Statin Induced Regression of Cardiomyopathy Trial: A Randomized, Placebo-controlled Double-blind Trial

• Published in: Heart views Vol. 17; no. 4; pp. 129 - 135
• Main Authors: Hersi, Ahmad, Giannoccaro, J Peter, Howarth, Andrew, Exner, Derek, Weeks, Sarah, Eitel, Ingo, Herman, R Cameron, Duff, Henry, Ritchie, Debbie, Mcrae, Maureen, Sheldon, Robert
• Format: Journal Article
• Language: English
• Published: India Medknow Publications and Media Pvt. Ltd 01.10.2016; Medknow Publications & Media Pvt. Ltd; Medknow Publications & Media Pvt Ltd; Wolters Kluwer Medknow Publications
• Subjects: Atorvastatin; Cardiomyopathy; Cardiovascular disease; Care and treatment; clinical trial; Complications and side effects; Dosage and administration; Flow velocity; Heart failure; Hypertension; hypertrophic cardiomyopathy; Myocardial diseases; NMR; Nuclear magnetic resonance; Original; Patients; regression; statin; Statins; Studies; United States; clinical trial; Atorvastatin; hypertrophic cardiomyopathy; statin; regression
• ISSN: 1995-705X; 0976-5123
• DOI: 10.4103/1995-705X.201784

Hypertrophic cardiomyopathy (HCM), characterized by a thickened, fibrotic myocardium, remains the most common cause of sudden cardiac death in young adults. Based on animal and clinical data, we hypothesized that atorvastatin would induce left ventricular (LV) mass regression. Statin Induced Regression of Cardiomyopathy Trial (SIRCAT) was a randomized, placebo-controlled study. The primary endpoint was change in LV mass measured by cardiac magnetic resonance imaging 12 months after treatment with once-daily atorvastatin 80 mg or placebo. A key secondary endpoint was diastolic dysfunction measured echocardiographically by transmitral flow velocities. SIRCAT is registered with www.clinicaltrials.gov (NCT00317967). Of 222 screened patients, 22 were randomized evenly to atorvastatin and placebo. The mean age was 47 ± 10 years, and 15 (68%) were male. All subjects completed the protocol. At baseline, LV masses were 197 ± 76 g and 205 ± 82 g in the placebo and atorvastatin groups, respectively. After 12 months treatment, the LV masses in the placebo and atorvastatin groups were 196 ± 80 versus 206 ± 92 g ( = 0.80), respectively. Echocardiographic indices were not different in the two groups at baseline. After 12 months, diastolic dysfunction as assessed using transmitral flow velocities E/E', A/A', and peak systolic mitral velocity showed no benefit from atorvastatin. In patients with HCM, atorvastatin did not cause LV mass regression or improvements in LV diastolic function.