ISCHAEMIC HEART DISEASE

(IHD)
• De nition: a group of pathophysiologically related syndromes resulting from myocardial
ischemia- an imbalance between the supply (perfusion) and demand of the heart for oxygenated
blood.
• In > 90% of cases, the cause of myocardial ischaemia is reduced blood ow due to obstructive
atherosclerotic lesions in the coronary arteries.
• Thus, IHD is often termed coronary artery disease (CAD) or coronary heart disease.
• 4 ischaemic syndromes:
1. Angina pectoris
2. Myocardial infarction
3. Chronic IHD with heart failure.
4. Sudden cardiac death.
Causes
1. Atherosclerotic narrowing of the coronary arteries with thrombotic occlusion (95-98%)
2. Coronary embolism
3. Coronary ostial stenosis in leutic aortitis
4. Coronary artery spasm
5. Dissecting aortic aneurysm extending back into wall of coronary arteries.
6. Coronary artery vasculitis e.g. Polyarteritis nodosa, temporal arteritis
7. Reduction of oxygen transport of the coronary blood. e.g. Severe anemia, chronic
obstructive airway diseases, congenital heart disease and carbon monoxide poisoning
8. Sudden inadequate perfusion following hypertensive crisis and shock.

ANGINA PECTORIS
• Angina pectoris (literally, chest pain) is characterized by paroxysmal and usually recurrent
attacks of substernal or precordial chest discomfort (constricting, squeezing, choking, or
knifelike) caused by transient (15 seconds to 15 minutes) myocardial ischaemia that falls short
of inducing myocyte necrosis.
• The three overlapping patterns of angina pectoris
1. Stable or typical angina,
2. Prinzmetal variant angina
3. Unstable or crescendo angina.

1. Stable angina
• The most common form, also called typical angina pectoris.
• Caused by an imbalanie in coronary perfusion (due to chronic stenosing coronary
atherosclerosis) relative to myocardial demand.
• Produced by physical activity, emotional excitement or increased cardiac workload.
• Typical angina pectoris - relieved by rest or nitroglycerin, a strong vasodilator.

2. Prinzmetal variant angina

• Uncommon form of episodic, myocardial ischaemia caused by coronary artery spasm.
• Although patients have signi cant coronary atherosclerosis, the anginal attacks are unrelated
to physical activity, heart rate, or blood pressure.
• Responds promptly to vasodilators.

3. Unstable or crescendo angina

• Increasingly frequent pain, often of prolonged duration,
• Pain - precipitated by progressively lower levels of physical activity or occurs at rest.
• Caused by the disruption of an atherosclerotic plaque with superimposed partial (mural)
thrombosis and embolization or vasospasm (or both).
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• Unstable angina serves as a warning that an acute MI may be imminent; (referred to as
preinfarction angina).
• Acute Coronary Syndrome (ACS) = Unstable Angina + Acute Myocardial Infarction

MYOCARDIAL INFARCTION (MI)

DEFINITION:
Usually results from sudden reduction or arrest of a signi cant portion of the coronary ow.
Also known as 'HEART ATTACK'.

INCIDENCE & RISK FACTOR:

1. AGE: any age
Frequency increases with increasing age (40 - 65yr)
Young person - in 1st 3 Decades with major risk factors for atherosclerosis- hypertension, D.M,
cigarette smoking, Hypercholesterolemia
2. SEX: Male greater risk
Female of reproductive age - protected
Post menopausal Female protected by Hormone Replacement Therapy
3. PERSONALITY TYPE: Type A - hard driving, impatient, competitive, compulsive, aggressive -
increased risk
4. ALCOHOL: moderate alcohol consumption - Protective role
Heavy use of Alcohol - increased risk
5. REGULAR EXERCISE: decreased risk

ETIOLOGY & PATHOGENESIS (CAUSES OF M.I)

1. Myocardial infarction is the result of sudden thrombotic occlusion of severely stenosed
coronary artery (75%)
precipitating cause of thrombosis - ulceration, ssure formation or intraplaque haemorrhage.
Major risk factors for atherosclerosis - hypertension, cigarette smoking, DM and hyperlipidemia (+)
2. Coronary embolism
3. Coronary osteal stenosis in leutic aortitis
4. Coronary artery spasm
5. Dissecting aortic aneurysm extending back into wall of coronary arteries.
6. Coronary artery vasculitis e.g. Polyarteritis nodosa, temporal arteritis
7. Reduction of oxygen transport of the coronary blood. e.g. Severe anemia, chronic
obstructive airway diseases, congenital heart disease and carbon monoxide poisoning
8. Sudden inadequate perfusion following hypertensive crisis and shock.

