The impact of low-level
carbon monoxide exposure on ventricular
arrhythmia frequency in patients with
ischemic heart disease has not been thoroughly studied. The issue is of concern because of the potential proarrhythmic effect of
carbon monoxide in patients with
ischemic heart disease. We studied 30 subjects with well-documented
coronary artery disease who had an average of at least 30
ventricular ectopic beats per hour over a 20-hour monitoring interval. By using appropriate inclusion and exclusion criteria, subjects were selected and enrolled in a randomized double-blind study to determine the effects of
carbon monoxide exposure on ventricular
arrhythmia frequency at rest, during exercise, and during ambulatory activities. The
carbon monoxide exposure was designed to result in 3% or 5%
carboxyhemoglobin levels, as measured by gas chromatography. The
carbon monoxide exposure protocol produced target levels in 60 minutes, and the levels were maintained for an additional 90 minutes to provide adequate time to assess the impact of
carbon monoxide on the frequency of
ventricular ectopic beats. The data on total and repetitive ventricular arrhythmias were analyzed for seven specific time intervals: (1) two hours before
carbon monoxide exposure; (2) during the two-hour
carbon monoxide or air exposure; (3) during a two-hour rest period; (4) during an exercise period; (5) during an exercise recovery period; (6) six hours after
carbon monoxide or air exposure; and (7) approximately 10 hours after exposure, or the remaining recording interval on the Holter monitor. There was no increase in ventricular
arrhythmia frequency after
carbon monoxide exposure, regardless of the level of
carboxyhemoglobin or the type of activity. During steady-state conditions at rest, the number of
ventricular ectopic beats per hour was 115 +/- 153 (SD) for room air exposure (0.7%
carboxyhemoglobin), 121 +/- 171 for the lower
carbon monoxide exposure (3.2%
carboxyhemoglobin), and 94 +/- 129 for the higher
carbon monoxide exposure (5.1%
carboxyhemoglobin). The frequency of complex ventricular ectopy was not altered at the levels of
carbon monoxide studied. Secondary analysis of the impact of
carbon monoxide on
ventricular ectopic beat frequency stratified by baseline ejection fraction, baseline
ventricular ectopic beat frequency, and exercise-induced ST-segment changes did not indicate an effect of
carbon monoxide on ventricular arrhythmias. In conclusion, low levels of
carbon monoxide exposure resulting in blood levels of 3.2% and 5.1%
carboxyhemoglobin, as measured by gas chromatography, do not have a proarrhythmic effect on patients with
coronary artery disease and frequent ventricular ectopy.(ABSTRACT TRUNCATED AT 400 WORDS)