Effects of valsartan on morbidity and mortality in patients with heart failure not receiving angiotensin-converting enzyme inhibitors
Aldo P. Maggioni, MD*,*,
Inder Anand, MD ,
Sidney O. Gottlieb, MD ,
Roberto Latini, MD ,
Gianni Tognoni, MD ,
Jay N. Cohn, MD|| the Val-HeFT Investigators
* ANMCO Research Center, Florence, Italy
Veterans Affairs Medical Center, Minneapolis, Minnesota, USA
Mid-Atlantic Cardiovascular Consultants, P.A., Baltimore, Maryland, USA
Mario Negri Institute, Milan, Italy
|| University of Minnesota, Minneapolis, Minnesota, USA

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Figure 1 (A) Kaplan-Meier curves for mortality in the valsartan (dotted line) and placebo (solid line) groups (n = 185 and 181, respectively) without angiotensin-converting enzyme (ACE) inhibitor background therapy (p = 0.017 by log-rank test). (B) Kaplan-Meier curves for the combined end point of mortality and morbidity in the valsartan (dotted line) and placebo (solid line) groups without ACE inhibitor background therapy (p < 0.001 by the log-rank test). Risk ratio (RR) and 95% confidence interval (CI) obtained using Cox regression.
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Figure 2 Echocardiographic changes over time. (A) Least squares mean (LSM) change (±SEM) from baseline in left ventricular ejection fraction (%). (B) LSM change from baseline in left ventricular internal diastolic diameter/body surface area (cm/m2). The p values refer to the LSM comparison between the valsartan (solid bars) and placebo (open bars) groups by analysis of co-variance. n = total number of patients in the valsartan and placebo treatment groups.
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Figure 3 Neurohormonal changes over time: least squares mean (LSM) changes from baseline in the plasma concentrations of norepinephrine (A) and BNP (B). The p values refer to the LSM comparison between the valsartan (solid bars) and placebo (open bars) groups by analysis of co-variance. n = total number of patients in the valsartan and placebo treatment groups.
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