 103 23.8 14 %

11-15 High 37 8.6 26 %

> 16 Very high 27 6.3 57.3 %

Total 432 100

MRS Mehran risk score, n no of patients, CIN contrast induced nephropathy.

The patients were followed for the development of CIN. Majority of the patients (61.3 %)

belonged to the low risk category (MRS < 5). Only 6.3 % patients belonged to very high risk

category (MRS > 16). (Figure 1)

 4

Figure 1: Categorisation of patients based on Mehran risk score (MRS)

Incidence of Contrast induced nephropathy (CIN)

Among the 432 patients who were followed for development of CIN, only 64 patients (14.8%)

developed CIN. (Figure 2)

Incidence of CIN

14.80%

85.20%

CINNO CIN

Figure 2: Incidence of CIN.

 4

Risk predictors of CIN

The known risk factors for development of CIN were analysed between the two groups – those

who developed CIN and those who did not. The traditional risk factors like age >75 years, sex,

hypertension, diabetes, smoking, periprocedural hypotension, use of IABP (intraaortic balloon

counterpulsation), heart failure anemia, contrast volume and eGFR were evaluated for the

development of CIN.

In our study of 432 patients, majority of patients i.e 307 (71.1%) were aged between 51-74 years.

103 (23.8%) were in age group of 26-50 years and 21 (4.9%) were in the age group of > 75 years

and only 1 patient (0.2%) was in the age group of < 25 years respectively. Incidence of CIN was

not significantly different across various age groups (p 0.435) (Table 7). Among patients with

age > 75 years, 28.6 % patients developed CIN compared to 14.1 % patients who had age less

than 75 years. However, the difference was not statistically significant. (Figure 3)

Table 7: Incidence of CIN across various age groups. (p 0.435)

Age (years) Non CIN group CIN group

< 25 years 1 (100 %) 0 (0 %)

26-50 92 (89.3 %) 11 (10.7%)

51-74 258 (84 %) 49 (16 %)

>75 years 17 (81%) 4 (19 %)

Total 368 (85.2 %) 64 (14.8 %)

CIN Contrast induced nephropathy

 4

Figure 3 : Comparison of age > 75 years with development of CIN (p value 0.074)

Among the males, 13.5 % patients developed CIN compared to 20.2 % females. However, the

difference was not statistically significant. (Figure 4)

 4

Figure 4: Comparison of males and females for development of CIN (p value 0.125)

Among the patients who had hypertension, 15.6 % patients developed CIN compared to 13.7

who didn’t have hypertension. However, the difference was not statistically significant.

(Figure 5)
 4

Figure 5: Comparison of hypertension for development of CIN (p value 0.679)

Among patients who had diabetes mellitus, 17.3 % patients developed CIN compared to 12.1

patients who didn’t have diabetes mellitus. However, the difference was not statistically

significant. (Figure 6)
 4

Figure 6: Comparison of diabetes mellitus with development of CIN ( p value 0.177)

Smokers had a lower incidence (10.6%) for development of CIN compared to non smokers

(18.8%). The difference was statistically significant. (Figure 7)

 4

Figure 7: Comparison of smokers and nonsmokers for development of CIN (p value 0.021)

Periprocedural hypotension was associated with development of CIN in 62.5 % patients

compared to 12 % patients who did not have it. The difference was statistically significant

(Figure 8)
 5

Figure 8: Periprocedural hypotension was significantly associated with development of CIN ( p

value <0.001).

Use of intraaortic balloon counterpulsation (IABP) was associated with development of CIN in

50 % of patients compared with 14.5 % patients in whom IABP was not used. However, the

difference was not statistically significant. (Figure 9)

 5

Figure 9: No significant association between use of IABP and development of CIN (p value

0.106)

Patients who had congestive heart failure had higher incidence (38.9%) of development of CIN

compared to those who didn’t have it (8 %) and the observed difference was statistically

significant (Figure 10)

 5

Figure 10: Congestive heart failure (CHF) was associated with higher risk of CIN (p < 0.001)

Anemic patients had higher incidence of CIN (25%) compared to non anemic patients (11.6 %),

and the difference was statistically significant. (p 0.001) (Figure 11)

 5

Figure 11: Anemia was significantly associated with development of CIN (p 0.001).

Univariate logistic regression analysis of different risk factors with development of CIN (Table

8)

Table 8: Univariate logistic regression analysis of various risk factors with development of CIN.

p value < 0.05 is significant.

Variable Patient Incidence p value Odds 95 % CI for OR

% of CIN % ratio
Lower Upper
(OR)

Age > 75 yrs Yes 4.9 28.6 0.074 2.434 0.908 6.530

No 9 14.1
 5

Sex Male 80.6 13.5 0.125 1.625 0.879 3.005

Female 19.4 20.2

Hypertension Yes 59.5 15.6 0.679 1.16 0.671 2.004

No 40.5 13.7

Diabetes mellitus Yes 48.1 17.3 0.177 1.465 0.858 2.501

No 51.9 12.1

Smoking Yes 48.1 10.6 0.021 .513 0.294 0.893

No 51.9 18.8

Hypotension Yes 5.6 62.5 < 0.001 12.211 5.072 29.399

No 94.4 12

IABP Yes 0.9 50 0.106 5.903 0.816 42.868

No 99.1 14.5

CHF Yes 22 38.9 < 0.001 7.324 4.143 12.949

No 78 8

Anemia Yes 24.1 25 0.001 2.544 1.456 4.444

No 75.9 11.6

CIN contrast induced nephropathy, OR Odds ratio, CI Confidence interval, IABP Intra aortic

balloon counterpulsation, CHF Congestive heart failure

Subsequently, multivariate logistic regression analysis of categorical variables with development

of CIN was studied after adjusting for the confounding factors. Table 9)
 5

Table 9: Multivariate logistic regression analysis of categorical variables with the development

of CIN. CHF Congestive heart failure. p value < 0.05 is considered significant.

Variable p value Odds ratio 95 % CI for odds ratio

Lower Higher

Age >75 yrs 0.660 1.312 0.392 4.392

Sex 0.310 1.493 0.689 3.233

Smoking 0.104 0.569 0.288 1.124

Hypotension < 0.001 6.706 2.514 17.891

CHF < 0.001 5.778 3.056 10.923

Anemia 0.047 1.926 1.009 3.677

CI Confidence interval, CHF Congestive heart failure

When the categorical variables were adjusted for other covariables, it was found out that

hypotension, congestive heart failure and anemia were significantly associated with development

of CIN, however, smoking was not significantly associated with development of CIN (p 0.104).

Estimated glomerular filtration rate (eGFR) with development of CIN

Among our study population of 432 patients, median eGFR was 96 ml/min/1.73 m 2 (Table 10).

Out of these, 64 patients who developed CIN, median eGFR was 58 ml/min/1.73 m 2 and among

the 368 patients who didn’t develop CIN had a median eGFR of 98 ml/min/1.73 m 2and the

difference between two groups was found to be statistically significant. (p < 0.001). (Table 11)
 5

Table 10: eGFR in our study population.

Variable eGFR

No. of patients, N 432

Median 96

Minimum 16

Maximum 143

Percentiles 25 63

75 110

eGFR Estimated glomerular filtration rate

Table 11: Comparison of eGFR between the CIN group and non CIN group. The difference was

statistically significant (p < 0.001).

No CIN CIN

No of patients 368 64

eGFR 98 58

Minimum 16 17

Maximum 143 136

Percentiles 25 72 37.25

75 110 98

CIN Contrast induced nephropathy, eGFR Estimated glomerular filtration

 5

Figure 12: Graphical representation of eGFR between CIN and non CIN groups (p < 0.001)

Among the 432 patients, who were enrolled in the study, the median use of contrast volume was

100 ml. (Table 12) Out of these who developed CIN, median use of contrast volume was 120 ml,

whereas those who didn’t develop CIN, median use of contrast volume was 100 ml, however, the

difference was not statistically significant (p 0.155). (Table 13) (Figure 13)

Table 12: Usage of contrast volume in our study population.

Variable Contrast volume (ml)

No. of patients, N 432

Median (ml) 100

 5

Minimum (ml) 50

Maximum (ml) 380

Percentiles 25 100

75 140

N number of patients, ml milliliter

Table 13: Comparison of usage of contrast volume between CIN and non CIN groups. The

difference was statistically insignificant (p 0.155)

Variable No CIN CIN

No. of patients 368 64

Median (ml) 100 120

Minimum (ml) 50 60

Maximum (ml) 380 280

Percentiles 25 100 100

75 140 150

CIN Contrast induced nephropathy ml milliliter

 5

Figure 13: Graphical representation of contrast volume use between CIN and non CIN groups. (p

0.155)

Incidence of CIN among various subgroups based on Mehran risk score (MRS) (Table 14)
 6

Table 14: Incidence of CIN across various MRS subgroups.

MRS subgroup No of patients CIN Total

No Yes

<5 N 248 17 265

% within MRS
93.6% 6.4% 100.0%
subgroup

6-10 N 87 16 103

% within MRS
84.5% 15.5% 100.0%
subgroup

11-15 N 27 10 37

% within MRS
73.0% 27.0% 100.0%
subgroup

>16 N 6 21 27

% within MRS
22.2% 77.8% 100.0%
subgroup

Total N 368 64 432

% of total
85.2% 14.8% 100.0%
patients

MRS Mehran risk score, CIN contrast induced nephropathy, N Number of patients
 6

Figure 14: Comparison of incidence of CIN across MRS subgroups. Higher MRS subgroups

were associated with increased incidence of CIN. (p <0.001)

Patients were categorized into four MRS subgroups based on Mehran Risk Score (MRS) as low

(< 5), intermediate (6-10), high (11-15), very high risk (> 16) and the incidence of CIN in each

subgroup was 6.4%, 15.5%, 27 % and 77.8 % respectively. Higher Mehran risk score was

associated with increased incidence of CIN, and the observation was statistically significant. (p

<0.001). Patients belonging to the low MRS risk subgroup had lowest incidence of CIN and

those belonging to very high risk group had the highest incidence of CIN respectively. (Table 14

, Figure 14).

The incidence of CIN was 2.7 fold higher (OR : 2.68, 95% CI : 1.299-5.540, p = 0.008), 5.4 fold

higher (OR : 5.403, 95% CI : 2.249-12.978, p <0.001) and 51 fold higher (OR : 51.059, 95% CI :
 6

18.195-143.278, p <0.001) in the intermediate (MRS 6-10), high (MRS 11-15) and very high

risk groups (MRS > 16) when compared to the low risk group (MRS < 5). (Table 15)

Table 15: Tabulated form of higher likelihood of CIN in intermediate, high and very high risk

groups as compared to the low risk group (MRS < 5) (reference group)

MRS subgroup P value Odds ratio 95 % CI for OR

(OR)
Lower Higher

Intermediate (MRS 6-10) 0.008 2.68 1.299 5.540

High (MRS 11-15) < 0.001 5.403 2.249 12.978

Very high risk ( > 16) < 0.001 51.059 18.195 143.278

.MRS Mehran risk score, OR Odds ratio, CI Confidence interval

RENAL REPLACEMENT

In our study of 432 patients, out of 64 patient who developed CIN, dialysis was required

only in 2 (3.1 %) patients with p value of 0.022.

 6

Discussion

The present prospective observational study titled ―Predicting contrast induced nephropathy

in post percutaneous intervention patients - A prospective observational cohort study.‖ was

conducted on 432 patients who were admitted with chronic stable angina and acute coronary

syndrome (unstable angina, NSTEMI and STEMI) for percutaneous coronary intervention in the

Department of Cardiology, Nizam’s Institute of Medical Sciences, Hyderabad, Telangana India

for a period of one year.

Incidence of Contrast induced nephropathy

In our study of 432 patients, who were followed for development of contrast induced

nephropathy (CIN), 64(14.8%) patients developed CIN whereas 368 (85.2 %) patients didn’t

develop CIN. Mehran et al (2004)43 in their study found an incidence of 13.1 % of contrast

induced nephropathy in post percutaneous intervention patients. ABMM Alam et al (2012)65 in

their study of Assessment of Acute Kidney Injury in Patients Undergoing Elective Coronary

Angiography and Percutaneous Coronary Intervention in 111 patients found AKI developed

11.7% of the study patient. Fei He et al (2012)66 in their retrospective case control study of risk

factors and outcomes of acute kidney injury after intracoronary stent implantation in 325 patients

observed that 51(15.7%) patients developed AKI. Nough H et al (2013)69 in their study of

Incidence and Main Determinants of Contrast-Induced Nephropathy following Coronary

Angiography or Subsequent Balloon Angioplasty, found an incidence of CIN in 12.8 %. Narula

A et al (2014)75 conducted a study on contrast-induced acute kidney injury after primary

percutaneous coronary intervention and found an incidence of 16.1%. Hamdy Shams-Eddin

Taher et al (2015)78 in their prospective cohort study of predicting contrast induced nephropathy
 6

post coronary intervention reported CIN was observed in 23 (11.5%) patients out of total of 200

patients. Taher HSE et al (2015)80 conducted an observational prospective cohort study with the

purpose to assess the incidence and predictors of contrast induced nephropathy (CIN) in

unselected patients undergoing coronary intervention either coronary angiography (CA) or

percutaneous coronary interventions (PCI) and found CIN incidence of 11.5 %. Shacham Y et

al. (2015)82 in their study of Myocardial Infarction patients treated with Primary Percutaneous

Intervention in 1656 patients found that AKI occurred in 168(10%) of patients. Ahmadreza

Assareh et al (2016)83 in cross-sectional and prospective study of Contrast induced nephropathy

among patients with normal renal function undergoing coronary angiography in 254 patients

reported CIN occurred in 27 patients (10.6%). Pérez-Topete SE et al (2016)85 did their study of

contrast-induced nephropathy in patients undergoing percutaneous coronary intervention, and

found incidence of CIN of 14.2 %. Gaurav Singhala et al (2017)87 conducted a study of

Incidence of contrast induced acute kidney injury in 300 patients undergoing percutaneous

coronary intervention in North Indian population and reported that CIN developed in 32 patients

(10.66%). Amrendra Mandal et al (2018)93 conducted an observational prospective study to

study the incidence of CIN in Nepalese populations and found CIN incidence of 13.2 %. Dileep

Kumar et al (2020)95 conducted an observational study in STEMI patients who underwent

primary PCI and found CIN incidence of 13.1 %.

