Myocardial infarction after electrocution

A case of acute anterior myocardial infarction in a 16-year-old boy who suffered electrocution is described. In spite of extensive electrocardiographic changes of transmural (Q-wave) infarction, left ventricular function was preserved well. Coronary angiography subsequently revealed normal coronary arteries.     

通心络对大鼠心肌梗死后神经重构和室颤阈值的影响

目的探讨通心络(TXL)对大鼠心肌梗死(MI)后神经重构和室颤阈值的影响。方法应用结扎冠状动脉前降支的方法制备大鼠MI模型,将大鼠随机分为3组:假手术组、MI组和TXL组(n=8),第6周应用超声心动图测定心脏结构和功能后进行室颤阈值测定;免疫组化法研究大鼠心室肌中生长相关蛋白43(GAP43)和酪氨酸羟化酶(TH)阳性神经纤维的分布和密度。结果与假手术组相比,MI组心室肌神经分布紊乱,神经纤维密度明显增高(P<0.05),室颤阈值明显降低(P<0.05);TXL组较MI组神经纤维密度明显降低(P<0.05),室颤阈值明显升高(P<0.05),并接近假手术组。结论TXL能改善MI后神经重构反应,提高室颤阈值,有预防MI后室性快速心律失常的潜在作用。     

通心络对大鼠心肌梗死后神经重构和室颤阈值的影响

目的 探讨通心络(TXL)对大鼠心肌梗死(MI)后神经重构和室颤阈值的影响. 方法 应用结扎冠状动脉前降支的方法制备大鼠MI模型,将大鼠随机分为3组:假手术组、MI组和TXL组(n=8),第6周应用超声心动图测定心脏结构和功能后进行室颤阈值测定;免疫组化法研究大鼠心室肌中生长相关蛋白43(GAP43)和酪氨酸羟化酶(TH)阳性神经纤维的分布和密度. 结果 与假手术组相比,MI组心室肌神经分布紊乱,神经纤维密度明显增高(P<0.05),室颤阈值明显降低(P<0.05);TXL组较MI组神经纤维密度明显降低(P<0.05),室颤阈值明显升高(P<0.05),并接近假手术组. 结论 TXL能改善MI后神经重构反应,提高室颤阈值,有预防MI后室性快速心律失常的潜在作用.     

诱导性室颤法在二尖瓣置换术中的心肌保护作用

目的探讨诱导性室颤状态下行体外循环二尖瓣置换术的心肌保护效果. 方法对照分析诱导室颤组（VF组,15例）和冷晶体停跳液组（CC组,15例）围手术期心肌肌钙蛋白（cTnI）、磷酸肌酸激酶同工酶（CK-MB）、脂质过氧化物产物丙二醛（MDA）和超氧化物歧化酶（SOD）的血清浓度变化. 结果两组术后血清cTnI,CK-MB,MDA和SOD水平均不同程度升高,CC组的cTnI,CK-MB在术后各时点均高于VF组（P＜0.01）,MDA值在心脏恢复搏动后6、24 h,SOD值在2 h分别高于VF组（P＜0.05）.cTnI值在恢复心搏后12 h、CK-MB值和MDA值在6 h、SOD值在2 h分别达高峰.除SOD外,其余指标值在48 h仍高于术前. 结论诱导性室颤法可明显减轻心肌缺血、缺氧及再灌注损伤,有较好的心肌保护效果.     

心肌桥引起冠状动脉痉挛、室颤1例报告

1临床资料患者男性,52岁,既往无高血压、糖尿病、高脂血症病史和长期吸烟、猝死家族史。2007年2月晨起或中度体力活动后感胸闷,休息十余分钟可自行缓解; 4月27日在上3层楼后出现心前区疼痛,伴全身出汗,无肩部放射痛、心悸、气促、晕厥,休息后缓解,当地医院急诊心电图示胸前导联V2-V6 ST斜下形压低0.05～0.3 mV,T波正负双向或倒置;5月初患者多次出现心前区疼痛,运动、休息时均出现,程度、持续时间、缓解方式与前相似,于5月4日来我科就诊。入院查体无阳性体征;心电图示窦性心律,无ST-T改变;心脏彩超未见异常。冠脉造影见左冠脉近端痉挛明显,狭窄90%左右,患者有明显胸痛,予冠脉内注入硝酸甘油后缓解;再次造影（图1）见冠脉呈左冠优势型,左前降支中段心肌桥(收缩期狭窄80%),左主干近段、左回旋支开口狭窄40%。     

