The purpose of this study is to determine if a drug called atorvastatin will reduce the size and stiffness of the muscle in the left ventricle of the heart.
Hypertrophic cardiomyopathy (HCM) is a primary disorder of the heart characterized by a thickened, fibrotic myocardium, with or without a dynamic left ventricular outflow tract gradient. It is a common heritable cardiovascular disease, with a population prevalence of 0.1% to 0.2%. Symptoms of congestive heart failure are extremely common in patients with HCM. Progression to disabling and debilitating symptoms \[New York Heart Association (NYHA) class III and IV\] is relatively common, occurring in 15% to 20% of unselected populations. The rate of progression to NYHA class III or IV or death from heart failure or stroke is high, with a relative risk 2.7. Management of symptoms can be very challenging, involve multiple medications, and 5% of patients may develop drug refractory heart failure, requiring invasive intervention. HCM is the most common cause of sudden death among young competitive athletes. Ventricular tachyarrhythmias appear to be the primary mechanism; however, other arrhythmias involved include asystole, rapid atrial fibrillation, and electrical mechanical dissociation. Patients may develop progressive myocardial wall thinning, a reduction in systolic performance, and an increase in left ventricular dimensions. Progressive wall thinning may be especially common in patients with initially severe hypertrophy. There is no cure for this condition. There is now evidence from both animal and human studies of a treatment that promises to reverse hypertrophy - HMG CoA reductase inhibitors. Clearly, studies of treatments that might cause regression of hypertrophy are timely and important.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
QUADRUPLE
Enrollment
22
80 mg pills daily
80 mg pills daily
University of Calgary, Faculty of Medicine
Calgary, Alberta, Canada
Change in left ventricular mass at 12 months from baseline
Time frame: 12 months
a decrease in maximal ventricular wall cross sectional width
Time frame: 12 months
a decrease in the incidence of nonsustained ventricular tachycardia
Time frame: 12 months
a decrease in T-wave alternans
Time frame: 12 months
a decrease in the volume of dense myocardial fibrosis
Time frame: 12 months
parameters of diastolic function
Time frame: 12 months
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