Abstract
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Coronary atherosclerosis is the dominant underlying cause of coronary artery disease (CAD) although nonatherosclerotic types of coronary (ischemic) heart disease do occur.
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Vulnerable coronary plaques usually have thin fibrous capsules and are prone to erosion, septum and thrombosis leading to acute myocardial ischemia.
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The clinical spectrum of CAD includes angina pectoris, myocardial infarction (MI), sudden cardiac death and chronic coronary heart disease. Fallowing coronary occlusion, irreversible myocardial ischemic injury beginner within 20–30 minutes in the subendocardium, and MI then progresses over 3 or more hours in a wavefront pattern through the myocardial bed-at-risk. MI is produced by ischemic myocardial cell death mediated by the distinction pathological processes of oncosis and apoptosis.
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The myocardium can be preconditioned resist the progression of MI by prior brief periods of reversible myocardial ischemic (myocardial preconditioning).
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The consequences to the myocardium of coronary reperfusion include reperfusion injury, salvage of myocardium, stumming and hibernation.
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Major cleternuinants of the prognosis of CAD are MI size and the quality of remodeling of the remaining visable myocardium.
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Distinctive pathobiological features are seen with established treatments for CAD, including coronary angioplasty and coronary artery surgery, and new approaches, including gene therapy and stem cell therapy, are under retina investigation.
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Maximilian Buja, L., McAllister, H.A. (2007). Coronary Artery Disease: Pathologic Anatomy and Pathogenesis. In: Willerson, J.T., Wellens, H.J.J., Cohn, J.N., Holmes, D.R. (eds) Cardiovascular Medicine. Springer, London. https://doi.org/10.1007/978-1-84628-715-2_25
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