Thiazide-induced hypokalemia. Association with acute myocardial infarction and ventricular fibrillation

Ten of 59 patients (17%) were receiving a thiazide preparation at the time of an acute myocardial infarction and ventricular fibrillation. Hypokalemia was present in seven of eight patients (87%) receiving thiazides, whereas it was observed in only one of 38 patients (2.6%) not receiving these medications. If hypokalemia is present in patients receiving thiazides who have had an acute myocardial infarction, it should be corrected so as to remove this predisposing cause of ventricular fibrillation.     

Life-threatening arrhythmias after intravenous lidocaine alone or with magnesium in myocardial infarction complicated by ventricular fibrillation

To compare the effects of Lidocaine (LID) alone or with Magnesium Sulfate (M) on life-threatening ventricular arrhythmias which followed cardioverted prolonged ventricular fibrillation (VF) during an acute myocardial infarction (AMI), we studied 34 (24.63%) out of 138 patients aged from 52 to 83 years (mean: 66.92 + 8.82) with an anterior AMI, who had cardioverted prolonged VF. Twenty patients (58.8%)--Group A--received LID 2 mg/min at constant-rate infusion through a subclavian catheter following a bolus of LID 100 mg, whereas 14 patients (14.2%)--Group B--received LID at the same dose + M 2.5 mg/min. All the patients had continuous monitoring and LID serum level was measured daily by means of immunofluorescent method (TDX Abbot; range 1.5-5 micrograms/ml). Group A had the following mean serum levels of LID; 250 + 0.9; 1.52; 245 +/- 0.9; 3.20 + 1.1. Group B showed: 2.65 + 1.2; 2.80 + 1.8; 3.10 + 1.2; 3.25 + 1.1. Continuous monitoring displayed the following arrhythmias respectively for Group A and Group B: VT 37 times vs 16(P less than 0.05, significant), transiently cardioverted VF during therapy 17 times vs 6(p less than 0.01, significant), 8 deaths from VF vs 6 - 3 from VF and 3 from asystole - (p = NS). LID + M treatment seemed to be more effective than LID alone to reduce life-threatening arrhythmias following cardioverted prolonged VF of AMI but not the deaths. In addition, M would raise moderately LID serum level and this fact, not yet well known, needs further investigation.     

辛伐他汀对大鼠心肌梗死后心室电重构及室颤阈值的影响

目的探讨心肌梗死(MI)后甲基羟戊二酰辅酶A还原酶抑制剂辛伐他汀对心室电重构及室颤阈值的影响。方法用结扎冠状动脉前降支的方法制备大鼠MI模型,将存活的大鼠随机分为MI组(n=8)、中等剂量辛伐他汀组(M-SIM组,n=8)、大剂量辛伐他汀组(H-SIM组,n=8);另设假手术组(Sham组,n=8),在相同位置只挂线不结扎。MI 24 h后,M-SIM组和H-SIM组分别以1 mg.kg-1.d-1和10 mg.kg-1.d-1辛伐他汀(溶于蒸馏水中)灌胃连续4周;MI组和Sham组则给予同体积蒸馏水灌胃。MI 4周后行超声心动图检查及在体电生理检查。结果各组大鼠MI前QTc间期比较,差异无统计学意义(P>0.05)。手术4周后与Sham组相比,MI组QTc间期明显延长(P<0.05),有效不应期(ERP)缩短,ERP-频率曲线下移;MI组诱发的室性快速心律失常(IVT)发生率升高,室颤阈值明显降低(均P<0.05);在MI组,S1S1间期为90 ms和80 ms时的ERP较S1S1间期为120 ms时明显延长(P<0.05)。M-SIM组及H-SIM组QTc间期均较MI组缩短(P<0.05),ERP-频率曲...     