The observation regarding the incidence of CIN in post percutaneous coronary

intervention patients is in accordance with the observations reported by the above

mentioned authors.
 6

AGE DISTRIBUTION

In our study of 432 patients, majority of patients i.e 307 (71.1%) were aged between 50-

75 years. 103 (23.8%) were in age group of 25-50 years and 21 (4.9%) were in the age group of

> 75 years and only 1 patient (0.2%) was in the age group of <25 years respectively. The mean

age of presentation was 57.2 + 10.43 years. Fei He et al (2012)66 in their retrospective case

control study of risk factors and outcomes of acute kidney injury after intracoronary stent

implantation in 325 patients observed that the age of participants ranged from 40 to 91 years

(mean age 65.57±10.66). Waqar Kashif et al (2013)73 in their study of 116 patients found that

mean age was 64.0 ± 11.5 years. Hamdy Shams-Eddin Taher et al (2015)78 in their prospective

cohort study of predicting contrast induced nephropathy post coronary intervention reported

mean age of 55.5±8.8 years in total of 200 patients. Ahmadreza Assareh et al (2016)83 in cross-

sectional and prospective study of 254 patients observed mean age of 56.6 ± 11.9 years. Sandeep

Kumar (2017)91 studied the incidence of CIN in post PCI patients and the mean age of the study

group was 56.6 ± 12.5 years. Amrendra Mandal et al (2018)93 conducted an observational

prospective study to study the incidence of CIN in Nepalese populations who underwent PCI,

and the mean age of study group was 58.5 ± 23 years. Dileep Kumar et al (2020)95 conducted

an observational study in which they included 282 patients who presented with STEMI and

underwent primary PCI, mean age of the group was 56.4 ± 9.1 years.

Incidence of CIN with age

In our study of 432 patients, none of the patients < 25 years, 11 patients (10.7 %) in age group of

26-50 years, 49 patients (16 %) in age group 51-75, and 4 patients (19 %) in age group of more
 6

than 75 years developed CIN. Though there was an increase in the incidence of CIN with

increasing age, however, the difference was not statistically significant. ((p 0.435). Dutta PK,

Mannan MM (2015)81 conducted a cross sectional observational study in a Tertiary hospital of

Bangladesh to assess the proportion of CI-AKI in post PCI patients and found that incidence of

CIN was more in age >50 years but the observation was not statistically significant (p >0.05).

Sandeep Kumar (2017)91 studied the incidence of CIN and its risk factors in patients

undergoing CAG and found that incidence of CIN was not different across various age groups.

The result of our study concerning the age involved are quite consistent with the results

made by above mentioned authors.

GENDER DISTRIBUTION

In our study of 432 patients, 348 patients (80.6%) were males and 84 (19.4%) patients

were females. Waqar Kashif et al (2013)73 in their study found that 84 (72%) patients were

males and 32 (28%) were females. Suma M Victor et al (2014)74 in their study found that

83.6% patients were males and 16.4 % were females. Sanjib Kumar Sharma et al (2014) 76 in

their study of Incidence and Predictors of Contrast Induced Nephropathy after Coronary

Intervention at College of Medical Sciences Teaching Hospital, Bharatpur in 330 patients

reported that 222 (67.2%) were male and 108 (32.7%) were female patients. Pradip Kumar

Dutta et al (2015)81 in their cross sectional observational study of risk factors of contrast

induced acute kidney injury -a single centre study in a Tertiary hospital of Bangladesh in 50

patients found that 34 (68%) were male patients and 16 (32%) were females.
 6

INCIDENCE OF CIN IN RELATION TO GENDER:

In our study of 432 patients, 47 (13.5 %) male patients developed CIN whereas 301 (86.5

%) male patients didn’t develop CIN. In female patients, 17 (20.2 %) had CIN and 67 (79.8 %)

didn’t develop CIN (p 0.125). Thus, there was no relation of gender to development of CIN. Fei

He et al (2012)66 in their retrospective case control study in 325 patients found that 37 male

patients had AKI whereas 190 male patients had no AKI. In female patients, 14 had AKI and 84

had no AKI. They also observed insignificant relationship between incidence of AKI and gender

with p>0.05. Insignificant association was also reported by Charanjit S. Rihal et al (2002)45,

Pradip Kumar Dutta et al (2015)81 and Ahmadreza Assareh et al (2016)83.

The observations concerning the sex ratio of our study patients are consistent to those

observed by above mentioned authors.

SMOKING

In our study of 432 patients, 208 patients (48.1 %) were smokers and 224 patients (51.9 %) were

non smokers. In univariate logistic regression analysis, smoking was found to be significant

predictor of CIN (p 0.021). However, in multivariate logistic regression analysis, after adjusting

for covariables, smoking was not a significant predictor of CIN (0.104). Yeong Cho (MD) et

al96 in his study on the effect of contrast-induced nephropathy on cardiac outcomes after use of

nonionic isosmolar contrast media during coronary procedure found smoking was present in

36.5% of patients in CIN group and 33.5 % patients in non CIN group, and the difference was

not statistically significant (p 0.615).

The observation made in our study was same as that observed by the above mentioned author.
 6

HYPERTENSION

In our study of 432 patients, hypertension was present in 257 patients (59.5%). CIN was

seen in 15.6 % patients in hypertensive group compared to 13.7 % patients in normotensive

group ( p 0.679). Fei He et al (2012)66 in their retrospective case control study in 325 patients

observed that AKI developed in 78.4% of hypertensive patients and in 75.9% of normotensive

patients with P value of >0.05. Kashif W et al. (2013)73 conducted a descriptive study to

evaluate the frequency and risk factors associated with clinically significant contrast-induced

nephropathy (CIN) in patients undergoing non-emergent coronary angiography and found

hypertension was not a significant predictor of CIN. (p 0.76) Pradip Kumar Dutta et al

(2015)81 in their study in 50 patients found that the CI-AKI was more in hypertensive patients

but it was not significant with P value of 0.860. Hamdy Shams-Eddin Taher et al (2015)78 in

their prospective cohort study of predicting contrast induced nephropathy post coronary

intervention reported that out of 71 hypertensive patients 9(38%) developed CIN and in 62

(35%) no CIN was seen (P value=0.66).

In our study, hypertension was not associated with development of CIN as the p

value was insignificant (p 0.679) and our observation was in accordance with the

observations recorded by above mentioned authors.

DIABETES MELLITUS

In our study of 432 patients, diabetes was present in 208 patients (48.1%). Among the diabetic

patients, incidence of CIN was 17.3 % as compared to 12.1 % in the non diabetic group,

however, the difference was not statistically significant (p 0.177). Kashif W et al. (2013)73

conducted a descriptive study to evaluate the frequency and risk factors associated with clinically
 6

significant contrast-induced nephropathy (CIN) in patients undergoing non-emergent coronary

angiography and found diabetes was not a significant predictor of CIN. Some authors have

suggested that diabetes alone may be an independent risk factor for the development of contrast-

induced nephropathy. More recent research has failed to corroborate this connection. Parfrey et

al47 in a prospective trial of patients with diabetes, showed that none of 85 patients with diabetes

and normal renal function developed clinically significant renal impairment (defined as an

increase of > 50% in serum creatinine levels).

The observations made by the above mentioned authors are comparable to our

observations.

HEART FAILURE

In our study of 432 patients, heart failure was present in 95 patients (22%). Among the

patients who had congestive heart failure, 38.9 % developed CIN compared to 8% patients who

did not have congestive heart failure. (p <0.001)

Rihal et al (2002)45 in their study regarding Incidence and Prognostic Importance of

Acute Renal Failure After Percutaneous Coronary Intervention found that history of congestive

heart failure significantly correlated with development of AKI in patients with P value of

<0.0001. Sana Shoukat et al (2010)64 in their study of Contrast-Induced Nephropathy in

Patients Undergoing Percutaneous Coronary Intervention observed that congestive heart failure

is an important non modifiable patient related risk factor. Tehrani et al (2013)72 in their study of

Contrast-induced acute kidney injury following PCI concluded that patients with congestive

cardiac failure are at risk of developing CI-AKI. Thomas T. Tsai et al (2014)77 developed risk

models for predicting acute kidney injury (AKI) and AKI requiring dialysis (AKI-D) after
 7

percutaneous coronary intervention (PCI) to support quality assessment and the use of

preventative strategies. In this study, they found that AKI was seen in 77072(11.6%) of patients

with congestive cardiac failure with P value of <0.001. Oren Caspi, MD, PhD (2017)90 aimed to

determine the causal association of contrast material exposure and the incidence of AKI

following primary percutaneous coronary intervention and found congestive heart failure as a

significant predictor of CIN.

Thus, in our study congestive heart failure was associated with risk of contrast

induced nephropathy and our observation was in accordance with the observations

recorded by the above mentioned authors.

HYPOTENSION

In our study of 432 patients, 29 (42.6%) patients with hypotension, developed AKI and

39 (57.4%) patients with hypotension had no AKI. AKI was seen in 23 (5.3%) patients without

hypotension and in 409 (94.7%) patients without hypotension, no AKI was seen with P value

<0.001. Fei He et al (2012)66 in their retrospective case control study in 325 patients observed

that intraoperative and postoperative hypotension were independent risk factors of AKI (P value

<0.05). Suma M. Victor et al (2014)74 in their prospective single center study of risk scoring

system to predict contrast induced nephropathy following percutaneous coronary intervention

identified that hypotension was independent predictor of CIN (P <0.0001).

The observations made by the above mentioned authors are comparable to our

observations.
 7

ANEMIA

In our study, anemic patients had higher incidence of CIN (25%) compared to non anemic

patients (11.6 %), and the difference was statistically significant. (p 0.001). Narula A et al

(2014)75 conducted a study on contrast-induced acute kidney injury after primary percutaneous

coronary intervention found that anemia was a significant predictor of CIN. Sharma SK et al

(2014)76 undertook an observational descriptive study to find the incidence of contrast induced

nephropathy in patients undergoing coronary angiography and angioplasty and found that anemic

patients were at high risk of contrast induced nephropathy. Pérez-Topete SE et al (2016)85 did

their study of contrast-induced nephropathy in patients undergoing percutaneous coronary

intervention and found that the presence of anemia had a higher incidence of CIN (OR 7.5,p =

0.006). Sanjai Pattu Valappil et al (2018)92 conducted a prospective observational study where

patients with an estimated glomerular filtration rate (eGFR) between 30 and 60 ml/mt underwent

elective percutaneous coronary intervention (PCI) and were evaluated for the development of

CIN found that on multivariate analysis, the presence of anemia (p = 0.007) was independent

predictor of CIN.

PREDICTED eGFR

eGFR was calculated based on MDRD formula. Serum creatinine is not an ideal predictor of

renal function. But still it is the most commonly used marker for assessment of renal function. In

our study of 432 patients, 64 (14.8%) CIN patients, median eGFR was 58 ml/min/1.73 m 2 and

amongst the 368 (85.2 %) patients who didn’t develop CIN, median eGFR was 98 ml/min/1.73

m2, and the difference was statistically significant (p < 0.001). Lower eGFR was associated with

increased risk of CIN compared to patients who had higher eGFR. Fei He et al (2012)66 in
 7

their retrospective case control study of risk factors and outcomes of acute kidney injury after

intracoronary stent implantation in 325 patients found that pre-operative lower estimated

glomerular filtration rate had a significant risk of development of CIN (OR=6.677, 95%

CI=1.167–38.193) with significant P value <0.001. Nough H et al (2013)69 in their study of

Incidence and Main Determinants of Contrast-Induced Nephropathy following Coronary

Angiography or Subsequent Balloon Angioplasty found that a low estimated glomerular

filtration rate at baseline significantly predicted CIN after these interventions.

Tehrani S et al. (2013)72 in their article to review the definition, pathogenesis and management

of CI-AKI found that preexisting renal impairment was significantly associated with

development of CIN. Kashif W et al. (2013)73 conducted a descriptive study to evaluate the

frequency and risk factors associated with clinically significant contrast-induced nephropathy

(CIN) in patients undergoing non-emergent coronary angiography. Multivariate analysis revealed

low GFR (p = 0.001) was found to be independent factor associated with CIN. Sharma SK et al

(2014)76 undertook an observational descriptive study to find the incidence of contrast induced

nephropathy and to identify risk factors for the development of contrast induced nephropathy in

patients undergoing coronary angiography and angioplasty found that baseline e-GFR was

independent predictor for Contrast induced nephropathy. Oren Caspi, MD, PhD (2017)90 aimed

to determine the causal association of contrast material exposure and the incidence of AKI

following primary PCI, an estimated lower eGFR was significantly associated with development

of CIN.

As the P value calculated in our study was <0.001 which is significant so our

observation that lower eGFR was associated with development of CIN and was in

accordance with the observations reported by above mentioned authors.

 7

VOLUME OF CONTRAST

In our study of 432 patients, those who developed CIN, median use of contrast volume

was 120 ml, whereas those who didn’t develop CIN, median use of contrast volume was 100 ml,

however, the difference was not statistically significant (p 0.155). Sharma SK et al (2014)76

undertook an observational descriptive study to find the incidence of contrast induced

nephropathy and to identify risk factors for the development of contrast induced nephropathy in

patients undergoing coronary angiography and angioplasty and found that the amount of the

contrast agent administered was similar for both groups of patients (138.20±91.34ml vs.

175.56±118.86ml; p =0.254) and no correlation was found between the amount of contrast agent

administered and development of CIN. Sandeep Kumar (2017)91 studied the incidence of CIN

and its risk factors in patients undergoing CAG and found that the total volume of contrast

administered to CIN group (175 ± 59.3) was not significant as compared to that of non-CIN

(159.1 ± 56) group (P = 0.334).

