Ischemic Heart Disease (IHD)

• Cause of Infraction Infarction in the heart is cell death due to insufficient arterial
blood supply for the tissue’s needs.
• Causes
– 95% Coronary artery atheroma
– Rarely: Insufficient blood supply due to other
causes, Shock, Massive LVH or cardiac
hypertrophy
• 3 main coronary arteries.
• Name them?
• Left coronary artery - 1.5cms and gives the
interventricular LAD and the (L) circumflex.
– The LAD supplies the apex, anterior 2/3 of
septum and the anterior wall of the LV.
• Right coronary artery classically the posterior wall
“inferior” in ECG.
– The right coronary artery usually supplies the
posterior of the septum

• In normal hearts or in cases of moderate (20-50%

stenosing) atheroma these are effectively end arteries.
• In abnormal hearts a collateral circulation may develop.
• Therefore paradoxically an acute event
e.g. thrombus complicating coronary atheroma may be
more catastrophic in a seemingly previously well patient.
e.g. STEMI V Non STEMI

• IHD • There are a number of clinical syndromes reflecting

varying pathology
• Angina pectoris
– Stable
– Unstable
• Myocardial infarction
• Chronic ischaemic heart disease

1. Stable Angina • Stable Angina

Usually chest pain caused by exercise and relieved by
rest and– often not clear-cut.
• Reflects “Significant” atheroma:
one vessel > 75% stenosis or 2 > 50% as rule of thumb.
Assessment via angiography. Often if autopsy done see
microscopic myocardial fibrosis.
Angina may be worsened by anaemia or increased
cardiac mass i.e. hypertrophy: therefore may reflect important
non-cardiac disease
 2. Unstable Angina • Unstable Angina
• Stable angina with recent progressively increasing
frequency.
• Precipitated with progressively less effort.
– Often occurs at rest, and tends to be of more
prolonged duration.
• Induced by disruption of an atherosclerotic plaque and
secondary thrombus.
• Increased risk of subsequent acute MI.

3. Prinzmental • Uncommon pattern of angina that occurs at rest and is

angina due to coronary artery spasm e.g. cocaine
• Indicative of transmural ischaemia or significant
coronary atherosclerosis.
• Anginal attacks are unrelated to physical activity, heart
rate, or blood pressure.
• Responds promptly to vasodilators.

• Sudden Cardiac Death • Defined as within an hour of onset of symptoms though

(SCD) often virtually instantaneous. Can arise as a result of :
• Sudden large coronary thrombosis on an atheromatous
plaque
• Secondary to an arrhythmia in chronic ischaemic heart
disease as defined above.
50% dead before arrival in hospital
Mechanism – ventricular Fibrillation.
(3) Coronary arterial spasm e.g. cocaine use

• Myocardial Infarction • Myocardial necrosis due to reduced blood supply:

Usually reflects unrelieved coronary artery occlusion evolving to
tissue death – dynamic process and can be reduced by coronary
reperfusion.
• Certain plaques more likely to thrombose – lipid rich
with fibrous cap cracks
• Of note statins stabilise plaques

Clinical Presentation of MI
• Crushing central chest pain, unrelieved by rest;
accompanied by weakness, sweating, nausea & vomiting
– Radiates commonly to left shoulder and jaw
• May be described as indigestion
• Can be painless - old/diabetes, pain may be atypical
abdominal.
• May be “silent” present as heart failure (esp in elderly)
arrhythmia – confusion – weakness.
• Need a high index of suspicion.
• Describe the Pathogenesis • Coronary atheroma and plaque rupture and subsequent
of MI thrombosis initiates ischaemia – possibly reversible for 6
– 12 hours.
• Necrosis of myocardium begins 30 mins after occlusion
but there is progression from the subendocardial
myocardium through the full thickness of the
myocardium to the pericardial zone. (Transmural
infarct)
• Why is it subendocardial?
• Most untreated episodes Transmural infarction.
• NB Subendocardial (AKA Non ST-elevation MI--
NSTEMI) infarction more likely in incomplete artery
occlusion or may develop in prolonged shock.

