الفهرس 
Acute myocardial infarctionOnly 14 pages are availabe for public view
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Abstract
Atherosclerosis, which involves the formation of fatty deposits or plaques in the inner wall of arteries, is now considered in many ways an inflammatory disorder of the blood vessels.
Inflammation not only affects the atherosclerotic phase of heart disease, but also the rupturing of plaques which can then travel and interfere with blood flow, causing acute myocardial infarction.
Many inflammatory markers are involved in the mechanism of plaque formation and rupture. One of these inflammatory markers, C- reactive protein (CRP), is shown to have prognostic significance, in both short and long term in acute myocardial infarction. Additionally, it has been suggested that elevated CRP levels after acute myocardial infarction is correlated with infarct size, and has predictive value for post-MI complications such as left ventricular failure or cardiac rupture.
White blood cells are involved in ischemic cardiovascular disease particularly in its acute phases by increased expression of neutrophil and monocyte adhesion molecules and other markers of polymorphonuclear and monocyte activation in peripheral blood. Recently, neutrophil invasion of atherosclerotic plaque has been described and has been shown in the culprit clinical plaques in patients with acute myocardial infarction and can facilitate plaque disruption. In addition together with platelets, they can aggregate when stimulated, contribute to the plugging of micro vessels and promote myocardial infarction.