Abstract 14110: The Plasma Renin Activity (PRA) Predicts Death from All Causes and Cardiovascular Events in Patients with Acute Decompensated Heart Failure (ADHF) Under Use of Renin-Angiotensin System Inhibitors
Background The renin-angiotensin-aldosterone system (RAAS) is activated in heart failure (HF) as a compensatory mechanism. However its over-activation leads to a vicious cycle and poor prognosis in HF. So inhibitors of RAAS are used as first-line drugs for HF. The plasma renin activity (PRA) is up-regulated by the use of RAAS blockers via a negative feedback mechanism. The clinical implication of PRA under use of RAAS inhibitors is poorly understood in ADHF. Method Of 459 consecutive patients with ADHF emergently admitted to our hospital, we investigated the impact of PRA on the prognosis of ADHF in 216 patients who had already received ACEI, ARBs or aldosterone antagonists or the combination of RAAS inhibitors before admission. None of them took direct renin inhibitors (DRIs). The patients were divided into 2 groups according to the median value of log PRA (≥ or <0.505 ng/ml/h). Kaplan-Meier survival analysis and Cox regression analysis with a proportional hazard model were performed to assess outcomes.
Result During a mean follow-up of 20.7 months, there were 82 deaths from all causes, including 46 deaths from cardiovascular causes. Kaplan-Meier analysis showed that all-cause death and cardiovascular death were significantly higher in patients with log PRA levels above the median than those with below (27% vs 49%; P<0.01 (Fig.), 14% vs 28%; P<0.01, respectively). Using univariate analysis, BMI, eGFR, log PRA and log BNP were significantly related to cardiovascular death (P<0.01). In a multivariate analysis, including clinical and laboratory variables, log PRA levels above the median was the only independent predictor for cardiovascular death (HR=2.06; 95% CI 1.30-3.28; P=0.0021). There is no difference in prevalence of β-blocker use in both groups (36% vs 31%).
Conclusion PRA was associated with increasing risk for adverse outcome for ADHF patients, even in those who are already receiving RAAS blockers, suggesting PRA would be useful biomarker in the treatment of ADHF.
- © 2012 by American Heart Association, Inc.