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Tachycardia mediated cardiomyopathy (TMC) is a reversible form of dilated cardiomyopathy that can occur with most supraventricular and ventricular arrhythmias. Despite the plethora of literature describing this entity in animal models, as well as humans, it remains poorly understood. Over the last decade, new etiologies of TMC, such as frequent premature ventricular complexes in normal hearts, have been identified. Recent advances in catheter-based ablation therapies, particularly for atrial fibrillation and ventricular arrhythmias, have added a new dimension to the treatment of this condition. This review describes the pathophysiology, proposed mechanisms, clinical features and management in various arrhythmic conditions.  相似文献   
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目的探究急诊时静脉注射胺碘酮治疗快速心律失常的临床治疗效果和安全性。方法选取2010年10月至2012年10月在本院接受治疗的快速心律失常患者50例,静脉注射胺碘酮治疗。记录治疗后患者显效、有效和无效的例数,以及出现不良反应的例数,然后计算有效率和不良反应的出现率。结果治疗之后,有40例显效,8例有效,2例无效,总有效率为96%,3例出现了不良反应,分别为2例静脉炎和1例窦性心动过缓。结论对快速心律失常的患者,可以静脉注射胺碘酮进行治疗,有效率高,不良反应的发生率低,值得在临床上推广。  相似文献   
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高翔 《职业与健康》2012,28(16):2045-2046
目的观察胺碘酮联合红花黄色素静脉注射治疗快速心律失常的临床疗效。方法将95例快速心律失常患者随机分为两组,在常规治疗的基础上,观察组(50例)使用胺碘酮联合红花黄色素,对照组(45例)使用胺碘酮。结果观察组总有效率88.0%,对照组总有效率71.1%,两组比较,差异有统计学意义(P0.05)。观察组起效时间短于对照组,治疗后心率较对照组慢,差异均有统计学意义。结论静脉联用胺碘酮与红花黄色素治疗快速心律失常安全且有效。  相似文献   
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目的 :进一步探讨房性快速心律失常发病机理。方法 :采用多普勒超声心动图和动态心电图检查方法对 12 0例心血管病人心房扩大和房性心律失常发生情况进行观察与分析。结果 :左心房扩大为主者房性快速心律失常发生率 (70 6 5 % )显著高于右心房扩大为主者 (18 18% )和心房内径正常者 (13 33% ) ,P <0 0 1;心房内径扩大越明显 ,房性快速心律失常的发生率越高 ,性质越严重 ;即便是速度相同的左心房扩大者 ,二尖瓣狭窄为主的瓣膜性心脏病其发生率也显著高于其他类型的瓣膜性心脏病 ,P <0 0 5。结论 :心房扩大 ,特别是左心房扩大是房性快速心律失常的最重要的病因之一 ,心房压力和心房肌张力增高是电生理紊乱产生的重要因素。  相似文献   
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An arrhythmogenic concentration of ouabain (1.37 × 10?6 m) was added to the media perfusing guinea-pig Langendorff hearts after a 60 min period for establishment of a steady-state. Within 15 min following the addition of ouabain, a significant though transient increase in ventricular cyclic-AMP occurred. The first appearance of electrocardiographic abnormalities occurred at a mean time of +22.6 (±5.1) min following ouabain, a fall in ATP, coronary flow and myocardial oxygen consumption (MVO2) at +28 min, tachycardia at +33.9 (±6.7) min, and asystole (due to fibrillation) at 42.2 (±2.6) min. When ATP levels, coronary flow and MVO2 declined, they remained depressed for the duration of the experiments. While these changes were occurring following ouabain, creatine kinase (CK) activity in the coronary effluent began a progressive increase at +45 min, as did lactate dehydrogenase (LDH) at +60 min, indicative of cellular damage. Electron microscopic analysis of tissues exposed to ouabain for 1 h revealed changes in the mitochondria (e.g. swelling, fragmentation or loss of cristae and loss of calcium granules) similar to those seen in anoxia and ischemia. The prior administration of propranolol (3.38 × 10?6 m) attenuated the rise in creatine kinase activity, and abolished all other effects elicited by ouabain. Neither increasing coronary flow, alpha-adrenergic blockade with phentolamine (1 × 10?6 m) nor “washing” preparations with drug-free media for 1 h affected the results observed with ouabain.On the basis of these results, we conclude that arrhythmogenic doses of ouabain activate the formation