Abnormalities of pulmonary function in patients with congestive heart failure, and reversal with ipratropium bromide

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Abstract

Patients with congestive heart failure (CHF) have baseline restrictive and obstructive abnormalities in pulmonary function. Thus, improvement of respiratory parameters may provide a new method for the treatment of CHF. Ipratropium is an inhaled anticholinergic bronchodilator with no reported cardiac or systemic effect. A pilot study was performed to investigate the acute effects of a 72 μg inhaled dose of ipratropium bromide on pulmonary function and pulmonary artery pressures in 18 nonsmokers and 11 smokers with severe (New York Heart Association class 2 or 3), stable CHF who were referred for orthotopic cardiac transplantation. An unmatched group of 10 healthy subjects (5 men and 5 women, mean age 36.8 ± 1.8 years) were studied with pulmonary function testing alone. Forced expiratory volume in 1 second (FEV1) in 15 of 18 nonsmokers with CHF showed a favorable response with a mean improvement of 5.1% (2.74 ± 0.20 to 2.89 ± 0.19 liter after drug treatment; p = 0.0026). Forced expiratory flow between 25 and 75% of the forced vital capacity (FEF25–75) improved by 19% (2.50 ± 0.25 to 3.09 ± 0.28 liter/s; p = 0.0013). Eight of 11 smokers with CHF responded with a 9.5% increase in FEV1 (2.32 ± 0.21 to 2.54 ± 0.19 liter; p = 0.0006) and a 23.2% increase in FEF25–75 (1.82 ± 0.38 to 2.37 ± 0.46 liter/s; p = 0.0029). Pulmonary artery pressures, cardiac output, systemic arterial pressures, and cardiac rate and rhythm were unaffected by administration of the drug. All normal subjects responded to ipratropium bromide. FEV1 increased by 3.8% (4.14 ± 0.3 to 4.29 ± 0.3 liter; p = 0.0002), and FEF25–75 increased by 15.2% (4.28 ± 0.39 to 4.94 ± 0.41 liter/s; p = 0.0005). It is concluded that the airway response to ipratropium bromide in patients with CHF is highly significant. Further study is needed to determine whether chronic therapy with ipratropium bromide in selected patients with CHF will lead to improvements in exertional breathlessness and effort tolerance.

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    This study was supported in part by Grant 1K11 HL02361 from the National Institutes of Health, Bethesda, Maryland, to Dr. Kindman and by a grant from the Boehringer Ingelheim Pharmaceutical Corporation, Ridgefield, Connecticut.

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