ISCHAEMIC HEART DISEASE

ISCHAEMIC HEART DISEASE

• IHD is as an acute or chronic form of cardiac
disability arising from imbalance between
the myocardial supply and demand for
oxygenated blood
• Coronary artery disease is narrowing or
obstruction of the coronary arterial system
leading to myocardial anoxia
• Coronary artery disease (CAD) is used
synonymously with IHD
Etiopathogenesis
1. Coronary atherosclerosis resulting in ‘fixed’
obstruction is the major cause of IHD
2. Some cases of acute coronary episodes are
caused by local aggregates of platelets on
the atheromatous plaque
Etiopathogenesis
3. Sudden changes in chronic plaques such as
plaque haemorrhage, fissuring or ulceration
that results in thrombosis and embolisation
of atheromatous debris
4. Vasospasm with or without atherosclerotic
coronary narrowing may cause angina or
myocardial infarction
Etiopathogenesis cont’d
3. Stenosis of coronary ostia due to syphilitic
aortitis or from aortic atherosclerotic
plaques encroaching on the opening
4. Arteritis i.e. inflammatory involvements of
coronary arteries like in rheumatic arteritis,
polyarteritis nodosa may contribute to
myocardial damage
Etiopathogenesis cont’d
5. Embolism from vegetations of bacterial
endocarditis, fat embolism and air embolism
of coronary circulation may occur
6. Trauma. Contusion of a coronary artery from
penetrating injuries may produce
thrombotic occlusion
Etiopathogenesis cont’d
7. Aneurysms. Extension of dissecting
aneurysm of the aorta into the coronary
artery may produce thrombotic coronary
occlusion
8. Compression of a coronary artery from
outside by a primary or secondary tumour
of the heart may result in coronary
occlusion
 EFFECTS OF MYOCARDIAL
ISCHAEMIA
1. Asymptomatic state
2. Angina pectoris (AP)
3. Acute myocardial infarction (MI)
4. Chronic ischaemic heart disease (CIHD)/
Ischaemic Cardiomyopathy/ Myocardial
fibrosis
5. Sudden cardiac death
 1. ANGINA PECTORIS
• Angina pectoris is a clinical syndrome of IHD
resulting from transient myocardial
ischaemia
• It is characterised by paroxysmal pain in the
substernal region of the chest
 1. ANGINA PECTORIS
• It is aggrevated by an increase in the
demand of the heart and relieved by a
decrease in the work of the heart
• Often, the pain radiates to the left arm, neck,
jaw or right arm
• It is more common in men past 5th decade of
life
Angina Pectoris cont’d
• There are 3 overlapping clinical patterns of
angina pectoris with some differences in
their pathogenesis
1. Stable or typical angina
2. Prinzmetal’s variant angina
3. Unstable or crescendo angina
 STABLE OR TYPICAL ANGINA
• This is the most common pattern
• It is characterised by attacks of pain following
physical exertion or emotional excitement
and is relieved by rest
Stable angina cont’d
• Pathogenesis
• The pathogenesis of condition lies in chronic
stenosing coronary atherosclerosis that
cannot perfuse the myocardium adequately
when the workload on the heart increases
Stable angina cont’d
• Diagnosis
• During the attacks, there is depression of ST
segment in the ECG due to poor perfusion of
the subendocardial region of the left
ventricle but there is no elevation of enzymes
in the blood as there is no irreversible
myocardial injury
 PRINZMETAL’S VARIANT ANGINA
• This angina is characterised by pain at rest and
has no relationship with physical activity
• Pathogenesis
• Pathogenesis of Prinzmetal’s angina is not
known
• It may occur due to sudden vasospasm of a
coronary trunk induced by coronary
atherosclerosis, or may be due to release of
humoral vasoconstrictors by mast cells in the
coronary adventitia
Prinzmetal’s variant angina cont’d
• Diagnosis
• ECG shows ST segment elevation due to
transmural ischaemia.
• The patients respond well to vasodilators like
nitrates, nifedepine
 UNSTABLE OR CRESCENDO ANGINA
• Also referred to as ‘pre-infarction angina’ or
‘acute coronary insufficiency
• It is characterised by more frequent onset of
pain of prolonged duration and occurring
often at rest
• It is thus indicative of an impending acute
myocardial infarction
Unstable angina cont’d
• Diagnosis
• Unstable angina may have non-ST segment
elevation Myocardial Infarction
Unstable angina cont’d
• Pathogenesis
• Stenosing coronary atherosclerosis
• Complicated coronary plaques (e.g.