辛伐他汀对大鼠心肌梗死后心室电重构及室颤阈值的影响

目的 探讨心肌梗死(MI)后甲基羟戊二酰辅酶A还原酶抑制剂辛伐他汀对心室电重构及室颤阈值的影响.方法 用结扎冠状动脉前降支的方法 制备大鼠MI模型,将存活的大鼠随机分为MI组(n=8)、中等剂量辛伐他汀组(M-SIM组,n=8)、大剂量辛伐他汀组(H-SIM组,n=8);另设假手术组(Sham组,n=8),在相同位置只挂线不结扎.MI 24 h后,M-SIM组和H-SIM组分别以1 mg·kg<'-1>·d<'-1>和10 mg·kg<'-1>·d<'-1>辛伐他汀(溶于蒸馏水中)灌胃连续4周;MI组和Sham组则给予同体积蒸馏水灌胃.MI 4周后行超声心动图检查及在体电生理检查.结果 各组大鼠MI前QTc间期比较,差异无统计学意义(P>0.05).手术4周后与Sham组相比,MI组QTc间期明显延长(P<0.05),有效不应期(ERP)缩短,ERP-频率曲线下移;MI组诱发的室性快速心律失常(IVT)发生率升高,室颤阈值明显降低(均P<0.05);在MI组,slsl间期为90 ms和80 ms时的ERP较SlSl间期为120 ms时明显延长(P<0.05).M-SIM组及H-SIM组QTc间期均较MI组缩短(P<0.05),ERP-频率曲线上移,各SlSl间期时对应的ERP值差异无统计学意义(P>0.05);且IVT发生率明显降低,室颤阈值明显升高(均P<0.05).M-SIM组与H-SIM组间各指标比较,差异无统计学意义(P>0.05).结论 辛伐他汀能改善大鼠MI后电生理重构,调整频率依赖适应性变化,提高室颤阈值而改善MI后室性心律失常.     

Dressler's syndrome after right ventricular infarction.

Undiagnosed myocardial infarction of the right ventricle presented as Dressler''s syndrome. Radioisotopic diagnostic procedures including first-pass and multigated acquisition nuclear angiography ( MUGA ) and thallium-201 perfusion studies enabled a retroactive diagnosis of myocardial infarction, showed it to be in the right ventricle, and clarified the aetiology of the unexplained fever and pleuropericarditis.     

急性ST段抬高型心肌梗死并心室颤动12例临床救治分析

目的总结基层医院急性ST段抬高型心肌梗死（STEMI）并心室颤动患者的救治体会。方法回顾性分析抢救12例符合溶栓条件的急性STEMI心室颤动患者的临床资料。结果在无直接经皮冠状动脉介入治疗（PCI）条件下,12例患者均采用及时的心脏电除颤和静脉溶栓治疗,11例获得成功,1例死亡。结论急性STEMI患者在无PCI条件的基层医院应及时积极采用静脉溶栓疗法,心室颤动时应首选电击除颤,以提高抢救效果。     

Left ventricular thrombi after acute myocardial infarction

Two-dimensional echocardiography was utilized in a prospective study to find the incidence, characteristics and natural history of left ventricular thrombus in 50 consecutive patients with acute myocardial infarction. The overall incidence of thrombosis was 14%; 19% in anterior and 5% in inferior infarction. The thrombus was detected at the apex in 4, along the ventricular septum in 2 and at both these sites in one patient. It was observed 3-10 days after the infarction. Thrombus at the ventricular septum, seen in this study, has not been reported previously in acute myocardial infarction. Development of apical and septal thrombi was significantly associated with akinesis of these sites. Only 2 patients with protruding thrombi had systemic embolism. We conclude that the apex as well as the septum are common sites for thrombosis in patients with severe wall motion abnormalities following acute anterior infarction. Careful observation of these sites during echocardiography may reveal thrombi prone for embolization.