MI is associated with tissue-specific activation of myocardial aldosterone synthesis. This increase is mediated primarily by cardiac angiotensin II via AT1-subtype receptor and may be involved in post-MI ventricular fibrosis and in control of tissue norepinephrine concentration.
No takes yet. Share an insight, caveat, or question.
Silvestre et al. (1999) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: