title: Aldosterone and cortisol predict medium-term left ventricular remodelling following myocardial infarction.
abstract: OBJECTIVE
  Mineralocorticoid receptor (MR) antagonists improve cardiovascular outcomes in patients with heart failure complicating acute myocardial infarction (AMI) and in chronic heart failure. It is unclear whether these beneficial effects are due solely to aldosterone blockade, as MR has a similar affinity for cortisol. We examined the relationships between plasma and urinary steroid hormones and left ventricular (LV) remodelling in patients with LV dysfunction following AMI.
  
  
  RESULTS
  Plasma concentrations of renin, aldosterone, and N-terminal pro-brain natriuretic peptide (NT-proBNP), and 24 h urinary excretion rates of tetrahydroaldosterone (THAldo) and total cortisol metabolites were measured in 93 patients at a mean of 46 h following AMI prior to contrast-enhanced cardiac magnetic resonance (ceCMR). Patients were then randomized to 24 weeks of placebo or eplerenone therapy in addition to standard treatment, after which ceCMR was repeated. In placebo-treated patients, aldosterone, NT-proBNP, and excretion rates of THAldo and total cortisol metabolites were univariate predictors of remodelling (i.e. change in LV end-systolic volume index); aldosterone (P = 0.040) and total cortisol metabolite excretion (P = 0.038) remained independent predictors on multivariate analysis. None of the measured biomarkers predicted remodelling in the presence of eplerenone. Plasma and urinary aldosterone measures, and urinary cortisol metabolites, were not only related to larger infarct volumes and greater infarct remodelling over time, but were also higher in patients with microvascular obstruction on baseline ceCMR.
  
  
  CONCLUSIONS
  Aldosterone and cortisol are associated with medium-term LV remodelling when measured early after AMI. The beneficial effects of MR antagonism may relate to blockade of both aldosterone- and cortisol-induced MR activation.
authors.affiliation: Cardiology Department, Western Infirmary, Glasgow, UK. robinweir75@hotmail.com
authors.forename: Robin A P
authors.initials: RA
authors.lastname: Weir
authors.forename: Ioannis K
authors.initials: IK
authors.lastname: Tsorlalis
authors.forename: Tracey
authors.initials: T
authors.lastname: Steedman
authors.forename: Henry J
authors.initials: HJ
authors.lastname: Dargie
authors.forename: Robert
authors.initials: R
authors.lastname: Fraser
authors.forename: John J V
authors.initials: JJ
authors.lastname: McMurray
authors.forename: John M C
authors.initials: JM
authors.lastname: Connell
mesh_terms: D000450:Aldosterone / Q000378:metabolism*; D015415:Biomarkers / Q000097:blood / Q000652:urine; D004311:Double-Blind Method; D004452:Echocardiography; D004562:Electrocardiography; D000077545:Eplerenone; D005260:Female; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use*; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy / Q000378:metabolism*; D011446:Prospective Studies; D013148:Spironolactone / Q000031:analogs & derivatives* / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D015415:Biomarkers; D000451:Mineralocorticoid Receptor Antagonists; D013148:Spironolactone; D000450:Aldosterone; D000077545:Eplerenone; D006854:Hydrocortisone