Abstract
Coronary atherosclerosis without acute thrombosis is generally a benign disease that is asymptomatic or presents as chronic stable angina. The great majority of patients can be treated pharmacologically. For those with intractable angina, percutaneous and surgical revascularization are available with high initial success and good long-term prognosis. Acute manifestations of coronary atherosclerosis either unstable angina, acute myocardial infarction, or sudden cardiac death share a common pathophysiologic phenomenon: acute coronary thrombosis. This life threatening complication occurs usually at the site of plaque fissure or rupture. Several studies have shown that plaque rupture plays a key role in the pathophysiology of acute coronary syndromes [1, 2].
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Moreno, P.R., Fallon, J.T. (1997). Inflammation in Acute Coronary Syndromes. In: Schultheiss, HP., Schwimmbeck, P. (eds) The Role of Immune Mechanisms in Cardiovascular Disease. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60463-8_19
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