Red cell distribution width as a novel prognostic marker in heart failure: data from the CHARM Program and the Duke Databank

G Michael Felker, Larry A Allen, Stuart J Pocock, Linda K Shaw, John J V McMurray, Marc A Pfeffer, Karl Swedberg, Duolao Wang, Salim Yusuf, Eric L Michelson, Christopher B Granger, CHARM Investigators, G Michael Felker, Larry A Allen, Stuart J Pocock, Linda K Shaw, John J V McMurray, Marc A Pfeffer, Karl Swedberg, Duolao Wang, Salim Yusuf, Eric L Michelson, Christopher B Granger, CHARM Investigators

Abstract

Objectives: The goal of this study was to identify potentially novel laboratory markers of risk in chronic heart failure patients.

Background: Although a variety of prognostic markers have been described in heart failure, a systematic assessment of routine laboratory values has not been reported.

Methods: All 2,679 symptomatic chronic heart failure patients from the North American CHARM (Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity) program had a wide range of laboratory measures performed at a core facility, enabling us to assess the relationship between routine blood tests and outcomes using a Cox proportional hazards model. We then replicated our findings in a cohort of 2,140 heart failure patients from the Duke Databank.

Results: Among 36 laboratory values considered in the CHARM program, higher red cell distribution width (RDW) showed the greatest association with morbidity and mortality (adjusted hazard ratio 1.17 per 1-SD increase, p < 0.001). Higher RDW was among the most powerful overall predictors, with only age and cardiomegaly showing a better independent association with outcome. This finding was replicated in the Duke Databank, in which higher RDW was strongly associated with all-cause mortality (adjusted hazard ratio 1.29 per 1 SD, p < 0.001), second only to age as a predictor of outcome.

Conclusions: In 2 large contemporary heart failure populations, RDW was found to be a very strong independent predictor of morbidity and mortality. Understanding how and why this marker is associated with outcome may provide novel insights into heart failure pathophysiology.

Source: PubMed

3
订阅