Plasma aldosterone levels have been shown to be associated with adverse clinical outcomes after ST-elevation myocardial infarction (STEMI). We investigated whether aldosterone levels in patients presenting with STEMI or non-STEMI, are predictive of mortality during prolonged follow-up. Aldosterone levels were assayed in plasma taken from 583 patients within 24–96 h following acute myocardial infarction (MI). The median plasma aldosterone level was 108 pmol/L and all values were below the upper limit of the normal range (800 pmol/L) except for five patients (0.9%). Aldosterone tertile was significantly associated with increasing plasma levels of NTproBNP (N-terminal pro-B-type natriuretic peptide), BNP (B-type natriuretic peptide), epinephrine, and endothelin-1 (P ≤ 0.010), but not ANP (atrial natriuretic peptide). Patients in the lowest aldosterone tertile had a significantly better survival, over 5 years’ follow-up, than those in the upper two tertiles (P = 0.0023). Multivariable analysis showed that aldosterone was a significant predictor of survival following adjustment for established predictors (tertile 1 vs. tertile 3; hazard ratio = 2.19, P = 0.018). Patients with above-median levels of both NTproBNP and aldosterone had significantly greater mortality than the remaining patients (above-median 39.8%, other patients ≥25.3% mortality, P ≥ 0.026). Plasma aldosterone levels post-MI are independent predictors of survival and hospitalization for heart failure over a 5-year-follow-up period.

Angiotensinogen M235T and T174M polymorphisms have individually been associated with elevated levels of plasma angiotensinogen, hypertension, and left ventricular hypertrophy. In this study, heart failure patients (n=451) were genotyped for the angiotensinogen M235T and T174M polymorphisms to investigate association with survival (recorded over 4 years of follow-up) and prognostic hormone markers. Patients carrying the 235TT genotype (n=86) were 3 years younger at admission ( P =0.011), and, in those with hypertension, diagnosis was made ≈10 years earlier than other patients. Patients carrying ≥1 174M allele (n=94) were more likely to have a previous history of heart failure ( P =0.044) and increased mortality during follow-up (risk ratio: 1.69, 95% CI: 1.03 to 2.79; P =0.038) compared with 174TT homozygotes (n=355), despite having a higher left ventricular ejection fraction ( P =0.009). “High-risk” genotype combinations (defined a priori as 235TT and/or ≥1 174M allele; n=144; 32%) were independently predictive of mortality, conferring a 2-fold greater risk of dying during the follow-up period (odds ratio: 2.0; 95% CI: 1.3 to 3.0; P =0.001). This study suggested that angiotensinogen gene variants M235T and T174M may provide prognostic information for long-term survival in heart failure patients.