The observations concerning the volume of contrast in our study are consistent to

those observed by above mentioned authors.

IABP

In our study of 432 patients, IABP was used in 2 patients who developed CIN and 2 patients who

didn’t develop CIN, however, the observed difference was not statistically significant. (p 0.106).

As the sample volume was very limited in both the groups, it may not be appropriate to

conclude the association of IABP with the development of CIN.

 7

RENAL REPLACEMENT

In our study of 432 patients, out of 64 patient who developed CIN, dialysis was required

only in 2 (3.1 %) patients with p value of 0.022. Charanjit S. Rihal et al (2002)45 in their study

regarding Incidence and Prognostic Importance of Acute Renal Failure After Percutaneous

Coronary Intervention in 7586 patients found that 20(7.8%) patients out of 254 patients with

AKI required renal replacement.

Renal requirement was required in less number of CIN patients in our study as

compared to above mentioned author. This can be attributed to large sample size in the

above mentioned study.

Predictability of Mehran Risk Score

In our study, it was seen that with increasing MRS the observed risk of CIN was exponentially

higher. The incidence of CIN was 2.7 fold higher (OR : 2.68, 95% CI : 1.299-5.540, p = 0.008)

in the intermediate group (MRS 6-10), 5.4 fold higher (OR : 5.403, 95% CI : 2.249-12.978, p

<0.001) in the high risk group (MRS 11-15) and 51 fold higher (OR : 51.059, 95% CI : 18.195-

143.278, p <0.001) in the very high risk groups (MRS > 16) when compared to the low risk

group (MRS < 5) respectively.

Our study and Mehran study were compared for the incidence of CIN across various MRS

subgroups, and it was found that the incidence of CIN across low, intermediate and high risk

groups were comparable between our study and Mehran study, however, the incidence of CIN

among very high risk group patients was substantially higher than the Mehran study.
 7

MRS < 5 MRS 6-10 MRS 11-15 MRS >16

Our study 6.4 % 15.5 % 27 % 77.8 %

Mehran study 7.5 % 14 % 26 % 57.3 %

Table 16: Comparison of observed risk of CIN in our study versus expected risk of CIN based on

Mehran risk score.

Mehran risk score was formulated and validated in the western population, but its applicability in

the Indian population holds true as well. The incidence of CIN in the very high risk group (MRS

> 16) was substantially higher in our study (77.8 %) as compared to same group in Mehran study

(57.3 %). Our observation was further validated by Sanjai Pattu Valappil et al92 who

conducted a study on the predictors of contrast induced nephropathy and the applicability of the

Mehran risk score in high risk patients undergoing coronary angioplasty—A study from a

tertiary care center in South India and found that the Mehran risk score prediction for CIN is

pertinent even in Indian population, however, the risk of CIN in high risk Mehran groups is

substantially higher in the Indian population than in the western population. The incidence of

CIN in the very high risk group (MRS > 16) was 83.3 % in their study which was comparable to

our study (77.8 %) but significantly higher than the Mehran study (57.3%).
 7

Summary

The present prospective study titled “Predicting contrast induced nephropathy in post

percutaneous coronary intervention patients – a prospective observational cohort study” was

conducted on 432 patients who were admitted with chronic stable angina and acute coronary

syndrome (unstable angina, NSTEMI and STEMI) for percutaneous coronary intervention

(Intracoronary stent implantation) in the Department of Cardiology, Nizam’s Institute of Medical

Sciences, Hyderabad, Telangana, India for a period of one year. In our study of 432 patients,

 64 (14.8 %) patients developed contrast induced nephropathy.

 Majority of patients, 307 (71.1%) were aged between 50-75 years. 103 (23.8%) were in

age group of 25-50 years and 21 (4.9%) were in the age group of > 75 years and only 1

patient (0.2%) was in the age group of <25 years respectively. The mean age of

presentation was 57.2 + 10.43 years. Contrast induced nephropathy didn’t differ between

various age groups.

 348 patients (80.6%) were males and 84 (19.4%) patients were females. There was no

gender predisposition for occurrence of contrast induced nephropathy.

 208 patients (48.1 %) were smokers and 224 patients (51.9 %) were non smokers.

Smoking was not associated with development of CIN.

 In our study of 432 patients, hypertension was present in 257 patients (59.5%). CIN was

seen in 15.6 % patients in hypertensive group compared to 13.7 % patients in

normotensive group ( p 0.679).

 7

 Diabetes was present in 208 patients (48.1%). Among the diabetic patients, incidence of

CIN was 17.3 % as compared to 12.1 % in the non diabetic group, however, the

difference was not statistically significant (p 0.177).

 Heart failure was present in 95 patients (22%). Among the patients who had

congestive heart failure, 38.9 % developed CIN compared to 8% patients who did not

have congestive heart failure. (p <0.001)

 29 (42.6%) patients with hypotension, developed AKI and 39 (57.4%) patients with

hypotension had no AKI. AKI was seen in 23 (5.3%) patients without hypotension and in

409 (94.7%) patients without hypotension, no AKI was seen with P value <0.001.

 Anemic patients had higher incidence of CIN (25%) compared to non anemic patients

(11.6 %), and the difference was statistically significant. (p 0.001).

 64 (14.8%) CIN patients, median eGFR was 58 ml/min/1.73 m 2 and amongst the 368

(85.2 %) patients who didn’t develop CIN, median eGFR was 98 ml/min/1.73 m 2, and the

difference was statistically significant (p < 0.001). Lower eGFR was associated with

increased risk of CIN compared to patients who had higher eGFR.

 In our study of 432 patients, those who developed CIN, median use of contrast volume

was 120 ml, whereas those who didn’t develop CIN, median use of contrast volume was

100 ml, however, the difference was not statistically significant (p 0.155).

 In our study of 432 patients, IABP was used in 2 patients who developed CIN and 2

patients who didn’t develop CIN, however, the observed difference was not statistically

significant. (p 0.106). As the sample volume was very limited in both the groups, it may

not be appropriate to conclude the association of IABP with the development of CIN.
 7

 Out of 64 patient who developed CIN, dialysis was required only in 2 (3.1 %) patients

with p value of 0.022.

 In our study, it was seen that with increasing Mehran risk score (MRS) the observed risk

of CIN was exponentially higher. The incidence of CIN was 2.7 fold higher (OR : 2.68,

95% CI : 1.299-5.540, p = 0.008) in the intermediate group (MRS 6-10), 5.4 fold higher

(OR : 5.403, 95% CI : 2.249-12.978, p <0.001) in the high risk group (MRS 11-15) and

51 fold higher (OR : 51.059, 95% CI : 18.195-143.278, p <0.001) in the very high risk

groups (MRS > 16) when compared to the low risk group (MRS < 5) respectively.

 The incidence of CIN in the very high risk group (MRS > 16) was substantially higher in

our study (77.8 %) as compared to same group in Mehran study (57.3 %).
 7

Limitations of the study

 This was a single center study which was conducted to analyze the incidence and

predictors of CIN in patients undergoing percutaneous coronary intervention.

 Other parameters for evaluation of post PCI renal dysfunction like Neutrophil galectin

associated lipocalyn {NGAL}, Cystatin C and Kidney injury molecule-1 (KIM-1) were

not included in this study.

 Latest Mehran study protocol was not included in this study.

 Very high risk group had less sample size.

 8

Conclusion
In our study of 432 patients,

 Incidence of contrast induced nephropathy was 14.8 %.

 Predictability of Mehran risk score for contrast induced nephropathy is pertinent even in

Indian population.

 Very high risk groups (MRS > 16) have a substantially higher incidence of contrast

induced nephropathy in Indian population as compared to western population, but the

difference may be because of the less sample size in very high risk group in our study

compared to the Mehran study.

 Periprocedural hypotension, anemia, congestive heart failure and baseline eGFR were

significant predictors of contrast induced nephropathy.

 Contrast induced nephropathy was associated with requirement of renal replacement

therapy.
 8

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Nephropathol. 2014; 3: 51-56.

63. Rudnick M, Feldman H. Contrast-Induced Nephropathy: What Are the True Clinical

Consequences? Clin J Am SocNephrol 2008; 3: 263–272.

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64. Shoukat S, Gowani SA, Jafferani A, and Dhakam SH. Contrast-Induced Nephropathy in

Patients Undergoing Percutaneous Coronary Intervention. Cardiology Research and

Practice.Volume 2010

65. Alam ABMM, Moniruzzaman M, Alam MB et al Assessment of Acute Kidney Injury in

Patients Undergoing Elective Coronary Angiography and Percutaneous Coronary

Intervention. Cardiovasc. J. 2012; 5(1): 37-43

66. Fei He, Jun Zhang, Zhong-qiu Lu et al Risk factors and outcomes of acute kidney injury after

intracoronary stent implantation. World J Emerg Med 2012; 3(3):197-201.

67. Perrin T, Descombes E, Cook S. Contrast-induced nephropathy in invasive cardiology.

Incidence, pathophysiology, diagnosis, prevention and prognosis. Swiss Med Wkly.

2012;142: w13608.

68. Salvatore Evola, Monica Lunetta, Francesca Macaion et al Risk factors for contrast induced

nephropathy: A study among Italian patients Indian Heart J. 2012 Sep; 64(5): 484–491.

69. Nough H, Eghbal F, Soltani M et al Incidence and Main Determinants of Contrast-Induced

Nephropathy following Coronary Angiography or Subsequent Balloon Angioplasty.

Cardiorenal Med 2013;3:128–135.

70. Neyra JA, Shah S, Mooney R, Jacobsen G et al Contrast-induced acute kidney injury

following coronary angiography: a cohort study of hospitalized patients withor without

chronic kidney disease. Nephrol Dial Transplant;2013: 1–10.

71. Islam N, Majumder AAS, Khalequzzaman M et al. Impact of blood glucose levels on

contrast induced nephropathy after percutaneous coronary intervention in patients not known

to be diabetic with acute coronary syndrome. Cardiovasc. J. 2013; 6(1): 23-30.

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72. Tehrani S, Laing C, Yellon DM et al Contrast-induced acute kidney injury following PCI

European Journal of Clinical Investigation 2013;43(5): 483-490

73. Kashif W, Khawaja A, Yaqub S, Hussain SA. Clinically Significant Contrast Induced Acute

Kidney Injury after Non-Emergent Cardiac Catheterization-Risk Factors and Impact on

Length of Hospital Stay. Journal of the College of Physicians and Surgeons Pakistan 2013,

Vol. 23 (12): 842-847.

74. Suma M. Victor, Anand Gnanaraj, Vijaya Kumar S. Risk scoring system to predict contrast

induced nephropathy following percutaneous coronary intervention Indian Heart J. 2014

Sep; 66(5): 517–524.

75. Narula A, Mehran R, Weisz G et al Contrast-induced acute kidney injury after primary

percutaneous coronary intervention: results from the HORIZONS-AMI substudy. European

Heart Journal (2014) 35, 1533–1540.

76. Sharma SL, Dubey L, Laudary S et al Incidence and Predictors of Contrast Induced

Nephropathy after Coronary Intervention at College of Medical Sciences Teaching Hospital,

Bharatpur. Nepalese Heart Journal 2014;11(1): 3-11.

77. Thomas T. Tsai, Uptal D. Patel, Tara I. Chang, et al Contemporary Risk Model of Acute

Kidney Injury in Patients Undergoing Percutaneous Coronary Interventions: Insights From

the National Cardiovascular Data Registry Cath-PCI Registry. J Am Heart Assoc. 2014;3:

1380.

78. Hamdy Shams-Eddin, TaherAyman, K.M. Hassan Salwa et al Predicting contrast induced

nephropathy post coronary intervention: A prospective cohort study The Egyptian Heart

Journal 2015;67 (4): 337-343.

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79. Rather FA, Najar SM, Malla HA et al Profile of acute kidney injury after open heart

surgeries in a tertiary care hospital. Saudi J Kidney Dis Transpl 2015;26(6):1177-1182

80. Taher HSE, Hassan AKM, Dimitry SR et al Predicting contrast induced nephropathy post

coronary intervention: A prospective cohort study The Egyptian Heart Journal 2015; 67:

337–343.

81. Dutta PK, Mannan MM. Risk factors of contrast induced acute kidney injury -a single centre

study in a Tertiary hospital of Bangladesh. Asian Journal of Science and Technology 2015;

6: 1080-1082.

82. Shacham Y, Leshem-Rubinow E, Gal-Oz A. Acute Cardio-Renal Syndrome as a cause for

Renal deterioration among Myocardial Infarction patients treated with Primary Percutaneous

Intervention. Canadian Journal of Cardiology 2015; 31:1240-1244.

83. Assareh A, Yazdankhah S, Majidi S et al. Contrast induced nephropathy among patients with

normal renal function undergoing coronary angiography. J Renal Inj Prev. 2016; 5(1): 21-24.

84. Farhan S, Vogel B, Tentzeris I, Jarai R et al Contrast induced acute kidney injury in acute

coronary syndrome patients: A single centre experience. European Heart Journal: Acute

Cardiovascular Care 2016;5(1): 55–61.

85. Pérez-Topete SE, Miranda-Aquino T, Gasca-Luna K et al Contrast-induced nephropathy in

patients undergoing percutaneous coronary intervention. Rev Mex Cardiol 2016; 27 (2): 64-

70.

86. Amin AP, Bach RG, Caruso ML et al Association of variation in contrast volume with acute

kidney injury in patients undergoing percutaneous coronary intervention. JAMA Cardiol.

2017; 2(9): 1007-1012.

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87. Singhala G, Pathak V, Kumar M. Incidence of contrast induced acute kidney injury in

patients undergoing percutaneous coronary intervention in North Indian population. Journal

of Indian College of Cardiology.2017; 7(4):143-148.

88. Tan CS, Tan CL, Mohammad, F et al Incidence and epidemiology of Contrast induced acute

kidney injury following percutaneous coronary Angiogram - single Centre experiences.

Kidney International Reports 2017; 2: S1–S41.

