Acute Coronary Syndrome

They are manifestations of atherosclerosis.

The onset of thrombosis usually accelerates.

acute, induced by rupture or erosion of a plate
atherosclerotic, with or without vasoconstriction, that
they cause a sudden and critical reduction in flow
sanguine

the clinical expression of a continuous spectrum and

dynamic myocardial ischemia

where

the balance between supply and demand is lost

of oxygen.
 CORONARY RISK FACTORS

HTA DIABETES METABOLIC SYNDROME SMOKING DYSLIPIDEMIAS OTHERS

PATHOPHYSIOLOGY ENDOTHELIAL DYSFUNCTION

Permeability INFLAMMATION THROMBOSIS

LDL cholesterol Oxidation + Procoagulants
Monocytes Immune response Anticoagulants
Lymphocytes Proteolysis
 Stable Thrombus Subocclusive or unstable thrombus
SICA without elevated ST, angina
PATHOPHYSIOLOGY SICA with STelevado
unstable

MAJOR CRITERIA:
• Active inflammation. MINOR CRITERIA
• Superficial calcified nodule.
• Thin cover with a large center
• Brilliant lipid core
lipid
• Intra bleeding
• Endothelial denudation
• Endothelial dysfunction
• Platelet aggregation.
• Positive remodeling
• Cracked plate.
• Stenosis > 90%
 THE CHARACTERISTICS OF CHEST PAIN WITH
SIGNS SYMPTOMS CORONARY PROFILE
Anxiety, Exhaustion
Nausea, Chest pain with exertion
Paleness, Restlessness, Sweating
Syncope or Pre-syncope
Tachycardia if state
adrenergic or IC
Bradycardia and activation of Acute Confusion
parasympathetic
Frequent mild hypotension ACV
Hypertension yes state Worsening of Insufficiency
adrenergic Cardiac
AC: 3rd and 4th Noise
Intense Weakness
Creaking Rales yes
Heart Failure
 DIAGNOSTICS
DIFFERENTIALS

Myocarditis HTP Dissection of the

aorta
Pericarditis TEP
Aneurysm
Tamponade Pulmonary infarction
aorta
cardiac Pneumonia Coarctation
Myopathies Pleurisy aortca
S. tako-tsubo Pneumothorax a ECV
tension
 Thoracic Pain

SICA

WITHOUT ELEVATION OF THE ST WITH ELEVATION OF THE ST

ABNORMALITIES ECG NORMAL O

ST ELEVATION
UNDETERMINED
Persistent ST

Elevation/Descent
Normal troponins
Of the Troponins

IAMEST
IAMSEST Unstable Angina
 SICA WITHOUT ELEVATED ST SICA WITH HIGH ST

Clinical data of unstable angina.

ST elevation of 1mm in 2 contiguous leads
anatomically or 2mm in 2 derivations
Elevation of cardiac enzymes necrosis precordial continuous
myocardial.
Be persistent myocardial necrosis and
persistent elevation of the ST segment they evolve to myocardial infarction with Q wave
dynamic
- changes in the sT segment
changes in the T wave (negativization, pointed appearance)
 Unstable Angina
DEFINITION
Type of ACS defined as a patient whose heart biomarkers do not
they meet criteria for IAM
Accentuated but not total obstruction.

CLINICAL EXPLORATION:
. Normal
. With signs:
affects a large part of VI: diaphoresis, paleness, coldness of skin, sinus tachycardia,
3R or 4R, basal crepitations, hypotension.

Zipes, D.P., Libby, P., Bonow, R. O., Mann, D. L., & Tomaselli, G. F. (Eds.). (2012). Braunwald. Treatise on cardiology: Text of cardiovascular medicine.
Elsevier Health Sciences.
CLINICAL PRESENTATION
. Women: 30-45%.
. Legal age
. BACKGROUND:
stable angina
DM
previous coronary revascularization
extra vascular disease
cardiac

