Author + information
- Received November 30, 1987
- Revision received April 5, 1988
- Accepted May 23, 1988
- Published online October 1, 1988.
- Kirkwood F. Adams, MD∗,a,b,
- Gary Koch, PhDa,b,
- Benu Chatterjee, MDa,b,
- George M. Goldstein, PhDa,b,
- John J. O'Neil, PhDa,b,
- Philip A. Bromberg, MDa,b,
- David S. Sheps, MD, FACCa,b,
- with technical assistance from Susan McAllister, Cynthia J. Price, Jill Bissettea
- ↵∗Address for reprints: Kirkwood F. Adams, MD, Division of Cardiology, University of North Carolina at Chapel Hill, 338 Burnett Womack Bldg, CB No. 7075, Chapel Hill, North Carolina 27599.
Acute exposure to carbon monoxide has the potential to impair exercise capacity in patients with ischemic heart disease. The effect of sufficient inhalation of this compound to gradually produce a level of 6% carboxyhemoglobin was studied in 30 nonsmoking patients with obstructive coronary artery disease and evidence of exercise-induced ischemia. After an initial training session, subjects were exposed to air or carbon monoxide on successive days in a randomized double-blind crossover fashion. Cardiac function and exercise capacity were assessed during symptomlimited supine radionuclide ventriculography. On the carbon monoxide day, mean postexposure carboxyhemoglobin was 5.9 ± 0.1% compared with 1.6 ± 0.1% (p < 0.01) after air exposure.
The mean duration of exercise was significantly longer after air compared with carbon monoxide exposure (626 ± 50 s for air versus 585 ± 49 s for carbon monoxide, p < 0.05). Actuarial methods suggested that subjects were likely to experience angina earlier during exercise on the day of carbon monoxide exposure (p < 0.05). Both the level (62 ± 2.4 versus 60 ± 2.4%, p = 0.05) and change in left ventricular ejection fraction at submaximal exercise (1.6 ± 1.6 versus −1.2 ± 1.6%, p = 0.05) were greater on the air exposure day compared with the carbon monoxide day. The peak exercise left ventricular ejection fraction was not different for the two exposures (57 ± 2.5% for both). These results demonstrate earlier onset of ventricular dysfunction, angina and poorer exercise performance in patients with ischemic heart disease after acute carbon monoxide exposure sufficient to increase blood carboxyhemoglobin to 6%.
☆ This study was supported in part by University of North Carolina-Environmental Protection Agency Cooperative Agreement CR 807392. The research described in this article has been reviewed by the Health Effects Research Laboratory, United States Environmental Protection Agency, Chapel Hill, and approved for publication. Approval does not signify that the contents necessarily reflect the views and policies of the Agency nor does mention of trade names or commercial products constitute endorsement or recommendation for use.
- Received November 30, 1987.
- Revision received April 5, 1988.
- Accepted May 23, 1988.