Aspirin worsens exercise performance and pulmonary gas exchange in patients with heart failure who are taking angiotensin-converting enzyme inhibitors

Background Pulmonary function abnormalities participate in causing exercise disability in patients with congestive heart failure (CHF). impaired pulmo nary gas transfer is one of these abnormalities. Angiotensin-converting enz yme (ACE) inhibitors improve diffusion for carbon monoxide and exercise cap acity, an effect that is seemingly mediated through prostaglandin activatio n because it is inhibited by cyclooxygenase blockade with aspirin. This sug gests the possibility that aspirin may disturb the pulmonary function and e xercise ability in CHF, at least in those patients who are taking ACE inhib itors. This study was aimed at probing this hypothesis. Methods A dose of 325 mg aspirin was given daily for 8 weeks to 26 consecut ive patients with primary dilated cardiomyopathy (New York Heart Associatio n class II or III) whose current outpatient antifailure therapy included (g roup 1, 18 cases) or did not include (group 2, 8 cases) an ACE inhibitor in addition to digoxin and furosemide. During the study ACE inhibition was co ntinued in group 1 by giving enalapril 20 mg daily. Results Tests repeated at 8 weeks proved that aspirin was deleterious in gr oup 1. Compared with run-in, rest carbon dioxide, peak exercise oxygen upta ke (peak VO2), and tidal volume levels were diminished in this group; the r atio of exercise minute ventilation to carbon dioxide production (VE/VCO2) was augmented and its variations were inversely related to those of peak VO 2. Similar results were not observed in group 2; however, once this part of the study was completed and enalapril was included in the current therapeu tic regimen, an inhibitory effect of aspirin on carbon dioxide, peak VO2, p eak tidal volume, and VE/VCO2 at 1 I levels become evident and was similar to that observed in group 1. Conclusions Aspirin does not affect ventilation efficiency and peak VO2 in patients with CHF not taking ACE inhibitors, but it worsens the pulmonary d iffusion for carbon monoxide, VO2, and the ventilatory response to exercise in the presence of ACE inhibition. This may be relevant in patients with C HF from ischemic heart disease. Whether the same may be true of smeller asp irin doses was nor investigated in this study.