Ischemic Heart Disease Flashcards
Define Ischemic heart disease.
IHD defined as acute or chronic form of cardiac
disability arising from imbalance between the myocardial supply and demand
for oxygenated blood.
Why is ischemic heart disease also called coronary artery disease?
Since narrowing or obstruction of the coronary arterial
system is the most common cause of myocardial anoxia, the alternate term ‘coronary artery disease (CAD)’ is used synonymously with IHD.
Etiopathogenesis
- Coronary Atherosclerosis (90% of cases)
- Superadded changes in Coronary Atherosclerosis
- Non-Atherosclerotic causes
Coronary Atherosclerosis
DISTRIBUTION
- Atherosclerotic lesions in coronary arteries are distributed in one or more of the three major coronary arterial trunks, the highest incidence being in the anterior descending branch of the left coronary, followed in decreasing frequency, by the right coronary artery and still less in circumflex branch of the left coronary.
LOCATION
- Almost all adults show atherosclerotic plaques scattered throughout the coronary arterial system. However, significant stenotic lesions that may produce chronic myocardial ischaemia show more than 75% (three-fourth) reduction in the cross-sectional area of a coronary artery or its branch.
FIXED ATHEROSCLEROTIC PLAQUES
- The atherosclerotic plaques in the coronaries are more often eccentrically located bulging into the lumen from one side.
- Occasionally, there may be concentric thickening of the wall of the artery.
- Atherosclerosis produces gradual luminal narrowing that may eventually lead to ‘fixed’ coronary obstruction.
Eccentric
Not placed centrally or not having its axis or other part placed centrally.
Superadded changes in Coronary Atherosclerosis.
ACUTE CHANGES IN CHRONIC ATHEROMATOUS PLAQUE
Though chronic fixed obstructions are the most frequent cause of IHD, acute coronary episodes are often precipitated by sudden changes in chronic plaques such as:
- plaque haemorrhage, fissuring, or ulceration that results in thrombosis and embolisation of atheromatous debris.
CORONARY ARTERY THROMBOSIS
- Transmural acute myocardial infarction is often precipitated by partial or complete coronary thrombosis. T
- he initiation of thrombus occurs due to surface ulceration of fixed chronic atheromatous plaque, ultimately causing complete luminal occlusion.
- The lipid core of plaque, in particular, is highly thrombogenic.
LOCAL PLATELET AGGREGATION AND CORONARY ARTERY SPASM
- Some cases of acute coronary episodes are caused by local aggregates of platelets on the atheromatous plaque, short of forming a thrombus.
- The aggregated platelets release vasospasmic mediators such as thromboxane A2 which may probably be responsible for coronary vasospasm in the already atherosclerotic vessel.
Non-Atherosclerotic Causes
These are:
Vasospasm, Stenosis of coronary ostia, Arteritis, Embolism, Thrombotic diseases, Trauma, Aneurysms and Compression.
What are the main clinical forms of IHD?
IHD is a consequence of atherosclerosis and develops when the coronary blood flow is inadequate to meet the needs of the myocardium. Ischemia that results from narrowing or obstruction of coronary arteries may be relative or absolute and will present itself in several clinical conditions:
- Asymptomatic state
- Angina pectoris (AP)
- Acute myocardial infarction (MI)
- Chronic ischaemic heart disease (CIHD)/ Ischaemic cardiomyopathy/ Myocardial fibrosis
- Sudden cardiac death
Angina Pectoris
Stable or typical angina
- This is the most common pattern.
- Stable or typical angina is characterised by attacks of pain following physical exertion or emotional excitement and is relieved by rest.
- The pathogenesis of condition lies in chronic stenosing coronary atherosclerosis that cannot perfuse the myocardium adequately when the workload on the heart increases.
- 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 pattern of angina is characterised by pain at rest and has no relationship with physical activity.
- The exact 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.
- ECG shows ST segment elevation due to transmural ischaemia.
- These patients respond well to vasodilators like nitroglycerin.
Crescendo or Unstable Angina
- Also referred to as ‘pre-infarction angina’ or ‘acute coronary insufficiency’, this is the most serious pattern of angina.
- 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.
- Distinction between unstable angina and acute MI is made by ST segment changes on ECG— acute MI characterised by ST segment elevation while unstable angina may have non-ST segment elevation MI.
- Multiple factors are involved in the pathogenesis of unstable angina which include: stenosing coronary atherosclerosis, complicated coronary plaques (e.g. superimposed thrombosis, haemorrhage, rupture, ulceration etc), platelet thrombi over atherosclerotic plaques and vasospasm of coronary arteries.
Acute Myocardial Infarction
Acute myocardial infarction (MI) is the most important and feared consequence of coronary artery disease. Many patients may die within the first few hours of the onset, while remainder suffer from effects of impaired cardiac function.
Incidence:
In developed countries, acute MI accounts for 10-25% of all deaths. Due to the dominant etiologic role of coronary atherosclerosis in acute MI, the incidence of acute MI correlates well with the incidence of atherosclerosis in a geographic area.
Age:
Acute MI may virtually occur at all ages, though the incidence is higher in the elderly. About 5% of heart attacks occur in young people under the age of 40 years, particularly in those with major risk factors to develop atherosclerosis like hypertension, diabetes mellitus, cigarette smoking and dyslipidaemia with familial hypercholesterolaemia.
Sex:
Males throughout their life are at a significantly higher risk of developing acute MI as compared to females. Women during reproductive period have remarkably low incidence of acute MI, probably due to the protective influence of oestrogen. After menopause, this sex difference gradually declines but the incidence of disease among women never reaches that among men of the same age.
Acute Myocardial Infarction; Etiopathogenesis- Notable features in the development of acute MI are?
- Myocardial Ischemia.
- Role of Platelets: Rupture of an atherosclerotic plaque exposes the subendothelial collagen to platelets which undergo aggregation, activation and release reaction. These events contribute to the build-up of the platelet mass that may give rise to emboli or initiate thrombosis.
- Acute Plaque Rupture: In general, slowly-developing coronary ischaemia from stenosing coronary atherosclerosis of high-grade may not cause acute MI but continue to produce episodes of angina pectoris. But acute complications in coronary atherosclerotic plaques in the form of superimposed coronary thrombosis due to plaque rupture and plaque haemorrhage is frequently encountered in cases of acute MI.
- Non-atherosclerotic causes:
Transmural VS Subendocardial Infarcts
- Transmural (full thickness) infarcts are the most common type seen in 95% cases. Critical coronary narrowing (more than 75% compromised lumen) is of great significance in the causation of such infarcts. Atherosclerotic plaques with superimposed thrombosis and intramural haemorrhage are significant in about 90% cases, and non-atherosclerotic causes in the remaining 10% cases.
- Subendocardial (laminar) infarcts have their genesis in reduced coronary perfusion due to coronary atherosclerosis but without critical stenosis (not necessarily 75% compromised lumen), aortic stenosis or haemorrhagic shock. This is because subendocardial myocardium is normally least well perfused by coronaries and thus is more vulnerable to any reduction in the coronary flow.