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The morphological correlate of acute coronary syndromes is a ruptured plaque with intraluminal thrombus formation. Furthermore, inflammation, coagulation, fibrinolysis, complement system, and corpuscular elements of the blood are activated. Certain markers as CRP, fibrinogen, plasminogen activator inhibitor or tissue-type plasminogen activator antigen are reported to have a prognostic impact to identify patients at risk. Morphological data provide evidence for the impact of inflammatory mechanisms for the rupture of an unstable plaque and an association of several infections with coronary syndromes was reported. To date it is not known to what extent the various patho-mechanisms influence the rupture of a plaque with the risk of consecutive formation of an occlusive thrombus. It can be assumed that a plaque rupture without critical occlusion of the vessel occurs frequently without symptoms, thus making the evaluation of causal relationships clinically difficult. Future studies should investigate the complex interactions of the different systems by determination of markers of activation in parallel during the acute phase of the disease. Furthermore, experiments should be designed to examine the relative impact of single factors for the pathophysiological process of plaque rupture in acute coronary syndromes including the meaning of infections agents. |
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