Clinical and Therapeutic Implications of Fibrosis in Hypertrophic Cardiomyopathy
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|ClinicalTrials.gov Identifier: NCT00879060|
Recruitment Status : Unknown
Verified April 2009 by Tufts Medical Center.
Recruitment status was: Recruiting
First Posted : April 9, 2009
Last Update Posted : April 9, 2009
Hypertrophic Cardiomyopathy (HCM) is the most common genetic cardiomyopathy and remains the leading cause of sudden cardiac death in young people and an important cause of heart failure symptoms and death at any age. In HCM, pathological remodeling of the left ventricle involving myocardial fibrosis is likely a major contributor to cardiac dysfunction and also a nidus for the generation of ventricular arrhythmias. Serum markers of collagen turnover have been shown to reliably reflect the magnitude of myocardial fibrosis in a variety of cardiovascular diseases. In addition, aldosterone antagonist drugs have been shown to decrease fibrous tissue formation in the myocardium in certain pathologic cardiovascular states in which aldosterone production is increased. In HCM, aldosterone production is up-regulated and has been implicated in the formation of myocardial fibrosis.
Therefore, the specific aims of this proposal are to:
- assess serum markers of collagen turnover at baseline and correlate these findings with a variety of clinical and morphologic disease parameters
- examine the effects of a 12-month treatment with the aldosterone antagonist spironolactone on magnitude of fibrosis as measured by serum markers of collagen turnover as well as changes in clinical and morphologic disease parameters.
The results of this proposal will offer important insights into the clinical significance of myocardial fibrosis in this primary genetic cardiomyopathy. The demonstration that spironolactone decreases fibrosis and improves clinical course would provide the rational for a larger multicenter clinical trial evaluating this novel therapy for improving clinical outcome in patients with HCM.
|Condition or disease||Intervention/treatment||Phase|
|Myocardial Fibrosis Hypertrophic Cardiomyopathy||Drug: spironolactone||Phase 4|
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||95 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||Quadruple (Participant, Care Provider, Investigator, Outcomes Assessor)|
|Official Title:||Clinical and Therapeutic Implications of Fibrosis in Hypertrophic|
|Study Start Date :||November 2007|
|Estimated Primary Completion Date :||November 2011|
|Estimated Study Completion Date :||November 2012|
U.S. FDA Resources
spironolactone 50mg daily
- changes in serum markers of collagen turnover [ Time Frame: one year ]
- measures of diastolic function by echocardiography [ Time Frame: one year ]
- cardiac mass and fibrosis by cardiac magnetic resonance imaging (CMR) [ Time Frame: one year ]
- exercise tolerance by exercise VO2max and Holter [ Time Frame: one year ]
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00879060
|Contact: Martin S Maron, MD||617 firstname.lastname@example.org|
|Contact: James E Udelson, MDemail@example.com|
|United States, Massachusetts|
|Tufts Medical Center||Recruiting|
|Boston, Massachusetts, United States, 02111|
|Contact: Martin S Maron, MD 617-636-8066 firstname.lastname@example.org|
|Contact: James E Udelson, MD 6176368066 email@example.com|
|Principal Investigator: Martin S Maron, MD|