Major cause of stroke, coronary artery disease, peripheral artery disease and aortic aneurysm.

Hardening of vessel due to loss of intimal and medial layer elasticity.

A major byproduct of a sedentary lifestyle and adverse dietary habits.

Atherosclerotic lesions typically form over years to decades, making it one of the longest incubation periods among human diseases.

Atherosclerosis is initiated decades prior to a clinical event.

Prevalence in young soldiers is about 50% with one or more traditional risk factors for coronary artery disease.

Total-body computerized tomograms of mummies found 1/3 of preindustrial populations, including preagricultural hunter-gatherers and evidence of atherosclerosis.

Coronary atherosclerosis multifactorial with endothelial injury and dysfunction with adhesion and migration of leukocytes from the circulation to arterial intima with migration of smooth muscle cells from the media to the intima initiating the formation of atherosclerotic plaque.

Progressive stenosis narrows the lumen of an atherosclerotic coronary artery such that small platelet thrombus could occlude the vessel completely and an occlusive process complicating a high-grade stenosis could arrest bloodflow causing a ST segment elevation myocardial infarction, while acute coronary syndromes without is a ST segment elevation would result from incomplete or transient obstruction of flow in the involved coronary artery at site of critical stenosis.

Two types of thrombi form after plaque rupture: a platelet rich clot (white clot) that forms in areas of high stress and only partly occludes the artery, or a fibrin rich clot (red clot) the result of an activated coagulation cascade and decreased flow in the artery.

Red clots are frequently superimposed on white clot and results in complete occlusion of the vessel.

Only white clots are found in unstable angina and non-STEMI, and STEMI associated with red clots (Sherman CT, DeWood MA).

Thrombotic coronary occlusion after rupture of a lipid-rich atheromatous plaque with only a thin layer of intima covering the thin cap fibroatheroma is the most common cause of MI and death from cardiac causes

When plaques of cholesterol, lipids and cellular debris form in the inner layers of the artery flexibility of the vessel is lost.

Infiltrates the arterial wall long before symptomatic obstruction of blood flow occurs.

Lesions are asymmetric thickenings of the intima and consist of cells, connective tissue, lipids and debris.

Inflammatory and immune cells are a major part of an atheroma with the remaining tissue endothelial and smooth muscle cells.

Adipose tissue in the epicardium is normally a source of cardiovascular development, regeneration, and nourishment, but when activated by systemic inflammation it becomes a source of pro inflammatory adipocytokines including leptin, tumor necrosis  factor, Interleukin 1-beta and interleukin-6 which are transmitted directly to underlying tissues.
If abnormal epicardial fat adjoins coronary vessels, it results in perivascular inflammation and accelerated coronary atherosclerosis.
If the biologic abnormality in the pericardium surrounds the left atrium it results in electro anatomical fragmentation and structured remodeling, leading to atrial myopathy which manifested clinical atrial fibrillation.
Dysfunctional epicardial adipose tissue abutting the left ventricle, results in a ventricle myopathy, which is characterized by impaired cardiac dispensability leading to heart failure with preserved ejection fraction.

Five factors are predictive and include hypertension, serum cholesterol greater than 297 mg/100mL, glucose intolerance, LVH and smoking.

Nearly three-fourths of deaths are related to atherosclerosis.

Majority of lesions associated with calcification of the arterial wall.

0.1 mm Increase in carotid intima-media thickness is associated with 18% and 15% increased risk for stroke and myocardial infarction, respectively.

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