Calcific aortic stenosis (AS) is the most common form of valvular heart disease in Europe and North
America. It is a progressive disease with a prolonged period of asymptomatic latency which eventually leads to
critical left ventricular outflow tract obstruction necessitating surgical replacement of the valve. Statins are lipidlowering
drugs with a robust evidence base demonstrating clinical benefit in atherosclerotic coronary artery disease.
There has therefore been significant interest in the potential benefit of statins in AS. Initial animal, retrospective
and non-randomized prospective studies suggested a beneficial effect of statins in AS. However, the
outcomes of 3 major randomized controlled clinical trials consistently failed to demonstrate any significant benefit
of lipid-lowering therapy on progression or clinical outcomes in AS. Consequently, statin therapy should not
be recommended if the sole purpose is prevention of AS progression and there is no other indication for lipidlowering
therapy. However, recent data have suggested that lipoprotein(a) (Lp(a)) may play a previously unknown
but critical role in the progression of AS. Lp(a) is not significantly modified by statin therapy and there is
therefore significant emerging interest in targeted reduction of Lp(a) with novel therapeutic agents such as
PCSK9 inhibitors and antisense oligonucleotides.
Keywords: Aortic stenosis, statins, HMG-CoA reductase, lipids, valvular heart disease, lipid-lowering drugs.
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