Dahms T E, Younis L T, Wiens R D, Zarnegar S, Byers S L, Chaitman B R
Department of Internal Medicine, Saint Louis University School of Medicine, Missouri 63110-0250.
J Am Coll Cardiol. 1993 Feb;21(2):442-50. doi: 10.1016/0735-1097(93)90687-v.
This study was designed to determine whether carbon monoxide has proarrhythmic effects at rest and during upright exercise in patients with myocardial ischemia and moderate baseline ectopic activity.
Exposure of patients with documented myocardial ischemia to low levels of carboxyhemoglobin (COHb) alters the myocardial response to exercise. Anecdotal reports from patients with myocardial ischemia have noted the development of arrhythmias related to carbon monoxide exposure. Increased frequency of arrhythmias related to carbon monoxide exposure in patients performing supine bicycle exercise has been recently reported.
Twenty-eight nonsmoking men and five nonsmoking women with documented coronary artery disease and a minimum of 30 ventricular ectopic beats/h over a 20-h period were studied. Subjects were exposed in a randomized double-blind fashion to either room air or sufficient carbon monoxide to elevate their COHb concentration to 3% or 5% in 1 h, followed by a maintenance exposure to carbon monoxide. The subjects then left the laboratory and resumed their normal daily activity to determine changes in ventricular ectopic beats after carbon monoxide exposure.
There was no significant change in the frequency of single ventricular ectopic beats at rest from 115 +/- 28 (in room air) to 121 +/- 31 at 3% COHb to 94 +/- 23 at 5% COHb. Exercise itself increased the frequency of ventricular ectopic beats, but there was no additional effect of carbon monoxide exposure on the exercise-induced increase in isolated ectopic beats or complex ectopic waveforms. Analysis of the data based on grouping of the subjects by the severity of disease (ventricular ectopic beat frequency, ejection fraction, presence of exercise-induced ischemia) indicated no proarrhythmic effect of carbon monoxide.
In patients with frequent ventricular ectopic activity (> or = 30 ectopic beats/h), exposure to carbon monoxide producing either 3% or 5% COHb does not increase arrhythmia frequency of single or multiple beats during rest or exercise.
本研究旨在确定一氧化碳在心肌缺血且基线异位活动中度的患者静息及直立运动时是否具有促心律失常作用。
有记录的心肌缺血患者暴露于低水平碳氧血红蛋白（COHb）会改变心肌对运动的反应。心肌缺血患者的轶事报道指出与一氧化碳暴露相关的心律失常的发生。最近有报道称，进行仰卧位自行车运动的患者中与一氧化碳暴露相关的心律失常频率增加。
对28名有记录的冠状动脉疾病且在20小时内至少有30次室性异位搏动/小时的非吸烟男性和5名非吸烟女性进行了研究。受试者以随机双盲方式暴露于室内空气或足够的一氧化碳中，使他们的COHb浓度在1小时内升至3%或5%，随后持续暴露于一氧化碳中。然后受试者离开实验室并恢复正常日常活动，以确定一氧化碳暴露后室性异位搏动的变化。
静息时单发性室性异位搏动频率从（室内空气时）115±28显著变化至COHb为3%时的121±31，再到COHb为5%时的94±23。运动本身增加了室性异位搏动的频率，但一氧化碳暴露对运动诱发的孤立性异位搏动或复合性异位波形增加没有额外影响。根据疾病严重程度（室性异位搏动频率、射血分数、运动诱发缺血的存在）对受试者进行分组后对数据的分析表明，一氧化碳没有促心律失常作用。
在室性异位活动频繁（≥30次异位搏动/小时）的患者中，暴露于产生3%或5% COHb的一氧化碳中不会增加静息或运动期间单发性或多发性搏动的心律失常频率。
