Abstract
The paradoxical occurrence of a high risk of stroke in some populations at low risk for coronary heart disease has long been known. Recently, evidence has appeared linking the paradoxical risk to population-based differences in diet, serum cholesterol, and alcohol intake. However, the pathophysiological mechanism of action that would explain this paradox is unlikely to be atherosclerosis alone. Several recent cross-sectional and prospective population studies have shown that hemostatic factors vary between populations in a manner consistent with the paradox. Studies have also shown that certain hemostatic factors are independent predictors of risk of coronary heart disease, ischemic stroke, and, probably, hemorrhagic stroke. Risk factors that enhance thrombosis and reduce fibrinolysis are capable of explaining the paradoxical occurrence of the incidence of coronary heart disease and stroke in certain populations.