The effect of intravenous ferric carboxymaltose on red cell distribution width: a subanalysis of the FAIR-HF study

<p>Aims: Red cell distribution width (RDW), a measure of variability in red blood cell size, is a novel prognostic marker in chronic heart failure (CHF). Iron deficiency contributes to elevated RDW. In the FAIR-HF trial, i.v. ferric carboxymaltose (FCM) improved the 6 min walk test (6MWT) distance in iron-deficient CHF patients. We studied the effect of FCM on RDW and the relationship between RDW and 6MWT distance.</p> <p>Methods and results: In FAIR-HF, iron-deficient CHF patients were randomized to FCM or placebo in a 2:1 ratio. From the total cohort (n = 459), we included 415 patients in whom RDW values and 6MWT distance were available for baseline and at least one follow-up visit (after 4, 12, and 24 weeks). Baseline RDW was higher in anaemic (haemoglobin &#60;12 g/dL) compared with non-anaemic patients [15.2% (14.0–16.8) vs. 14.2% (13.4–15.4), P &#60; 0.0001, median (interquartile range)]. In multivariate analysis, RDW was significantly associated with transferrin saturation (P &#60; 0.001) and C-reactive protein levels (P = 0.002). Treatment with FCM led to a biphasic response; RDW increased within 4 weeks (+0.54% absolute change from baseline, P = 0.01) but fell to values below the placebo group after 24 weeks (–1.0 %, P = 0.03). The 6MWT distance and RDW were inversely related at baseline (r = –0.30, P &#60; 0.0001). In all patients, the increase in 6MWT distance after 24 weeks was significantly correlated with a decrease in RDW (r= –0.25, P &#60; 0.0001), even after adjustment for changes in haemoglobin.</p> <p>Conclusions: Iron deficiency in CHF is associated with high RDW, even after adjustment for the presence of anaemia. Treatment with i.v. FCM in iron-deficient CHF patients decreases RDW.</p

The effect of intravenous ferric carboxymaltose on red cell distribution width: a subanalysis of the FAIR-HF study

&lt;p&gt;Aims: Red cell distribution width (RDW), a measure of variability in red blood cell size, is a novel prognostic marker in chronic heart failure (CHF). Iron deficiency contributes to elevated RDW. In the FAIR-HF trial, i.v. ferric carboxymaltose (FCM) improved the 6 min walk test (6MWT) distance in iron-deficient CHF patients. We studied the effect of FCM on RDW and the relationship between RDW and 6MWT distance.&lt;/p&gt; &lt;p&gt;Methods and results: In FAIR-HF, iron-deficient CHF patients were randomized to FCM or placebo in a 2:1 ratio. From the total cohort (n = 459), we included 415 patients in whom RDW values and 6MWT distance were available for baseline and at least one follow-up visit (after 4, 12, and 24 weeks). Baseline RDW was higher in anaemic (haemoglobin &#60;12 g/dL) compared with non-anaemic patients [15.2% (14.0–16.8) vs. 14.2% (13.4–15.4), P &#60; 0.0001, median (interquartile range)]. In multivariate analysis, RDW was significantly associated with transferrin saturation (P &#60; 0.001) and C-reactive protein levels (P = 0.002). Treatment with FCM led to a biphasic response; RDW increased within 4 weeks (+0.54% absolute change from baseline, P = 0.01) but fell to values below the placebo group after 24 weeks (–1.0 %, P = 0.03). The 6MWT distance and RDW were inversely related at baseline (r = –0.30, P &#60; 0.0001). In all patients, the increase in 6MWT distance after 24 weeks was significantly correlated with a decrease in RDW (r= –0.25, P &#60; 0.0001), even after adjustment for changes in haemoglobin.&lt;/p&gt; &lt;p&gt;Conclusions: Iron deficiency in CHF is associated with high RDW, even after adjustment for the presence of anaemia. Treatment with i.v. FCM in iron-deficient CHF patients decreases RDW.&lt;/p&gt

Effects of the long-term administration of nebivolol on the clinical symptoms, exercise capacity, and left ventricular function of patients with diastolic dysfunction: results of the ELANDD study

AIMS: We hypothesized that nebivolol, a beta-blocker with nitric oxide-releasing properties, could favourably affect exercise capacity in patients with heart failure and preserved left ventricular ejection fraction (HFPEF). METHODS AND RESULTS: A total of 116 subjects with HFPEF, in New York Heart Association (NYHA) functional class II-III, with left ventricular ejection fraction (LVEF) >45%, and with echo-Doppler signs of LV diastolic dysfunction, were randomized to 6 months treatment with nebivolol or placebo, following a double-blind, parallel group design. The primary endpoint of the study was the change in 6 min walk test distance (6MWTD) after 6 months. Nebivolol did not improve 6MWTD (from 420 ± 143 to 428 ± 141 m with nebivolol vs. from 412 ± 123 to 446 ± 119 m with placebo, P = 0.004 for interaction) compared with placebo, and the peak oxygen uptake also remained unchanged (peakVO(2); from 17.02 ± 4.79 to 16.32 ± 3.76 mL/kg/min with nebivolol vs. from 17.79 ± 5.96 to 18.59 ± 5.64 mL/kg/min with placebo, P = 0.63 for interaction). Resting and peak blood pressure and heart rate decreased with nebivolol. A significant correlation was found between the change in peak exercise heart rate and that in peakVO(2) (r = 0.391; P = 0.003) for the nebivolol group. Quality of life, assessed using the Minnesota Living with Heart Failure Questionnaire, and NYHA classification improved to a similar extent in both groups, whereas N-terminal pro brain natriuretic peptide (NT-pro BNP) plasma levels remained unchanged. CONCLUSIONS: Compared with placebo, 6 months treatment with nebivolol did not improve exercise capacity in patients with HFPEF. Its negative chronotropic effect may have contributed to this result