title: Plasma renin activity is a strong and independent prognostic indicator in patients with acute decompensated heart failure treated with renin-angiotensin system inhibitors.
abstract: BACKGROUND
  The renin-angiotensin system (RAS) is activated in heart failure (HF) as a compensatory mechanism, being related to cardiac remodeling and poor prognosis. Although RAS inhibitors are used as first-line drugs for HF, plasma renin activity (PRA) is upregulated by RAS inhibitors via a negative feedback mechanism. The clinical significance of PRA during RAS inhibitor therapy is poorly understood in acute decompensated HF (ADHF). Therefore we examined the impact of PRA in HF patients already receiving RAS inhibitors.
  
  
  RESULTS
  Of 611 consecutive patients with ADHF and emergency admission to hospital, we studied the impact of PRA on the prognosis of ADHF in 293 patients already receiving RAS inhibitors before admission. The patients were divided into 2 groups according to median PRA (≥ vs. <3.4 ng·ml(-1)·h(-1)). During a mean follow-up of 29.0 months, there were 124 deaths from all causes. Kaplan-Meier analysis showed that all-cause and cardiovascular mortality were significantly higher in patients with high PRA than low PRA (log-rank P=0.0002 and P<0.0001, respectively). Log PRA was an independent predictor of all-cause and cardiovascular death (HR, 1.194; 95% CI: 1.378-2.678, P<0.0001; and HR, 2.559; 95% CI: 1.610-4.144, P<0.0001, respectively).
  
  
  CONCLUSIONS
  PRA was associated with an increased risk of all-cause and cardiovascular mortality in ADHF patients already receiving RAS inhibitors, suggesting that PRA would be a useful biomarker during ADHF treatment.
authors.affiliation: First Department of Internal Medicine, Nara Medical University.
authors.forename: Tomoya
authors.initials: T
authors.lastname: Ueda
authors.forename: Rika
authors.initials: R
authors.lastname: Kawakami
authors.forename: Taku
authors.initials: T
authors.lastname: Nishida
authors.forename: Kenji
authors.initials: K
authors.lastname: Onoue
authors.forename: Tsunenari
authors.initials: T
authors.lastname: Soeda
authors.forename: Satoshi
authors.initials: S
authors.lastname: Okayama
authors.forename: Yukiji
authors.initials: Y
authors.lastname: Takeda
authors.forename: Makoto
authors.initials: M
authors.lastname: Watanabe
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kawata
authors.forename: Shiro
authors.initials: S
authors.lastname: Uemura
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Saito
mesh_terms: D000208:Acute Disease; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D000368:Aged; D000450:Aldosterone / Q000097:blood; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000401:mortality; D015897:Comorbidity; D004359:Drug Therapy, Combination; D025461:Feedback, Physiological; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000097:blood* / Q000188:drug therapy / Q000401:mortality / Q000503:physiopathology; D006801:Humans; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D010359:Patient Readmission / Q000706:statistics & numerical data; D011379:Prognosis; D016016:Proportional Hazards Models; D012083:Renin / Q000097:blood*; D012084:Renin-Angiotensin System / Q000187:drug effects; D012307:Risk Factors; D049994:Sodium Potassium Chloride Symporter Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D020257:Ventricular Remodeling
chemical_list: D000319:Adrenergic beta-Antagonists; D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D015415:Biomarkers; D049994:Sodium Potassium Chloride Symporter Inhibitors; D000450:Aldosterone; D012083:Renin