
doi: 10.3233/ch-2011-1498
pmid: 22214719
The role of viscosity, and of interindividual variations in this parameter, in the pathophysiology of cardiovascular disease remain incompletely understood. Any speculation regarding the possible impact of “hemorheological” therapies is therefore even more complex. In the last years, the debate regarding the relationship between increased viscosity and atherogenesis has been opened again. While the traditional view postulates that an increased blood viscosity has invariably a negative impact on tissue perfusion and therefore should be considered as a risk factor (when not as a true disease), a more recent hypothesis has been formulated based on the observation that small increases in viscosity actually have vasodilatory effects, potentially improving tissue perfusion.
Chest Pain, Adenosine, Platelet Aggregation, Vasodilator Agents, Models, Cardiovascular, Blood Pressure, Coronary Disease, Myocardial Reperfusion Injury, Dipyridamole, Platelet Glycoprotein GPIIb-IIIa Complex, Blood Viscosity, Vasodilation, Oxidative Stress, Hematocrit, Risk Factors, Humans, Endothelium, Vascular, Blood Flow Velocity, Thrombectomy
Chest Pain, Adenosine, Platelet Aggregation, Vasodilator Agents, Models, Cardiovascular, Blood Pressure, Coronary Disease, Myocardial Reperfusion Injury, Dipyridamole, Platelet Glycoprotein GPIIb-IIIa Complex, Blood Viscosity, Vasodilation, Oxidative Stress, Hematocrit, Risk Factors, Humans, Endothelium, Vascular, Blood Flow Velocity, Thrombectomy
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