Superimposed thrombosis, haemorrhage,
rupture, ulceration etc)
• Platelet thrombi over atherosclerotic plaques
• vasospasm of coronary arteries
• More often, the lesions lie in a branch of the
major coronary trunk so that collaterals prevent
infarction
2. ACUTE MYOCARDIAL INFARCTION
(MI)
• Immediately after an acute coronary occlusion,
blood flow ceases in the coronary vessels
beyond the occlusion except for small amounts
of collateral flow from surrounding vessels
• The area of muscle that has either zero flow or
so little flow that it cannot sustain cardiac
muscle function is said to be infarcted
• The overall process is called a myocardial
infarction
Myocardial infarction cont’d
• Myocardial infarction is the most important
and feared consequence of coronary artery
disease
• Many patients die within the first few hours
of the onset
• While remainder suffer from effects of
impaired cardiac function
Pathogenesis of MI
• After onset of the infarction, small amounts of
collateral blood begin to seep into the infarcted
area
• This is combined with progressive dilation of
local blood vessels causing the area to become
overfilled with stagnant blood
• Simultaneously the muscle fibers use the last
little oxygen in the blood, causing the
hemoglobin to become totally de-oxygenated.
Pathogenesis of MI cont’d
• The infarcted area takes on a bluish-brown
colour and the blood vessels of the area appear
to be engorged despite lack of blood flow
• In later stages, the vessel walls become highly
permeable and the local muscle tissue becomes
edematous
• The cardiac muscle cells begin to swell because
of diminished cellular metabolism
• Within a few hours of almost no blood supply,
the cardiac muscle cells die
Acute myocardial infarction cont’d
• A significant factor that may prevent or
diminish the myocardial damage is the
development of collateral circulation through
anastomotic channels over a period of time
• Etiopathogenesis is similar to coronary heart
disease
 3. CHRONIC ISCHAEMIC HEART
DISEASE
• Ischaemic cardiomyopathy or myocardial
fibrosis
• It is found in elderly patients with progressive
IHD with a history of angina and MI
• The patients have gradually developing CHF
due to decompensation over a period of
years.
• Occasionally cardiac arrhythmias or infarction
may supervene and cause death
Etiopathogenesis of CIHD
• Myocardial fibres in a small area undergo slow
degeneration due to myocardial ischaemia.
• These fibres lose their myofibrils but nuclei
remain intact
• These foci are infiltrated by macrophages and
eventually are replaced by proliferating
fibroblasts and collagen
• This explains the focal or diffuse fibrosis in the
myocardium characteristically found in elderly
patients of progressive IHD
 4. SUDDEN CARDIAC DEATH
• This is sudden death within 24 hours of the
onset of cardiac symptoms
Etiology
• The most important cause is coronary
atherosclerosis
1. Coronary vasospasm
2. Calcific aortic stenosis
3. Myocarditis of various types
4. Hypertrophic cardiomyopathy
5. Mitral valve prolapse
6. Endocarditis
7. Hereditary and acquired defects of the
conduction system
Sudden cardiac death cont’d
• Pathogenesis
• The most common causes of death after acute
myocardial infarction are
1. Decreased cardiac output
2. Damming of blood in the pulmonary blood
vessels
3. Death resulting from pulmonary edema
4. Fibrillation of the heart
5. Rupture of the heart
Pathogenesis cont’d
• When some of the cardiac muscle fibres are
not functioning and others are too weak to
contract with great force, the overall
pumping ability of the affected ventricle is
proportionately depressed
Pathogenesis cont’d
• when the normal portions of the ventricular
muscle contract, the ischemic portion of the
muscle instead of contracting is forced
outward by the pressure that develops inside
the ventricle
• Therefore much of the pumping force of the
ventricle is dissipated by bulging of the area
of non functional cardiac muscle
Pathogenesis cont’d
• When the heart becomes incapable of
contracting with sufficient force to pump
enough blood into the peripheral arterial tree,
cardiac failure and death of peripheral tissues
ensue as a result of peripheral ischemia
• This leads to coronary shock, cardiogenic
shock, cardiac shock, or low cardiac output
failure