MORPHOLOGY:
GROSS:
Morphological evidence of M.I not possible if death occur with minutes or few hours of infarct.
2 types: 1.TRANSMURAL INFARCT and 2.SUBENDOCARDIAL INFARCT

TRANSMURAL INFARCT
• involves at least portion of L.V & interventricular septum
• full thickness infarction extending from endocardium to epicardium
• coronary artery usually occluded or non occlusive and associated with coronory plaque
rupture, thrombosis.
• if due to vasospasm or lysed thrombus → coronary arteries - appear normal
• Occasionally severe stenosis without infarction - due to collateral.
• S/t severe stenosis or occlusion of right coronary artery causes infarction in the area supplied
by left anterior descending coronary artery due to development of collaterals - known as
PARADOXICAL INFARCT OR INFARCTION AT A DISTANCE
• Transmural infarct involves entire area perfused by occluded coronary artery.
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 SUBENDOCARDLAL INFARCT:
• limited to inner 1/3 of L.V wall & multifocal & cover circumference of LV
• Stenosing coronary atherosclerosis. No superimposed occlusive thrombus
• Extend beyond the distribution of single coronary artery

LOCATION, SIZE & MORPHOLOGY OF AMI DEPEND ON:

1. Location, severity & rate of development of coronary atherosclerotic occlusion
2. Size of area perfused by obstructed vessels
3. Duration of occlusion
4. Metabolic & O2 needs of myocardium
5. Extent of collaterals
6. Presence, site & severity of coronary spasm
7. Other factors - B.P, H.R, rhythm

GROSS
6-12 Hours: inapparent on gross exam:
High lighted by immersion in solution of Triphenyltetrazolium chloride (TTC)
Normal area: brick red color due to presence of dehydrogenase enzyme
infarct area: unstained pale zone
18-24 Hours: pallor or red blue hue due to stagnated trapped blood
24 Hours: infarct - more sharply de ned, yellow softened due to fatly change.
10 Days -2 weeks: rimmed by hyperemic zone of highly vascularized granulation tissues.
Central area - yellow & softened due to fatty change
central necrotic tissue - soft
Maximally soft - 5-8 Days (MYOMALACIA CORDIS)
6 Wks later : brous scar
OVERLYING PERICARDIUM: Fibrinous pericarditis

HISTOLOGY:
4 - 12 Hours : light microscope with routine stain (H &E) - coagulation necrosis not detectable.
1. wavy bres present at periphery of infarct due to loss of normal contractility of necrotic
myocardial cells.
2. myocytolysis or vacuolar degeneration: large vacuoles within the cells containing H2O
within 24 Hours: Coagulation necrosis - cytoplasm - deeply hyaline eosinophilic with loss of
nuclei & cross striation - indistinct.
2-3 Days: acute in ammation in necrotic muscle
5 - 10 Days: macrophage removes the necrotic cell
2 -4 weeks: ingrowth of highly vascularized granulation t/s - become less vascularized & more
brous
End of 6 wks: advanced scar (acellular, avascular collagenous scar)

INFARCT MODIFICATION BY THROMBOLYSIS:

Thrombolytic agents remove thrombus in 70% Reperfusion of myocardium
1. within 15 -20 minutes after onset - prevent all necrosis
2. after longer interval - prevent some necrosis
3. reperfusion of an area of ischaemia - contraction band (Lethally injured muscle)

