Effect of Losartan in Patients With Nonobstructive Hypertrophic Cardiomyopathy

This study has been completed.
Sponsor:
Information provided by (Responsible Party):
Michael A. Fifer, MD, Massachusetts General Hospital
ClinicalTrials.gov Identifier:
NCT01150461
First received: June 22, 2010
Last updated: September 3, 2013
Last verified: September 2013

June 22, 2010
September 3, 2013
February 2007
July 2010   (final data collection date for primary outcome measure)
Percentage Change From Baseline in Extent of Left Ventricular Fibrosis at 1 Year as Assessed by Magnetic Resonance Imaging. [ Time Frame: Baseline and 1 year ] [ Designated as safety issue: No ]
Extent of left ventricular myocardial fibrosis as assessed by magnetic resonance imaging. [ Time Frame: One Year ] [ Designated as safety issue: No ]
Complete list of historical versions of study NCT01150461 on ClinicalTrials.gov Archive Site
Percentage Change From Baseline in Left Ventricular Mass at 1 Year as Assessed by Magnetic Resonance Imaging. [ Time Frame: Baseline and 1 year ] [ Designated as safety issue: No ]
Left ventricular mass as assessed by magnetic resonance imaging. [ Time Frame: 1 year ] [ Designated as safety issue: No ]
Not Provided
Not Provided
 
Effect of Losartan in Patients With Nonobstructive Hypertrophic Cardiomyopathy
Effect of Losartan in Patients With Nonobstructive Hypertrophic Cardiomyopathy

The purpose of this study is to determine whether taking losartan helps people with hypertrophic nonobstructive cardiomyopathy feel better by decreasing the amount of heart muscle thickening and/or the amount of heart muscle scarring.

Hypertrophic cardiomyopathy (HCM) is characterized by idiopathic cardiac hypertrophy, heart failure, ischemia even in the absence of epicardial coronary artery disease, and arrhythmias. The pathological features of HCM include hypertrophy and disarray, interstitial fibrosis, and increased arteriolar wall thickness. Hypertrophy and fibrosis are major determinants of morbidity and mortality in hypertrophic cardiomyopathy. Some investigators have demonstrated that interstitial fibrosis and hypertrophy occur secondarily, in response to trophic and mitotic factors in the heart. Therefore, blocking trophic factors may attenuate or potentially reverse hypertrophy and fibrosis in HCM.

Angiotensin II has trophic and profibrotic effects on the heart, and blockade of angiotensin II type I receptors has been shown to attenuate myocardial hypertrophy and fibrosis in acquired cardiac disease in humans and animal models.

We hypothesize that treatment with the selective angiotensin II type receptor antagonist, losartan, will decrease both hypertrophy and fibrosis, improve diastolic function, reduce symptoms, and improve functional status in patients with HCM.

Interventional
Phase 2
Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator)
Primary Purpose: Treatment
Hypertrophic Cardiomyopathy
  • Drug: losartan
    Losartan 50 mg b.i.d
    Other Names:
    • Angiotensin II receptor antagonist
    • Cozaar
  • Drug: placebo
    Placebo b.i.d.
    Other Name: Placebo tablet
  • Experimental: losartan
    Losartan 50 mg b.i.d.
    Intervention: Drug: losartan
  • Placebo Comparator: placebo
    Placebo b.i.d.
    Intervention: Drug: placebo
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
20
July 2010
July 2010   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Patients with hypertrophic cardiomyopathy
  • Left ventricular outflow tract (LVOT) gradient less than 30 mm Hg at rest
  • Age 18 years or older

Exclusion Criteria:

  • Contraindication to losartan
  • Already taking losartan
  • Contraindication to MRI
  • Hemodynamic instability
Both
18 Years and older
No
Contact information is only displayed when the study is recruiting subjects
United States
 
NCT01150461
2006P002232/7
No
Michael A. Fifer, MD, Massachusetts General Hospital
Massachusetts General Hospital
Not Provided
Principal Investigator: Michael A Fifer, MD Massachusetts General Hospital
Massachusetts General Hospital
September 2013

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP