Blood rheology was studied in patients with acute myocardial infarction (AMI) and essential hypertension (EH), and the results were correlated with in vivo hemodynamic functions. Blood viscosity (ηB) was elevated as a result of sequential changes of a number of parameters, including increases in hematocrit, plasma fibrinogen and α2-globulin, an enhancement of red cell aggregation and a reduction of red cell filterability in plasma. Total peripheral resistance (TPR) was elevated upon admission, due to increases in both the vascular hindrance (Zs) and ηB. During recovery, the ηB became normalized; alterations in ηB were accompanied by parallel changes in TPR and an inverse change in plasma volume (PV). In EH patients, the increase in ηB showed a correlation with arterial pressure. For both established and borderline hypertensives, the rheological changes were most prominent in the high renin subgroups. In mild EH, the elevation of ηB was compensated by a decrease in Zs (vasodilation), keeping the TPR essentially normal. In EH with higher arterial pressure, the elevation of ηB was accompanied by a normal Zs without compensatory vasodilation, and hence TPR rose to exacerbate the hypertension. These results suggest that the elevation of ηB may be an early event in the development of EH and that its role must be considered with concurrent cardiovascular functions. In EH there is a significant correlation between left ventricular mass and ηB. Experimental manipulations of the hematocrit level in spontaneously hypertensive rats led to a corresponding variation of arterial pressure. The available data implicate a significant role of ηB in the pathophysiology of AMI and EH. Further interdisciplinary, longitudinal studies are needed tin order to unravel the complicated pathophysiological changes in myocardial infarction and hypertension.
