Platelet hyperresponsiveness in familial hypercholesterolemia appears to arise from an alteration in the coupling mechanism between thrombin binding and response, allowing platelets to respond at lower receptor occupancy.
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Altered coupling may underlie platelet hyperresponsiveness in familial hypercholesterolemia; leaves open differential lipid effects on thrombotic risk in rare dyslipidemias.
Harmon et al. (1986) studied this question.
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