临床药物治疗杂志
臨床藥物治療雜誌
림상약물치료잡지
CLINICAL MEDICATION JOURNAL
2013年
5期
22-25
,共4页
和渝斌%郭晓东%王长华%曾晓林%林月
和渝斌%郭曉東%王長華%曾曉林%林月
화투빈%곽효동%왕장화%증효림%림월
急性心肌梗死%冠状动脉痉挛%血栓%D-二聚体
急性心肌梗死%冠狀動脈痙攣%血栓%D-二聚體
급성심기경사%관상동맥경련%혈전%D-이취체
D-dimer%Acute myocardial infarction%Coronary thrombosis%Coronary artery spasm
目的:分析D-二聚体(D-dimer)水平在溶栓治疗急性心肌梗死时的水平,探讨其在治疗过程中演变的意义。方法:连续随机选择急性心肌梗死患者90例,根据是否进行溶栓治疗及溶栓后冠状动脉造影结果,将入选患者分为冠状动脉狭窄溶栓再通组(A, n=23)、无冠状动脉明显狭窄再通组(B, n=25)、非再通组(C, n=24)及非溶栓组(D, n=18)。各组患者在治疗前后测定血清D-dimer水平。治疗前测定磷酸肌酸激酶同工酶、肌钙蛋白I、总胆固醇、甘油三酯、低密度脂蛋白胆固醇、血糖、凝血酶原时间及活化部分凝血活酶时间。溶栓组用rt-PA进行静脉溶栓,非溶栓组静脉滴注等量生理盐水。经冠状动造影对溶栓效果进行评价。结果:各组患者磷酸肌酸激酶同工酶及肌钙蛋白I水平均明显增高,各再通组患者磷酸肌酸激酶同工酶峰值小于13h,A组及B组D-dimer水平在溶栓后1.0h快速升高,但A组血中D-dimer水平明显高于B组(溶栓后1~8h, P<0.05~0.001),A组D-dimer水平峰值出现在溶栓后4h,而B组D-dimer峰值出现在溶栓后2h,明显早于前者。但非溶栓组在相同时间内无上述变化。结论: D-dimer水平变化在冠状动脉痉挛及或血栓形成引起急性心肌梗死时显著不同,通过分析D-dimer水平变化有助于判断急性心肌梗死的形成原因,利于指导临床治疗。
目的:分析D-二聚體(D-dimer)水平在溶栓治療急性心肌梗死時的水平,探討其在治療過程中縯變的意義。方法:連續隨機選擇急性心肌梗死患者90例,根據是否進行溶栓治療及溶栓後冠狀動脈造影結果,將入選患者分為冠狀動脈狹窄溶栓再通組(A, n=23)、無冠狀動脈明顯狹窄再通組(B, n=25)、非再通組(C, n=24)及非溶栓組(D, n=18)。各組患者在治療前後測定血清D-dimer水平。治療前測定燐痠肌痠激酶同工酶、肌鈣蛋白I、總膽固醇、甘油三酯、低密度脂蛋白膽固醇、血糖、凝血酶原時間及活化部分凝血活酶時間。溶栓組用rt-PA進行靜脈溶栓,非溶栓組靜脈滴註等量生理鹽水。經冠狀動造影對溶栓效果進行評價。結果:各組患者燐痠肌痠激酶同工酶及肌鈣蛋白I水平均明顯增高,各再通組患者燐痠肌痠激酶同工酶峰值小于13h,A組及B組D-dimer水平在溶栓後1.0h快速升高,但A組血中D-dimer水平明顯高于B組(溶栓後1~8h, P<0.05~0.001),A組D-dimer水平峰值齣現在溶栓後4h,而B組D-dimer峰值齣現在溶栓後2h,明顯早于前者。但非溶栓組在相同時間內無上述變化。結論: D-dimer水平變化在冠狀動脈痙攣及或血栓形成引起急性心肌梗死時顯著不同,通過分析D-dimer水平變化有助于判斷急性心肌梗死的形成原因,利于指導臨床治療。
목적:분석D-이취체(D-dimer)수평재용전치료급성심기경사시적수평,탐토기재치료과정중연변적의의。방법:련속수궤선택급성심기경사환자90례,근거시부진행용전치료급용전후관상동맥조영결과,장입선환자분위관상동맥협착용전재통조(A, n=23)、무관상동맥명현협착재통조(B, n=25)、비재통조(C, n=24)급비용전조(D, n=18)。각조환자재치료전후측정혈청D-dimer수평。치료전측정린산기산격매동공매、기개단백I、총담고순、감유삼지、저밀도지단백담고순、혈당、응혈매원시간급활화부분응혈활매시간。용전조용rt-PA진행정맥용전,비용전조정맥적주등량생리염수。경관상동조영대용전효과진행평개。결과:각조환자린산기산격매동공매급기개단백I수평균명현증고,각재통조환자린산기산격매동공매봉치소우13h,A조급B조D-dimer수평재용전후1.0h쾌속승고,단A조혈중D-dimer수평명현고우B조(용전후1~8h, P<0.05~0.001),A조D-dimer수평봉치출현재용전후4h,이B조D-dimer봉치출현재용전후2h,명현조우전자。단비용전조재상동시간내무상술변화。결론: D-dimer수평변화재관상동맥경련급혹혈전형성인기급성심기경사시현저불동,통과분석D-dimer수평변화유조우판단급성심기경사적형성원인,리우지도림상치료。
Objective: To assess the level of D-dimer during thrombolytic therapy in patients with acute myocardial infarction (AMI) and to understand its significance. Method:A total of 90 patients with AMI were randomly assigned to coronary artery stenosis reperfusion (group A, n=23), or no obvious stenosis in coronary artery reperfusion (group B, n=25), or no reperfusion (group C, n=24), or no-thrombolytic (group D, n=18) according to the evaluation of coronary angiography before or after thrombolytic therapy during 2001 to 2010. D-dimer was tested at 1, 2, 4, 8, 24, 48 hours after treatment, as did myocardial enzyme, Troponin I, PT, APTT, TC, TG, LDL-C and glucose before treatment. Al of patients did coronary angiography to assess the treatment effect. The thrombolytic patients treated with thrombolytic rt-PA and the no-thrombolytic patients treated with same volume 0.9% NaCl as control at same time. Result:The level of CK-MB and Troponin I was significantly higher than normal in al patients. The CK-MB peak was less than 13 hours after AMI in al reperfusion patients. And the serum D-dimer went up at 1.0 hour after thrombolytic treatment in group A and group B. But the D-dimer was significantly higher in group A than in group B (from 1 to 8 hours when thrombolytic treatment begin, p<0.05~0.001). However the peak of D-dimer occurred earlier in group B (at 2 hours) than in group A (at 4 hours). Meanwhile the D-dimer level did not change obviously in no-thrombolytic treatment group (p>0.05). Conclusion: The D-dimer is real y different in patients with AMI due to coronary artery spasm and / or thrombosis. This difference could help us to analyze the causes of AMI and to guide the clinical treatment.