SUMMARY
Aim:To assess the effect of chronotropic incompetence on functional capacity in chronic heart failure (CHF) patients, as evaluated as NYHA and peak oxygen consumption (pVO 2 ), focusing on the presence and dose of β-blocker treatment. Methods: Nine hundred and sixty-seven consecutive CHF patients were evaluated, 328 of whom were discarded because they failed to meet the study criteria. Of the 639 analyzed, 90 were not treated with β-blockers whereas the other 549 were. The latter were further subdivided in high (n = 184) and low (n = 365) β-blockers daily dose group in accordance with an arbitrary cut-off of 25 mg for carvedilol and of 5 mg for bisoprolol. Failure to achieve 80% of the percentage of maximum age predicted peak heart rate (%Max PHR) or of HR reserve (%HRR) constituted chronotropic incompetence. Results: No differences were found in NYHA or pVO2 between patients with and without β-blockers and, similarly, between high and low β-blocker dose groups. Twenty and sixty-nine percent of not β-blocked patients showed chronotropic incompetence according to %Max PHR and %HRR, respectively, whereas this prevalence rose to 61% and 84% in those on β-blocker therapy. Patients taking β-blockers without chronotropic incompetence, as inferable from both %Max PHR and %HRR, showed higher NYHA and pVO2 regardless of drug dose, whereas, in not β-blocked patients, only %HRR revealed a difference in functional capacity. At multivariable analysis, HR increase during exercise ( HR) was the variable most strongly associated to pVO2 (β: 0.572; SE: 0.008; P < 0.0001) and NYHA class (β: −0.499; SE: 0.001; P < 0.0001). Conclusions: HR is a powerful predictor of CHF severity regardless of the presence of β-blocker therapy and of β-blocker daily dose.
Multidetector computed tomography is feasible, safe, and accurate for identification of idiopathic versus ischemic DCM, and may represent an alternative to coronary angiography.
Aims: To evaluate whether carvedilol influences exercise hyperventilation and the ventilatory response to hypoxia in heart failure (HF). Methods and results: Fifteen HF patients participated to this double blind, randomised, placebo controlled, cross-over study. Patients were evaluated by quality of life questionnaire, echocardiography, pulmonary function and cardiopulmonary exercise tests (ramp and constant workload) both in normoxia (FiO 2 = 21%) and hypoxia (FiO 2 = 16%, equivalent to a simulated altitude of 2000m). Carvedilol improved clinical condition and reduced left ventricle size, but had no effect on lung mechanics. In normoxia during exercise, ventilation was lower, V CO 2 unchanged and PaCO 2 (constant workload) or PetCO 2 (ramp) higher with carvedilol, exercise capacity was unchanged (peak workload 92 T 22 and 90 T 22W for placebo and carvedilol, respectively). Abnormal V E /V CO 2 slope was reduced by carvedilol. Hypoxia increased ventilation but less with carvedilol; exercise capacity decreased to 87 T 21 W (placebo) and to 80 T 11W (carvedilol, p < 0.01). With hypoxia, carvedilol decreased V E /V CO 2 slope. At constant workload exercise with hypoxia, PaO 2 decreased to 69 T 6 mm Hg (placebo) and to 64 T 5 (carvedilol, p < 0.01). Conclusion: Carvedilol reduced hyperventilation possibly by reducing peripheral chemoreflex sensitivity as suggested by PaCO 2 increase with normoxia and PaO 2 decrease with hypoxia without V CO 2 and V D /V T changes. Lessening hyperventilation is beneficial when breathing normally, but detrimental when hyperventilation is needed for exercise at high altitude.
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