Complications
Early complications
1. Sudden Cardiac Death: Occur within 1 -2 Hours in 20% of patient.
2. Cardiac arrhythmias & conduction disturbance due to damage to conducting system.
Heart block, sinus bradycardia, sinus tachycardia, ventricular tachycardia, ventricular brillation.
Ventricular brillation - most lethal & impair vent: lling.
3. Cardiogenic shock
occur in large infarct (>40% of L.V)
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70% mortality rate
4. LVF with hypotension, pulmonary congestion & edema due to L.V dysfunction → respiratory
embarrassment, hypostatic Pneumonia
5. CCF → congestive cardiac failure

LATE COMPLICATION:
PERICARDIUM:
6. Fibrinous or brino haemorrhagic pericarditis
occur on 2nd - 3rd day. Localized to region overlying infarct or generalized. may be usually
resolved but occasionally organized brous adhesions
MYOCARDIUM:
7. Cardiac rupture $
◦ Rupture of ventricular free wall: _Hemopericardium & cardiac temponade, occur in 4th - 7th
day due to myomalacia cordis
◦ Rupture of IVS→ Lt to Rt shunt → RHF
◦ Rupture of papillary muscle_ acute onset of severe acute mitral regurgitation
8. Infarct extension: New necrosis adjacent to existing infarct.
9. Infarct expansion: Disproportionate stretching, thinning & dilatation of infarct region.
10. Ventricular aneurysm: results from large infarct with resultant large area of thin scar tissue
that bulge during systole & later aneurysm formation→ rupture & mural thrombus formation.
ENDOCARDIUM:
11. Mural thrombosis & thromboembolism: (15 -40 %)
mural thrombus → systemic embolism & a ect Brain, Kidney, Spleen, GIT, Lower extremities
Prolonged bed rest, impaired circulatory state, stasis & hypercoagulability state→Deep Vein
Thrombosis → Pulmonary embolism
GENERAL:
12. Post MI syndrome (Dressler’s syndrome)
Occur a month after M.I due to autoimmune reaction to necrotic myocardium characterized by
persistent fever, Pericarditis, & pleurisy.
13. Shoulder hands syndrome
14. Recurrence
15. Psychological

Diagnosis
I. CLINICAL FEATURES: /
1. AGE: 55-65yrs, SEX: Male > Female
PREDISPOSING FACTOR - smoking, obesity, D.M, Hypertension
2. Sudden onset of severe substernal or precordial pain which may radiate to Lt Shoulder, arm &
jaw. Pain is severe, constricting, crushing or burning characteristic accompanied by sweating,
nausea, vomiting or breathlessness, not relieved by rest or nitroglyceride. Sometimes, burning
substernal or epigastric discomfort misinterpreted as indigestion or Heart burn.
3. 10 - 15% - asymptomatic
4. 20% - Sudden Cardiac Death within 1 -2 hrs Because of complications such as arrhythmia,
cardiogenic shock, LVF, CCF.

II. LABORATORY INVESTIGATION:

A. ECG changes
1. New Q wave
2. S T elevation
3. T inversion
4. Arrhythmias
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B. Enzyme diagnosis
done because soluble cytoplasmic
cytoplasmic enzymes leak out of fatally damaged myocardial cells.
Ideal markers
Troponins: protein that regulate calcium mediated contraction of cardiac & skeletal muscle
Troponin I ( Tnl) & Troponin T (TnT ) : normally not detectable in circulation.
In acute MI, both Tn I & Tn T levels arise at about the same time as CK - MB & sensitivity is similar
to that of CK - MB, remain elevated for 7 - 10 Days after acute event - allowing the Diagnosis of
Acute MI long after CK - MB levels has returned to normal.
Unchanged levels of CK-MB and troponin over a period of 2 days essentially excludes the
diagnosis of MI.

CHRONIC I. H. D
Often but not exclusively elderly patients who insidiously develop C H F., following ischaemic
myocardial damage. History of angina or MI present or not or may be silent.
Clinically called ISCHAEMIC CARDIOMYOPATHY.

SUDDEN CARDIAC DEATH

DEFINITION:
Unexpected death from cardiac causes within 1 hour after or without the onset of symptoms.