Abstract
Myocardial infarction refers to the death of myocardium in a region of the heart in which blood flow is insufficient to sustain cell viability. The underlying pathology of acute myocardial infarction in man most commonly is due to atherosclerotic stenosis of the coronary arteries {1}. The exact process by which the coronary blood flow is interrupted, however, is still controversial. It is debatable as to whether thrombus formation is the primary event or if occlusion occurs by some other mechanism such as coronary spasm followed by thrombus formation. Coronary thrombi, especially those overlying ruptured plaque, are frequently found in autopsies of transmural infarctions {1} and recently, De Wood et al. {2} reported that coronary angiography revealed an occluding thrombosis in 86% of acute myocardial infarction patients in the first 6 h following the onset of symptoms. Another aspect of this problem is that coronary spasm commonly occurs just distal to a fixed obstructive lesion {3}. The pathological explanation of this finding may be that the tunica media of the mildly sclerotic artery remains normal or even hypertrophic {4,5} while the severly sclerotic artery has an atrophic tunica media {4,6}. Therefore, the exact sequence of events that bring about a rapid coronary obstruction remain unresolved. Regardless of the sequence of events, recent clinical experience reveals that perfusion can be restored in a large number of these patients by early intervention with thrombolytic agents.
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Miura, T., Yellon, D.M., Downey, J.M. (1989). Myocardial Infarction. In: Sperelakis, N. (eds) Physiology and Pathophysiology of the Heart. Developments in Cardiovascular Medicine, vol 90. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0873-7_47
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