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[Cardiac consequences of primary hyperaldosteronism]
1Département de médecine interne et hypertension artérielle, hôpital Lapeyronie, 371, avenue du Doyen-Gaston-Giraud, 34295 Montpellier cedex 5, France. g-du_cailar@chu-montpellier.fr
Annales De Cardiologie Et D'Angeiologie
|August 5, 2004
Summary
Excess aldosterone, often from Conn adenoma, causes significant cardiac hypertrophy and fibrosis, independent of blood pressure. This leads to accelerated heart disease and diastolic dysfunction.
Area of Science:
- Cardiology
- Endocrinology
- Nephrology
Context:
- Aldosterone hypersecretion's cardiac effects are understudied.
- Experimental hyperaldosteronism causes cardiac hypertrophy and fibrosis.
- Conn adenoma is a primary source of aldosterone excess in humans.
Purpose:
- To assess cardiac consequences of hyperaldosteronism in Conn adenoma patients.
- To compare cardiac changes in hyperaldosteronism versus primary hypertension.
- To correlate plasma aldosterone levels with cardiac structural changes.
Summary:
- Patients with Conn adenoma showed more prominent cardiac hypertrophy than hypertensive patients at similar blood pressure levels.
- Plasma aldosterone positively correlated with left ventricular wall thickness and myocardial fibrosis.
- Echocardiography revealed concentric left ventricular hypertrophy and increased myocardial fibrosis, suggesting excess collagen.
Impact:
- Conn adenoma accelerates cardiac disease, partly independent of blood pressure.
- Identifies aldosterone as a key driver of cardiac remodeling and dysfunction.
- Highlights the importance of quantifying myocardial fibrosis in hyperaldosteronism.