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.