Heartbeat: therapeutic targets for prevention of calcific aortic valve stenosis

Current management of calcific aortic valve stenosis (CAVS) is limited to palliation of end-stage disease with valve replacement to relieve left ventricular outflow obstruction. Rather than treating the mechanical consequences of severe CAVS, identification of causal disease pathways at the tissue level might lead to medical therapies that could actually prevent or delay the pathological changes in the valve leaflets. Serum levels of lipoprotein-associated phospholipase A2 (Lp-PLA2) activity are associated with the presence of CAVS; however, it has been unclear whether this association is due to a cause–effect relationship. In this issue of Heart, Perrot and colleagues1 used genetic association studies from eight cohorts to show that CAVS was not associated with any of four single nucleotide polymorphisms that are associated with Lp-PLA2 activity or mass. These findings suggest that although Lp-PLA2 activity is a biomarker for CAVS unfortunately, it is unlikely to be a therapeutic target...

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