Antiphospholipid antibodies may increase heart disease risk in healthy people umich jamanetworkopen
Vascular endothelial dysfunction has also been suggested to play an essential role in aPL-mediated CVD. aPL can activate endothelial cells through ApoER2, impairing nitric oxide production and causing a proadhesive and proinflammatory endothelial phenotype.These mechanisms—focused mainly on the IgG isotype of criteria aPL—have primarily been studied in the context of systemic autoimmune diseases. The potential role of noncriteria aPL in promoting CVD in a healthy population has not been studied.
Furthermore, we could not evaluate potential associations between circulating aPL and some well-recognized APS clinical manifestations, such as venous thrombosis and pregnancy morbidity, as DHS was designed to capture only ASCVD events. Acknowledging those limitations, we emphasize that the goal of our study was not to classify APS, but rather to ask whether the presence of some aPL by solid-phase assays at a single time point in the general population might associate with future ASCVD risk.
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