AIMS: Exercise intolerance predicts mortality in patients with chronic heart failure (CHF). Recently, increased red cell distribution width (RDW) has emerged as an additional powerful predictor of poor outcome. We investigated the relationship between RDW and exercise capacity in patients with CHF. In addition, the association between training-induced improved maximal aerobic capacity (VO(2)peak) and RDW was studied. METHODS AND RESULTS: Stable and optimally treated CHF patients (n = 118) with a left ventricular ejection fraction (LVEF) <40% were included. RDW and cardiopulmonary exercise testing were obtained at baseline and after 6 months of exercise training (n = 71) or a sedentary lifestyle (n = 47). At baseline, log[RDW] was inversely related to VO(2)peak (P = 0.003), independently of disease severity [LVEF, New York Heart Association class, N-terminal pro brain natriuretic peptide (NT-proBNP)] and haemoglobin. Exercise training was associated with a decrease in RDW compared with controls (P < 0.0001 for interaction), independent of baseline VO(2)peak, haemoglobin, and NT-proBNP levels. The change in RDW after 6 months was significantly related to the change in VO(2)peak (r= -0.248, P = 0.009). CONCLUSIONS: Higher RDW is independently related to impaired exercise capacity in CHF patients. Increased VO(2)peak following exercise training relates to the observed changes in RDW. Whether increased RDW is a marker of impaired exercise tolerance, or plays a pathophysiological role in impaired oxygen transport, deserves further investigation.
AIMS: Exercise intolerance predicts mortality in patients with chronic heart failure (CHF). Recently, increased red cell distribution width (RDW) has emerged as an additional powerful predictor of poor outcome. We investigated the relationship between RDW and exercise capacity in patients with CHF. In addition, the association between training-induced improved maximal aerobic capacity (VO(2)peak) and RDW was studied. METHODS AND RESULTS: Stable and optimally treated CHFpatients (n = 118) with a left ventricular ejection fraction (LVEF) <40% were included. RDW and cardiopulmonary exercise testing were obtained at baseline and after 6 months of exercise training (n = 71) or a sedentary lifestyle (n = 47). At baseline, log[RDW] was inversely related to VO(2)peak (P = 0.003), independently of disease severity [LVEF, New York Heart Association class, N-terminal pro brain natriuretic peptide (NT-proBNP)] and haemoglobin. Exercise training was associated with a decrease in RDW compared with controls (P < 0.0001 for interaction), independent of baseline VO(2)peak, haemoglobin, and NT-proBNP levels. The change in RDW after 6 months was significantly related to the change in VO(2)peak (r= -0.248, P = 0.009). CONCLUSIONS: Higher RDW is independently related to impaired exercise capacity in CHFpatients. Increased VO(2)peak following exercise training relates to the observed changes in RDW. Whether increased RDW is a marker of impaired exercise tolerance, or plays a pathophysiological role in impaired oxygen transport, deserves further investigation.