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Published on: May 21, 2017
Statins in Aortic Stenosis
Karl Norrington1, Emmanuel Androulakis2, Evangelos Oikonomou3
1Cardiology Department, Barts Health NHS Trust, London,United Kingdom.
Insights
Statins do not prevent the progression of calcific aortic stenosis (AS). Novel therapies targeting lipoprotein(a) (Lp(a)) show promise for managing this common heart valve disease.
Area of Science:
- Cardiology
- Vascular Biology
- Pharmacology
Background:
- Calcific aortic stenosis (AS) is a prevalent valvular heart disease in Western countries, characterized by progressive obstruction requiring valve replacement.
- Statins, widely used for coronary artery disease, were investigated for their potential to slow AS progression.
- Previous studies yielded conflicting results regarding statin efficacy in AS.
Purpose of the Study:
- To evaluate the effectiveness of statin therapy in preventing the progression of calcific aortic stenosis.
- To explore emerging therapeutic targets for AS, particularly lipoprotein(a) (Lp(a)).
Main Methods:
- Review of evidence from animal studies, retrospective analyses, and non-randomized prospective trials.
- Analysis of outcomes from three major randomized controlled trials (RCTs) of statin therapy in AS.
- Consideration of recent research on the role of lipoprotein(a) in AS pathogenesis.
Main Results:
- Three major RCTs demonstrated no significant benefit of statin therapy on AS progression or clinical outcomes.
- Statin therapy is not recommended solely for preventing AS progression without other indications for lipid-lowering.
- Lipoprotein(a) (Lp(a)) has emerged as a critical factor in AS progression, independent of statin effects.
Conclusions:
- Current evidence does not support the use of statins to prevent AS progression.
- Targeted therapies aimed at reducing Lp(a) levels, such as PCSK9 inhibitors and antisense oligonucleotides, represent a promising new avenue for AS management.
Abstract:
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.
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