Study of Myocardial Interstitial Fibrosis in Hyperaldosteronism
NCT02938910 · Status: COMPLETED · Type: OBSERVATIONAL · Enrollment: 80
Last updated 2016-10-19
Summary
Animal models have demonstrated the role of aldosterone in left ventricular remodeling involving fibrosis, apoptosis and hypertrophy. Myocardial fibrosis is a risk factor for serious arrhythmia and sudden death in ischemic and idiopathic hypertrophic heart disease. It is accepted that patients with primary aldosteronism have a higher prevalence of LV hypertrophy , arterial involvement and increased cardiovascular risk. In humans, a link has been demonstrated between aldosterone and heart failure as well as the benefit of the administration of an anti -aldosterone drug to lower mortality in this population , regardless of blood pressure level . The administration of spironolactone ( aldosterone ) in hypertensive rats has prevented the occurrence of aortic fibrosis . Plasma aldosteronism in humans has been associated with inflammation, fibrosis and aortic stiffness . However, primary aldosteronism is generally associated with so-called secondary hypertension . Chronic hypertension alone is a recognized etiological factor of myocardial hypertrophy ( myocardial fibrosis very advanced ) . The purpose of this study is to investigate the effects of MRI hyperaldosteronism on the heart.
Conditions
- Primary Hyperaldosteronism
- Secondary Hyperaldosteronism
- Essential Hypertension
- Healthy
Interventions
- OTHER
-
non interventional study
Non invasive imaging study without interventional procedures
Sponsors & Collaborators
-
Assistance Publique - Hôpitaux de Paris
lead OTHER
Principal Investigators
-
Elie MOUSSEAUX, MD, PhD · Assistance publique des hopitaux de Paris
-
Alban REDHEUIL, MD,PhD · Assistance publique des hopitaux de Paris
Eligibility
- Min Age
- 18 Years
- Max Age
- 75 Years
- Sex
- ALL
- Healthy Volunteers
- Yes
Timeline & Regulatory
- Start
- 2012-11-30
- Primary Completion
- 2014-10-31
- Completion
- 2014-10-31
Countries
- France
Study Locations
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