Guazzi M, Agostoni P, Matturri M, Pontone G, Guazzi M D
Istituto di Cardiologia dell'Università degli Studi, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione Monzino, IRCCS, Milano, Italy.
Am Heart J. 1999 Sep;138(3 Pt 1):460-7. doi: 10.1016/s0002-8703(99)70148-1.
Chronic heart failure causes disturbances in ventilation and pulmonary gas transfer that participate in limiting peak exercise oxygen uptake (VO(2p )). The beta-adrenergic receptor blocker carvedilol improves left ventricular (LV) function and not VO(2p). This study was aimed at investigating the pulmonary response to changes in LV performance produced by carvedilol in patients with chronic heart failure.
Twenty-one patients with New York Heart Association class II to III heart failure were randomly assigned (2 to 1) to carvedilol (25 mg twice daily, n = 14) or placebo (n = 7) for 6 months. Rest forced expiratory volume (FEV(1)), vital capacity, total lung capacity, carbon monoxide diffusing capacity, its alveolar-capillary membrane component, pulmonary venous and transmitral flows (for monitoring changes in LV end-diastolic pressure), LV diastolic and systolic dimensions, stroke volume, ejection fraction, and fiber shortening velocity were measured at baseline and at 3 and 6 months. VO(2p), peak ratio of dead space to tidal volume (VD/VT(p)), ventilatory equivalent for carbon dioxide production (VE/VCO(2)), and VO(2) at anaerobic threshold (VO(2at)) were also determined.
FEV(1), vital capacity, total lung capacity, carbon monoxide diffusing capacity, and the alveolar-capillary membrane component were impaired in chronic heart failure compared with 14 volunteers and did not vary with treatment. Carvedilol reduced end-diastolic pressure, end-diastolic diameter, and end-systolic diameter and increased ejection fraction, stroke volume, and fiber shortening velocity without affecting VO(2p), VO(2at), VD/VT(p), or VE/VCO(2) at 3 and 6 months. Placebo did not produce significant changes.
In chronic heart failure carvedilol ameliorates LV function at rest and does not significantly affect ventilation and pulmonary gas transfer or functional capacity. These results suggest that improvement in cardiac hemodynamics with carvedilol does not reverse pulmonary dysfunction. Persistent lung impairment might have some role in the failure of carvedilol to improve exercise performance.
慢性心力衰竭会导致通气和肺气体交换障碍，这些障碍会限制运动峰值摄氧量（VO₂p）。β-肾上腺素能受体阻滞剂卡维地洛可改善左心室（LV）功能，但对VO₂p无影响。本研究旨在探讨慢性心力衰竭患者中卡维地洛引起的左心室功能变化所导致的肺部反应。
21例纽约心脏病协会心功能II至III级的心力衰竭患者被随机分组（2∶1），分别给予卡维地洛（每日2次，每次25mg，n = 14）或安慰剂（n = 7），为期6个月。在基线、3个月和6个月时测量静息用力呼气容积（FEV₁）、肺活量、肺总量、一氧化碳弥散量、其肺泡-毛细血管膜成分、肺静脉和二尖瓣血流（用于监测左心室舒张末期压力变化）、左心室舒张和收缩内径、每搏量、射血分数以及纤维缩短速度。还测定了VO₂p、死腔与潮气量峰值比（VD/VT(p)）、二氧化碳产生的通气当量（VE/VCO₂）以及无氧阈时的VO₂（VO₂at）。
与14名志愿者相比，慢性心力衰竭患者的FEV₁、肺活量、肺总量、一氧化碳弥散量及肺泡-毛细血管膜成分均受损，且不受治疗影响。卡维地洛在3个月和6个月时降低了舒张末期压力、舒张末期直径和收缩末期直径，增加了射血分数、每搏量和纤维缩短速度，但未影响VO₂p、VO₂at、VD/VT(p)或VE/VCO₂。安慰剂未产生显著变化。
在慢性心力衰竭中，卡维地洛可改善静息时的左心室功能，且对通气、肺气体交换或功能能力无显著影响。这些结果表明，卡维地洛改善心脏血流动力学并不能逆转肺功能障碍。持续的肺功能损害可能在卡维地洛未能改善运动表现中起到一定作用。
