Background-Recent studies have supported the hypothesis that calcific aortic stenosis is the product of an active inflammatory process, with similarities to atherosclerosis. We sought to determine whether therapy with hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) might slow the progression of aortic stenosis. Methods and Results-A retrospective study of 174 patients (mean age 68Ϯ12 years) with mild to moderate calcific aortic stenosis was conducted. Patients required normal left ventricular function, Յ2ϩ aortic regurgitation, and Ն2 echocardiograms performed at least 12 months apart. Fifty-seven patients (33%) received treatment with a statin; the remaining 117 (67%) did not. The statin group was older and had a higher prevalence of hypertension, diabetes mellitus, and coronary disease. During a mean follow-up of 21 months, patients treated with statin had a smaller increase in peak and mean gradient and a smaller decrease in aortic valve area. When annualized, the decrease in aortic valve area for the nonstatin group was 0.11Ϯ0.18 cm 2 compared with 0.06Ϯ0.16 cm 2 for those treated with a statin (Pϭ0.03). In multivariate analysis, statin usage was a significant independent predictor of a smaller decrease in valve area (Pϭ0.01) and a lesser increase in peak gradient (Pϭ0.02). Conclusions-Statin-treated patients, despite a higher risk profile for progression, had reduced aortic stenosis progression compared with those not treated with a statin. These data provide justification for a prospective randomized trial to substantiate whether statin therapy slows the progression of aortic stenosis.

Prior epidemiologic studies have shown that increasing body mass index (BMI) is associated with higher total cholesterol and low-density lipoprotein cholesterol (LDL). However, these studies were limited by underrepresentation of obese subjects. The aim of this study was to determine whether there is an association between BMI and lipid profiles in a population of patients with a broad spectrum of BMI values. A case-control study was performed involving patients seen at the Cleveland Clinic Florida. Cases (BMI >30 kg/m(2)) were obtained from the obesity surgery database between August 31, 2000, and April 4, 2002. Controls (BMI ≤ 30 kg/m(2)) were obtained from a database of primary care physicians between May 1, 2004, and November 18, 2004. Pearson correlation coefficients were used to assess the relationship between BMI and lipid fractions. Multiple linear regression was performed to assess the independent effect of BMI on lipid levels while adjusting for potential confounders and propensity scores. Six hundred thirty-seven patients were analyzed (females, n = 362, 57%). There was no association between higher BMI and LDL (r = 0.19 p = 0.07), a negative association with high-density lipoprotein cholesterol (HDL; r = 0.45, p < 0.001), and a positive association with the log transformation of triglycerides (r = 0.32, p = 0.005).Higher BMI was inversely associated with HDL and directly associated with TG. BMI showed no significant association with LDL. Although the association between BMI and both HDL and TG may be explained by insulin resistance, the lack of a significant association between BMI and LDL remains an unexpected finding that requires further investigation.

Nitroprusside rapidly and markedly improves cardiac function in patients with decompensated heart failure due to severe left ventricular systolic dysfunction and severe aortic stenosis. It provides a safe and effective bridge to aortic-valve replacement or oral vasodilator therapy in these critically ill patients.

In this large population-based cohort, approximately 9% of subjects with aortic sclerosis progressed to aortic stenosis over a 5-year follow-up period. There was no association between CRP levels and the presence of calcific aortic-valve disease or incident aortic stenosis. C-reactive protein appears to be a poor predictor of subclinical calcific aortic-valve disease.