Etiology of Myocardial Infarction
Atherosclerosis is the disease primarily responsible for most acute coronary syndrome (ACS) cases. Approximately 90% of myocardial infarctions result from an acute thrombus that obstructs an atherosclerotic coronary artery. Plaque rupture and erosion are considered to be the major triggers for coronary thrombosis. Following plaque erosion or rupture, platelet activation and aggregation, coagulation pathway activation, and endothelial vasoconstriction occur, leading to coronary thrombosis and occlusion.
Within the coronary vasculature, flow dynamics and endothelial shear stress are implicated in the pathogenesis of vulnerable plaque formation. Evidence indicates that in numerous cases, culprit lesions are stenoses of less than 70% and are located proximally within the coronary tree. Coronary atherosclerosis is especially prominent near branching points of vessels. Culprit lesions that are particularly prone to rupture are atheromas containing abundant macrophages, a large lipid-rich core surrounded by a thinned fibrous cap.
Non-modifiable risk factors for atherosclerosis include the following:
• Age
• Sex
• Family history of premature coronary heart disease
• Male-pattern baldness
In addition, myocardial infarction can result from hypoxia due to carbon monoxide poisoning or acute pulmonary disorders. Infarcts due to pulmonary disease usually occur when demand on the myocardium dramatically increases relative to the available blood supply.