非开胸法建立持续性单形性室性心动过速动物模型的研究

探讨运用经皮球囊冠状动脉成形术 (PTCA)球囊堵闭猪冠状动脉造成急性心肌梗死 (AMI)后数周建立持续性单形性室性心动过速 (VT)的非开胸法动物模型的方法。猪 1 3只 ,体重 30± 5kg ,运用PTCA球囊堵闭猪左前降支(LAD)形成AMI。存活猪在AMI后数周内进行心室程序电刺激诱发持续性单形性VT ,观察VT诱发、终止的方式及VT诱发的时间窗等。结果 :9/ 1 3只猪形成AMI,经左心室造影及心脏超声检查证实左室心尖、前间隔、左室前壁室壁瘤形成。术后 2～ 2 0周内 9只猪接受平均 1～ 2次电生理检查 ,运用程序电刺激方法 ,8只猪共成功诱发出 1 6种单形性持续性VT ,1只猪仅诱发出非持续性短阵VT。VT周长为 2 54± 65ms ,持续时间 1 8± 1 6min,最长达 62min。程序电刺激和直流电复律可终止VT ,1 0种VT表现为室房分离 ,6种VT室房均为 1∶1逆传 ;9种呈左束支阻滞型 ,7种呈右束支阻滞型。结论 :运用PTCA球囊堵闭冠状动脉造成MI后室壁瘤形成 ,通过程序电刺激的方法可成功建立持续性单形性VT非开胸动物模型 ,成功率较高 ,VT诱发的时间窗长。     

非开胸法建立室壁瘤动物模型的实验研究

目的　探讨运用PTCA球囊封堵猪冠状动脉建立急性心肌梗死后室壁瘤的动物模型的实验方法。方法　选用家猪 7只 ,麻醉后经颈总动脉或股动脉置入PTCA球囊至左前降支 (LAD)第一对角支远端 ,对堵血流 15 0分钟。观察 :心电图、心肌酶、心脏二维超声检查及冠状动脉和左心室造影。结果　 7只猪均完成LAD的封堵 ,2只分别在堵闭 12 0分钟和 2 0分钟后因心室纤颤死亡。存活的 5只猪成功建立左室前壁急性心肌梗死模型 ,术后 6周造影复查示左室前壁、心尖部室壁瘤形成 ,4只猪堵闭的LAD远端闭塞。心电图显示急性心肌梗死的典型图形和动态演变过程。cTnI明显升高并呈动态演变。术后 1小时超声检查出现间隔上部及前壁局部运动异常 ,术后 2周即有室壁瘤形成。结论　运用PTCA球囊封堵冠状动脉可成功建立急性心肌梗死后室壁瘤的动物模型 ,与开胸法相比更接近人体的状态 ,具有创伤小、动物成活率高、生存时间长、技术要求不高等优点 ,可为进一步的研究提供较好的实验模型。     

全层心肌线性消融术治疗室壁瘤相关室性心动过速

目的:探讨一种标准化的全层心肌线性消融术治疗室壁瘤相关室性心动过速的有效性。方法:左侧开胸冠状动脉结扎法建立猪心肌梗死后室壁瘤相关室性心动过速的疾病模型,使用双极射频消融钳从室壁瘤中心放射状向室壁瘤边缘区进行"米"字形消融。消融后诱发室性心动过速,评价同时心内膜-心外膜全层心肌线性消融术后的即刻有效性。结果:20只实验猪建模6周后14只伴室壁瘤形成。其中10只可诱发持续性室性心动过速。所有模型猪均在心脏不停跳下顺利完成了全层心肌消融术,每只猪8条线性消融损伤,无手术死亡。消融术后再次诱发室性心动过速,全层心肌消融术的即刻有效可达80%。结论:标准化的"米"字形全层心肌消融术可有效遏制猪室壁瘤相关室性心动过速。     

Carto标测下双极射频消融术治疗实验猪室壁瘤相关室性心动过速的研究

目的:探索Carto标测指导下,双极射频消融术治疗室壁瘤相关室性心动过速的可行性。方法:14头实验猪利用左侧肋间小切口冠状动脉缝扎法建立猪急性心肌梗死(AMI)模型。建模6~8周后对左心室造影证实有室壁瘤的模型猪诱发持续室性心动过速(VT)。将可诱发VT的模型猪随机分为射频组和对照组。射频组行基质标测,解剖定位缓慢传导区,然后进行双极射频消融术(BRF)。BRF后,两组模型猪再次诱发VT。评价BRF的可行性。结果:14头猪建模6~8周后存活10头,左心室造影证实8头形成室壁瘤,其中7头可诱发持续VT。射频组5头,对照组2头。射频组均成功施行了基质标测下BRF,无手术死亡。术后射频组80%模型猪VT不可诱发,而对照组100%可诱发VT(P0.05)。结论:Carto标测指导下BRF在室壁瘤相关VT模型的应用是可行的,即刻控制VT是有效的。     

