Aldosterone: Cardiovascular assault

Background Blocking the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitors has improved cardiovascular morbidity and mortality rates. However, because of aldosterone “escape,” the effectiveness of this blockade decreases over time. Methods Various in vitro and in vivo...

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Bibliographic Details
Published in:The American heart journal 2002-11, Vol.144 (5), p.S2-S7
Main Author: Struthers, Allan D.
Format: Article
Language:English
Subjects:
ACE inhibitors
Aldosterone - physiology
Autonomic Nervous System Diseases - etiology
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Cardiomegaly - etiology
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
Drug therapy
Endothelium, Vascular - physiopathology
Fibrinolysis
Fibrosis - etiology
Heart attacks
Heart Failure - complications
Heart Failure - drug therapy
Humans
Magnesium - metabolism
Medical sciences
Mineralocorticoid Receptor Antagonists - therapeutic use
Mortality
Myocardium - pathology
Necrosis
Potassium - metabolism
Rodents
Sodium - metabolism
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Summary:Background Blocking the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitors has improved cardiovascular morbidity and mortality rates. However, because of aldosterone “escape,” the effectiveness of this blockade decreases over time. Methods Various in vitro and in vivo studies were evaluated to determine the mechanisms by which aldosterone contributes to morbidity and mortality. Results Aldosterone has several deleterious properties. It causes a vasculopathy with both endothelial dysfunction and a reduction in fibrinolysis, leading to heart, brain, and kidney damage. Aldosterone causes myocardial hypertrophy and fibrosis, autonomic imbalance, and electrolyte abnormalities, contributing to myocardial dysfunction, arrhythmias, and sudden cardiac death. Studies have shown that all of these deleterious effects can, at least in part, be reversed by aldosterone receptor blockade. This may explain why adding an aldosterone blocker to standard heart failure therapy, including angiotensin-converting enzyme inhibitors, reduces morbidity and mortality rates by an additional 30% compared with standard therapy alone. Conclusions Eplerenone is a selective aldosterone blocker whose role in reducing morbidity and mortality rates in patients with cardiovascular disease is being investigated. (Am Heart J 2002;144:S2-7.)
ISSN:0002-8703
1097-6744
DOI:10.1067/mhj.2002.129969