Survival and heart failure therapy in chronic dialysis patients with heart failure and reduced left ventricular ejection fraction: an observational retrospective study.

AIMS: We retrospectively followed 250 patients who started dialysis between 2005 and 2009 to clarify the prevalence, the prognosis and the prescribed heart failure treatment of systolic heart failure patients on dialysis. METHODS AND RESULTS: This cohort was divided according to left ventricular ejection fraction (LVEF): group A with a reduced LVEF (< or = 45%, n = 45) versus group B with a preserved LVEF (> 45%, n = 205). Patients in group A had a significantly worse survival after 12 and 24 months (68.9% and 55.5% vs. 87.3% and 73.0%, respectively, P = 0.0001). Hazard ratio for all-cause mortality was 2.70 (C.I. 95% 1.6 - 4.56, P = 0.0002). In the subgroup of patients with a LVEF < 30% the hazard ratio increased to 3.45 (C.I. 95% 1.71 - 6.94, P = 0.0005). The cumulative incidence of cardiovascular death was significantly higher in group A (hazard ratio: 4.78 (C.I. 95% 1.99- 11.50, P = 0.0005), especially in the subgroup with a LVEF < 30%. In group A 71%, 31% and 9% of the patients received a beta blocker, an ACE inhibitor and an angiotensin-receptor blocker, respectively. Only 27% were treated with the combination of a beta blocker and a RAAS inhibitor, while 18% did not receive any heart failure therapy. Most patients only received a low dose of neurohormonal blockers (< or = 25% of the recommended daily dose). The use of these heart failure medications was not significantly different between group A and B. CONCLUSION: After initiation of dialysis, patients with heart failure and reduced LVEF have a bad prognosis. Only a minority of these patients receive adequate specific heart failure treatment.

Chemoreflex and metaboreflex control during static hypoxic exercise.

To investigate the effects of muscle metaboreceptor activation during hypoxic static exercise, we recorded muscle sympathetic nerve activity (MSNA), heart rate, blood pressure, ventilation, and blood lactate in 13 healthy subjects (22 +/- 2 yr) during 3 min of three randomized interventions: isocapnic hypoxia (10% O(2)) (chemoreflex activation), isometric handgrip exercise in normoxia (metaboreflex activation), and isometric handgrip exercise during isocapnic hypoxia (concomitant metaboreflex and chemoreflex activation). Each intervention was followed by a forearm circulatory arrest to allow persistent metaboreflex activation in the absence of exercise and chemoreflex activation. Handgrip increased blood pressure, MSNA, heart rate, ventilation, and lactate (all P < 0.001). Hypoxia without handgrip increased MSNA, heart rate, and ventilation (all P < 0.001), but it did not change blood pressure and lactate. Handgrip enhanced blood pressure, heart rate, MSNA, and ventilation responses to hypoxia (all P < 0.05). During circulatory arrest after handgrip in hypoxia, heart rate returned promptly to baseline values, whereas ventilation decreased but remained elevated (P < 0.05). In contrast, MSNA, blood pressure, and lactate returned to baseline values during circulatory arrest after hypoxia without exercise but remained markedly increased after handgrip in hypoxia (P < 0.05). We conclude that metaboreceptors and chemoreceptors exert differential effects on the cardiorespiratory and sympathetic responses during exercise in hypoxia.