Patients with acute heart failure (AHF) are at high risk of HF re-hospitalization and death within 30 days of admission [1]. Accurate risk stratification at the acute phase could support physicians to select the most appropriate treatment strategies, which might lead to a better prognosis for these patients [2]. However, existing predictive models are of limited clinical use because they are not very accurate, especially for readmissions [3].
In this retrospective analysis of the Value of Endothelin Receptor Inhibition with Tezosentan in
Acute heart failure (VERITAS) studies [4], the value of adding BNP and troponin I to conventional prognostic markers was evaluated. For this purpose, multivariable prognostic models including baseline clinical data were created for:
a) the composite of death, in-hospital worsening HF, or HF re-hospitalization at 30 days,
b) death or HF re-hospitalization at 30 days,
c) death at 90 days.
Excluding biomarker data, the multivariable model included age, heart rate, respiratory rate, SBP, history of COPD, history of DM, history congestive HF, history of renal impairment, dyspnea severity by visual analogue scale (dyspnea VAS) at baseline, albumin, blood urea nitrogen (BUN), hemoglobin, and sodium.
The data of 1347 patients (93%) in the VERITAS studies were analyzed. They had been enrolled within 24 hours from admission for AHF, and were randomized to intravenous tezosentan, an endothelin antagonist, or placebo. BNP and troponins were measured retrospectively on stored plasma, because they had been measured in only 20% of patients when the study was ongoing. Moreover, troponin I, and not troponin T, was used for this analysis, because a higher number of troponin T values were missing, and troponin I and T values were highly correlated.
Note: the VERITAS program was discontinued prematurely because of the low probability of achieving a significant treatment effect.
For AHF patients in the VERITAS studies, the predictive value of conventional clinical assessments made shortly after admission was poor at identifying death or readmission at 30 days, but somewhat better at predicting all-cause mortality at 90 days. Measurement of BNP and troponin I at admission did not substantially improve the prediction of any of the specified outcomes.
1. O’Connor CM, AbrahamWT, Albert NM, et al. Predictors of mortality after discharge in patients hospitalized with heart failure: an analysis from the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF). Am Heart J 2008;156:662–673.
2. O’Connor CM, Mentz RJ, Cotter G, et al. The PROTECT in-hospital risk model: 7-day outcome in patients hospitalized with acute heart failure and renal dysfunction. Eur J Heart Fail 2012;14:605–612.
3. Lassus J, Gayat E, Mueller C, et al; GREAT-Network. Incremental value of biomarkers to clinical variables for mortality prediction in acutely decompensated heart failure: The Multinational Observational Cohort on Acute Heart Failure (MOCA) study. Int J Cardiol 2013;168:2186–2194.
4. McMurray JJ, Teerlink JR, Cotter G, et al; VERITAS Investigators. Effects of Tezosentan on Symptoms and Clinical Outcomes in Patients with Acute Heart Failure. The VERITAS Randomized Controlled Trials. JAMA 2007;298:2009–2019.
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