Why the study?
Do patients with chronic stable angina and coronary artery disease have abnormal blood rheology compared to normal controls?
Do patients with chronic stable angina and coronary artery disease have abnormal blood rheology compared to normal controls?
Patients with stable angina exhibit significant rheologic abnormalities, including increased blood viscosity and red cell aggregation, which may contribute to disturbed blood flow and an enhanced tendency for coronary arterial thrombosis.
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Rheologic abnormalities may promote thrombosis in stable angina; leaves open whether viscosity modification improves outcomes.
We investigated several rheologic variables in 17 patients (11 men, six women, mean age = 52.1 +/- 9.8 years) with chronic stable angina. None took any medication except for sublingual nitroglycerin for 2 weeks before the study, and all had angiographically proven coronary artery disease with no history of myocardial infarction. Rheologic measurements included hematocrit, whole blood and plasma viscosity (750 and 1500 sec-1), degree of red cell aggregation via the zeta sedimentation ratio, and the extent and rate of red cell aggregation after stasis (Myrenne aggregometer). Compared with normal control donors, salient observations in the patients as a group included: a small (6%) but significant increase in hematocrit, a significant elevation in plasma viscosity (9%), significant increases in whole blood viscosity at both shear rates (14% and 16%), significant increases in the degree (12%), the extent (41%), and the rate (28% faster time constant) of red cell aggregation, an elevated alpha 2 level (15% increase) and a significantly increased fibrinogen concentration (25% increase), both of which correlated with the enhanced red cell aggregation. Rheologic abnormalities were evident when patients with disease in either one vessel or two to three vessels were compared with controls, but differences between these subgroups of patients were not significant. We conclude that patients with angina have rheologic abnormalities that are compatible with disturbed blood flow and an enhanced tendency for coronary arterial thrombosis.
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Rainer et al. (1987) studied this question.
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