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Published on: January 14, 2014
Multimodality Imaging in Aldosterone-Induced Cardiomyopathy: Early Detection and Prognostic Implications
Francesca Zoccatelli1, Gabriele Costa1, Matteo Merlo1
1Unit of Internal Medicine B, Department of Medicine, University of Verona School of Medicine, Azienda Ospedaliera Universitaria Integrata Verona, Policlinico "G.B. Rossi", 37134 Verona, Italy.
Insights
Primary aldosteronism (PA) causes cardiac remodeling beyond high blood pressure. Multimodality cardiac imaging helps assess this damage, but more research is needed on early detection and treatment impacts.
Area of Science:
- Cardiology
- Endocrinology
- Medical Imaging
Background:
- Primary aldosteronism (PA) is the leading cause of secondary hypertension.
- Aldosterone excess independently drives adverse cardiac remodeling, including fibrosis and hypertrophy.
- This leads to a distinct, often underdiagnosed, cardiomyopathy.
Purpose of the Study:
- To review the pathophysiology of aldosterone-induced cardiac remodeling.
- To assess the role of multimodality cardiac imaging in PA.
- To evaluate treatment effects and identify research gaps.
Main Methods:
- Narrative review of current literature.
- Focus on echocardiography and cardiac magnetic resonance (CMR) techniques (T1 mapping, LGE).
- Analysis of pathophysiological mechanisms and imaging biomarkers.
Main Results:
- Aldosterone excess causes myocardial fibrosis, hypertrophy, and diastolic dysfunction.
- Echocardiography and CMR enable non-invasive assessment of cardiac changes.
- Gaps exist in understanding subclinical changes, long-term prognosis, and treatment impacts.
Conclusions:
- Multimodality imaging is crucial for assessing PA-related cardiac damage.
- Standardized criteria and further research on prognostic biomarkers and treatment effects are needed.
- Personalized care and improved outcomes in PA patients require integrated imaging strategies.
Abstract:
Primary aldosteronism (PA), the most common cause of secondary hypertension, is increasingly recognized as an independent driver of adverse cardiac remodeling, mediated through mechanisms beyond elevated blood pressure alone. Chronic aldosterone excess leads to myocardial fibrosis, left ventricular hypertrophy, and diastolic dysfunction via mineralocorticoid receptor activation, oxidative stress, inflammation, and extracellular matrix dysregulation. These changes culminate in a distinct cardiomyopathy phenotype, often underrecognized in early stages. Multimodality cardiac imaging, led primarily by conventional and speckle-tracking echocardiography, and complemented by exploratory cardiac magnetic resonance (CMR) techniques such as T1 mapping and late gadolinium enhancement, enables non-invasive assessment of structural, functional, and tissue-level changes in aldosterone-mediated myocardial damage. While numerous studies have established the diagnostic and prognostic relevance of imaging in PA, several gaps remain. Specifically, the relative sensitivity of different modalities in detecting subclinical myocardial changes, the long-term prognostic significance of imaging biomarkers, and the differential impact of adrenalectomy versus medical therapy on cardiac reverse remodeling require further clarification. Moreover, the lack of standardized imaging-based criteria for defining and monitoring PA-related cardiomyopathy hinders widespread clinical implementation. This narrative review aims to synthesize current knowledge on the pathophysiological mechanisms of aldosterone-induced cardiac remodeling, delineate the strengths and limitations of existing imaging modalities, and critically evaluate the comparative effects of surgical and pharmacologic interventions. Emphasis is placed on early detection strategies, identification of imaging biomarkers with prognostic utility, and integration of multimodal imaging into clinical decision-making pathways. By outlining current evidence and highlighting key unmet needs, this review provides a framework for future research aimed at advancing personalized care and improving cardiovascular outcomes in patients with PA.
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