Article Comprehensive Overview of Myocardial Infarction: Etiology, E...

Area of necrosis of myocardiocytes and formation of scar tissue to cover that area & that infarcted area balloons while every systolic contraction and can be ruptured if the area is considerably extensive & cause sudden death ! But if the infarcted area is clinacally considered small almost nothing may happen !

Sequence of events in MI ::

Erosion /ulceration /rupture of plaque - activate plaque induced thrombogenesis - sudden thrombus formation - sudden occulssion of lumen -Ischaemia and Infarction if event happens acutely

Atheromatous plaque rupture, erosion-thrombosis-sudden thrombus formation-sudden oclussion of lumen-ischaemia and infarction ifevent occurs suddenly.

Atheromatous plaque deposited in wall of artery with due course of time , if plaque get ruptured coagulation cascade ativated - thrombosis of artery - Ischemia - Myocardial Infarction and choice of treatmemt is reperfusion thérapy

The pathophysiological mechanism of CAD:

The underlying pathophysiologic mechanisms for coronary artery disease commence with atherosclerosis. Atherosclerosis is a low-grade inflammatory state of the intima (inner lining) of medium-sized arteries that is accelerated by eminent risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and genetics. In the case of coronary atherosclerosis, this slow progression leads to the gradual thickening of the inner layer of the coronary arteries, which may over time narrow the lumen of the artery to various degrees. (Ambrose and Singh 2015)

Previously considered a cholesterol storage disease, recent studies showed inflammation also contributes to the local, myocardial, and systemic complications of atherosclerosis. When the arterial endothelium encounters certain bacterial products or risk factors as diverse as dyslipidemia, hypertension hyperglycemia, or obesity promotes the sticking of blood leukocytes to the inner surface of the arterial wall. Transmigration of the adherent leukocytes largely depends on the expression of chemoattractant cytokines regulated by signals associated with traditional and emerging risk factors for atherosclerosis. Once it resides in the arterial intima, the blood leukocytes primarily mononuclear phagocytes and T lymphocytes connect with endothelial and smooth muscle cells (SMCs), the endogenous cells of the arterial wall. Key messages shared among the cell types engaged in atherogenesis depend on mediators of inflammation and immunity, including small molecules that include lipid mediators. Recently, protein mediators of inflammation and immunity have gained much attention. During the inflammatory process, SMCs migrate towards intima and endothelial cells secret matrix metalloproteinases (MMPs) in response to various oxidative, hemodynamic, inflammatory, and autoimmune signals. The extracellular matrix (notably proteoglycans) binds with lipoproteins, prolonging their residence in the intima. As the lesion progresses, calcification may then occur through mechanisms similar to those in bone formation. In addition to proliferation, cell death (including apoptosis) commonly occurs in the established atherosclerotic lesion. The death of lipid-laden macrophages can lead to extracellular deposition of tissue factor (TF), some in particulate form. The extracellular lipid that accumulates in the intima can coalesce and form the classic, lipid-rich “necrotic” core of the atherosclerotic plaque. During this course of plaque formation, a patient can be asymptomatic. Patients can be diagnosed at any stage of disease course and with medication symptoms will be stable (Libby and Theroux 2005; Libby and Lee 2000; Geng and Libby 2002).

Main Culprit for MI is atheromatous plaque and initiate thromgenic cascade and lead to ischeamia and Infarction