Affiliations: I. Medical Department, City Hospital, Ingolstadt, Germany | Division for Clinical Chemistry, Technical University, Munich, Germany | Division of Angiology, I. Medical Department, Johann Wolfgang Goethe‐University, Frankfurt, Germany
Note: [] Corresponding author: Rupert M. Bauersachs, Department of Angiology, Center of Internal Medicine, Johann Wolfgang Goethe‐University, Theodor‐Stern‐Kai 7, 60590 Frankfurt, Germany. E‐mail: Bauersachs @ em. uni‐frankfurt.de.
Abstract: The objective of the study was to identify the relative importance of erythrocyte flow resistance and aggregation in acute and chronic coronary syndromes. 117 subjects in five groups were studied: (1) 34 patients shortly after acute myocardial infarction (AMI) before reperfusion therapy; (2) 27 patients with unstable and (3) 21 with stable angina pectoris (AP); (4) 14 age‐matched control patients and (5) 21 healthy volunteers. Single erythrocyte transit times were measured using the Cell Transit Analyser. Shear dependent elongation and aggregation was measured by a modified computerized Myrenne aggregometer. Leukocyte count was increased in coronary artery disease (CAD), especially in acute syndromes (mean \pm SD for groups 1–5): 12.2 \pm 4.5; 10.0 \pm 5.4; 8.0 \pm 2.0; 8.0 \pm 3.7; 7.0 \pm 2.0 (pl^{-1})). Platelets, hematocrit, fibrinogen, \alpha_{2}‐macroglobulin did not differ between the groups. Plasma viscosity (mPa s) was elevated in AMI and stable AP: 1.34 \pm 0.10; 1.30 \pm 0.09; 1.32 \pm 0.08; 1.27 \pm 0.07; 1.27 \pm 0.05. Erythrocyte filtrability was not different as was the shear dependent deformation. Aggregation parameters such as \gamma T_{\min} were elevated in CAD: 180 \pm 70; 159 \pm 60; 166 \pm 59; 115 \pm 43; 113 \pm 51 (s^{-1}). Erythrocyte deformability, measured with two independent methods, does not appear to contribute to the pathophysiology of acute coronary syndromes. Erythrocyte aggregation and plasma viscosity were again found increased both in unstable and stable coronary disease. It is unlikely that increased red cell aggregation contributes to emergence of AMI.