89. Yuan Y, Qiu H, Hu XY et al Risk Factors of Contrast-induced Acute Kidney Injury in

Patients Undergoing Emergency Percutaneous Coronary Intervention. Chin Med J 2017;

130:45-50.

90. Oren Caspi, MD, PhD; Manhal Habib, MD, PhD; Yuval Cohen, MD Acute Kidney Injury

After Primary Angioplasty: Is Contrast-Induced Nephropathy the Culprit? J Am Heart

Assoc. 2017; 6: 5715

91. Sandeep Kumar, Ranjith K Nair, Naveen Aggarwal Risk factors for contrast-induced

nephropathy after coronary angiography Saudi Journal of Kidney diseases and

transplantation 2017; 28 (2): 318-324

92. Sanjai Pattu Valappila, Sivaprasad Kunjukrishnapillai, Mathew Iypea et al Predictors of

contrast induced nephropathy and the applicability of the Mehran risk score in high risk

patients undergoing coronary angioplasty—A study from a tertiary care center in South India

Indian Heart Journal 2018; 70: 399–404

93. Amrendra Mandal, Mukesh S. Paudel, Paritosh Kafle et al Contrast-induced Nephropathy

Following Percutaneous Coronary Intervention at a Tertiary Cardiac Center in Nepal Cureus

2018; 10(9): 3331

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94. Kazumasa Kurogi, MD, PhD; Masanobu Ishii, MD, PhD; Kenji Sakamoto, MD, PhD et al

Persistent Renal Dysfunction in Patients Undergoing Primary Percutaneous Coronary

Intervention for Acute Myocardial Infarction. J Am Heart Assoc. 2019; 8: e014096.

95. Dileep Kumar , Hussain Liaquat , Jawaid A. Sial et al Risk Factors Associated With Contrast

Induced Nephropathy after Primary Percutaneous Coronary Intervention Cureus 2020; 12(8):

e9721.

96. Jae Yeong Cho (MD), Myung Ho Jeong (MD, PhD), Su Hwan Park (MS) et al Effect of

contrast-induced nephropathy on cardiac outcomes after use of nonionic isosmolar contrast

media during coronary procedure Journal of cardiology 2010; 56: 300-306.

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9
 9

INFORMED CONSENT FORM

Study title: Predicting contrast induced nephropathy in post percutaneous coronary intervention
patients – A prospective observational cohort study.

Study number:

Subject name: s/o, w/o, d/o:

Date of birth/age:

Qualification:

Address:

Occupation: student/self employed/service/house wife/others

Name and address of the nominee(s) and the relation to the subject:

1. I confirm that I have read and understood the information sheet dated (dd/mm/yy)
for the above study and had the opportunity to ask questions.

2. I understand that my participation is voluntary and that I am free to withdraw at any time,
without giving any reason without any medical care or legal rights being affected.

3. I understand that the ethics committee will not need any permission to look at my health
records both in respect of the present study or any further research that may be conducted in
relation to it even if I withdraw from the study. I agree to this access. However, I understand that
my identity will not be revealed in any information released to the third parties or published.

4. I agree not to restrict the use of any data or result that arises from this study provided such a
use is only for scientific purpose(s).

5. I agree to participate in the above study and received a copy of this consent form.

Name of the subject Signature/thumb Impression

Name of the legally acceptable Signature/thumb Impression

representative or impartial witness

Name of the investigator Signature

 9

सचू ित सहमचत प्रपत्र

अध्ययन का शीर्षक: 7 ` 7` ी 7 ` के रोचगयों में चिपरीत प्रेररत नेफ्रोपैथी की
भचिष्यिाणी - एक संभाचित अिलोकन संबंधी अध्ययन।
अध्ययन संख्या:
चिर्य का नाम: s / o, w / o, d / o:
चिर्य के शरुु
आती: जन्म चतचथ /
आय:ु योग्यता:
पता:
व्यिसाय: छात्र / स्ियं कायषरत / सेिा / गह पत्नी / अन्य
नामांचकत व्यचि का नाम और पता और चिर्य
के संबंध: ना पत्र dated (dd / mm / yy) को पढा और समझा है और उसे
1. मैं पचु ि करता ह ं चक मैंने उपरोि
अध्ययन के चलए सिू
प्रश्न पछने का अिसर चमला।
2. मैं समझता ह ं चक मेरी भागीदारी स्िैचछछक है और मैं चबना चकसी चिचकत्सकीय देखभाल या काननू ी
अचधकारों को प्रभाचित चकए चबना चकसी भी समय िापस लेने के चलए स्ितंत्र ह। ं
3. मैं समझता ह ं चक ितषमान अध्ययन के संबंध में नैचतक सचमचत को मेरे स्िास््य ररकॉडष को देखने के चलए चकसी भी
अनमु चत की आिश्यकता नहीं
होगी या अध्ययन से हटने पर भी इसके संबंध में चकए जा सकने िाले चकसी भी अन्य शोध के से सहमत हालााँचक मैं
बारे में पता िलेगा। मैं इस पह¸ि समझता ह ं चक तीसरे पक्ष को जारी चकसी भी जानकारी ह।
में मेरी पहिान उजागर नहीं की जाएगी या प्रकाचशत नहीं की जाएगी।
4. मैं इस अध्ययन से उत्पन्न चकसी भी डेटा या पररणाम के उपयोग को प्रचतबंचधत नहीं करने के चलए सहमत ह ं, बशते
ऐसा उपयोग के िल िैज्ञाचनक उद्देश्य के चलए हो।
5. मैं उपरोि अध्ययन में भाग लेने के चलए सहमत ह ं और इस सहमचत पत्र की एक प्रचत प्राप्त की।

चिर्य का नाम हस्ताक्षर/ अंगठू े का चनशान चदनांक

काननू ी रूप से स्िीकायष का नाम

7 हस्ताक्षर/ अंगूठे का चनशान चदनांक

अन्िेर्क का नाम हस्ताक्षर/ अंगठू े का चनशान चदनांक

 9

ఇన్ఫర్మేడ్ కన్జ ెంట్ ఫారెం

అధ్యయన్ెం శీర్షి క: పోస్ట ్ పెర్క్యయటేనియస్ కొరోన్రీ ఇెంటర్వెన్ి న్ రోగులలో కెంట్రా స్ట ్ ప్రే ర్షత
న్ఫ్రే పతీని హెంచడెం - భావి పర్షశీలనాతేక స్మన్ెయ అధ్యయన్ెం.
ic

స్ట డీ స్ెంఖ్య:

విషయెం ప్రర్క్: s / o, w / o, d / o:

విషయెం యొకయ ప్రే రెంభాలు:

పుట్టట న్ / వయస్సు తేదీ:

అరహ తలు:

చిర్క్నామా:

వృత్తి : విద్యయర్షి / స్ెయెం ఉప్రధి / సేవ / హౌస్ భారయ / ఇతర్క్లు

నామినీ (లు) యొకయ ప్రర్క్ మర్షయు చిర్క్నామా మర్షయు విషయెంతో స్ెంబెంధ్ెం:

1. పె అధ్యయన్ెంలో నేను
dated స్మాచార షీట్ను చదివి అరి ెం చేస్సకునాును మర్షయు పే శ్ులను అడగడానికి
(dd / mm / yy )

ఉెందని నిర్ధా ర్షస్సి అవకశ్ెం

నాును.

2. నా భాగస్వెమయెం స్ెచఛెందమని నేను అరి ెం చేస్సకునాును మర్షయు ఏ స్మయెంలోన్ై నా

ఉపస్ెంహర్షెంచుకోవడెం నాకు ఉచితెం ఏ వై దయ స్ెంరక్షణ లేద్య చటట పరమై న్ హకుయలు లేకుెండా ఏ కరణెం
,

లేకుెండానే.

3. అధ్యయన్ెం నుెండి నేను ఉపస్ెంహర్షెంచుకునాు కూడా పే స్సి త అధ్యయన్ెం లేద్య ఏ ఇతర

పర్షశోధ్నానికి స్ెంబెంధిెంచి నా ఆరోగయెం ర్షకర్క్ు లను పర్షశీలెంచడానికి ఎథికు్ కమిటీకి ఏ
అనుమత్త అవస్రెం లేదని నేను అరి ెం
 9
చేస్సకునాును. నేను ఈ యాక్సుస్సయ అెంA కర్షస్సి నాును. అయితే నా గుర్షత ెంపు మూడవ పకి లకి
విడుదల చేయబడిన్ లేద్య పే చుర్షెంచబడిన్ ఏదై నా స్మాచార్ధనిు బహరగ తెం చేయదని నేను అరి ెం
చేస్సకునాును.

4. అట్నవెంట్ట ఉపయోగెం శాస్త్ి ీయ పే యోజన్ెం కోస్ెం మాతా మే అెందిెంచిన్ ఈ అధ్యయన్ెం నుెండి

ఉతపన్ుమయ్యయ ఏదై నా డేట్ర లేద్య ఫలతానిు ఉపయోగెంచడానిు నేను పర్షమితెం చేయన్ని అెంAకర్షస్సి
నాును.

5. పె అధ్యయన్ెంలో ప్రల్గగ న్డానికి నేను అెంA కర్షస్సి నాును మర్షయు ఈ స్మేత్త రూపెం యొకయ కపీని
అెందుకునాును.

విషయెం యొకయ ప్రర్క్ స్ెంతకెం / వేలు ముదే తేదీ

చటట పరెంగా ఆమోదయోగయమై న్ ప్రర్క్ స్ెంతకెం / వేలు ముదే

తేదీ పే త్తనిధి లేద్య నిషపక్షప్రత

స్వకిి

పర్షశోధ్కుడి ప్రర్క్ స్ెంతకెం / వేలు ముదే తేదీ

 9

PROFORMA
Patient details
Name
Age Sex
IP NO : CR NO :
Address and phone number:

Presenting complaints:

H/O past illness:

Personal history: Family history :

General examination : Vital data :

Sytemic examination :

Investigations:

CBC : Hb: TLC: PLT: HCT :

KFT (before procedure) : e GFR ( before procedure) :

