Abstract
Despite significant advances in understanding the pathophysiology of acute coronary insufficiency, myocardial infarction remains a serious health problem for Western society and accounts for approximately one fourth of all deaths in the United States. The most common underlying mechanism is coronary thrombosis superimposed on an atherosclerotic plaque which has been disrupted. Non atherosclerotic mechanisms of infarction account for a minority of clinical events and are of varied etiology (Table 1) (1). Conceptually, these can be considered as those disease processes which lead to luminal obstruction with subsequent ischemia and those which do not involve intrinsic compromise of the lumen. The former group includes entities such as vasculitis and storage disorders which cause diffuse or focal obstruction, while the latter group includes sudden coronary embolus, myocardial oxygen supply-demand mismatch without obstructive coronary disease, hyperviscosity and hypercoagulability states, and trauma. The emphasis of this chapter will be on the events preceding and following the rupture of an atherosclerotic coronary plaque.
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© 1994 Springer Science+Business Media New York
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Ferrell, M., Fuster, V. (1994). Mechanisms of Acute Myocardial Infarction. In: Becker, R.C. (eds) The Modern Era of Coronary Thrombolysis. Developments in Cardiovascular Medicine, vol 160. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2618-6_1
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DOI: https://doi.org/10.1007/978-1-4615-2618-6_1
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