[Atherothrombosis and inflammation].
Alterations of coagulation, fibrinolysis, platelets and low grade inflammation are causal pathophysiological factors in atherosclerosis. Considerable activation of several involved pathways occurs during the acute progression of atherosclerotic lesions, which is characterized by an occluding thrombus, and local and systemic inflammatory reactions as in patients with acute coronary syndromes. These patients become clinically compromised due to the reduction in coronary flow. Furthermore, a frequent occurrence of non-occluding thrombi may be assumed as a progression factor in atherosclerotic diseases. Both the extrinsic and the intrinsic pathway of coagulation are involved, resulting in a hypercoagulative state. Furthermore, an inflammatory acute phase reaction occurs in addition to the activation of several other inflammatory pathways in patients with unstable angina pectoris or acute myocardial infarction. Exposure of tissue factor by the ruptured plaque together with a systemic hypercoagulative state, local and systemic inflammation as well as stimulated platelets and endothelial dysfunction are involved in the pathophysiology of acute coronary syndromes. In the following paper the current knowledge on activation of these pathways and on the various complex interactions is discussed.
Hoffmeister
H M
HM
Medizinische Universitätsklinik Abteilung Innere Medizin III Otfried-Müller-Strasse 10 72076 Tübingen, Germany.
D003324:Coronary Artery Disease / Q000503:physiopathology*; D003328:Coronary Thrombosis / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology; D005342:Fibrinolysis / Q000502:physiology; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D009203:Myocardial Infarction / Q000503:physiopathology; D015539:Platelet Activation / Q000502:physiology; D018746:Systemic Inflammatory Response Syndrome / Q000503:physiopathology*
D018836:Inflammation Mediators