Correspondence

Bronchial Hyperresponsiveness in Heart Failure

N Engl J Med 1993; 328:1424-1425May 13, 1993

Article

To the Editor:

The role of bronchial hyperresponsiveness in the pathophysiology of dyspnea in congestive heart failure has been a subject of considerable interest1-3. Although there is no doubt that patients with heart failure have increased airways resistance, and that many have bronchial hyperreactivity to inhaled methacholine at rest, the contribution of airways obstruction to exercise limitation has not been established.

Cabanes et al. (June 18, 1992, issue)4 observed that exercise performance improved in patients with left ventricular dysfunction after they inhaled methoxamine, but did not produce evidence of exercise-induced changes in spirometric variables, and their conclusion that methoxamine alters exercise tolerance through its effects on airways resistance remains speculative. The potential for improvement in exercise tolerance with the use of bronchodilators had already been recognized5.

In an attempt to determine whether exercise-induced changes in airway resistance actually occur in heart failure, we investigated the effects of maximal exercise on spirometric variables in patients with stable congestive heart failure, and we also investigated the effects of pretreatment with a nebulized beta-agonist (albuterol, 2.5 mg; Ventolin, Allen and Hanburys) and an anticholinergic agent (ipratropium bromide, 0.5 mg; Atrovent, Boehringer Ingelheim) in a randomized, double-blind crossover study of nine patients. Three patients were in functional class II of the New York Heart Association, and six were in class III. The mean daily dose of furosemide or its equivalent was 58 mg; eight patients were taking an angiotensin-converting-enzyme inhibitor. We found no evidence of exercise-induced bronchoconstriction; instead, we observed small increases in the forced expiratory volume in one second (FEV₁) and the peak expiratory flow rate at peak exercise with both control (saline) and bronchodilator pretreatment (Table 1Table 1Mean (±SD) Results of Spirometry in Nine Patients with Congestive Heart Failure, after the Administration of Saline and Bronchodilator.). Pretreatment with these agents had only minor effects on spirometric values at rest and did not influence exercise ventilation, oxygen saturation, spirometric variables at peak exercise or recovery, or exercise duration. We conclude from these data that exercise-induced bronchoconstriction does not significantly limit exercise performance in patients with heart failure.

David P. Moore, M.B., Ch.B., M.R.C.P.
Adele Weston, M.Sc.
J. Michael B. Hughes, M.D., F.R.C.P.
Celia M. Oakley, M.D., F.R.C.P.
John G.F. Cleland, M.D., F.R.C.P.
Hammersmith Hospital, London W12 ONN, United Kingdom

5 References

1. 1

   Cabanes LR, Weber SN, Matran R, et al. Bronchial hyperresponsiveness to methacholine in patients with impaired left ventricular function. N Engl J Med 1989;320:1317-1322
   Full Text | Web of Science | Medline

2. 2

   Cardiac asthmaLancet 1990;335:693-694
   CrossRef | Web of Science | Medline

3. 3

   Fishman AP. Cardiac asthma -- a fresh look at an old wheeze. N Engl J Med 1989;320:1346-1348
   Full Text | Web of Science | Medline

4. 4

   Cabanes L, Costes F, Weber S, et al. Improvement in exercise performance by inhalation of methoxamine in patients with impaired left ventricular function. N Engl J Med 1992;326:1661-1665
   Full Text | Web of Science | Medline

5. 5

   Kindman LA. Bronchial hyperresponsiveness in cardiac failure. N Engl J Med 1989;321:1756-1757
   Full Text | Web of Science | Medline

Author/Editor Response

The authors reply:

To the Editor: We agree with Moore et al. that since we did not perform spirometric testing at peak exercise, our finding that inhaled methoxamine improved exercise capacity in patients with left ventricular failure does not provide direct evidence that this was achieved by a decrease in airways resistance.

In our study we selected subjects whose limiting symptom in the activities of daily life was dyspnea; furthermore, the patients performed a symptom-limited, maximal-exercise test with a constant workload protocol specifically designed to reproduce dyspnea as the limiting factor. The protocol being truly maximal, the patients were unable to perform a satisfactory forced expiration at peak exercise, and we could not therefore obtain reliable FEV₁ measurements. Moore et al. do not provide data about how their patients were selected or about their exercise protocol. It is possible that under less strenuous conditions, FEV₁ can be reliably measured; but in that situation, bronchial obstruction may no longer be an important contributor to exertional dyspnea.

The fact that albuterol did not enhance exercise duration is in agreement with our own findings. In a previous study 1 we showed that this drug had only a moderate effect on bronchial hyperresponsiveness, whereas pretreatment with methoxamine was able to suppress this phenomenon completely. We have no experience with the use of atropine. Although we could not directly assess airway resistance at peak exercise, we propose that the prevention of exercise-induced bronchial obstruction is a likely mechanism for the effects of methoxamine on exercise duration, since methoxamine can completely prevent methacholine-induced bronchial obstruction in patients with heart failure.1

Laure Cabanes, M.D.
Frederic Costes, M.D.
Simon Weber, M.D.
Hopital Cochin, 75679 Paris, France

1 References

1. 1

   Cabanes LR, Weber SN, Matran R, et al. Bronchial hyperresponsiveness to methacholine in patients with impaired left ventricular function. N Engl J Med 1989;320:1317-1322
   Full Text | Web of Science | Medline

Citing Articles (2)

Citing Articles

1. 1

   Nathaniel M. Hawkins, Mark C. Petrie, Michael R. MacDonald, Pardeep S. Jhund, Leonardo M. Fabbri, John Wikstrand, John J.V. McMurray. (2011) Heart Failure and Chronic Obstructive Pulmonary Disease. Journal of the American College of Cardiology 57:21, 2127-2138
   CrossRef

2. 2

   Klaus K.A Witte, Alyn Morice, John G.F Cleland, Andrew L Clark. (2004) The reversibility of increased airways resistance in chronic heart failure measured by impulse oscillometry. Journal of Cardiac Failure 10:2, 149-154
   CrossRef