: Dilated cardiomyopathy (DCM) is an underrecognized yet potentially reversible cardiac complication of primary aldosteronism (PA), the most prevalent cause of secondary hypertension. Beyond its well-established hypertensive and profibrotic effects, chronic aldosterone excess exerts direct myocardial toxicity, driving progressive left ventricular remodeling. This remodeling follows a characteristic trajectory, evolving from concentric remodeling to eccentric hypertrophy with diastolic dysfunction, and ultimately culminating in overt systolic impairment. Importantly, these pathological changes result from mechanisms extending beyond mere pressure overload, including mineralocorticoid receptor overactivation, inflammation, oxidative stress, and myocardial fibrosis. This state-of-the-art review integrates current epidemiological data, mechanistic insights, and therapeutic outcomes from both clinical and experimental studies on PA-related DCM. We critically assess the pathophysiological cascade linking aldosterone excess to adverse cardiac remodeling and evaluate the comparative impact of adrenalectomy and mineralocorticoid receptor antagonists on myocardial recovery. Special emphasis is placed on diagnostic challenges, clinical implications, and the importance of early recognition. By consolidating available evidence and highlighting key knowledge gaps, this review aims to inform clinical decision-making and stimulate future research in the emerging field of endocrine cardiomyopathy.
Dilated cardiomyopathy in primary aldosteronism: A state-of-the-art of mechanistic insights, therapeutic strategies, and future perspectives
Zoccatelli, FrancescaWriting – Original Draft Preparation
;Friso, SimonettaSupervision
2025-01-01
Abstract
: Dilated cardiomyopathy (DCM) is an underrecognized yet potentially reversible cardiac complication of primary aldosteronism (PA), the most prevalent cause of secondary hypertension. Beyond its well-established hypertensive and profibrotic effects, chronic aldosterone excess exerts direct myocardial toxicity, driving progressive left ventricular remodeling. This remodeling follows a characteristic trajectory, evolving from concentric remodeling to eccentric hypertrophy with diastolic dysfunction, and ultimately culminating in overt systolic impairment. Importantly, these pathological changes result from mechanisms extending beyond mere pressure overload, including mineralocorticoid receptor overactivation, inflammation, oxidative stress, and myocardial fibrosis. This state-of-the-art review integrates current epidemiological data, mechanistic insights, and therapeutic outcomes from both clinical and experimental studies on PA-related DCM. We critically assess the pathophysiological cascade linking aldosterone excess to adverse cardiac remodeling and evaluate the comparative impact of adrenalectomy and mineralocorticoid receptor antagonists on myocardial recovery. Special emphasis is placed on diagnostic challenges, clinical implications, and the importance of early recognition. By consolidating available evidence and highlighting key knowledge gaps, this review aims to inform clinical decision-making and stimulate future research in the emerging field of endocrine cardiomyopathy.| File | Dimensione | Formato | |
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Trends Cardiovasc Med 2025_Dilated cardiomyopathy_Marzano_Friso.pdf
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