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Published on: December 2, 2016
Left ventricular anatomy and function in primary aldosteronism and renovascular hypertension
A C Pessina1, A Sacchetto, G P Rossi
1Department of Clinical & Experimental Medicine, University of Padua Medical School.
Insights
Left ventricular hypertrophy (LVH) is linked to hypertension and poor outcomes. Studying rare conditions like primary aldosteronism and renovascular hypertension helps understand the roles of the renin-angiotensin system and aldosterone in developing LVH.
Area of Science:
- Cardiology
- Nephrology
- Endocrinology
Background:
- Left ventricular hypertrophy (LVH) is a significant complication of hypertension, increasing morbidity and mortality.
- The renin-angiotensin system (RAS) and aldosterone excess are implicated in LVH pathogenesis.
- Secondary hypertension models offer unique insights into human cardiac remodeling.
Purpose of the Study:
- To review cardiac changes in primary aldosteronism and renovascular hypertension.
- To elucidate the roles of RAS and aldosterone in the pathogenesis of LVH.
- To utilize 'exceptions' in hypertension to understand disease mechanisms.
Main Methods:
- Review of clinical data on LV changes in primary aldosteronism.
- Analysis of studies on LVH in renovascular hypertension.
- Comparative analysis of hypertensive subtypes to understand specific pathway contributions.
Main Results:
- Experimental data show angiotensin II induces myocardial hypertrophy.
- Aldosterone excess is linked to extracellular matrix deposition and myocardial fibrosis.
- Secondary hypertension models highlight distinct contributions of RAS and aldosterone to LVH.
Conclusions:
- The renin-angiotensin system and aldosterone play critical roles in the development of left ventricular hypertrophy.
- Studying rare secondary forms of hypertension provides valuable insights into LVH pathogenesis.
- Understanding these mechanisms is crucial for managing hypertensive heart disease.
Abstract:
Left ventricular hypertrophy (LVH) is a common finding in hypertension and represents a detrimental outcome since it is associated with increased morbidity and mortality. For similar elevation of blood pressure the severity and type of LVH vary considerably in relation to several factors. Compelling evidence suggests that both the renin-angiotensin system (RAS) and the aldosterone excess play an important role in the pathogenesis of LVH, since experimentally angiotensin II has been found to cause myocardial cells hypertrophy and/or hyperplasia and excess aldosterone has been related to extracellular matrix and collagen deposition and therefore to myocardial fibrosis. Secondary forms of hypertension offer models for investigating the relative role of the RAS and aldosterone on the heart in humans. Being rare in the population of hypertensive patients, they furnish an example of the so called Bateson's approach to the understanding of diseases "Treasure your exceptions." In this paper, we review the data concerning the LV changes in primary aldosteronism and renovascular hypertension and discuss the insight that they have provided into the pathogenesis of LVH.
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