中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2009年
6期
460-461
,共2页
中毒%有机磷化合物%心房颤动
中毒%有機燐化閤物%心房顫動
중독%유궤린화합물%심방전동
Poisoning%Organophosphorlls compounds,Atrial fibrillation
目的 探讨急性有机磷中毒与心房颤动(房颤)的关系. 方法 回顾分析322例老年急性有机磷中毒患者的临床资料,选取其中36例发生房颤患者,同时选取年龄和性别均匹配的38例非房颤患者作为对照.对两组患者的胆碱酯酶(ChE)、心肌损伤标志物如肌酸肌酶(CK)及其同工酶(CK-MB)、肌钙蛋白(cTn-Ⅰ)进行对比分析. 结果 两组患者ChE均降低,房颤组ChE 10～3300U/L,平均(1126.42±1047.02)U/L,非房颤组ChE(178～3700)U/L,平均(1604.82±934.06)U/L,房颤组低于非房颤组(t=2.077,P=0.041).CK、CK-MB、cTn-Ⅰ两组患者均有不同程度增高.CK:房颤组(80～2212)U/L,平均(609.97±597.84)U/L;非房颤组50～2200 U/L,平均(462.84±530.71)U/L,两组差异无统计学意义(t=1.121,P=0.266).CK-MB:房颤组8～468 U/L,平均(97.31±104.50)U/L;非房颤组6～300 U/L,平均(55.16±69.62)U/L,房颤组高于非房颤组(t=2.052,P=0.044).cTn-Ⅰ:房颤组1.2～5.0 μg/L,平均(2.39±0.88)μg/L,非房颤组0.1～6.0 μg/L,平均(1.81±1.38)μg/L,房颤组高于非房颤组(t=2.132,P=0.036). 结论 急性有机磷中毒致房颤与ChE活力降低、乙酰胆碱(ACh)蓄积、心肌损伤可能有密切关系.
目的 探討急性有機燐中毒與心房顫動(房顫)的關繫. 方法 迴顧分析322例老年急性有機燐中毒患者的臨床資料,選取其中36例髮生房顫患者,同時選取年齡和性彆均匹配的38例非房顫患者作為對照.對兩組患者的膽堿酯酶(ChE)、心肌損傷標誌物如肌痠肌酶(CK)及其同工酶(CK-MB)、肌鈣蛋白(cTn-Ⅰ)進行對比分析. 結果 兩組患者ChE均降低,房顫組ChE 10～3300U/L,平均(1126.42±1047.02)U/L,非房顫組ChE(178～3700)U/L,平均(1604.82±934.06)U/L,房顫組低于非房顫組(t=2.077,P=0.041).CK、CK-MB、cTn-Ⅰ兩組患者均有不同程度增高.CK:房顫組(80～2212)U/L,平均(609.97±597.84)U/L;非房顫組50～2200 U/L,平均(462.84±530.71)U/L,兩組差異無統計學意義(t=1.121,P=0.266).CK-MB:房顫組8～468 U/L,平均(97.31±104.50)U/L;非房顫組6～300 U/L,平均(55.16±69.62)U/L,房顫組高于非房顫組(t=2.052,P=0.044).cTn-Ⅰ:房顫組1.2～5.0 μg/L,平均(2.39±0.88)μg/L,非房顫組0.1～6.0 μg/L,平均(1.81±1.38)μg/L,房顫組高于非房顫組(t=2.132,P=0.036). 結論 急性有機燐中毒緻房顫與ChE活力降低、乙酰膽堿(ACh)蓄積、心肌損傷可能有密切關繫.
목적 탐토급성유궤린중독여심방전동(방전)적관계. 방법 회고분석322례노년급성유궤린중독환자적림상자료,선취기중36례발생방전환자,동시선취년령화성별균필배적38례비방전환자작위대조.대량조환자적담감지매(ChE)、심기손상표지물여기산기매(CK)급기동공매(CK-MB)、기개단백(cTn-Ⅰ)진행대비분석. 결과 량조환자ChE균강저,방전조ChE 10～3300U/L,평균(1126.42±1047.02)U/L,비방전조ChE(178～3700)U/L,평균(1604.82±934.06)U/L,방전조저우비방전조(t=2.077,P=0.041).CK、CK-MB、cTn-Ⅰ량조환자균유불동정도증고.CK:방전조(80～2212)U/L,평균(609.97±597.84)U/L;비방전조50～2200 U/L,평균(462.84±530.71)U/L,량조차이무통계학의의(t=1.121,P=0.266).CK-MB:방전조8～468 U/L,평균(97.31±104.50)U/L;비방전조6～300 U/L,평균(55.16±69.62)U/L,방전조고우비방전조(t=2.052,P=0.044).cTn-Ⅰ:방전조1.2～5.0 μg/L,평균(2.39±0.88)μg/L,비방전조0.1～6.0 μg/L,평균(1.81±1.38)μg/L,방전조고우비방전조(t=2.132,P=0.036). 결론 급성유궤린중독치방전여ChE활력강저、을선담감(ACh)축적、심기손상가능유밀절관계.
Objective To explore the relationship between acute organophosphate poisoning and atrial fibrillation (AF). Methods Three hundred and twenty-two acute organophosphorus poisoning of elderly patients treated from January 2000 to June 2008 in our hospital were analyzed. Among these patients, 36 cases with AF were selected as case group and 38 age-gender-matched cases without AF were selected as control group. Serum cholinesterase (ChE), myocardial damage markers such as creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB) and Troponin- Ⅰ (cTn-Ⅰ) were compared between the two groups. Results ChE was decreased in the two groups, and ChE was lower in case group than in control group [(1126. 42±1047.02) vs. (1604.82±934.06)U/L, t= 2.07, P=0. 0414]. CK, CK-MB and cTn-Ⅰ were increased in different degree in the two groups. There was no difference in CK between the two groups [(609.97±597.84) U/L vs. (462.84± 530. 71)U/L, t= 1. 121, P= 0. 266]. CK-MB and cTn-I were higher in case group than in control group [(97.31±104.50) vs. (55. 16±69.62)U/L, t=2. 052,P=0. 0438; (2.39±0. 88) vs. (1.81± 1.38) μg/L, t = 2. 132, P = 0. 036, respectively9 . Conclusions AF caused by acute organophosphate poisoning may be related to the decrease of ChE activity, acetylcholine accumulation and myocardial injury.
