Pulmonary function, cardiac function, and exercise capacity in a follow- up of patients with congestive heart failure treated with carvedilol

M. Guazzi, P. Agostani, M. Matturri, G. Pontone, M. D. Guazzi

Research output: Contribution to journalArticle

71 Citations (Scopus)

Abstract

Background: Chronic heart failure causes disturbances in ventilation and pulmonary gas transfer that participate in limiting peak exercise oxygen uptake (VO(2p)). The β-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. Methods: 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. Results: 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. Conclusions: 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.

Original languageEnglish
Pages (from-to)460-467
Number of pages8
JournalAmerican Heart Journal
Volume138
Issue number3 I
DOIs
Publication statusPublished - 1999

Fingerprint

Heart Failure
Exercise
Lung
Total Lung Capacity
Pulmonary Ventilation
Vital Capacity
Carbon Monoxide
Left Ventricular Function
Stroke Volume
Gases
Placebos
Blood Pressure
Anaerobic Threshold
Adrenergic Antagonists
Membranes
Tidal Volume
Forced Expiratory Volume
carvedilol
Carbon Dioxide
Adrenergic Receptors

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Pulmonary function, cardiac function, and exercise capacity in a follow- up of patients with congestive heart failure treated with carvedilol. / Guazzi, M.; Agostani, P.; Matturri, M.; Pontone, G.; Guazzi, M. D.

In: American Heart Journal, Vol. 138, No. 3 I, 1999, p. 460-467.

Research output: Contribution to journalArticle

@article{704e5a64fec14191889bf0c9a666f78c,
title = "Pulmonary function, cardiac function, and exercise capacity in a follow- up of patients with congestive heart failure treated with carvedilol",
abstract = "Background: Chronic heart failure causes disturbances in ventilation and pulmonary gas transfer that participate in limiting peak exercise oxygen uptake (VO(2p)). The β-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. Methods: 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. Results: 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. Conclusions: 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.",
author = "M. Guazzi and P. Agostani and M. Matturri and G. Pontone and Guazzi, {M. D.}",
year = "1999",
doi = "10.1016/S0002-8703(99)70148-1",
language = "English",
volume = "138",
pages = "460--467",
journal = "American Heart Journal",
issn = "0002-8703",
publisher = "Mosby Inc.",
number = "3 I",

}

TY - JOUR

T1 - Pulmonary function, cardiac function, and exercise capacity in a follow- up of patients with congestive heart failure treated with carvedilol

AU - Guazzi, M.

AU - Agostani, P.

AU - Matturri, M.

AU - Pontone, G.

AU - Guazzi, M. D.

PY - 1999

Y1 - 1999

N2 - Background: Chronic heart failure causes disturbances in ventilation and pulmonary gas transfer that participate in limiting peak exercise oxygen uptake (VO(2p)). The β-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. Methods: 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. Results: 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. Conclusions: 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.

AB - Background: Chronic heart failure causes disturbances in ventilation and pulmonary gas transfer that participate in limiting peak exercise oxygen uptake (VO(2p)). The β-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. Methods: 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. Results: 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. Conclusions: 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.

UR - http://www.scopus.com/inward/record.url?scp=0032845314&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032845314&partnerID=8YFLogxK

U2 - 10.1016/S0002-8703(99)70148-1

DO - 10.1016/S0002-8703(99)70148-1

M3 - Article

C2 - 10467196

AN - SCOPUS:0032845314

VL - 138

SP - 460

EP - 467

JO - American Heart Journal

JF - American Heart Journal

SN - 0002-8703

IS - 3 I

ER -