Abstract
Primary aldosteronism (PA), the most common form of secondary hypertension, has been considered for decades as a “benign” form of hypertension, but evidences progressively built up to show that patients with PA had an excess rate of cardiovascular damage as compared to blood pressure-matched essential hypertensive patients. This review provides an updated view of structural and electrical cardiac remodeling and of vascular changes in hyperaldosteronism, and how they can favor development of cardiovascular events. The link between hyperaldosteronism and resistant hypertension is also examined, and the impact of targeted treatment of hyperaldosteronism on cardiovascular changes is finally discussed.
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