Zipes, D.P., Libby, P., Bonow, R. O., Mann, D. L., & Tomaselli, G. F. (Eds.). (2012). Braunwald. Textbook of cardiology: Cardiovascular medicine.
Elsevier Health Sciences.
ANGINA CLASSIFICATION
UNSTABLE (Canadian
Cardiovascular Society
UNSTABLE ANGINA - BRAUNWALD CRITERIA
Based on the
medical history
presence or
absence of
changes in the ECG and
intensity of the
treatment
antagonistic
 TESTS
NON-INVASIVE:
ECG:
transient descent or elevation
Ischemia and prognosis: >0.1 mV
Prior to the episode:
Decrease ST of 0.05mV
Elevación transitoriaST: riesgo
height of future episodes

Wave T: >0.3mV
Inferolateral inversion
from the symmetrical T
deep with a
Zipes, D.P., Libby, P., Bonow,deviation
R. O., Mann,ofD. L., &
ST segment
Tomaselli, G. F. (Eds.). (2012). Braunwald. Treaty
of cardiology: Text of cardiovascular medicine.
Elsevier Health Sciences.
Continuous EKG monitoring:
Objective: to identify
A. Arrhythmias
B. Recurrent deviations of ST
Stress tests: after 24 hours of stabilization. Without ST alteration
Contraindication: pain at rest, hemodynamic instability, arrhythmia,
Resting problems: perfusion tests, echocardiogram, test of
pharmacological effort

HIGH RISK MARKERS:

EKG: Sign of ischemia, ventricular tachyarrhythmia
Rest or overload: left ventricle dysfunction

Zipes, D.P., Libby, P., Bonow, R. O., Mann, D. L., & Tomaselli, G. F. (Eds.). (2012). Braunwald. Treatise on cardiology: Text of cardiovascular medicine. Elsevier.
Health Sciences.
 Image tests:
. ECIV: broken plates of positive remodeling and areas
of larger plates.
. Angiography in CT: broken plate, low density,
calcium deposition in the form of speckling. With
contrast: Vulnerable plates.
. RMC (sequence T2): allows precise localization
of SCA, acute and chronic IM.
. pulmonary edema

Laboratory tests
Serum lipid group: cholesterol (high density and low density) and triglycerides.
Measured at the time of the initial presentation.
Zipes, D.P., Libby, P., Bonow, R. O., Mann, D. L., & Tomaselli, G. F. (Eds.). (2012). Braunwald. Treatise on cardiology: Text of cardiovascular medicine. Elsevier
Health Sciences.
 PRINZMETAL ANGINA Cause: VASOSPASM, narrowing
coronary arteries caused by contraction of
of

smooth muscle of the vessel wall.

4% of patients with unstable angina

Prevalence: 5 to 1 (Male-Female)
Edad:40-50 años
Factors: Cigarette, alcohol and cocaine

SYMPTOMS: midnight and early morning,

rest
DIAGNOSIS:
coronary angiography
Echocardiograms with dobutamine

ECG: ST segment elevation.

Troponin I: elevated if there is myocardial damage
 ST-Elevation Myocardial Infarction

It is the necrosis of myocardial cells as a consequence of ischemia.

prolonged caused by the reduction of coronary blood flow,
it compromises one or more areas of the myocardium

Evidence of myocardial necrosis: elevation and subsequent decline

of the levels of necrosis markers
In the definition of an IAM,
requires the presence of two of the
following criteria Clinical picture of ischemia: presence of at least one of the
next:
• Symptoms consistent with ischemia.
• Changes in the ECG compatible with acute ischemia
(changes in the ST or T wave or left bundle branch block
• Development of new pathological waves.
• loss of viable tissue in imaging tests.
• Sudden cardiac death, usually
preceded by symptoms compatible with a heart attack
Clinical classification of IM positions
Type 1: Spontaneous myocardial infarction related to ischemia due to a coronary event
primary

Type 2: Secondary IAM to ischemia due to increased O demand2o

decrease in its contribution

Type 3: Unexpected sudden death, including cardiac arrest, frequently.

with suggestive symptoms of myocardial ischemia but that death has
occurred before the blood sampling

Type 4a: IAM associated with percutaneous coronary intervention.