Amount of contrast : Type of contrast used :
Hypotension : IABP:
CHF : Anemia:
Diabetes :
CIN RISK :
KFT (24 hours) : KFT (48 hours):
CIN : YES / NO
DIAGNOSIS :
ECG :
ECHO :
PROCEDURE DETAILS :
COMPLICATIONS :
S.NO Name Age Sex HTN DM Smoker OTHERS Diagnosis HypotensioIABP CHF Age > 75 yrAnemia eGFR Contrast v Creat (baseCreat (48 hCIN Dialysis MRS ECG ECHO CAG PTCA
1 Jaganath 48 M N Y Y AWMI Y N Y N N 120 150 0.73 0.94 Y N 14 N S S LAD
2 Azmath 55 M N N Y AWMI N N Y N N 110 170 0.82 0.89 N N 6N S S LAD
3 Kamalamma 60 F N N N NSTEMI N N Y N N 50 100 2.12 2.2 N N 10 N MO S RCA
4 SHOBA 46 F N N N NSTEMI N N N N Y 102 100 0.89 0.83 N N 4N N D LCX
5 SATTAIAH 55 M` Y Y Y IWMI Y N Y N N 56 60 1.28 1.7 Y N 15 CHB S D LCX
6 ANGAIAH 62 M Y Y N CVA CSA N N N N N 110 100 0.8 0.78 N N 4N N T RCA
7 SHANKARAIAH 65 M N Y N NSTEMI N N N N N 108 100 0.88 0.82 N N 4N M D LAD
8 SUBBA REDDY 65 M Y Y N CSA N N N N N 121 300 0.69 0.8 N N 6N N D LAD
9 MUDALI 60 M Y N Y AWMI N N N N N 116 110 0.99 1N N 4N MO S LAD
10 VENKANNA 49 M N N N CSA N N N N N 117 150 0.89 0.84 N N 1N N S LAD
11 KHAJA 76 F Y N N PWMI N N N Y N 36 200 1.14 2.1 Y N 10 N M S OM1
12 REDDY SWAMY 57 M Y Y Y CSA N N N N N 120 80 0.9 0.92 N N 3N N S LAD
13 YESANNA 48 M N Y N IWMI N N N N N 118 80 1 1.1 N N 3N N S RCA
14 VENKATAIAH 66 M Y Y Y COPD UA N N N N N 126 200 0.97 1.09 N N 5N N T RCA
15 NIRMALA 63 F Y Y N HYPOTHYR NSTEMI N N N N N 98 100 0.84 0.86 N N 4N N D LAD/LCX
16 SHAIK HUSSAIN 48 M Y N N AWMI N N N N N 110 200 0.7 0.8 N N 2N MO S LAD
17 MALLA CHARY 63 M N N N CSA N N N N N 108 200 0.7 0.78 N N 2N N D LCX/RCA
18 LAL SINGH 45 M N N Y IWMI N N N N N 104 100 0.74 0.79 N N 1N M S PDA
19 ABDUL KALAM 55 M N N N AWMI N N N N N 110 100 0.9 0.89 N N 1N M S LAD
20 CHANDRAIAH 65 M N Y N AWMI N N Y N N 96 200 0.8 1.3 Y N 10 N S T LAD
21 J CHANDRAIAH 70 M N Y N AWMI N N Y N N 89 200 1.04 1.5 Y N 10 N S T LAD
22 AHMED HUSSAIN 66 M Y Y N NSTEMI N N N N N 98 200 1.21 1.11 N N 7N N LM DVD LM LAD
23 LAXMI 65 M Y N N COPD CSA N N N N N 100 250 0.64 0.52 N N 2N N LM LM
24 B PULLAIAH 66 M Y N Y NSTEMI N N N N N 92 100 0.63 0.81 Y N 1N M S LAD
25 GADDAM 46 F N N N CSA N N N N N 126 100 0.77 0.78 N N 1N N S LAD
26 SANJEEVULU 50 M Y Y N AWMI N N N N N 118 100 0.87 0.89 N N 4N S D LAD,RCA
27 TARANNA 65 F Y Y N IWMI Y N N N N 98 90 0.64 1.1 Y N 8 1 HB M D RCA
28 I MALLAIAH 64 M Y Y N CSA N N N N N 98 1.2 0.87 0.9 N N 4N N D LCX
29 PINJARI 65 M Y N Y AWMI N N N N N 102 1.5 0.83 0.86 N N 1N MO S LAD
30 VENKATA SETTY 70 M N Y N CSA N N N N N 100 0.5 1.03 0.96 N N 4N N S RCA
31 MURALI KRISHNA 51 M Y N N IWMI N N N N N 99 1.5 0.76 0.8 N N 1N M D LCX
32 GOGULOTHU 65 M N N Y UA N N N N N 96 1 0.91 0.87 N N 1N N S LAD
33 SEEPELLY 36 M N N Y IWMI N N N N N 126 1.2 0.85 0.79 N N 1N M S RCA
34 SHAIK SAHANA 55 F Y Y N HYPOTHYR CSA N N N N N 89 1.2 1.06 1.09 N N 4N N S RCA
35 MD JAFFER 67 M Y Y Y IWMI N N N N N 50 0.8 1.12 1.06 N N 5N S T LCX
36 NAGABHUSHANANAN 63 M Y N N HYPOTHYR CSA N N N N Y 104 1 0.95 0.96 N N 4N N S RCA
37 B SRINU 35 M N N Y AWMI N N N N N 130 1 1.06 1.05 N N 1N MO S LAD
38 YOUSUF 58 M Y Y N PSORIASIS CSA N N N N N 87 1 0.9 1N N 4N N D LAD,RCA
39 MALLAIAH DODDE 58 M Y N Y CSA N N N N N 88 1 0.6 0.7 N N 1N N S RCA
40 BHASKAR 57 M N Y Y CSA N N N N N 86 1.2 1 1N N 4N N S LAD
41 MARYAMMA 70 M Y Y N UA N N Y N Y 36 1.3 1.3 1.9 Y N 15 N MO D LAD,RCA
42 PIDUGU 83 F Y Y N UA N N N Y Y 56 1 0.84 0.83 N N 13 N N S LAD
43 NARAYANA 70 M Y Y N CSA N N N N N 89 1 1 1 N N 4N N S LAD
44 MURTHI 66 M Y Y N NSTEMI N N Y N N 55 1.5 1.1 1.4 Y N 11 N S D LAD,LCX
45 SRISHA 48 F N N N UA N N N N N 110 1 0.5 0.52 N N 1N N D LAD,LCX
46 JAFER 53 M Y Y N UA N N N N N 113 1 0.8 0.9 N N 4N N S RCA
47 SHALLIMAYA 65 M Y N N AWMI N N N N N 0 1.5 0.78 0.75 N N 1N MO S LAD
48 PUSHPALATHA 60 F Y Y N HYPOTHYR CSA N N N N N 0 1.5 1.1 1.3 N N 4N N S LAD
49 MULTAMMA 60 F Y Y N OSA UA N N N N N 0 1.2 0.69 0.55 N N 4N M S RCA
50 SAHANA 55 F Y Y N HYPOTHYR CSA N N N N N 0 1.3 1 1.32 N N 4N N S RCA
51 NAGESWARA 57 M N N N AWMI N N N N N 0 1 0.95 0.86 N N 1N N S LAD
52 RAMACHANDER 55 M Y N N NSTEMI N N N N N 0 1 0.95 0.97 N N 1N N S LAD
53 MARY 62 F N N N UA N N N N N 0 1 1 1.1 N N 1N N S LCX
54 NAGENDRA 68 M Y Y N UA N N N N N 4 2 1.6 2.1 N N 9N S S LCX
55 HEMELI 50 F Y N N UA N N N N N 0 1 0.8 0.9 N N 1 TRIGEMINY N S LAD
 56 SANGABOI 65 M Y N N AWMI N N N N N 0 1 0.9 1 N N 1N S D LAD,RCA
57 RAMULAMMA 85 F N N N AWMI N N N N Y 0 1 0.57 0.62 N N 7N S D LAD,RCA
58 MURTHI 66 M Y Y N NSTEMI N N Y N N 2 1.5 1.1 1.4 Y N 11 N S D LAD,LCX
59 PRAVEEN KUMAR 33 M N N N AWMI N N N N N 120 100 0.72 0.61 N N 1N M S LAD
60 B YELLAIAH 65 M Y N Y CSA N N N N N 85 100 0.9 0.82 N N 1N N D LAD,D1
61 T SHANKARAIAH 56 M Y Y N NSTEMI Y N Y N N 4 2 1.3 1.9 Y N 19 N S T LAD,LCX
62 BUJJAMMA 60 F Y Y N CSA N N N N N 110 100 0.56 0.4 N N 4N N S LCX
63 D VENKAT REDDY 73 M N N N IWMI N N N N N 90 110 0.87 0.9 N N 1N N D LAD,RCA
64 RAMACHANDER 65 M Y Y Y AWMI N N N N N 92 100 1.04 1.2 N N 4N MO D LAD,LCX
65 K SARADA 76 F N N N AWMI N N N Y N 50 100 1.1 1.23 N N 7N M S LAD
66 SHAREEF 66 M Y N Y UA N N N N N 56 120 1.15 1.23 N N 1N N D LAD,RCA
67 CHANDRAMMA 60 F Y Y N CSA N N N N N 70 140 0.99 1.1 N N 4N N S LAD
68 SYED ALI 80 M N N Y COPD AWMI Y N Y Y N 6 120 1.7 2.5 Y N 21 N S S LAD
69 SATYANARAYANA 47 M Y N Y AWMI N N N N N 115 130 0.9 1 N N 1N MO S LAD
70 RAJDEVI 50 F Y Y N CVA AWMI N N N N N 130 200 0.8 0.85 N N 5 N,LBBB MO D LAD,D1
71 SABEERA BEGUM 60 F Y Y N NSTEMI N N N N N 70 180 1 1.1 N N 4N MO D LAD,LCX
72 MD BASHEER 45 M Y N N NSTEMI N N N N N 130 110 0.85 0.88 N N 1N N D LAD,LCX
73 M VEERAIAH 70 M Y Y Y CSA N N N N N 55 150 1.2 1.25 N N 6N S T LCX,RCA
74 PHOOL CHAND 65 M Y N N AWMI N N N N N 70 120 0.98 1.1 N N 1N MO D LAD,LCX
75 M KANDA RAO 65 M Y Y N CSA N N N N N 58 120 1.25 1.2 N N 5N M S LCX
76 B NARSIMHA 54 M Y Y N NSTEMI N N N N Y 6 2 1.7 2.3 Y N 15 N M D LAD,RCA
77 B NARSAMMA 55 F Y Y N AWMI N N N N Y 0 1 0.6 0.7 N N 8N MO S LAD
78 KAMALAMMA 64 F N N N IWMI N N N N N 0 1 0.6 0.6 N N 1N M S RCA
79 SHIVRANI 46 F Y Y N CSA N N N N Y 0 1 0.7 0.8 N N 8N N D LM-LCX, RCA
80 S CHANDRAIAH 50 M Y Y Y AWMI N N N N N 0 1 0.8 0.8 N N 4N N S LAD
81 RENUKA 52 F Y Y N CSA N N N N N 0 1.2 0.7 0.58 N N 4 N,LBBB N S LAD
82 SIMHACHALAM 52 M Y Y N NSTEMI N N Y N Y 4 1.5 1.32 1.9 Y N 16 N,LBBB MO S RCA
83 RAJAIAH 55 M N N Y AWMI Y N N N N 4 1.5 1.7 1.46 N N 10 N S S LAD
84 SHANKARAIAH 70 M Y Y N HYPOTHYR UA N N N N N 0 1 0.79 0.82 N N 4N N D LAD,RCA
85 NARAHARI 45 M N N N AWMI N N N N Y 6 1 3.5 3.7 N N 11 N MO S LAD
86 LAXMAIAH GOUD 46 M Y Y N NSTEMI N N Y N Y 4 1 1.4 1.9 Y N 17 N MO D LCX,RCA
87 SIRISHA 48 F N N N UA N N N N N 0 1 0.38 0.4 N N 1N N D LAD,RCA
88 SAILU 34 M N N Y AWMI N N N N N 2 1 1.1 1.4 Y N 3N MO S LAD
89 VENKAT SUBBA RAO 52 M N N N CSA N N N N N 0 1 0.7 0.78 N N 1N M S RCA
90 P LAXMAMMA 52 F N Y N CSA N N N N Y 0 1 0.65 0.7 N N 8N N S LAD
91 RAVINDER 59 M N N Y UA N N N N N 0 1 0.74 0.8 N N 1N N S RCA
92 B YELLAIAH 75 M N N N IWMI Y N N Y Y 4 1 1.4 1.8 Y N 18 N M S RCA
93 PARIJATHA 70 F Y Y N AWMI N N N N N 0 1 0.6 0.7 N N 4N MO D LAD,RCA
94 SOMAIAH 47 M N N N AWMI N N N N N 0 1 0.61 0.6 N N 1 2:1 AV MO S LAD
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95 NAGARAJU 56 M N N Y IWMI N N N N N 0 1 0.85 0.82 N N 1N M S RCA
96 JAYA LAKHSMI 72 F Y N N CSA N N N N N 0 1 0.78 0.91 N N 1N N D LCX,RCA
97 SATYAMMA 70 F Y N N CSA N N N N N 0 1 0.69 0.67 N N 1N N S LCX
98 N PADMAVATHI 69 F N N N UA N N N N N 0 1 0.6 0.62 N N 1N N S LCX
99 SHAMBAMMA 70 F Y N N OSA UA Y N N N Y 4 1 1.2 1.5 Y N 14 N N S LAD
100 KHAIRUNNISA 51 F Y Y N IWMI N N N N N 0 1 0.52 0.5 N N 4N N S RCA
101 B SRINIVAS RAJU 55 M Y Y N CSA N N N N N 0 1.2 0.8 0.78 N N 4N N S LAD
102 Y BEGUM 65 F N Y N HYPOTHYR IWMI N N N N N 4 1.5 1.6 2.02 Y N 8N N S LCX
103 P PARIJATHA 70 F Y Y N STEMI N N N N N 100 80 0.78 0.8 N N 3N MO D LAD,RCA
104 RANGAMMA 40 F Y Y N IWMI N N N N N 0 1.5 0.34 0.5 N N 4N M D LCX,RCA
105 M MOULANA 52 M N N N IWMI N N N N N 0 1 0.99 0.95 N N 1N S D RCA,LAD
106 LAXMI BAI 75 F Y Y N IWMI N N N Y N 0 1.3 0.82 1.06 N N 7N M D LAD,RCA
107 T RAJA RAO 59 M Y Y N UA N N N N N 0 1 1 1.1 N N 4N N D LAD,LCX
108 D KISHORE BABU 43 M Y Y Y CSA N N N N N 0 1.2 0.6 0.53 N N 4N M S LAD
109 J SUDEEPINI 56 F Y Y N CSA N N N N Y 0 1.2 0.57 0.63 N N 8N N D LAD,LCX
110 M YELLAIAH 53 M Y N N HYPOTHYR CSA N N N N N 0 1 0.8 0.9 N N 1N N S LAD
111 CHINCHAIAH 54 M Y N N CVA AWMI N N N N N 120 70 0.98 0.99 N N 0N M S LAD
112 A BAKAIAH 70 M N N N IWMI N N N N N 2 1 1.27 1.44 N N 3N MO D LCX,RCA
113 B KAMALAMMA 55 F Y Y N AWMI N N Y N Y 6 1 1.6 2 Y N 19 N N S LAD
114 SUGREEV PRASAD 54 M N N N CSA N N N N N 0 1 0.78 0.92 N N 1 CHB N S LAD
115 RANGA RAO 52 M N N N CSA N N N N N 0 1 0.95 0.92 N N 1N N S LAD
116 KISHTAMMA 65 F N N N IWMI N N N N N 98 90 0.89 0.86 N N 0N N S LM LCX
117 KHAN AYUB 50 M Y N N NSTEMI N N N N N 106 90 0.88 0.9 N N 0N N S LAD
118 GOVIND KUMAR 45 M N Y N AWMI N N N N N 0 1.5 0.9 1 N N 4N MO S LAD
119 BASAPPA 49 M N N Y AWMI N N N N N 0 1.2 0.7 0.9 N N 1N MO D RCA,LAD
120 M JOSEPH 31 M N N Y AWMI N N N N N 0 1 0.83 0.9 N N 1N M S LAD
121 RAVI BABU 46 M N Y N NSTEMI N N N N N 0 1 0.8 0.9 N N 1N N D LAD,LCX
122 J NARSIMULU 57 M N N Y AWMI N N N N N 100 70 1.09 0.89 N N 0N MO S LAD
123 RAMCHANDER 50 M N N Y AWMI N N N N N 110 90 0.76 0.81 N N 0N M S LAD
124 G NARSIMULU 41 M Y N Y AWMI N N N N N 96 80 0.8 0.81 N N 0N MO S LAD
125 M HAMEED 53 M Y Y N COPD IWMI N N N N N 0 1 0.84 0.76 N N 4N N S RCA
126 BAI MASHAMMI 50 M N N Y AWMI N N N N N 98 60 0.78 0.8 N N 0N MO D LAD,RCA
127 IBRAHIM 51 M Y N Y HYPOTHYR AWMI N N N N N 4 1.5 1.7 1.9 N N 5N M D LAD,LCX
128 S NAMPALLY 65 M N N Y AWMI N N N N N 99 70 0.59 0.64 N N 0N MO D LAD,LCX
