Effect of hydroxymethylglutaryl coenzyme a reductase inhibitors on the progression of calcific aortic stenosis.
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.


RESULTS
A retrospective study of 174 patients (mean age 68+/-12 years) with mild to moderate calcific aortic stenosis was conducted. Patients required normal left ventricular function, </=2+ aortic regurgitation, and >/=2 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 0.11+/-0.18 cm(2) compared with 0.06+/-0.16 cm(2) for those treated with a statin (P=0.03). In multivariate analysis, statin usage was a significant independent predictor of a smaller decrease in valve area (P=0.01) and a lesser increase in peak gradient (P=0.02).


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.
Novaro
G M
GM
Department of Cardiology, Section of Preventive Cardiology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA.
Tiong
I Y
IY
Pearce
G L
GL
Lauer
M S
MS
Sprecher
D L
DL
Griffin
B P
BP
D000368:Aged; D001024:Aortic Valve Stenosis / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy*; D000069059:Atorvastatin; D002114:Calcinosis / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D018450:Disease Progression; D004452:Echocardiography; D004562:Electrocardiography / Q000187:drug effects; D005229:Fatty Acids, Monounsaturated / Q000627:therapeutic use; D005260:Female; D000077340:Fluvastatin; D005500:Follow-Up Studies; D006538:Heptanoic Acids / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007211:Indoles / Q000627:therapeutic use; D008148:Lovastatin / Q000627:therapeutic use; D008297:Male; D015999:Multivariate Analysis; D017035:Pravastatin / Q000627:therapeutic use; D011758:Pyrroles / Q000627:therapeutic use; D012189:Retrospective Studies; D012307:Risk Factors; D019821:Simvastatin / Q000627:therapeutic use; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood; D014654:Vascular Patency / Q000187:drug effects
D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005229:Fatty Acids, Monounsaturated; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D011758:Pyrroles; D014280:Triglycerides; D000077340:Fluvastatin; D008148:Lovastatin; D000069059:Atorvastatin; D019821:Simvastatin; D017035:Pravastatin