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Effect of Losartan in Patients With Nonobstructive Hypertrophic Cardiomyopathy

2014-08-27 03:12:42 | BioPortfolio

Summary

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.

Description

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.

Study Design

Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Caregiver, Investigator), Primary Purpose: Treatment

Conditions

Hypertrophic Cardiomyopathy

Intervention

losartan, placebo

Location

Massachusetts General Hospital
Boston
Massachusetts
United States
02114

Status

Active, not recruiting

Source

Massachusetts General Hospital

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:12:42-0400

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Medical and Biotech [MESH] Definitions

An autosomal dominant inherited form of HYPERTROPHIC CARDIOMYOPATHY. It results from any of more than 50 mutations involving genes encoding contractile proteins such as VENTRICULAR MYOSINS; cardiac TROPONIN T; ALPHA-TROPOMYOSIN.

A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).

A form of CARDIAC MUSCLE disease, characterized by left and/or right ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR; HYPERTROPHY, RIGHT VENTRICULAR), frequent asymmetrical involvement of the HEART SEPTUM, and normal or reduced left ventricular volume. Risk factors include HYPERTENSION; AORTIC STENOSIS; and gene MUTATION; (FAMILIAL HYPERTROPHIC CARDIOMYOPATHY).

An autosomal recessively inherited glycogen storage disease caused by GLUCAN 1,4-ALPHA-GLUCOSIDASE deficiency. Large amounts of GLYCOGEN accumulate in the LYSOSOMES of skeletal muscle (MUSCLE, SKELETAL); HEART; LIVER; SPINAL CORD; and BRAIN. Three forms have been described: infantile, childhood, and adult. The infantile form is fatal in infancy and presents with hypotonia and a hypertrophic cardiomyopathy (CARDIOMYOPATHY, HYPERTROPHIC). The childhood form usually presents in the second year of life with proximal weakness and respiratory symptoms. The adult form consists of a slowly progressive proximal myopathy. (From Muscle Nerve 1995;3:S61-9; Menkes, Textbook of Child Neurology, 5th ed, pp73-4)

Isoforms of MYOSIN TYPE II, specifically found in the ventricular muscle of the HEART. Defects in the genes encoding ventricular myosins result in FAMILIAL HYPERTROPHIC CARDIOMYOPATHY.

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