129 KAMESHWAR RAO 75 M Y Y Y DYSLIPIDE UA N N N Y N 78 80 1.06 1 N N 7 2:1 AVB N S LAD
130 A BABURAO 63 M Y Y Y IWMI N N N N N 39 175 0.89 0.96 N N 4N M D RCA,LCX
131 M SHAKIR 40 M Y N Y AWMI N N N N N 130 90 0.99 0.95 N N 0N M S LAD
132 S SWAMY 59 M Y N N CSA N N N N N 90 90 0.68 1.12 Y N 0N N S LAD
133 MAHMUDA BEGUM 56 F Y Y N UA N N N N N 89 100 0.7 1.1 Y N 4 N,LBBB MO S LCX
134 T P LAXMI 75 F Y Y N AWMI Y Y Y Y N 88 80 1 3.5 Y Y 22 N S S LAD
135 N SRINIVAS 49 M N Y N AWMI N N N N N 0 1.2 0.9 0.9 N N 4N MO D LAD,LCX
136 B NUKARAJU 54 M N N N AWMI N N N N N 0 1 0.9 0.9 N N 1N MO D LAD,PDA
137 SUSAI MARY 65 F Y N N HYPOTHYR CSA N N N N Y 52 100 1.2 0.9 N N 7 CHB N D LAD,RCA
138 SHANKAR 53 M N N Y LWMI N N N N N 90 120 0.68 0.7 N N 1N M S LCX
139 YOUSUF 70 M Y Y N NSTEMI N N N N N 50 150 1.18 1.4 N N 6N N D LM-LCX,LAD
140 L VASUDEVA 72 M Y N N CSA N N N N N 70 100 0.83 0.76 N N 1N N S RCA
141 MOINUDDIN 61 M Y Y N CSA N N N N N 80 120 0.96 0.98 N N 4N N S RCA
142 MD JABBAR 65 M N Y N AWMI N N N N N 100 90 0.77 0.77 N N 3N M S LAD
143 SARADHA 64 F Y Y N CSA N N N N N 35 120 2.27 1.9 N N 8N N S LAD
144 CHINNNA 60 M N Y Y IWMI N N N N N 45 180 1.5 1.2 N N 6N N S RCA
145 BALAKRISHNA 50 M N N Y NSTEMI N N N N N 56 100 1.1 0.8 N N 3N N S LM-LAD
146 BHAVA NARAYANA 54 M N N N AWMI N N N N N 110 120 0.9 0.9 N N 1N MO S LAD
147 B VENKATAIAH 73 M Y N N IWMI N N N N N 59 130 1.1 0.9 N N 3N N S RCA
148 KHAJA MIYA 72 M Y N Y AWMI N N N N N 39 150 0.9 1.42 Y N 4N MO D LAD,RCA
149 VENKAT NARSAMMA 64 F N Y N CSA N N N N N 90 120 7 0.65 N N 4N MO D LAD,RCA
150 UPPALAIAH 65 M N N N CSA N N N N N 100 120 0.96 1.02 N N 1N M S LAD
151 CHILAKAMMA 70 F Y Y N CSA N N N N N 82 110 0.65 0.75 N N 4N N S LAD
152 A SURYA PRAKASH 67 M Y N N AWMI Y N Y N N 112 120 0.68 0.8 N N 11 N S S LAD
153 MD SALEEM 45 M Y N N AWMI N N N N N 108 90 0.89 0.88 N N 0N MO S LAD
154 K RAMULU 38 M N N Y IWMI N N N N N 58 110 1.1 1.2 N N 3N N S RCA
155 P S ARO 62 M Y N Y NSTEMI N N N N N 90 120 1.06 1.12 N N 1N N S RCA
156 VEERA VEKATESH 71 M Y N Y UA N N N N N 57 120 1.2 1.25 N N 3N N S RCA
157 SARASWATHI 45 F Y Y N AWMI N N N N N 100 120 1.18 0.97 N N 4N MO S RCA
158 J VENKATAIAH 46 M Y Y N CVA AWMI N N N N N 100 110 0.73 0.71 N N 4N N S LAD
159 M VIJAYALAXMI 62 F Y Y N HYPOTHYR CSA N N N N Y 50 130 1.3 0.9 N N 10 N N S LAD
160 PARVEEN 52 F Y Y N NSTEMI N N N N Y 100 130 8 0.73 N N 8N MO D LAD,LCX
161 SHIVA REDDY 55 M N N Y IWMI N N N N N 110 120 0.81 0.86 N N 1N M S RCA
162 L SRIRAM 50 M N N N IWMI N N N N N 110 150 0.89 1 N N 1N N T LAD,RCA
163 C MURALI KRISHNA 55 M Y N Y UA N N N N N 50 120 1.5 1.3 N N 3N M D RCA
164 T V REDDY 52 M Y N N CSA N N N N N 78 140 1 1 N N 1N N D LAD,RCA
165 R DEVITA 58 F Y Y N HYPOTHYR IWMI N N N N Y 100 130 0.8 0.71 N N 8N N S LCX
166 SHANKAR 49 M N N N AWMI N N N N N 108 150 0.79 0.8 N N 1N N D LAD,RCA
167 ANJAIAH 50 M N N Y AWMI N N N N N 58 170 1.3 1.3 N N 3N MO S LAD
168 G SARAIAH 40 M N Y N IWMI N N N N N 130 120 0.7 0.82 N N 4N N S LAD
169 B TAVUDU 66 M Y Y N CVA IWMI N N N N Y 120 120 0.83 0.79 N N 8N N D LCX,RCA
170 G SARAIAH 4 M N Y N IWMI N N N N N 108 140 0.7 0.82 N N 4N N S LAD
171 MD SABBIR 59 M N N N AWMI N N N N N 88 130 0.9 1 N N 1N MO S LAD
172 PERUMAL 52 M Y Y Y AWMI N N N N N 128 140 0.9 0.77 N N 4N MO SVD RCA
173 G KRISHNAIAH 56 M Y N N UA N N N N N 110 90 0.92 1 N N 0N N S RCA
174 MD JAFFER 66 M Y Y Y CSA N N N N N 58 100 1.2 1.1 N N 6N MO D LAD,LCX
175 B KESHAVULU 37 M Y N N CSA N N N N N 90 180 1.12 1.2 N N 1N M LM LM
176 OMERDARAZ KHAN 52 M N N N AWMI N N Y N N 90 170 1 1.42 Y N 6N S S LAD
177 KEDARNATH 64 M N N Y IWMI N N N N N 88 80 0.8 0.84 N N 0N M TVD LAD,LCX
178 G PEDDA KRISHNA 52 M Y N N AWMI N N N N N 120 80 0.7 0.7 N N 0N MO S LAD
179 P RAJESHWARI 39 F N Y N UA N N N N N 130 80 0.6 0.64 N N 3N N S RCA
180 D VEERABHADRA 76 M N N Y IWMI N N N N Y 110 80 0.8 0.82 N N 8N MO S RCA
181 GOVARDHAN 35 M N N N NSTEMI N N Y N N 82 100 0.92 1 N N 6N N S RAMUS
182 POONAM DEVI 63 F Y Y Y HYPOTHYR NSTEMI N N Y N N 98 80 0.7 0.8 N N 8N MO T LAD
183 BOJJU ADELLU 45 F Y N N IWMI N N N N Y 56 130 1.2 1.25 N N 6N M S LCX
184 T BUCHAMMA 60 F Y Y Y AWMI N N N N Y 54 120 1.32 1.35 N N 10 N MO S LAD
185 MUMTAZ BEGUM 76 F Y Y N AWMI N N N Y N 84 70 0.9 0.91 N N 7N MO S LAD
186 MANNAP REDDY 60 M Y N Y HEPATITIS AWMI N N Y N N 98 100 0.9 0.94 N N 6N MO S LAD
187 KOMURAIAH 60 M N N Y AWMI N N N N N 38 100 2.2 2.1 N N 5N MO D LAD,LCX
188 KUMARA SWAMY 37 M N N Y AWMI N N N N N 110 120 0.8 0.8 N N 1N MO S LAD
189 SRNIVAS REDDY 30 M N N Y NSTEMI N N N N N 126 110 1 1 N N 1N N S LAD
190 B V SUBBA REDDY 66 M Y N N CSA N N N N N 38 200 1.5 1.56 N N 6N N S LAD
191 VENKATAIAH 34 M N N N AWMI N N Y N N 58 80 1.4 1.32 N N 7N MO S LAD
192 M J KRISHNA 60 M Y N N NSTEMI N N N N N 98 110 0.9 0.8 N N 1N N D LAD,RCA
193 RAJANNA 55 M N Y Y AWMI N N N N N 102 120 0.9 1 N 4N MO S LAD
194 JAHANGEER 57 M Y N N NSTEMI N N N N N 39 200 1.56 1.6 N N 6N N D LAD,LCX
195 T RAJESHWAR RAO 36 M N N Y AWMI N N N N N 128 110 0.95 0.9 N N 1N M S LAD
196 KRISHNA 59 M Y N Y AWMI N N N N N 124 140 0.81 0.89 N N 1N M S LAD
197 G MADDILITI 45 M N N Y AWMI N N N N N 118 100 0.99 1.24 Y N 1N MO S LAD
198 B YADAMMA 53 F N Y N AWMI N N N N N 114 90 0.8 0.8 N N 3N MO S LAD
199 K VENKATA SUBBAIAH 47 M N N Y IWMI N N N N N 110 160 0.9 0.9 N N 1N MO D LAD,RCA
200 ABDUL SALAM 55 M N N Y CVA IWMI N N N N N 57 150 1.2 1.25 N N 3N MO S RCA
201 SHIVA REDDY 55 M N N Y IWMI N N N N N 98 110 0.81 0.86 N N 1N M S RCA
202 PARVEEN BEGUM 52 F Y Y N NSTEMI N N N N Y 90 150 0.8 0.73 N N 8N MO D LAD,LCX
203 AFSAR ALI 55 M Y Y Y IWMI N N N N N 102 90 0.91 0.94 N N 3N N D RCA,CX
204 B HANUMANTHU 61 M N N Y IWMI N N N N N 115 80 0.9 1 N N 0N N S RCA
205 AUGUSTEIN 76 M N Y N AWMI N N N N N 98 70 0.89 0.91 N N 7N S S RCA
206 SHANKAR 45 M N N N HEPATITIS AWMI N N Y N N 92 120 0.9 0.89 N N 6N S S LAD
207 NARAYAN 70 M Y N Y PSORIASIS AWMI N N N N N 102 180 0.9 1.4 N N 1N MO D LAD,LCX
208 N SRINIVAS 49 M N Y N AWMI N N N N N 98 150 0.9 1.06 N N 4N MO S LAD
209 M GOPAL 40 M N N Y AWMI N N N N N 120 140 0.87 1.2 Y N 1N MO S LAD
210 VENKAT LAXMI 65 F Y Y Y AWMI N N N N Y 27 150 2.31 2.37 N N 8N M D LAD,RCA
211 B BUTCHAIAH 60 M Y Y Y NSTEMI N N N N N 100 100 0.68 0.7 N N 4N N S LAD
212 LAXMI N GOUD 49 M Y N N AWMI N N N N N 54 110 1.4 1.5 N N 3N MO S LAD
213 KEDAR RAM 65 M Y Y N LWMI Y N Y N N 50 120 1.25 1.7 Y N 16 N MO S LAD
214 NARHIMHARAO 36 M Y Y N AWMI Y Y Y N N 101 90 1 1.5 Y N 18 N S S LAD
215 SATYANARAYANA 45 M N Y Y HYPOTHYR AWMI N N N N N 58 100 1.4 1.46 N N 6N MO S LAD
216 P CHANDRASHEKHAR 42 M Y N N IWMI N N N N N 116 140 0.67 0.75 N N 1N N S RCA
217 MD FAKURDDIN 39 M N N N AWMI Y N N N N 126 110 0.84 1.14 Y N 6N MO S LAD
218 MA HAMEED 53 M Y Y Y COPD IWMI N N N N N 114 120 0.84 0.76 N N 4N N S RCA
219 J ANANDAM 42 M N N Y IWMI N N Y N N 56 120 1.37 1.1 N N 6N MO S LM-LAD
220 CH SURESH 46 M N Y Y AWMI N N Y N N 118 140 0.71 0.81 N N 9N S S LAD
221 S SRINIVAS 46 M N N Y AWMI N N N N N 117 100 0.96 0.95 N N 1N MO S LAD
222 KHADARPASHA 42 M N N Y AWMI N N N N N 123 110 0.9 0.98 N N 1N MO D LAD,RCA
223 N SAVITHA 66 F Y N N AWMI N N N N Y 48 150 1.09 1.6 Y N 7N M D LAD,RCA
224 DAYAKAR 50 M N N N NSTEMI N N N N N 58 90 1.13 1.14 N N 2N N S RAMUS
225 D RAJENDER 76 M Y Y Y COPD NSTEMI N N Y Y N 80 130 0.71 0.99 Y N 13 N MO S RCA
226 SYED HANEEF 56 M Y N N AWMI N N N N N 92 100 1.03 0.96 N N 1N MO S LAD
227 V KANAKAIAH 85 M Y Y N HYPOTHYR IWMI N N N N N 110 100 1.05 1.08 N N 8N M D LCX,RCA
228 K LALITHA 76 F Y Y Y CVA IWMI N N N Y Y 56 120 1.15 1.2 N N 12 CHB M S RCA
229 K NAGA RAJU 55 M Y N Y IWMI N N N N N 98 90 0.7 0.9 N N 0 CHB N S RCA
230 M ROCK 35 M N N Y AWMI N N Y N N 98 150 1 1.4 Y N 6N S D LAD,LCX
231 ANJANEYLU 48 F N N N NSTEMI N N N N N 92 120 0.8 0.9 N N 1N N D LAD,RCA
232 S NARSAMMA 50 F N Y N AWMI N Y Y N N 100 100 0.9 1 N N 13 N S S LAD
233 NAGESWARA 64 M Y Y N HYPOTHYR IWMI N N N N Y 58 100 1.2 1.3 N N 9N N T RCA
234 YAKAMMA 52 F Y Y N CSA N N N N Y 98 150 0.9 1.3 Y N 8N N S RCA
235 SUDANANDHAM 55 M Y Y N AWMI N N N N N 59 180 1.17 1.16 N N 6N S D LAD,LCX
236 SATYA REDDY 52 M Y Y Y IWMI N N N N N 120 130 0.86 0.87 N N 4N M S LCX
237 JEHANGIR BEE 70 F Y N N NSTEMI N N N N N 110 160 0.9 1 N N 1N M D RCA,LAD
238 RAVINDER 55 M N N Y AWMI N N N N N 118 100 0.7 0.91 N N 1N MO S LAD
239 MD TAJUDDIN 45 M N N Y AWMI N N N N N 120 100 0.86 0.9 N N 1N M D LAD,LCX
240 BAL CHANDRAIAH 65 M N N Y IWMI N N N N N 110 150 0.8 0.9 N N 1N N S RCA
241 TUNNA KUMAR 35 M N N Y CSA N N N N N 120 120 0.7 0.75 N N 1N N S RCA
242 M MOHAN 63 M Y Y N AWMI N N Y N Y 50 100 1.4 1.8 Y N 16 N S S LAD
243 B MADHU SUDAN 65 M N Y Y CSA N N N N N 80 60 0.9 1 N N 3N N S LAD
244 NALLANGARU 45 M N Y Y IWMI N N N N N 126 80 0.85 0.9 N N 3N M S RCA
245 MD MOINUDDIN 62 M Y Y N CVA CSA N N N N N 98 50 0.76 0.8 N N 3N N S LCX
246 BV SUBBA REDDY 66 M Y N N CSA N N N N N 94 200 0.96 0.98 N N 2N N S LM-LAD
247 VENKATAIAH 34 M N N Y AWMI N N N N N 89 50 1.2 0.99 N N 0N M S LAD
248 L YADAIAH 57 M Y N N IWMI N N N N N 56 150 1.1 1.17 N N 3N M D RCA,LCX
249 YASHODA 76 F N Y N AWMI N N N Y N 46 100 1 0.96 N N 10 N M S LAD
250 VAIJANATH SWAMY 62 M N N Y IWMI N N N N N 59 100 1 0.9 N N 3N M D RCA,LAD
251 YAHDIYA BEGUM 60 F N N N NSTEMI N N Y N Y 18 100 2 2.58 Y N 16 N MO S LAD
252 BUJJA ADELLU 45 M Y N N IWMI N N N N N 122 50 0.8 0.84 N N 0N M S LCX
253 A SRINIVAS 45 M N N Y AWMI N N N N N 110 100 0.89 0.96 N N 1N M D LAD,LCX
254 SWAROOPA RANI 65 F Y N N AWMI N N Y N N 100 70 0.9 0.82 N N 6N S S LAD
255 J ISAK 55 M Y N N AWMI N N N N N 56 100 1.28 1.32 N N 3N MO S LM-LAD
256 K VENKATESHAM 40 M N N N AWMI Y N N N N 120 120 0.7 0.78 N N 6N MO S LAD
257 PANDARINATH 48 M N N Y UA N N N N N 72 100 1.1 1.15 N N 1N N S LAD,RAMUS
