Key result
Rosuvastatin linked to ~50% slower aortic stenosis progression vs. no statin.
Why the study?
Recent retrospective studies suggested statins slow aortic stenosis progression, but prospective evaluation of an HMG CoA reductase inhibitor on progression of moderate to severe aortic stenosis was needed.
Does rosuvastatin slow the echocardiographic progression of moderate to severe aortic stenosis in asymptomatic patients?
Cohort (n=121)
Open-label
Does rosuvastatin slow the echocardiographic progression of moderate to severe aortic stenosis in asymptomatic patients?
Absolute Event Rate: -0.05% vs -0.1%
p-value: p=0.041
Prospective treatment with rosuvastatin targeted at elevated LDL significantly slowed the hemodynamic progression of asymptomatic moderate to severe aortic stenosis.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“That may be because of the potentially different genetics in the patients studied or it may be that the timing of the treatment [was too late]. If you start the statins early in the patients that have a very high LDL cholesterol level and you start to modify those levels, there may be a chance to slow progression of aortic valve disease.”
“Following the negative statin trials, people abandoned the theory that LDL lowering could play a role reducing the risk of in aortic valve disease. But their study hints that aortic valve disease is a '2-step disease': an early atherosclerotic process related to high LDL cholesterol and a secondary calcification process, wherein statins are no longer effective 'and it's too late to turn the tables on the disease.'”
Should not yet change practice in aortic stenosis; leaves open whether early LDL-lowering modifies progression and outcomes.
The objective of this study was to test the effect of a 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor on the progression of moderate to severe aortic stenosis as measured by echocardiography. Recent retrospective studies support the hypothesis that statins slow the progression of aortic stenosis. We performed an open-label, prospective study evaluating 121 consecutive patients with asymptomatic moderate to severe aortic stenosis (aortic valve area ≥ 1.0 cm 2 ; mean age 73.7 ± 8.9 years; 57 men and 64 women), treated with and without rosuvastatin according to the National Cholesterol Education Program Adult Treatment Panel III guidelines. Echocardiographic, serum lipid, and inflammatory markers were measured at baseline and every 6 months for 18 months. Sixty-one patients (50.4%) with elevated LDL (159.7 ± 33.4 mg/dl), aortic valve velocity (3.65 ± 0.64 m/s), and aortic valve area (1.23 ± 0.42 cm 2 ) received rosuvastatin (20 mg/day), and 60 (49.6%) with a normal LDL (118.6 ± 37.4 mg/dl), aortic valve velocity (3.62 ± 0.61 m/s), and aortic valve area (1.20 ± 0.35 cm 2 ) received no statin. During a mean follow-up of 73 ± 24 weeks, the change in aortic valve area in the control group was −0.10 ± 0.09 cm 2 /year versus −0.05 ± 0.12 cm 2 /year in the rosuvastatin group (p = 0.041). The increase in aortic valve velocity was 0.24 ± 0.30 m/s/year in the control group and 0.04 ± 0.38 m/s/year in the rosuvastatin group (p = 0.007). There was significant improvement in serum lipid and echocardiographic measures of aortic stenosis in the statin group. Prospective treatment of aortic stenosis with rosuvastatin by targeting serum LDL slowed the hemodynamic progression of aortic stenosis. This is the first prospective study that shows a positive effect of statin therapy for this disease process.
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Moura et al. (2007) conducted a cohort in Asymptomatic moderate to severe aortic stenosis (n=121). Rosuvastatin vs. No statin was evaluated on Change in aortic valve area (cm2/year) (p=0.041). Rosuvastatin slowed the hemodynamic progression of aortic stenosis compared to no statin, with a change in aortic valve area of -0.05 vs -0.10 cm2/year (p=0.041).
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