汽车废气吸入对冠心病患者的影响

Title: Ischemic and Thrombotic Effects of Dilute Diesel-Exhaust Inhalation in Men with Coronary Heart Disease

汽车废气吸入对冠心病患者缺血和局部血栓形成的影响
ABSTRACT
Background Exposure to air pollution from traffic is associated with adverse cardiovascular events. The mechanisms for this association are unknown. We conducted a controlled exposure to dilute diesel exhaust in patients with stable coronary heart disease to determine the direct effect of air pollution on myocardial, vascular, and fibrinolytic function.
为了揭示交通引发的大气污染与心血管事件负相关。这种关联的机制现在不清楚。我们控制稳定型的冠心病患者吸入汽车废气，来确定大气污染对心肌，血管和溶解纤维蛋白的功能的直接影响。
Methods In a double-blind, randomized, crossover study, 20 men with prior myocardial infarction were exposed, in two separate sessions, to dilute diesel exhaust (300 礸 per cubic meter) or filtered air for 1 hour during periods of rest and moderate exercise in a controlled-exposure facility. During the exposure, myocardial ischemia was quantified by ST-segment analysis using continuous 12-lead electrocardiography. Six hours after exposure, vasomotor and fibrinolytic function were assessed by means of intraarterial agonist infusions.
进行随机双盲交叉实验，20名男性心梗患者 在2个不同的房间，分别暴露于汽车废气（300 礸/立方米）或者滤过空气1小时，同时对照组在实验室进行休息和适度的锻炼。在此期间，心梗患者用12导连的心电图持续检测，进行ST段定量分析。吸入汽车废气后6小时，血管收缩和溶解纤维蛋白的功能通过输入动脉激动剂药物进行分析。
Results During both exposure sessions, the heart rate increased with exercise (P<0.001); the increase was similar during exposure to diesel exhaust and exposure to filtered air (P=0.67). Exercise-induced ST-segment depression was present in all patients, but there was a greater increase in the ischemic burden during exposure to diesel exhaust (–22±4 vs. –8±6 millivolt seconds, P<0.001). Exposure to diesel exhaust did not aggravate preexisting vasomotor dysfunction, but it did reduce the acute release of endothelial tissue plasminogen activator (P=0.009; 35% decrease in the area under the curve).
在2个不同条件，锻炼的心率增加了(P<0.001);吸入汽车废气和滤过空气组心率稍有增加(P=0.67)。锻炼引起的ST段降低在所有的患者都存在，但是吸入汽车废气组的患者心肌缺血明显增加（P<0.001)。吸入汽车废气组没有加重血管舒缩功能障碍，但是减少了内皮组织纤维蛋白溶酶原激活剂的急性释放(P=0.009; 曲线面积减少35%)。
Conclusions Brief exposure to dilute diesel exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart disease. Our findings point to ischemic and thrombotic mechanisms that may explain in part the observation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events.
(ClinicalTrials.gov number, NCT00437138 [ClinicalTrials.gov] .)
稳定型冠心病男性患者直接暴露吸入汽车废气促进急性心肌缺血，抑制内源性溶解纤维蛋白功能。我们的发现意味着燃烧产生的大气污染和心血管事件呈负相关。

编译：

汽车废气吸入对冠心病患者缺血和局部血栓形成的影响

最近研究发现交通引发的大气污染与心血管事件呈负相关，但是这种关联的机制现在不清楚。研究者通过控制稳定型的冠心病患者吸入汽车废气，来确定大气污染对心肌，血管和溶解纤维蛋白的功能的直接影响。（NEJM, Volume 357:1075-1082 , September 13, 2007 ）

对20名男性心梗患者进行随机双盲交叉实验，分别暴露于汽车废气（300 礸/立方米）和滤过空气得2个不同的房间1小时，同时对照组在实验室进行休息和适当的锻炼。在此期间，心梗患者用12导连的心电图持续监测，进行ST段定量分析。吸入汽车废气后6小时，通过输入动脉激动剂药物分析血管收缩和溶解纤维蛋白的功能。

在2种不同的条件下，锻炼者心率增加了(P<0.001);吸入汽车废气和滤过空气组心率稍有增加(P=0.67)。锻炼引起的ST段降低在所有的患者都存在，但是吸入汽车废气组的患者心肌缺血明显增加（P<0.001)。吸入汽车废气组没有加重血管舒缩功能障碍，但是减少了内皮组织纤维蛋白溶酶原激活剂的急性释放。 (P=0.009; 曲线面积减少35%)。

稳定型冠心病男性患者吸入汽车废气能促进急性心肌缺血，抑制内源性溶解纤维蛋白的功能。我这一发现意味着燃烧产生的大气污染和心血管事件呈负相关。