期刊
EUROPEAN JOURNAL OF HEART FAILURE
卷 8, 期 4, 页码 420-427出版社
WILEY
DOI: 10.1016/j.ejheart.2005.10.003
关键词
ventilatory response; heart failure; cardiopulmonary exercise testing; interstitial pulmonary oedema; risk stratification
Background: Patients with chronic heart failure (CHF) present with exercise-induced hyperpnea, but its pathophysiological mechanism has not been thoroughly investigated. We aimed to determine the relationship between exercise-induced hyperpnea, resting haemodynamic measurements and the validity of ventilatory response (V-E/V-CO2 slope) as a mortality predictor in CHF patients. Methods: Ninety-eight CHF patients (90M/8F) underwent a symptom-limited treadmill cardiopulmonary exercise test (CPET). Right heart catheterization and radionuclide ventriculography were performed within 72 h of CPET. Results: Twenty-seven patients died from cardiac causes during 20 +/- 6 months follow-up. Non-survivors ' had a lower peak oxygen consumption (V(O2)p), (16.5 +/- 4.9vs. 20.2 +/- 6,1, ml/kg/min,p=0.003), a steeper V-E/V-CO2 slope (34.8 +/- 8.3 vs. 28.9 +/- 4.8, p < 0.001) and a higher pulmonary capillary wedge pressure (PCWP) (19.5 +/- 8.6 vs. 11.7 +/- 6.5 min Hg, p=0.008) than survivors. By multivariate survival analysis, the V-E/V-CO2 slope as a continuous variable was an independent prognostic factor (chi(2) : 8.5, relative risk: 1. 1, 95% CI: 1.03 -1.18, p = 0.004). Overall mortality was 52% in patients with V-E/V-CO2 slope >= 34 and 18% in those with V-E/V-CO2 slope < 34 (log rank: 18.5, p < 0.001). In a subgroup of patients (V(O2)p: 10-18 ml/kg/min), V-E/V-CO2 slope was a significant predictor of mortality (relative risk: 6.2, 95% CI: 1.7-22.2, p=0.002). Patients with high V-E/V-CO2 slope had higher resting PCWP (19.9 +/- 9.1 vs. 11.3 +/- 5.7 mmHg, p < 0.001) and V-E/V-CO2 slope correlated significantly with PCWP (r: 0.57, p < 0.001). Conclusions: The V-E/V-CO2 slope, as an index of ventilatory response to exercise, improves the fisk stratification of CHF patients. Interstitial pulmonary oedema may be a pathophysiological mechanism of inefficient ventilation during exercise in these patients. (c) 2005 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
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