Pathogenesis of Myocardial Ischaemia

• Plaque rupture/fissure
• Exposure of lipid, smooth muscle foam cells
• Thrombin generation and fibrin platelet aggregates
• Intra coronary artery thrombus
• Ischaemia or infarction

• Signs of cardiac failure • Vital Signs:

– HR
– BP
– RR
– Sats
• Cardiovascular Examination:
• Signs of right heart failure
– Raised JVP
– Bilateral Lower limb oedema
– Hepatomegaly and ascites if severe
• Signs of left heart failure
• Low BP
• Weak thready pulse
• Bibasal creps/rales on auscultation
• Cold peripheries
• Cardiogenic shock
• Signs of Mechanical Complications:
– Murmurs: VSD, MR

• Dx MI • Clinical
• ECG (EKG): quick, easy and gives information about site
and vessel involved as well as information about
arrhythmias.
• Lab Evaluation : Troponin-I (TNI) and Troponin used
most commonly.
 • Also MB fraction of creatine kinase (enzyme) cardiac
specific structural proteins

Troponin 2 advantages
(1) More specific.
(2) Stays elevated for 7-10 days.
Enzyme levels give some idea of extent of infarct, latter
depending on location of obstruction, significance of vessel,
degree of myocardial hypertrophy and presence of a collateral
coronary circulation.
Where do troponins come from?

Other conditions associated with raised troponins (any cause of

myocardial necrosis)
• Cardiac surgery
• Cardiac contusion
• Myocarditis
• HOCM
• Cardiomyopathy
• Chemotherapy
i.e. Troponins are a marker of all heart muscle cell necrosis

Morphological changes of MI: think of necrosis,

inflammation and wound healing

Think of lectures on inflammation and repair and wound healing.

• Day 1: Myocardium
Coagulation necrosis with hypereosinophilia and wavy
fibres. Dead vessels – haemorrhage.
Macroscopically - Dark Red Firm
 • Day 2 – 7:
Beside necrotic area – inflammation – neutrophils and
oedema. If marked can get fever and raised WCC (bad
prognosis).
Macroscopically – Soft yellowish/tan tissue.

• Day 7 – 14:
Ongoing repair process with resorption of dead tissue
and granulation tissue at edges.
Macro – depressed area with red edges.
• Week 2-8:
Evolving fibrosis and decreasing vascularity.
Macro – grey white tissue
• Week 8:
Dense fibrosis – depressed thinned myocardium and
scar.
Why is the myocardium thinned??

• Explain the Acute

Coronary Syndromes;

ACS: Signs and Symptoms

The cardinal symptom of critically decreased blood flow to the
heart is
chest pain, experienced as tightness around or over the chest
radiating to the left arm and the left angle of the jaw.
diaphoresis (sweating), nausea and vomiting, as well as
shortness of breath. palpitations, anxiety
STEMI
• May be no collateral circulation.
• May be reversible if achieve reperfusion (PCI)
• PCI percutaneous coronary intervention and
thrombolysis

NON STEMI
• Often bad coronary atheroma
• Still a lumen in coronary artery
• Often good collaterals
• Less likely sudden death
• PCI not as urgent
• Describe the Pathology Of
MI– Macroscopic &
Microscopic

Microscopic features of myocardial infarction and its repair.

One-day-old infarct showing coagulative necrosis along with
wavy fibers (elongated and narrow), compared with adjacent
normal fibers (at right). Widened spaces between the dead
fibers contain edema fluid and scattered neutrophils.

Necrotic myocardium with polymorphs

Microscopic features of myocardial infarction and its repair.

Granulation tissue characterized by loose collagen and abundant
capillaries.
 Microscopic features of myocardial infarction and its repair.
• Important point
Well-healed myocardial infarct with replacement of the necrotic
fibers by dense collagenous scar. A few residual cardiac muscle
cells are present

• The cause of an MI is almost always coronary artery

ischaemia/occlusion due to thrombus occurring
following rupture of an atheromatous plaque leading to
partial or complete occlusion of the artery
• Evaluation of the heart at autopsy includes
• Assessment of
– coronary arteries
– myocardium

Rare causes of coronary occlusion

Vasculitis
• Thrombus due to hypercoagulability
• Vasospasm eg Cocaine or other drugs
• Trauma
• Almost never emboli
• Can any other condition of the heart predispose to an
MI?