258 SK AKBAR HUSSAIN 56 M Y Y Y CSA N N N N Y 110 90 0.7 0.75 N N 7N N S RCA
259 V NARSIMHA 52 M Y Y Y AWMI N N N N N 68 50 1 1.14 N N 3N M S LAD
260 BALLI MALLAIAH 50 M N N Y NSTEMI N N N N N 90 120 1 1.08 N N 1N N S LCX
261 E BALANNA 76 M Y N N UA N N N N N 38 250 1 1.3 N N 6N N S LAD,LCX
262 D MADHUKAR 68 M Y N N CSA N N N N N 84 150 0.9 1 N N 1N N D LAD,RCA
263 MD MUSTAFA 48 M Y Y Y LWMI N N N N N 127 50 0.89 0.9 N N 3N M S LCX
264 S LAXMA NARSA 49 M Y N N NSTEMI N N N N N 58 200 1 1.35 Y N 4Y M S LCX
265 D SAMBA SIVA RAO 69 M Y Y N PARKINSO UA N N N N N 98 100 0.7 0.6 N N 4N N S RCA
266 B PADMA 57 F Y Y N CVA UA N N N N N 94 110 0.7 0.8 N N 4N N S LAD
267 D RAJESHWAR 61 M Y Y N UA N N N N N 92 120 0.9 1 N N 4N N S LCX
268 G NARSIMULU 42 M Y N N UA N N N N N 110 80 0.8 0.9 N N 0N N S LAD
269 GUNTI BASANTH 69 M Y Y N HEPATITIS AWMI N N N N N 39 100 1.5 1.3 N N 8N MO D LCX,RCA
270 J RAM REDDY 70 M Y Y Y IWMI N N Y N Y 38 100 1.7 2.25 Y N 17 CHB M S RCA
271 RAVI 57 M Y Y N NSTEMI Y N Y N N 38 200 1.3 2 Y N 19 N S T LAD,LCX
272 MANOJ 63 M Y Y N AWMI N N Y N Y 38 200 1.4 1.8 Y N 17 N S S LAD
273 ALI 80 M N N Y COPD AWMI Y N Y Y N 18 120 1.7 2.5 Y N 21 N S S LAD
274 SIMON 52 M Y Y N NSTEMI N N Y N Y 37 150 1.32 1.9 Y N 16 N,LBBB MO S RCA
275 JAVAGAL 46 M N Y Y AWMI Y N Y N N 120 150 0.73 0.8 N N 14 N S S LAD
276 SATYA 52 M` Y Y Y IWMI Y N Y N N 58 60 1.28 1.8 Y N 15 CHB S D LCX
277 FEHMEENA 60 F N Y N NSTEMI N N Y N Y 18 100 2 2.58 Y N 18 N MO S LAD
278 MARYAM 73 F Y Y N UA N N Y N Y 38 80 1.3 1.9 Y N 15 N MO D LAD,RCA
279 PARAMESH 84 M Y Y N UA N N N Y Y 58 100 0.84 0.83 N N 13 N N S LAD
280 MD SHAFI 66 M Y Y N NSTEMI N N Y N N 52 150 1.1 1.02 N N 11 N S D LAD,LCX
281 MANOHAR 66 M Y Y N NSTEMI N N Y N N 48 150 1.1 1.05 N N 11 N S D LAD,LCX
282 LAXMAN 46 M Y Y N NSTEMI N N Y N Y 36 100 1.4 1.38 N N 16 N MO D LCX,RCA
283 MOHIT 63 M Y Y N AWMI Y N Y N Y 50 100 1.4 1.36 N N 19 N S S LAD
284 B NARSIMHA 54 M Y Y N NSTEMI N N N N Y 19 200 1.7 1.8 N N 14 N M D LAD,RCA
285 YOGI 75 M N N N IWMI Y N N Y Y 37 100 1.4 1.3 N N 17 N M S RCA
286 NAVJOT 45 M N N N AWMI N N N N Y 18 100 3.5 3.7 N N 11 N MO S LAD
287 MAHENDER 63 M Y Y N AWMI N N Y N Y 36 100 1.4 1.99 Y N 16 N S S LAD
288 SHANTI 70 F Y N N OSA UA Y N N N Y 36 100 1.2 1.1 N N 13 N N S LAD
289 SURYA 67 M Y N N AWMI Y N Y N N 112 120 0.68 0.8 N N 11 N S S LAD
290 SAMEEN 60 F N Y N NSTEMI N N Y N Y 18 90 2 2.6 Y N 17 N MO S LAD
291 RAJIV 76 M Y Y Y COPD NSTEMI N N Y Y N 80 130 0.71 0.69 N N 13 N MO S RCA
292 KALA 76 F Y Y Y CVA IWMI N N N Y Y 56 120 1.15 1.2 N N 11 CHB M S RCA
293 KAMALI 55 F Y Y N AWMI N N Y N Y 6 1 1.6 2.2 Y N 19 N N S LAD
294 VENKAT LAXMI 65 F Y Y Y AWMI N N N N Y 27 150 2.31 2.37 N N 8N M D LAD,RCA
295 MAHARAJ 63 M Y Y N AWMI N N Y N Y 50 100 1.4 1.46 N N 16 N S S LAD
296 ANAND 42 M N N Y IWMI N N Y N N 56 120 1.37 1.1 N N 6N MO S LM-LAD
297 BADRUNNISA 60 F N N N NSTEMI N N Y N Y 18 100 2 1.8 N N 16 N MO S LAD
298 LATA 52 F Y Y N CSA N N N N Y 98 150 0.9 1.3 Y N 8N N S RCA
299 SRI KRISHNA 65 M Y Y N LWMI Y N Y N N 50 120 1.25 1.7 Y Y 16 N MO S LAD
300 NARAYANA 36 M Y Y N AWMI Y Y Y N N 101 90 1 0.98 N N 18 N S S LAD
301 PRABHAKAR 57 M N N N AWMI N N N N N 66.00 100 1.20 1.30 N N 1.00 N N S LAD
302 M.LUNKER 83 M N N Y CSA N N N Y Y 76.00 100 1.00 0.88 N N 8.00 N N S LAD
303 O.MALLAIAH * 56 M N N N AWMI N N Y N Y 67.00 100 1.20 2.25 Y N 9.00 N S S LAD
304 A.LINGAIAH * 57 M N N N CSA N N N N Y 106.00 100 0.85 0.93 N N 4.00 N N D LCX
305 A.BABU 57 M Y N Y CSA N N N N N 66.00 100 1.20 0.72 N N 1.00 CHB N D LCX
306 KAITHA SHANKARI 58 M Y N Y CSA N N Y N N 92.00 100 0.90 0.93 N N 6.00 N S T RCA
307 BOINA POCHAIAH 58 M N N Y CSA N N N N N 35.00 100 2.10 2.18 N N 1.00 N N D LAD
308 RAJAIAH.C 57 M Y Y Y CSA N N N N N 97.00 150 0.86 1.03 N N 4.00 N N D LAD
309 KUMARA SWAMI.B 58 M Y Y Y CSA N N Y N N 97.00 100 0.86 3.09 Y N 8.00 N S S LAD
310 M.RAJAIAH * 58 M N N Y CSA N N N N N 72.00 150 1.12 1.09 N N 1.00 N N S LAD
311 NAGARAJU.A 57 M Y N N CSA N N N N N 82.00 150 1.00 0.91 N N 1.00 N N S OM1
312 D.DAMODAR * 58 M Y N Y CSA N N N N N 119.00 120 0.72 0.77 N N 1.00 N N S LAD
313 J.SAMBHAIAH * 57 M N Y Y AWMI N N N N N 134.00 150 0.70 0.76 N N 4.00 N N S LAD
314 A.RAMBABU 56 M Y Y Y CSA N N N N N 82.00 100 1.00 0.76 N N 4.00 N N T RCA
315 BINGI RAJAIAH 57 M Y Y Y IWMI N N Y N N 106.00 200 0.80 0.91 N N 9.00 N S S RCA
316 T.ANJANAYULU 59 M Y Y Y CSA N N Y N N 94.00 100 0.88 0.89 N N 9.00 N S S LAD
317 P.RAMA RAO 62 M N Y Y IWMI N N Y N Y 38.00 100 1.90 1.04 N N 11.00 N S D LCX/RCA
318 BODDU NARSAIAH * 57 M N Y Y IWMI N N N N Y 112.00 100 0.76 0.84 N N 4.00 N N S PDA
319 R.BHOOMAIAH 58 M N N Y CSA N N N N Y 92.00 100 0.90 0.87 N N 1.00 N N S LAD
320 K.PANDU 58 M N N Y CSA N N N N Y 38.00 100 1.20 1.00 N N 1.00 N N T LAD
321 B.ANAND 57 M N Y Y CSA N N N N Y 126.00 250 0.69 0.70 N N 5.00 N N T LAD
322 K.KRISHNA MURTHY 85 M Y Y Y CSA N N N Y Y 68.00 150 1.10 1.18 N N 14.00 N N LM DVD LM LAD
323 GUDI. SUDHANSHU RE 58 M Y N Y UA N N N N Y 73.00 100 1.00 1.20 N N 4.00 N N LM LM
324 K.LASUMAIAH 58 M Y N Y CSA N N N N Y 39.00 100 1.90 0.82 N N 4.00 N N S LAD
325 NARAYANA TADURI 58 M N Y Y CSA N N N N Y 106.00 280 0.80 0.90 N N 7.00 N N S LAD
326 B.NARSAIAH 58 M Y N Y CSA N N Y N Y 139.00 100 0.68 0.71 N N 8.00 N S D LAD,RCA
327 SISTER MARIA REINE 81 F Y N N UA N N Y Y Y 85.00 100 0.70 0.70 N N 12.00 1 HB S D RCA
328 k.CHANDRA SHEKHAR 68 M Y Y N UA N N N N N 90.00 100 0.89 0.57 N N 4.00 N N D LCX
329 SHANKAR MADDALLA 57 M Y N Y AWMI N N N N N 94.00 100 0.89 0.97 N N 1.00 N N S LAD
330 RAJAIAH.I 57 M N Y Y CSA N N N N N 99.00 150 0.85 0.67 N N 4.00 N N S RCA
331 PRABHAKAR RANTALA 52 M Y Y Y AWMI N N N N N 105.00 100 0.82 0.85 N N 4.00 N N S LAD
332 MOHD HUSSAIN * 55 M N Y Y CSA N N N N N 107.00 100 0.80 0.86 N N 4.00 N N S LAD
333 A.RAJASHEKHAR 70 M N N Y AWMI N N N N N 136.00 150 0.62 1.24 Y N 1.00 N N S RCA
334 GEORGE NICHOLAS 50 M Y Y Y CSA N N Y N N 86.00 100 0.98 0.98 N N 4.00 N S S RCA
335 T.MALADRI * 45 M Y Y Y CSA N N Y N N 70.00 120 1.20 0.84 N N 4.00 N S T LCX
336 J .GANGADHAR 55 M Y N Y CSA N N Y N N 96.00 100 0.80 0.96 N N 1.00 N S S RCA
337 RAMAKRISHNA * 39 M N Y Y CSA N N N N N 143.00 380 0.66 0.57 N N 6.00 N N S LAD
338 LAXMAIAH.D 50 M Y Y Y AWMI N N N N N 101.00 150 0.85 1.04 N N 4.00 N N D LAD,RCA
339 PRABHAKAR RENTALA 53 M Y Y Y AWMI N N N N N 67.00 100 1.20 0.83 N N 4.00 N N S LAD
340 SINGHU BACHAN * 58 M N N Y CSA N N N N N 66.00 100 1.20 0.86 N N 1.00 N N S LAD
341 MALLESH.M 72 M Y Y Y CSA N N N N N 46.00 150 0.60 3.56 Y N 4.00 N N D LAD,RCA
342 MR.VENKATESHWARA 48 M Y Y Y CSA N N Y N N 72.00 120 1.18 1.21 N N 9.00 N S S LAD
343 BONDILA VIJAYA SINGH 58 M Y N Y CSA N N N N N 70.00 100 0.79 0.85 N N 1.00 N N S LAD
344 VEERANNA .B 47 M Y N Y CSA N N N N Y 110.00 110 0.80 1.20 Y N 1.00 N N D LAD,LCX
345 HUSSAIN SAYEED 54 M N Y N CSA N N N N Y 53.00 150 1.46 1.41 N N 7.00 N N D LAD,LCX
346 P.VENKATESHWARLU 56 M Y N Y CSA N N Y N Y 128.00 120 0.68 1.20 Y N 9.00 N S S RCA
347 JAYANTHI.M 45 F Y Y N CSA N N Y N Y 115.00 150 0.60 0.66 N N 11.00 N S S LAD
348 VINOD PRASAD DUBEY 53 M Y Y N CSA N N N N N 90.00 180 0.93 0.97 N N 4.00 N N S LAD
349 B.MALLAIAH 56 M Y Y Y CSA N N N N N 103.00 100 0.82 0.88 N N 4.00 N N S RCA
350 L.RAMDAS 57 M Y N Y CSA N N N N N 106.00 250 0.80 1.34 Y N 4.00 N N S RCA
351 MALLAIAH 56 M N N Y CSA N N Y N Y 122.00 280 0.71 1.99 Y N 10.00 N S S LAD
352 C.DUBBAIAH 56 M Y N Y CSA N N Y N Y 183.00 150 0.50 0.58 N N 12.00 N S S LAD
353 K.BHEEMAIAH 57 M N Y Y CSA N N N N N 130.00 100 0.67 0.69 N N 4.00 N N S LCX
354 MAHMOOD VALI 57 M Y Y N CSA N N N N N 124.00 100 0.70 0.77 N N 4.00 N N S LCX
355 G.VENKATESHWARULU 58 M Y N Y IWMI N N N N N 119.00 120 0.72 0.70 N N 1.00 TRIGEMINY N S LAD
356 G.SHANKARAIAH 50 M Y N Y IWMI N N N N N 96.00 100 0.89 0.82 N N 1.00 N N D RCA
357 E.SARAIAH 58 M N N Y CSA N N N N N 107.00 100 0.79 0.75 N N 1.00 N N D LAD,RCA
358 M.ILLAIAH 59 M Y Y Y CSA N N Y N Y 58.00 150 1.34 1.20 N N 12.00 N S D LAD,LCX
359 RAYALINGU.K 57 M N N Y CSA N N Y N Y 96.00 150 0.89 1.09 N N 9.00 N S S LAD
360 A.PULLAIAH 56 M Y N Y IWMI N N N N Y 174.00 100 1.09 1.10 N N 4.00 N N D RCA
361 B.SATANARAYANA 57 M Y N Y AWMI N N N N N 106.00 100 0.80 0.94 N N 1.00 N N T LAD
362 N.DANAMMA 59 M Y Y N AWMI N N N N N 78.00 100 0.80 0.82 N N 4.00 N N S LAD
363 GORLA GURAVAIAH 59 M N N N CSA N N N N N 92.00 100 0.80 1.60 Y N 1.00 N N D LAD,RCA
364 CHELLA RAJI REDDY 59 M Y N Y CSA N N N N N 121.00 150 0.71 0.84 N N 1.00 N N D LAD,LCX
365 BODDU NARSAIAH 57 M N Y Y UA N N N N N 122.00 100 0.71 0.84 N N 4.00 N N S LAD
366 K.RAJA MOULI 58 M Y N Y CSA N N Y N N 83.00 100 0.98 0.94 N N 6.00 N S D LAD,RCA
367 J.RADHA KRISHNA 57 M Y Y Y CSA N N Y N Y 84.00 100 0.98 0.99 N N 12.00 N S S LAD
368 A.POSHAMALLU 57 M N Y Y CSA N N Y N Y 109.00 100 0.78 0.74 N N 12.00 N MO S LAD
369 V.LINGAIAH 58 M Y N Y CSA N N N N Y 92.00 100 0.90 0.86 N N 4.00 N N S LAD
370 N.MAHARAJU 61 M Y N Y CSA N N N N Y 97.00 100 0.85 1.07 N N 4.00 N,LBBB N D LAD,D1
371 P.BAPANNA 58 M Y N Y CSA N N N N Y 112.00 100 0.76 0.84 N N 4.00 N N D LAD,LCX
372 CHANDRAIAH VANGA 57 M Y Y Y CSA N N Y N N 111.00 120 0.77 0.85 N N 4.00 N MO D LAD,LCX
373 M.ILLAIAH 57 M Y Y Y CSA N N N N N 126.00 100 0.69 0.73 N N 4.00 N N T LCX,RCA
374 P.MOHAMMED FEROZ 58 M Y Y Y CSA N N N N N 50.00 150 1.52 1.54 N N 6.00 N N D LAD,LCX
375 GATTAIAH KAKKERLA 57 M Y N Y CSA N N Y N Y 67.00 200 1.19 1.14 N N 10.00 N MO S LCX
376 MOHAMMED SHOUKA 57 M Y N Y CSA N N N N Y 109.00 200 0.78 1.01 N N 5.00 N N D LAD,RCA
377 N.SAVITHRI 58 F Y N N CSA N N N N N 76.00 100 0.82 2.85 Y N 1.00 N N S LAD
378 VSP RAO 82 M N N N CSA N N N Y N 68.00 200 1.10 1.27 N N 6.00 N N S RCA
379 M.VENKATESHWARLU 52 M Y Y Y CSA N N Y N N 69.00 140 1.18 1.24 N N 9.00 N MO D LM-LCX, RCA

