P Srinivas1, C N Manjunath2, Shaheena Banu3, K S Ravindranath4. 1. Post-Graduate, Sri Jayadeva Institute of Cardiovascular Sciences and Research , Bangalore, India . 2. Director and HOD, Department of Cardiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research , Bangalore, India . 3. HOD, Department of Biochemistry, Sri Jayadeva Institute of Cardiovascular Sciences and Research , Bangalore, India . 4. Professor, Department of Cardiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research , Bangalore, India .
Abstract
BACKGROUND: Heart failure (HF) is a growing public health problem. Patients often present to emergency department (ED) with acute onset dyspnea where a rapid triage is required to avoid misdiagnosis and to institute appropriate therapy. An objective risk-stratification in the ED is warranted to identify patients at high risk of adverse outcomes, so that more intensive therapy and vigilant follow-up after discharge are instituted. METHODS AND RESULTS: Fifty two consecutive acute HF (AHF) patients in NYHA class III/IV were enrolled for the present study. N-terminal pro B-type natriuretic peptide (NT-proBNP), high-sensitivity cardiac troponin T (hsTropT), high-sensitivity C-reactive protein (hsCRP) and Uric acid (UA) were evaluated at admission; a second sample for NT-proBNP and hsTropT was obtained 48h later. The end-point of the study, a composite of cardiovascular death, rehospitalisation for worsening HF symptoms and refractory HF was reached in 32.7% of patients during a median follow-up of 4.8mnth. Although, hsTropT (>0.014ng/ml), hsCRP (>0.5mg/dl) and UA (>5.6mg/dl for females and >7 mg/dl for males) were elevated in the vast majority of patients (92.3%, 75% and 63.5% respectively), baseline and changing patterns of NT-proBNP following treatment were the only predictors of adverse outcomes on follow-up. A significant correlation between hsTropT, hsCRP and UA was observed suggesting a link between inflammation, myocyte injury and oxidative stress in AHF. CONCLUSION: Baseline and changing patterns of NT-proBNP predicted adverse outcomes on follow-up suggesting that a strategy of serial measurement of NT-proBNP could prove invaluable in early risk stratification. Further research is needed to understand the link between inflammation, myocyte injury and oxidative stress in AHF which could provide potential therapeutic targets.
BACKGROUND:Heart failure (HF) is a growing public health problem. Patients often present to emergency department (ED) with acute onset dyspnea where a rapid triage is required to avoid misdiagnosis and to institute appropriate therapy. An objective risk-stratification in the ED is warranted to identify patients at high risk of adverse outcomes, so that more intensive therapy and vigilant follow-up after discharge are instituted. METHODS AND RESULTS: Fifty two consecutive acute HF (AHF) patients in NYHA class III/IV were enrolled for the present study. N-terminal pro B-type natriuretic peptide (NT-proBNP), high-sensitivity cardiac troponin T (hsTropT), high-sensitivity C-reactive protein (hsCRP) and Uric acid (UA) were evaluated at admission; a second sample for NT-proBNP and hsTropT was obtained 48h later. The end-point of the study, a composite of cardiovascular death, rehospitalisation for worsening HF symptoms and refractory HF was reached in 32.7% of patients during a median follow-up of 4.8mnth. Although, hsTropT (>0.014ng/ml), hsCRP (>0.5mg/dl) and UA (>5.6mg/dl for females and >7 mg/dl for males) were elevated in the vast majority of patients (92.3%, 75% and 63.5% respectively), baseline and changing patterns of NT-proBNP following treatment were the only predictors of adverse outcomes on follow-up. A significant correlation between hsTropT, hsCRP and UA was observed suggesting a link between inflammation, myocyte injury and oxidative stress in AHF. CONCLUSION: Baseline and changing patterns of NT-proBNP predicted adverse outcomes on follow-up suggesting that a strategy of serial measurement of NT-proBNP could prove invaluable in early risk stratification. Further research is needed to understand the link between inflammation, myocyte injury and oxidative stress in AHF which could provide potential therapeutic targets.
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