of cyclic-AMP, lending support to the hypothesis that increased levels of the nucleotide may act as a triggering event for the subsequent development of arrhythmias. The sequence of events obtained suggests that arrhythmogenic doses of ouabain produce an oxygen deficit similar to that observed in ischemia, as evidenced by the fall in coronary flow, MVO2 and ATP, the rise in released LDH and CK, and changes in mitochondrial ultrastructure. This deficit, at least in part, appears to be responsible for the development and maintenance of arrhythmias induced by the concentration of ouabain used in this model.  相似文献   
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目的 探讨射频导管消融(radiofrequency catheter ablation,RFCA)治疗儿童快速型心律失常的有效性及安全性.方法 用体表心电图的大体定位及常规心内电生理检查,寻找消融靶点,采用温度控制方式进行RFCA.结果 心内电生理检查显示房室折返性心动过速(atrioventricular reentrant tachycardia,AVRT)10例,房室结折返性心动过速(atrioventricular nodal reentrant tachycardia,AVNRT)10例,房性心动过速(atrial tachycardia,AT)3例,特发性室性心动过速(idiopathic ventricular tachycardia,IVT)2例(1例起源于左后分支、1例起源于右心室流出道).手术即刻成功25例.术中1例在放置ABL导管时机械性的压迫希氏束出现一过性的Ⅱ~Ⅲ度房室传导阻滞(auriculo-ventricular block,AVB),给予异丙肾上腺素、阿托品、糖皮质激素处理,2 h后恢复正常的房室传导;2例放置希氏束电极时,出现Ⅰ度AVB,未经处理自行恢复正常的房室传导;22例平均随访(2.8±1.3)年未复发,3例半年后复发,其中AVNRT 2例,AVRT 1例,再次消融均获得成功.结论 RFCA治疗儿童快速型心律失常技术成熟、安全、疗效好.术后复发可能与消融点准确性、消融能量及消融时间趋于保守有关.  相似文献   
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BACKGROUND: Conventional mapping of ventricular tachycardia (VT) after myocardial infarction is limited in patients with hemodynamically untolerated or noninducible VT. OBJECTIVES: The purpose of this study was to develop a unique strategy using noncontact unipolar mapping to define infarct substrate and VT circuits. METHODS: Dynamic substrate mapping (DSM) was performed in seven pigs with healed anterior myocardial infarction. This technique defined substrate as the intersection of low-voltage areas identified in sinus rhythm and during pacing around the infarct. Pacing was also performed within the substrate to determine exit sites. RESULTS: Anteroapical transmural scar was identified in all animals. A mean of three pacing sites was used for substrate definition. The mean area (+/- SD) was 18.4 +/- 8.8 cm2 by DSM and 15.4 +/- 6.9 cm2 by pathology (P >.5). A mean of 4.5 sites was paced within substrate. Ten of 18 paced wavefronts exited substrate adjacent to the pacing area, seven exited at distant areas, and one had two exits. VT was induced in five animals (1.6 morphologies per animal). Except for one VT, circuit exit sites were identified at substrate borders on the endocardium. VT exit sites were at (n = 6) or near (n = 3) a pacing exit site. Electrogram voltages differed significantly between substrate, border, and nonsubstrate areas in infarcted animals and in comparison with control animals. No substrate was identified in two control animals. CONCLUSION: DSM is a reliable method for infarct substrate localization in this model. Pacing within substrate can predict VT exit sites and may prove useful for ablation of unmappable VT after myocardial infarction.  相似文献   
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目的探索盐酸胺碘酮治疗冠心病快速心律失常患者的临床治疗效果。方法将收集到的62例冠心病快速心律失常患者随机分为治疗组和对照组两组,对照组采用普罗帕酮进行治疗,治疗组采用盐酸胺碘酮进行治疗,比较两组的临床治疗疗效。结果两组患者临床疗效比较:治疗组显效18例,有效8例,无效5例;对照组显效8例,有效11例,无效12例。两组临床疗效比较组间资料采用χ2检验,P=0.0273<0.05,两组资料比较差异有统计学意义。结论采用盐酸胺碘酮治疗急诊冠心病快速心律失常的治疗效果优于使用普罗帕酮的治疗效果,且不良反应相对较少,胺碘酮是治疗此类疾病的理想的药物之一,值得在临床上推广使用。  相似文献   
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