Type 4b: IAM associated with vascular endoprosthesis thrombosis (stent),
demonstrated by angiography or autopsy.
Type 4c: restenosis
Type 5: IAM associated with coronary artery bypass surgery
 Clinic
The pain has anginal characteristics (oppressive), usually lasts more than 20 minutes and does not
responds completely to rest or nitroglycerin.

On rare occasions it may not be present, although it is not uncommon for it to present.
atypical characteristics (diabetics, elderly).

It usually occurs at rest (sometimes during or after exercise) and is more frequent in
first hour of the morning

It is common to be accompanied by vegetative symptoms (cold sweating, nausea,

vomiting, anxiety, and a sense of impending death.

Important data is given in the possibility of irradiation to areas such as the neck,
jaw, shoulder, arm, wrist, or the back

Patient presents a facial expression of suffering

Risk classifications
CLINICAL RESULT
COMPLEMENTARY TESTS:
Electrocardiogram
• NSTEMI (Non-ST Elevation Myocardial Infarction):
In the form of a descent of the ST as
translation of subendocardial injury due to
subtotal occlusion of artery.

Are there sharp changes?

ST segment elevation
Inversion of the T wave
Presence of Q waves
• IAM With ST elevation: Reciprocal depression of the ST segment
Convex elevation shape of the ST Are there signs of previous myocardial infarction?
transmural lesion due to
complete occlusion of coronary artery
We have a previous ECG for comparison.
ELECTROCARDIOGRAPHIC EVOLUTION

A. Normal

B. T hyperacute (high and wide), prolonged QT

C. Supradesnivel of the ST marked with hyperacute T

D. Q wave appears of necrosis, the ST elevation is

younger, the T wave is inverted

E. Pathological Q wave and negative T

Pathological Q wave and positive T wave

ELECTROCARDIOGRAPHIC EVOLUTION

Initially, tall T waves are produced and

sharp drops (hyperacute ischemia) that continue
of ST segment elevation (current of
subepicardial injury) and negativization of the
wave T (deep and symmetric).
 ELECTROCARDIOGRAPHIC EVOLUTION

• Hyperacute phase (4 to 6 hours): Elevation of

ST segment with positive T waves.

• Acute phase (6 hours to 2-3 weeks):

Development of Q waves. Supradesnivel of
ST segment and gradual negation of
wavesT.

• Subacute phase (3rd week onwards): The

ST returns to its baseline level with T waves
. The Q wave may decrease in
amplitude.

• Chronic phase (after 2-3 months): The

persistent pathological Q wave. The T wave
can remain negative, isoelectric or
recover your positivity.
LOCATION OF THE IAM

The elevation of the ST allows for the localization of the area

affected

High lateral lead: I - aVL

Low side car: V5 - V6

Previous face: V2 - V4

Sept: VI - V2

Inferior leads: II – III – aVF

Posterior view: ST depression in V1-

V2, like a mirror image.

Right ventricle: Derivations

specials V3R and V4R
DA: descendente anterior - Cx: circunfleja - CD: coronaria derecha
SUPPLEMENTARY TESTS:
Cardiac Enzymes

CPKy its more specific fraction CPK-MB mass

It rises in 4-6 hours
Disappears in 48 - 72 hours
It has greater specificity (it can be elevated in
situations of non-ischemic myocardial damage

TROPONIN
But more specific
They rise in 4 to 6 hours
• TnI: 7 days
• TnT: 14 days

MYOGLOBIN
Very early elevation (2nd hour)
Little specific
It normalizes in 24 hours
COMPLICATIONS: Mechanical COMPLICATIONS: Electrical

They usually appear after the first 24 hours of the heart attack.
1. Supraventricular arrhythmias:
They are experiencing a sudden destabilization.
• Sinus tachycardia
• The difference must be highlighted:
• Sinus bradycardia
• Aneurysm: it has the normal layers of the
• Atrial fibrillation and flutter
ventricle
• Pseudoaneurysm: contained cardiac rupture
2. Ventricular extrasystoles
through thrombus and incomplete rupture of the
ventricular wall
3. Ventricular arrhythmias
• Ventricular tachycardia
• Ventricular fibrillation
• Torsades de pointes