Sun Zhong-ji, Yang Chao-bin, Wang Hui, Li Ying
Department of Emergency, Army's Logistics Institute, Tianjin, China.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2011 Dec;23(12):739-42.
To examine the serum level of myocardial injury markers in patients with carbon monoxide (CO) poisoning, the correlation between these markers and the severity of the disease, and the therapeutic effects of L-carnitine administration.
69 patients, chosen from 309 cases of acute carbon monoxide poisoning (ACOP) for abnormally high level of serum myocardial injury markers (myoglobin, Mb; MB isoenzyme of creatine kinase, CK-MB; cardiac troponin-I, cTnI) at the time of admission, were randomly divided into control group (n = 34) and observation group (n = 35). The patients in control group were given Xingnaojing (20 ml/d i.v. drip), and the observation group Xingnaojing (20 ml/d)+L-carnitine (2 g/d i.v. drip), in addition to the conventional oxygen supply and symptom-focused therapy. The plasma concentration of carboxyhemoglobin (HbCO, as index for CO poisoning severity), Mb, CK-MB, and cTnI in these patients were further examined 24 hours, 72 hours and 1 week after the treatment, for difference between the two groups, and the correlation between the serum level of HbCO and the myocardial injury markers.
At the time of admission, the incidence of abnormal findings in myocardial injury markers were 2.5% (5/204), 46.8% (36/77) and 100.0% (28/28) in patients with mild (HbCO: 10% ~ 19%), moderate (20% ~ 39%) and severe (≥40%) CO poisoning, respectively. The incidence of abnormal findings in injury markers was significantly correlated to the HbCO concentration (x(2)=170.3549, P < 0.0001). Before the treatment, no significant difference was found in any of the indexes [HbCO: (31.1 ± 17.6)%, (32.3 ± 16.9)%, Mb (μg/L): 154.2 ± 51.8, 165.4 ± 48.6, CK-MB (μg/L): 8.7 ± 3.3, 9.6 ± 3.8), and cTnI (μg/L): 2.7 ± 1.2, 2.8 ± 1.5, all P > 0.05] between the control and observation group. However, it was found in: Mb (24 hours: 74.0 ± 36.5 vs. 97.1 ± 35.8, 72 hours: 40.1 ± 6.8 vs. 69.0 ± 11.2), cTnI (24 hours: 1.9 ± 0.5 vs. 2.3 ± 0.7, 72 hours: 1.2 ± 0.3 vs. 1.8 ± 0.4) both 24 hours and 72 hours after the treatment, and CK-MB, 24 hours after treatment (10.6 ± 4.1 vs. 13.0 ± 3.9) with the values in observation group significantly lower (P < 0.05 or P < 0.01); 1 week after the treatment, the concentration of all the injury markers returned to the normal levels with no significant difference between the two groups. Meanwhile, no significant difference was found between the two groups in HbCO concentration throughout the due-course of the therapy.
The incidence of abnormal findings in serum myocardial injury markers was positively correlated with HbCO concentration after CO poisoning. L-carnitine may protect the myocardium and striated muscles against injury in patients with CO poisoning.
检测一氧化碳（CO）中毒患者血清心肌损伤标志物水平，分析这些标志物与病情严重程度的相关性以及左卡尼汀治疗的效果。
从309例急性一氧化碳中毒（ACOP）患者中选取69例入院时血清心肌损伤标志物（肌红蛋白，Mb；肌酸激酶同工酶MB，CK-MB；心肌肌钙蛋白I，cTnI）异常升高者，随机分为对照组（n = 34）和观察组（n = 35）。对照组患者给予醒脑静（20 ml/d静脉滴注），观察组患者给予醒脑静（20 ml/d）+左卡尼汀（2 g/d静脉滴注），同时进行常规吸氧及对症治疗。治疗后24小时、72小时和1周检测患者血浆中碳氧血红蛋白（HbCO，作为CO中毒严重程度指标）、Mb、CK-MB和cTnI浓度，比较两组差异及HbCO血清水平与心肌损伤标志物的相关性。
入院时，轻度（HbCO：10%19%）、中度（20%39%）和重度（≥40%）CO中毒患者心肌损伤标志物异常检出率分别为2.5%（5/204）、46.8%（36/77）和100.0%（28/28）。损伤标志物异常检出率与HbCO浓度显著相关（x(2)=170.3549，P <0.0001）。治疗前，两组各项指标[HbCO：(31.1±17.6)%，(32.3±16.9)%；Mb（μg/L）：154.2±51.8，165.4±48.6；CK-MB（μg/L）：8.7±3.3，9.6±3.8；cTnI（μg/L）：2.7±1.2，2.8±1.5，均P>0.05]比较，差异无统计学意义。但治疗后24小时和72小时，观察组Mb（24小时：74.0±36.5 vs. 97.1±35.8，72小时：40.1±6.8 vs. 69.0±11.2）、cTnI（24小时：1.9±0.5 vs. 2.3±0.7，72小时：1.2±0.3 vs. 1.8±0.4）及治疗后24小时CK-MB（10.6±4.1 vs. 13.0±3.9）均显著低于对照组（P <0.05或P <0.01）；治疗1周后，所有损伤标志物浓度均恢复正常水平，两组间差异无统计学意义。同时，治疗全过程两组患者HbCO浓度比较，差异无统计学意义。
CO中毒后血清心肌损伤标志物异常检出率与HbCO浓度呈正相关。左卡尼汀可能对CO中毒患者心肌和横纹肌具有保护作用，减轻损伤。
