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Samuel Vaisrub, MD

JAMA. 1975;234(4):417.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Heightened platelet sensitivity to aggregating agents— adenosine diphosphate (ADP), epinephrine, collagen—has been reported in some diseases that are not primarily disorders of hemostasis, but that often predispose to abnormal thrombotic complications. Is the increased platelet aggregation incidental, or is it a factor in this predisposition?

Thirty years ago, Duguid¹ suggested that continual laying down of microthrombi on the arterial intima is a fundamental cause of atherosclerosis, but this hypothesis still awaits definitive confirmation. Sano et al² demonstrated an eightfold increase in platelet sensitivity to the aggregating action of ADP in 12 patients during acute myocardial infarction and stroke. Increased sensitivity to platelet aggregants has been noted also as late as 16 months³ after myocardial infarction, as well as in angina without infarction.⁴ And, curiously, the enhanced sensitivity has been observed in hyperbetalipoproteinemia⁵—a genetic trait conducive to atherosclerosis.

Interpretation of these observations is somewhat complicated . . . [Full Text PDF of this Article]

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