Study to Determine if Atorvastatin Reduces Size and Stiffness of Muscle in the Left Ventricle of the Heart

Hypertrophic Cardiomyopathy Clinical Trial

Official title:

Statin Induced Regression of Cardiomyopathy Trial - SirCat

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00317967
• Other study ID #: 1-Sheldon
• Status: Completed
• Phase: Phase 3
• First received: April 24, 2006
• Last updated: December 5, 2013
• Start date: April 2007
• Est. completion date: November 2010

Study information

• Verified date: December 2013
• Source: University of Calgary
• Contact: n/a
• Is FDA regulated: No
• Health authority: Canada: Health Canada
• Study type: Interventional

Clinical Trial Summary

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.

Description:

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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 22
• Est. completion date: November 2010
• Est. primary completion date: October 2010
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 18 Years and older

Eligibility

Inclusion Criteria:

• 18 years and over with HCM in the absence of another cardiac or systemic disease capable of producing a prespecified wall thickening

Exclusion Criteria:

• Required use of statin therapy or intolerance

• A clinical diagnosis of hypertension

• Indication for statin therapy for primary or secondary prevention of coronary artery disease

• Current or anticipated indication in = 1 year for implantable cardioverter defibrillators or other metallic devices preventing cardiac magnetic resonance imaging (MRI).

Study Design

Allocation: Randomized, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor), Primary Purpose: Treatment

Related Conditions & MeSH terms

• Cardiomyopathies
• Cardiomyopathy, Hypertrophic
• Hypertrophic Cardiomyopathy
• Hypertrophy

Intervention

Drug:
• Atorvastatin
80 mg pills daily
• Placebo
80 mg pills daily

Locations

Country	Name	City	State
Canada	University of Calgary, Faculty of Medicine	Calgary	Alberta

Sponsors (2)

Lead Sponsor	Collaborator
University of Calgary	Heart and Stroke Foundation of Canada

Country where clinical trial is conducted

Canada, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Change in left ventricular mass at 12 months from baseline		12 months	No
Secondary	a decrease in maximal ventricular wall cross sectional width		12 months	No
Secondary	a decrease in the incidence of nonsustained ventricular tachycardia		12 months	No
Secondary	a decrease in T-wave alternans		12 months	No
Secondary	a decrease in the volume of dense myocardial fibrosis		12 months	No
Secondary	parameters of diastolic function		12 months	No