Ischemic Heart Disease Overview

Study Notes

Ischemic heart disease (IHD) is a group of related syndromes arising from insufficient blood supply to the myocardium relative to its functional demand.
An imbalance exists between myocardial oxygen supply and demand.
Coronary artery diseases (CAD) are a key component of IHD.

Myocardial ischemia can result from vessel occlusion (e.g., coronary atherosclerosis, coronary emboli, myocardial vessel inflammation, vascular spasm).
Increased myocardial demand (e.g., myocardial hypertrophy, increased heart rate), hypoxemia, and systemic hypotension can also cause myocardial ischemia.

IHD is the leading cause of death worldwide, accounting for 11.2% of global deaths in 2011.
Russia, the USA, and Ukraine have the highest numbers of IHD-related deaths.
IHD affects men more frequently than pre-menopausal women.
Incidence is similar in white and black populations.
Specific regional data (e.g., Maiduguri, Ilorin, Benin) show varying prevalence rates and demographics.

Risk factors are multiplicative, not additive.
Risk factors are classified as absolute and relative.
Absolute risk factors include male gender, age, and positive family history.
Relative risk factors include smoking, hypertension, diabetes mellitus, haemostatic factors, physical activity, alcohol, other dietary factors, personality types and social deprivation.

IHD can manifest as one or more overlapping clinical syndromes, including acute myocardial infarction, angina pectoris, chronic ischemic heart disease with heart failure, and sudden cardiac death.

Coronary artery disease is central to IHD pathogenesis.
Atherosclerosis (a progressive inflammatory disease of the arterial wall) is the primary cause of IHD, with lipid-rich deposits (atheromas) forming in the arterial walls.

Atherosclerosis often begins in the second to third decade of life.
Sites of involvement are commonly vessel bifurcations.
Initial stages involve abnormal endothelial function.
Inflammatory cells attach to the endothelium, migrating into the intima.
Oxidized LDL is taken up by macrophages, leading to the formation of foam cells.
Lipid accumulation, smooth muscle migration, and plaque formation lead to asymptomatic atheromatous plaques.

Macrophages and smooth muscle cells are crucial components of established atheromas.
Smooth muscle mediates repair, and macrophages mediate inflammation.
Cytokines released by macrophages contribute to degradation of smooth muscle over the plaque.
Plaque erosion, fissuring, and rupture expose plaque contents to blood, triggering platelet aggregation, thrombosis, and eventual occlusion/embolization.

Myocardial infarction is the death of cardiac muscle due to prolonged ischemia.
10% of infarcts occur in people younger than 40, and 45% in those under 65.
Pathogenesis is due to coronary arterial occlusion (90%), vasospasm, emboli or ischemia with no detectable atherosclerosis or thrombosis.
The resulting occlusion, ischemia, and infarct result in damage to the myocardium.

Gross morphology:
Fresh MIs (< 12 hours) are not obvious macroscopically.
Time dependent Gross findings include pallor (<12 hours), then a red-blue area of hemorrhage(<24 hours), yellow tan with soft neutrophils (3-7 days), and a fibrous scar (>10 days).
Microscopic morphology:
Early findings include wavy myocardial fibers, staining defects, coagulation necrosis, edema, hemorrhage and infiltration with neutrophilic cells.
Progressively, pyknosis of nuclei, marginal contraction bands, and total loss of nuclei and striations are noted.
Macrophages and mononuclear cells infiltrate the area.
Fibrovascular response and prominent granulation tissue eventually become apparent.

IHD is a leading global cause of mortality and morbidity, with overlapping syndromes.
Acute MID is difficult to diagnose at autopsy without special stains.
Lifestyle interventions can reduce incidence.