Bharathi Upadhya1, Michael Rocco1, Cora E Lewis1, Suzanne Oparil1, Laura C Lovato1, William C Cushman1, Jeffrey T Bates1, Natalie A Bello1, Gerard Aurigemma1, Lawrence J Fine1, Karen C Johnson1, Carlos J Rodriguez1, Dominic S Raj1, Anjay Rastogi1, Leonardo Tamariz1, Alan Wiggers1, Dalane W Kitzman2. 1. From the Cardiovascular Medicine Section (B.U., C.J.R., D.W.K.), Nephrology Section, Department of Internal Medicine (M.R.), and Biostatistics (L.C.L.), Wake Forest School of Medicine, Winston-Salem, NC; Division of Preventive Medicine (C.E.L.) and Division of Cardiovascular Disease (S.O.), Department of Medicine, University of Alabama, Birmingham; Preventive Medicine Section, Veterans Affairs Medical Center, Memphis, TN (W.C.C.); Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, TX (J.T.B.); Cardiovascular Division, Department of Medicine, Columbia University Medical Center, New York, NY (N.A.B.); Department of Cardiology, University of Massachusetts Medical School, Worcester (G.A.); Clinical Applications and Prevention Branch, Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, MD (L.J.F.); Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis (K.C.J.); Department of Medicine-Nephrology, George Washington University School of Medicine, DC (D.S.R.); Division of Nephrology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles (A.R.); University of Miami Miller School of Medicine, FL and Veterans Affairs Medical Center, Miami, FL (L.T.); and UH Harrington Heart and Vascular Institute, Cleveland Medical Center, OH (A.W.). 2. From the Cardiovascular Medicine Section (B.U., C.J.R., D.W.K.), Nephrology Section, Department of Internal Medicine (M.R.), and Biostatistics (L.C.L.), Wake Forest School of Medicine, Winston-Salem, NC; Division of Preventive Medicine (C.E.L.) and Division of Cardiovascular Disease (S.O.), Department of Medicine, University of Alabama, Birmingham; Preventive Medicine Section, Veterans Affairs Medical Center, Memphis, TN (W.C.C.); Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, TX (J.T.B.); Cardiovascular Division, Department of Medicine, Columbia University Medical Center, New York, NY (N.A.B.); Department of Cardiology, University of Massachusetts Medical School, Worcester (G.A.); Clinical Applications and Prevention Branch, Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, MD (L.J.F.); Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis (K.C.J.); Department of Medicine-Nephrology, George Washington University School of Medicine, DC (D.S.R.); Division of Nephrology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles (A.R.); University of Miami Miller School of Medicine, FL and Veterans Affairs Medical Center, Miami, FL (L.T.); and UH Harrington Heart and Vascular Institute, Cleveland Medical Center, OH (A.W.). dkitzman@wakehealth.edu.
Abstract
BACKGROUND:Acute decompensated heart failure (ADHF) was a frequent common outcome in SPRINT (Systolic Blood Pressure Intervention Trial). We examined whether there was differential reduction in ADHF events from intensive blood pressure [BP] treatment among the 6 key, prespecified subgroups in SPRINT: age ≥75 years, prior cardiovascular disease, chronic kidney disease, women, black race, and 3 levels of baseline systolic BP (≤132 versus >132 to <145 versus ≥145 mm Hg). METHODS AND RESULTS:ADHF was defined as hospitalization for ADHF, confirmed and formally adjudicated by a blinded events committee using standardized protocols. At 3.29 years follow-up, there were 103 ADHF events (2.2%) among 4683 standard arm participants and 65 ADHF events (1.4%) among 4678 intensive arm participants (Cox proportional hazards ratio, 0.63; 95% confidence interval, 0.46-0.85; P value =0.003). In multivariable analyses, including treatment arm, baseline covariates that were significant predictors for ADHF included chronic kidney disease, cardiovascular disease, age≥75 years, body mass index, and higher systolic BP. The beneficial effect of the intervention on incident ADHF was consistent across all prespecified subgroups. Participants who had incident ADHF had markedly increased risk of subsequent cardiovascular events, including a 27-fold increase (P<0.001) in cardiovascular death. CONCLUSIONS: Targeting a systolic BP<120 mm Hg, compared with <140 mm Hg, significantly reduced ADHF events, and the benefit was similar across all key, prespecified subgroups. Participants who developed ADHF had markedly increased risk for subsequent cardiovascular events and death, highlighting the importance of strategies aimed at prevention of ADHF, especially intensive BP reduction. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01206062.
RCT Entities:
BACKGROUND: Acute decompensated heart failure (ADHF) was a frequent common outcome in SPRINT (Systolic Blood Pressure Intervention Trial). We examined whether there was differential reduction in ADHF events from intensive blood pressure [BP] treatment among the 6 key, prespecified subgroups in SPRINT: age ≥75 years, prior cardiovascular disease, chronic kidney disease, women, black race, and 3 levels of baseline systolic BP (≤132 versus >132 to <145 versus ≥145 mm Hg). METHODS AND RESULTS:ADHF was defined as hospitalization for ADHF, confirmed and formally adjudicated by a blinded events committee using standardized protocols. At 3.29 years follow-up, there were 103 ADHF events (2.2%) among 4683 standard arm participants and 65 ADHF events (1.4%) among 4678 intensive arm participants (Cox proportional hazards ratio, 0.63; 95% confidence interval, 0.46-0.85; P value =0.003). In multivariable analyses, including treatment arm, baseline covariates that were significant predictors for ADHF included chronic kidney disease, cardiovascular disease, age≥75 years, body mass index, and higher systolic BP. The beneficial effect of the intervention on incident ADHF was consistent across all prespecified subgroups. Participants who had incident ADHF had markedly increased risk of subsequent cardiovascular events, including a 27-fold increase (P<0.001) in cardiovascular death. CONCLUSIONS: Targeting a systolic BP<120 mm Hg, compared with <140 mm Hg, significantly reduced ADHF events, and the benefit was similar across all key, prespecified subgroups. Participants who developed ADHF had markedly increased risk for subsequent cardiovascular events and death, highlighting the importance of strategies aimed at prevention of ADHF, especially intensive BP reduction. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01206062.
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