Statins for aortic stenosis? Still waiting for answers


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Abstract

SYNOPSISBACKGROUNDExperimental and retrospective studies have indicated that statins might inhibit aortic valve calcification and, therefore, slow the progression of aortic stenosis (AS).OBJECTIVETo examine whether rosuvastatin slows disease progression in patients with moderate to severe AS.DESIGNThe Rosuvastatin Affecting Aortic Valve Endothelium (RAAVE) study was a prospective, open-label, observational study conducted at the cardiology clinic of the Hospital Pedro Hispano in Matosinhos, Portugal. All participants were asymptomatic and had an aortic valve area of 1.0-1.5 cm2. Patients were excluded if they were taking angiotensin-enzyme-converting inhibitors, but those on antihypertensive medication, anti-diabetic agents, or insulin were enrolled. Other exclusion criteria included history of coronary artery disease, evidence of rheumatic mitral valve disease, congenital heart disease, chronic liver disease, subaortic obstruction, aortic valve regurgitation, previous aortic valve surgery, previous statin treatment, and a creatinine level of 2.0 mg/dl or higher.INTERVENTIONPatients were managed according to National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) III guidelines. Those with LDL-cholesterol levels higher than 130 mg/dl received rosuvastatin therapy, while those with LDL levels of 130 mg/dl were not treated. Patients underwent echocardiographic assessment and measurement of serum high-sensitivity C-reactive protein, interleukin-6, and CD40 at baseline and at 6, 12, and 18 months after study entry.OUTCOME MEASURESThe primary outcome measures were progression of AS and reduction in LDL-cholesterol levels. Improvements in levels of inflammatory markers were also assessed.RESULTSA total of 121 patients participated in the study, 61 of whom received rosuvastatin. The mean age of patients was 73.7 years and 53% were female. The mean baseline LDL-cholesterol level was 158.2 mg/dl (± 31.7 mg/dl) in patients treated with rosuvastatin and 116.5 mg/dl (± 20.9 mg/dl) in the untreated group. There was one death in the rosuvastatin group (sudden death), and four among untreated patients (sepsis [n = 2], malignancy [n = 2]). One patient who received rosuvastatin became symptomatic and underwent aortic valve replacement. After a mean follow-up period of 73 weeks, the aortic valve area had decreased to a greater extent among untreated patients than in rosuvastatin-treated patients (−0.10 cm2/year vs −0.05 cm2/year; P = 0.041). Those in the statin group had lower annualized change in peak aortic valve velocity (0.04 m/s/year vs 0.24 m/s/year; P = 0.007), peak gradient (2.13 mmHg/year vs 7.57 mmHg/year; P = 0.010) and mean gradient (2.08 mmHg/year vs 5.06 mmHg/year; P = 0.049) than patients who did not receive treatment. Rosuvastatin was also associated with significant decreases in levels of total cholesterol (P <0.001), LDL-cholesterol (P < 0.001), triglycerides (P = 0.003), high-sensitivity C-reactive protein (P = 0.030), interleukin 6 (P <0.001), and CD40 (P <0.001) from baseline values.CONCLUSIONRosuvastatin is associated with a reduced rate of progression of AS in patients with LDL-cholesterol levels above 130 mg/dl.

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