Affiliations: [a] Medizinische Universitätsklinik III (Kardiologie), Ruprecht-Karls Universität, Bergheimerstr. 58, 6900 Heidelberg, FRG | [b] Zentrum für Innere Medizin, Abteilung Kardiologie, Justus-Liebig-Universität, Klinikstr. 36, 6300 Gießen, FRG
Note: [*] Own studies were supported by grants from the Wilhelm Sandet-Stiftung, 84.007/1-3, Munchen, and from the Deutsche Forschungsgemeinschaft, SFB 320, Bonn, FRG
Note: [**] A.L. Copley Lecture Awardee
Abstract: The role of blood fluidity in acute coronary syndromes is still unclear. Various studies have revealed hemorheological abnormalities in unstable angina and myocardial infarction. These hemorheological abnormalities are basically independent of risk factor profile and extent of coronary artery lesions. In unstable angina they are related to the risk of myocardial infarction. This suggests that the hemorheological abnormalities have some link to the pathogenesis of the disease. Due to alterations of the atherosclerotic plaque, acute coronary syndromes are characterized by continuous or intermittent impairment of flow. This leads to an intensive interaction of platelets and white blood cells with the vessel wall causing release of interleukins 1 and 6. The resulting expression of acute phase reactants in hepatocytes induces an increase in plasma viscosity and red cell aggregation. Experimental evidence suggests that hemorheological abnormalities may in turn impede nutritional coronary flow. In addition, the increase in red cell aggregation promotes the interaction of other blood formed elements with the vessel wall, which is the prime event of ischemic microvascular injury. Therefore, hemorheological abnormalities in acute coronary syndromes may represent both, cause and consequence of the disease.
