Anemia in heart failure patients was associated with significantly lower peak VO2 (971 vs 1243 ml/min, P<0.001), with each 1 g/dl increase in hemoglobin correlating to a 109 ml/min increase in VO2.
Observational (n=704)
No
Does resting hemoglobin concentration correlate with peak oxygen uptake in patients with chronic heart failure?
In patients with chronic heart failure, resting hemoglobin concentration is directly correlated with peak oxygen uptake, suggesting that changes in hemoglobin significantly impact exercise capacity.
Effect estimate: Slope 109 ml/min/g/dl
Absolute Event Rate: 971% vs 1243%
p-value: p=<0.001
Anemia is frequent in chronic heart failure (HF). To calculate what change in peak oxygen uptake ( VO(2)) should be expected in the event of changes in hemoglobin concentration, we studied the correlation between peak VO(2) and hemoglobin concentration in a large HF population. We carried out retrospective analysis of all cardiopulmonary exercise tests (CPET) performed in our HF Clinic between June 2001 and March 2009 in HF patients who had a resting hemoglobin concentration measurement taken within 7 days of the CPET. We collected 967 CPETs, 704 tests were considered maximal and analyzed. We identified 181 patients (26%) as anemic. Peak VO(2) was lower (P < 0.001) in anemic patients (971 +/- 23 ml/min) compared with nonanemic (1243 +/- 18 ml/min). The slope of the VO(2) vs. hemoglobin ratio was 109 ml/min/g/dl at peak exercise. This correlation remained significant also when several confounding variables were analyzed by multivariate analysis. As an average, each gram of hemoglobin accounts, at peak exercise, for 109 ml/min change in VO(2) which is equivalent to 0.97 ml/min/kg. Therefore, in HF patients anemia treatment should increase VO(2) by 109 ml/min for each g/dl of hemoglobin increase.
Agostoni et al. (Tue,) conducted a observational in Chronic heart failure (n=704). Anemia vs. Nonanemic was evaluated on Peak oxygen uptake (VO2) (Slope 109 ml/min/g/dl, p=<0.001). Anemia in heart failure patients was associated with significantly lower peak VO2 (971 vs 1243 ml/min, P<0.001), with each 1 g/dl increase in hemoglobin correlating to a 109 ml/min increase in VO2.