CARDIOVASCULAR CONSEQUENCES IN PRIMARY ALDOSTERONISM

Irida Kecaj1, Ergita Nelaj*, Ilir Gjermeni1, Kei Xhixhabesi and Ina Refatllari

ABSTRACT

Aldosterone, beyond its fundamental role in maintaining water, sodium, and potassium balance, significantly impacts cardiovascular physiology and pathology. Excess aldosterone contributes to endothelial dysfunction, promotes inflammatory cell infiltration, and accelerates the progression of atherosclerosis by increasing plaque instability, arterial stiffness, and calcification. At the cardiac level, it exacerbates inflammation, fibrosis, and myocardial hypertrophy. Clinically, elevated aldosterone levels correlate with a higher risk of cardiovascular events and mortality, particularly in conditions like primary aldosteronism, where its secretion is dysregulated relative to renin levels and sodium intake. Clinical studies indicate that mineralocorticoid receptor antagonists (MRAs) effectively lower cardiovascular mortality in individuals with heart failure with preserved ejection fraction, but the effects on myocardial infarction and atrial fibrillation remain less clear. In cases of primary aldosteronism, treatments like adrenalectomy or MRAs significantly reduce cardiovascular risks, including mortality and atrial fibrillation. This review compiles key preclinical and clinical research on the detrimental cardiovascular effects of aldosterone and the protective role of MRAs in managing cardiovascular disease and primary aldosteronism.

Keywords: Aldosterone, vascular system, left ventricular hypertrophy, heart failure, arrhythmias.