Hemorheological abnormalities in stable angina and acute coronary syndromes.

摘要

I read with interest the manuscript of Lee et al. [1] in the last issue of Clinical Hemorheology and Microcirculation. In this study the authors found continuous progress in alternations of red blood cell (RBC) aggregation, blood viscosity adjusted to a hematocrit of 40%, plasma viscosity and yield shear stress values from stable angina (SA) to unstable angina (UA) and acute myocardial infarction (AMI). In the same issue of Clinical Hemorheology and Microcirculation Zorino et al. [2] noted that erythrocyte hyperaggregability is associated with a increased risk of AMI in young patients. In reference to this original observations, continuity of hemorheological abnormalities can be extended on patients with lack of tissue reperfusion following successful recanalisation of the infarct-related epicardial artery defined as the achievement of TIMI grade-3 flow. Closely related to fibrinogen concentration, RBC aggregation, plasma viscosity and yield shear stress are the major contributors that cause an increase in vascular resistance especially in the presence of endothelial cell blebbing, white cell infiltration and extravascu-lar edema cased by ischemia and reperfusion injury [3].