Leaf D A, Kleinman M T
Department of Medicine, West Los Angeles V.A. Medical Center, California 90073, USA.
Arch Environ Health. 1996 Jul-Aug;51(4):283-90. doi: 10.1080/00039896.1996.9936027.
Environmental exposure to inhaled carbon monoxide (CO) increases coronary artery disease risk. Sudden cardiac death, a frequent manifestation of coronary artery disease, is usually a result of ventricular dysrhythmia. The effect of exposure to CO at sea level (CO/SL) and simulated high (2.1 km) altitudes (CO/HA) on the incidence of cardiac ectopy in subjects with coronary artery disease was investigated. A double-blind crossover study was conducted, with random-order assignment, and each subject served as his own control. Seventeen men with documented coronary artery disease and stable angina pectoris performed cardiopulmonary exercise stress tests after random exposure to either CO or clean air (CA) at sea level (CA/SL) or at a simulated 2.1-km high altitude (CA/HA). The individual CO and HA exposure conditions were each selected to reduce the percentage of oxygen saturation of the subjects' arterial blood by 4%. Subjects' blood carboxyhemoglobin levels were increased from an average of 0.62% after clean-air exposure to 3.91% of saturation after CO exposure. The percentage of oxygen saturation in arterial blood was reduced from a baseline level of 98% to approximately 94% after CO/SL or CA/HA and to approximately 90% after CO/HA. Compared with the CA/SL (i.e., 10 premature ventricular contractions [PVCs]), the average incidence of exercise-induced ventricular ectopy was approximately doubled after all exposures (CO/SL = 18 PVCs, CA/HA = 16 PVCs, and CO/HA = 19 PVCs), and a significant trend (p < .05) of increased ectopy with decreased oxygen saturation in arterial blood was observed. Yet, among subjects who were free from ectopy (n = 11) on CA/SL, only 2 subjects developed ectopy after CO/HA. No episodes of ventricular tachycardia or fibrillation occurred. The findings indicated that exposure to increased levels of hypoxemia, resulting from hypoxic and/or CO exposures, increased the susceptibility to ventricular ectopy during exercise in individuals with stable angina pectoris; however, this risk was nominal for those without ectopy.
环境中吸入一氧化碳（CO）会增加冠状动脉疾病风险。心源性猝死是冠状动脉疾病的常见表现，通常是室性心律失常的结果。本研究调查了海平面（CO/SL）和模拟高海拔（2.1千米）（CO/HA）环境下接触CO对冠状动脉疾病患者心脏异位搏动发生率的影响。进行了一项双盲交叉研究，采用随机顺序分配，每位受试者作为自身对照。17名有冠状动脉疾病记录且稳定型心绞痛的男性在随机暴露于海平面（CA/SL）或模拟2.1千米高海拔（CA/HA）的CO或清洁空气（CA）后，进行心肺运动应激试验。每个个体的CO和HA暴露条件均选择使受试者动脉血氧饱和度百分比降低4%。受试者血液中碳氧血红蛋白水平从清洁空气暴露后的平均0.62%增加到CO暴露后的饱和度3.91%。动脉血氧饱和度百分比从基线水平98%在CO/SL或CA/HA后降至约94%，在CO/HA后降至约90%。与CA/SL（即10次室性早搏[PVCs]）相比，所有暴露后运动诱发的室性异位搏动平均发生率约增加一倍（CO/SL = 18次PVCs，CA/HA = 16次PVCs，CO/HA = 19次PVCs），并且观察到随着动脉血氧饱和度降低异位搏动有显著增加趋势（p <.05）。然而，在CA/SL时无异位搏动的受试者（n = 11）中，只有2名受试者在CO/HA后出现异位搏动。未发生室性心动过速或颤动发作。研究结果表明，低氧和/或CO暴露导致的低氧血症水平升高，增加了稳定型心绞痛患者运动期间对室性异位搏动的易感性；然而，对于无异位搏动的患者，这种风险很小。