380 D.NIRANJANI 68 M Y N N CSA N N Y N Y 169.00 100 0.40 0.66 N N 9.00 N MO S LAD

381 J.MADHAVA RAO 59 M Y Y N CSA N N N N Y 87.00 200 0.94 0.98 N N 6.00 N,LBBB N S LAD
382 GATTAIAH KAKKERLA 57 M Y N Y CSA N N N N N 73.00 200 1.11 1.18 N N 2.00 N,LBBB N S RCA
383 BALLAM SHANTAIAH 58 M N N Y CSA N N N N N 92.00 110 0.90 1.00 N N 1.00 N N S LAD
384 YALLAIAH .K 58 M Y Y Y CSA N N Y N N 92.00 120 0.90 0.86 N N 9.00 N MO D LAD,RCA
385 NCH NAGESHWAR RAO 65 M N N Y CSA N N Y N Y 90.00 100 0.90 0.82 N N 9.00 N MO S LAD
386 A.RAJA KOMARAIAH 57 M Y Y Y CSA N N N N Y 124.00 130 0.70 0.77 N N 7.00 N N D LCX,RCA
387 GUMMADI RAJAIAH 59 M N N Y CSA N N N N Y 105.00 200 0.80 0.98 N N 5.00 N N D LAD,RCA
388 M.PADMA 59 F N Y N CSA N N N N N 101.00 100 0.64 0.68 N N 4.00 N N S LAD
389 TORREM POSHAM 57 M N N Y CSA N N N N N 110.00 140 0.60 0.72 N N 1.00 N N S RCA
390 K.SURENDER 60 M N N Y CSA N N Y N N 81.00 250 1.00 0.96 N N 7.00 N MO S LAD
391 V.LAXMI NARAYANA 57 M N Y Y CSA N N Y N N 120.00 170 0.82 0.98 N N 9.00 N MO S RCA
392 P.RAMA RAO 55 M N N Y CSA N N N N Y 126.00 100 0.70 1.25 Y N 4.00 N N S RCA
393 SHEKAR REDDY 48 M Y Y Y CSA N N N N N 97.00 150 0.89 0.81 N N 4.00 N N D LAD,RCA
394 CHANDRAMAULI 59 M N Y Y UA N N Y N N 119.00 250 0.72 0.72 N N 10.00 2:1 AV bloc MO S LAD
395 K.SUDHARSHAN RAO 61 M N N Y CSA N N Y N Y 82.00 100 0.99 0.89 N N 9.00 N MO S RCA
396 N.VENKATESHWAR RA 64 M Y Y Y CSA N N N N Y 119.00 280 0.71 0.74 N N 8.00 N N D LCX,RCA
397 AFZAL MOHAMMED 55 M Y N Y CSA N N N N N 124.00 180 0.90 0.77 N N 1.00 N N S LCX
398 RAJU.M 58 M N N Y CSA N N Y N N 123.00 150 0.70 0.77 N N 6.00 N MO S LCX
399 S.MADHU SUDHAN RA 57 M Y N Y CSA N N Y N N 124.00 200 0.70 0.71 N N 7.00 N MO S LAD
400 CHINNA RATTA GANGA 73 F Y N N CSA N N N N N 72.00 120 0.83 0.88 N N 1.00 N N S RCA
401 B.LAXMAIAH 58 M Y Y Y CSA N N N N Y 52.00 200 4.48 1.66 N N 7.00 N N S LAD
402 K.RAMULU 57 M N Y Y CSA N N Y N Y 130.00 180 0.67 0.76 N N 12.00 N MO S LCX
403 Y.PRAKASH 45 M Y N Y CSA N N N N N 61.00 110 1.34 1.16 N N 1.00 N N D LAD,RCA
404 RAVINDER KATHERA 57 M Y Y Y CSA N N N N N 43.00 100 0.76 0.83 N N 4.00 N N D LCX,RCA
405 D.MALLESH 57 M N N Y CSA N N Y N N 44.00 100 0.70 0.71 N N 6.00 N MO D RCA,LAD
406 ANJAIAH * 50 M Y Y Y CSA N N N N N 73.00 100 1.13 1.33 N N 4.00 N N D LAD,RCA
407 J.MURLIDHAR * 56 M Y Y Y CSA N N N N Y 93.00 100 0.90 0.99 N N 4.00 N N D LAD,LCX
408 GANGARAM.R * 57 M Y N Y CSA N N N N N 62.00 100 1.27 1.30 N N 1.00 N N S LAD
409 RAJENDRA .M * 57 M Y Y Y CSA N N Y N Y 148.00 100 0.60 0.68 N N 12.00 N MO D LAD,LCX
410 BINGI RAJAIAH * 57 M Y N Y CSA N N N N N 95.00 100 0.88 0.91 N N 1.00 N N S LAD
411 L.SAMUEL 58 M Y Y Y CSA N N N N N 92.00 100 0.90 0.69 N N 4.00 N N S LAD
412 RAMA KRISHNA * 52 M N N Y CSA N N Y N N 124.00 100 0.71 0.79 N N 5.00 N MO D LCX,RCA
413 VENKATESHWARLU 47 M Y N Y CSA N N N N N 124.00 100 0.27 0.75 N N 1.00 N N S LAD
414 KOMARA BATTINA 67 F N N N CSA N N N N Y 120.00 100 0.70 0.89 N N 4.00 CHB N S LAD
LAX
415 CH.VEERASHAM 65 M N Y Y CSA N N N N Y 85.00 100 0.92 1.00 N N 7.00 N N S LAD
416 P.SHEKAR REDDY 32 M N Y Y CSA N N N N Y 105.00 100 0.89 0.81 N N 7.00 N M S LM LCX
417 J CHANDRAIAH 70 M Y N Y CSA N N N N N 46.00 100 1.59 1.89 N N 3.00 N M S LAD
418 P.YADAMMA 50 F N Y N CSA N N N N N 130.00 120 0.35 0.83 Y N 4.00 N M S LAD
419 J YELLAIAH 54 M N N N CSA N N N N Y 125.00 100 0.70 0.82 N N 4.00 N M D RCA,LAD
420 KUMARA SWAMI.B 68 M N N N CSA N N Y N Y 102.00 100 0.80 1.81 Y N 9.00 N MO S LAD
421 MURALI KRISHNA 51 M N N Y CSA N N N N N 115.00 100 0.76 2.02 Y N 1.00 N M D LAD,LCX
422 B.YADGIRI 68 M N Y Y CSA N N N N N 92.00 150 0.89 0.85 N N 4.00 N M S LAD
423 M.LAXMI * 65 F N Y N CSA N N N N N 44.00 100 1.30 0.75 N N 6.00 N M S LAD
424 K.RAJENDRA REDDY 45 M Y Y N CSA N N N N Y 75.00 250 1.12 1.04 N N 8.00 N M S LAD
425 M LAXMINARAYAN 57 M Y Y Y CSA N N N N Y 87.00 100 0.95 1.11 N N 7.00 N M S RCA
426 T MALLAIH 58 M N N Y CSA N N N N N 106.00 100 0.80 0.73 N N 1.00 N M D LAD,RCA
427 R SARAIAH 58 M Y Y Y CSA N N N N N 82.00 180 1.00 0.80 N N 4.00 N M D LAD,LCX
428 N NARASINGA RAO 65 M N Y N CSA N N N N N 109.00 100 0.76 0.88 N N 4.00 N M D LAD,LCX
429 B SATYANARAYAN 57 M Y N Y CSA N N N N N 106.00 250 0.80 0.87 N N 2.00 2:1 AVB M S LAD
430 MALLAIAH 50 M Y Y N AWMI N N Y N N 33.00 100 2.25 2.02 N N 15.00 N MO S LAD
431 K VENKATA REDDY 68 M Y Y N CSA N N Y N Y 105.00 150 0.78 0.85 N N 12.00 N MO S LAD
432 K SAMBAIAH 57 M N Y N CSA N N N N Y 118.00 150 0.73 0.76 N N 7.00 N M S LAD