Send to

Choose Destination
Trends Cardiovasc Med. 2011 Feb;21(2):42-7. doi: 10.1016/j.tcm.2012.02.003.

Cardiomyocyte mineralocorticoid receptor function post myocardial infarction.

Author information

Klinik fuer Kardiologie und Angiologie, Medizinische Hochschule Hannover, D-30175 Hannover, Germany.


Clinical trials have clearly demonstrated that mineralocorticoid receptor (MR) blockade improves outcome in patients with chronic systolic heart failure and left ventricular dysfunction after myocardial infarction; however, the underlying mechanisms as well as the cell-specific functional role of MR activation are still under investigation. Extrarenal effects of MR blockade on cardiovascular extracellular matrix turnover and oxidative stress, on myocardial structural and electrical remodeling, and on sympathoadrenergic stimulation, platelet activation, endothelial dysfunction, and macrophage polarization appear to be important mechanisms. Recent scientific advances, involving mice with cardiomyocyte-restricted inactivation of the MR gene suggest that the clinical benefits of MR blocking therapy in myocardial infarction and heart failure are mediated largely via cardiomyocyte-dependent mechanisms, and they provide strong evidence that more favorable effects on cardiac dysfunction and failure can be achieved by early initiation of MR blockade postinfarction.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center