Am J Cardiovasc Dis 2012;2(1):50-57
Original Article
Aldosterone and aldosterone antagonists in cardiac disease: what is known,
what is new
Cristiana Catena, GianLuca Colussi, Gabriele Brosolo, Lorenzo Iogna-Prat, Leonardo A. Sechi
Internal Medicine, Hypertension Unit, Department of Experimental and Clinical Medicine, University of Udine, 33100 Udine,
Italy.
Received November 9, 2011; accepted November 25, 2011; Epub January 1, 2012; published January 15, 2012
Abstract: Experimental and clinical studies indicate that exposure to high aldosterone concentrations causes cardiac
damage independent of the blood pressure level. In recent years, it has become clear that the effects of aldosterone on the
heart are mediated by actions on a variety of cell types and intracellular mechanisms that contribute to regulation of specific
tissue responses, leading to hypertrophy and fibrosis. Most cardiac effects of aldosterone are mediated by activation of
mineralocorticoid receptors that are detected in cardiac myocytes and fibroblasts. Clinical evidence of the unfavorable
cardiac effects of aldosterone has been established in landmark studies that have tested the benefits of aldosterone
antagonists in patients with heart failure and decreased ejection fraction. However, evidence of benefits of aldosterone
antagonists occurring independent of the renal effects of these agents is not limited to patients with systolic heart failure. In
this article, we briefly summarize the current knowledge on the effects of aldosterone antagonists on cardiac protection and
highlight the most recent findings that have been obtained in different cardiac conditions with use of these drugs.
(AJCD1111001).
Keywords: Aldosterone, aldosterone antagonists, atrial fibrillation, diastolic cardiac failure, essential hypertension, primary
aldosteronism
Full Text PDF
Address all correspondence to:
Cristiana Catena, MD PhD
Clinica Medica, University of Udine
University Hospital, Building 8, 1st floor
33100 Udine, Italy.
Phone: +39 0432 559804
E-mail: cristiana.catena@uniud.it
Original Article
Aldosterone and aldosterone antagonists in cardiac disease: what is known,
what is new
Cristiana Catena, GianLuca Colussi, Gabriele Brosolo, Lorenzo Iogna-Prat, Leonardo A. Sechi
Internal Medicine, Hypertension Unit, Department of Experimental and Clinical Medicine, University of Udine, 33100 Udine,
Italy.
Received November 9, 2011; accepted November 25, 2011; Epub January 1, 2012; published January 15, 2012
Abstract: Experimental and clinical studies indicate that exposure to high aldosterone concentrations causes cardiac
damage independent of the blood pressure level. In recent years, it has become clear that the effects of aldosterone on the
heart are mediated by actions on a variety of cell types and intracellular mechanisms that contribute to regulation of specific
tissue responses, leading to hypertrophy and fibrosis. Most cardiac effects of aldosterone are mediated by activation of
mineralocorticoid receptors that are detected in cardiac myocytes and fibroblasts. Clinical evidence of the unfavorable
cardiac effects of aldosterone has been established in landmark studies that have tested the benefits of aldosterone
antagonists in patients with heart failure and decreased ejection fraction. However, evidence of benefits of aldosterone
antagonists occurring independent of the renal effects of these agents is not limited to patients with systolic heart failure. In
this article, we briefly summarize the current knowledge on the effects of aldosterone antagonists on cardiac protection and
highlight the most recent findings that have been obtained in different cardiac conditions with use of these drugs.
(AJCD1111001).
Keywords: Aldosterone, aldosterone antagonists, atrial fibrillation, diastolic cardiac failure, essential hypertension, primary
aldosteronism
Full Text PDF
Address all correspondence to:
Cristiana Catena, MD PhD
Clinica Medica, University of Udine
University Hospital, Building 8, 1st floor
33100 Udine, Italy.
Phone: +39 0432 559804
E-mail: cristiana.catena@uniud.it
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