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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.

Are hemostatic factors responsible for the paradoxical risk factors for coronary heart disease and stroke?