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To the Editor: Dr Bodary and colleagues¹ found that leptin contributed to arterial thrombosis following photochemical vascular injury in mice. Recently, Konstantinides et al² reported similar results with the ferric chloride model of carotid artery injury. A common factor of these findings may be the ability of leptin to enhance platelet aggregation through the stimulation of the long form of its receptor on the platelet membrane.^2-4

The findings of Bodary et al provide further support to the hypothesis that a direct adipocyte-platelet interaction contributes to the excess risk of cardiovascular events in obesity. However, Bodary et al state that "these findings raise the possibility that therapeutic strategies aimed at reducing plasma leptin levels may reduce cardiovascular events." Although they acknowledge the potential adverse effects of a drug-induced leptin reduction, they invoke "a strategy specifically targeting the leptin receptor on the platelet."

We think that studies in this field are still . . . [Full Text of this Article]