Massive hypertrophy as more muscle mass to be oxygenated

• Complications of an MI
• Sudden death What causes this?
• Arrhythmias Within 48 hours usually (posterior MI
usually)
• Left ventricular failure and pulmonary oedema
• Cardiogenic shock
• Ventricular rupture and haemopericardium (After 4
days)
• Chordae tendineae/papillary muscle rupture
• Aneurysm formation and +/- emboli
• Pericarditis (acute or chronic) and Dressler’s syndrome
A) Sudden Death in MI
• Arrhythmias eg Ventricular fibrillation
– Esp in posterior/inferior MI (on ECG)
• Cardiac rupture and Haemopericardium
• Ie Cardiac Tamponade

B) Myocardial cell death causes pump failure which leads

to Left ventricular failure (LVF)
• Signs of LVF:Mild: sinus tachycardia but normal BP and
good tissue perfusion
• Moderate: dyspnoea with clinical/radiological evidence
of pulmonary oedema.
• Severe=Cardiogenic shock hypotension, poor tissue
perfusion and markedly decreased ejection fraction on
ECHO
• What is the ejection fraction?
• What is pulmonary oedema?

C) Pulmonary oedema
• Pulmonary oedema is fluid (transudate) in the alveolar
spaces.
• Due to left atrial or left ventricular failure which causes
pulmonary venous hypertension
• Increased hydrostatic pressure in pulmonary capillaries
• Pulmonary oedema (fluid in alveolar spaces)
• Dyspnoea
• Why does the patient have dyspnoea?
• Why does the patient have peripheral oedema in RVF?

D) Cardiogenic shock
• Cardiogenic shock is due to poor cardiac output due to
poor muscle pump or/and arrhythmia

E) Pump Failure
• May be spectrum from mild left ventricular failure to
intractable hypotension known as Cardiogenic Shock :
very poor outlook.

F) NB
• Pump problems are particularly associated with anterior
MI
• Conduction difficulties with posterior MI.
• Combination of both suggests very extensive damage
and ominous prognosis.

G) Muscle Rupture post MI

• If through free wall (usually after 4 days)-
haemopericardium.
• If septum – ventricular septal defect.
 • Papillary muscles - acute valve dysfunction – intractable
heart failure.
• Why? Valve won’t close

• Later problems include weakening of the area of

scarring leading to a Ventricular Aneurysm, increasing
risk of chronic heart failure, arrhythmias and mural
thrombosis.
• Mural Thrombosis in aneurysm sac → systemic emboli.
• Dressler’s syndrome

Summary Complications of MI
• Sudden death What causes this?
• Arrhythmias Within 48 hours usually (posterior MI
usually)
• Left ventricular failure and pulmonary oedema
• Cardiogenic shock
• Ventricular rupture and haemopericardium (After 4
days)
• Chordae tendineae/papillary muscle rupture
• Aneurysm formation and +/- emboli
• Pericarditis (acute or chronic) and Dressler’s syndrome

Summary :
Chronic Ischemic Heart Disease
May be due to chronic angina or past myocardial infarction.
Clinically – progressive heart failure
Pathology – usually big heart, with combination of hypertrophy, dilatation, narrowed coronaries and
myocardial fibrosis.
Summary – crucial topic – primary prevention vital.
Eg non invasive coronary imaging – statin treatment, angioplasty and improvements in heart failure
management.
Perhaps heart transplant in the future

Heart is a pump, understand these concepts

• Pump pumps fluid out of 1 system into another (venous blood → lungs → aorta)
• If the left Ventricle Outflow eg aortic stenosis is narrowed
– Pump has to work harder
 • If Fails – decreased cardiac output – LVF, myocardial ischaemia exacerbates
the situation
• Obstruction to fluid coming into left ventricle eh mitral stenosis→ pulmonary
venous congestion and pulmonary oedema and RVF

• Elevated JVP
• Cause
• Due to obstruction to return of venous blood to the right side of the heart
• Causes
– Right ventricular failure
– Pericardial effusion
– Mass obstructing SVC e.g. lymphoma

• Bilateral ankle oedema

• Failure of venous return usually due to right ventricular failure