特发性室性心动过速的心电图特点

室性心动过速是恶性心律失常的一种,常见于器质性心脏病的病人,正常人罕见。而心电图呈完全性右束支传导阻滞(RBBB)伴心电轴左偏(LAD)的特发性室性心动过速却常见于正常人,现将我们遇到的7     

急性心肌梗死后室壁瘤形成患者炎性指标水平的临床分析

目的 探讨急性心肌梗死(AMI)患者的高敏C反应蛋白(hs-CRP)等炎性指标水平和左心室室壁瘤(LVA)形成的关系.方法 将68例AMI患者经心脏超声和(或)左心室造影检查确诊为LVA形成,并符合纳入标准的患者分为LVA组,另设68例为对照组行配对研究,测定血清hs-CRP、血沉(ESR)、白细胞(WBC)计数和中性粒细胞百分率,并做超声心动图和(或)左心室造影检查,评定左心室功能和室壁运动情况.结景 LVA组患者的血清hs-CRP、ESR、中性粒细胞百分率明显高于对照组(P<0.001),WBC虽高于对照组,但差异无统计学意义(P0.05).结论 hs-CRP炎性指标水平增高与AMI后LVA形成密切相关.     

重组人肿瘤坏死因子受体融合蛋白对大鼠急性心肌梗死室性心律失常的影响

目的:通过大鼠急性心肌梗死(AMI)模型探讨重组人肿瘤坏死因子受体融合蛋白(rhTNFR:Fc)对AMI室性心律失常发生的影响.方法:将240只大鼠随机分为假手术组(Sham组)、AMI组和rhTNFR:Fc组.Sham组开胸后不结扎冠状动脉;AMI组开胸后结扎冠状动脉左前降支(LAD),建立AMI模型;rhTNFR:Fc组结扎LAD前24 h腹腔注射rhTNFR:Fc.于结扎前10 min和结扎后10 min、20 min、30 min、60 min、3 h、6 h、12 h,记录心电图,观测程序刺激诱发的室性心律失常;通过免疫组化法检测各时间点各组心肌TNF-a的表达水平.结果:AMI组和rhTNFR:Fc组结扎后10 min即可诱发室性心律失常,30 min内诱发性室性心律失常的发生最频繁,峰值在15～25 min,以后逐渐减少,1 h后很少能诱发;急性缺血心肌TNF-a分泌的时间窗规律与上述基本一致.rhTNFR:Fc组心肌检测出的TNF-a及室性心律失常发生次数均明显少于AMI组(P＜0.05).Sham组无明显变化.结论:rhTNFR:Fc能明显降低大鼠AMI室性心律失常的发生.     

射频消融治疗束支折返性室性心动过速一例

一例室性心动过速患者无扩型心肌病或缺血性心肌病基础,有明确的希-浦系统传导障碍,电生理检查可诱发两种室速:一种呈左束支传导阻滞型,心内激顺序为左束支-His束-心室;另一种呈右束支传导阻滞型,心内激动顺序为His束-左束支-心室。确诊为束支折返性室性心动过速,通过消融右束支治疗成功。     

第20课束支折返性室性心动过速

束支折返性心动过速是室性心动过速(室速)的一种罕见类型,由双侧束支组成折返环路。该心律失常通常见于获得性心脏病和(心脏)传导系统显著受损的患者,但亦曾报道见于心脏结构正常的患者。在窦性心律时,体表心电图特征性地显示心室内传导障碍。由于(该)室性心动过速伴>200次/m in的快心室率,患者典型表现为晕厥先兆、晕厥或猝死。室性心动过速时QRS波群呈典型的束支传导阻滞型,常显示左束支传导阻滞,其形态可与窦性心律时一致。大多数束支折返性室性心动过速患者在窦性心律时H-V间期延长,但尚有部分患者H-V间期可在正常范围内。束支折返性…     

急性心肌梗死后左心室壁瘤形成机制、并发症及治疗

左心室壁瘤（LVA）是急性心肌梗死（AMI）后常见的严重并发症之一。急性心肌梗死后梗死区白细胞释放炎症介质导致心肌细胞坏死,纤维瘢痕组织形成,心肌变薄及纤维化,引起左心室重构,在心室压力作用下室壁局部向外膨出是室壁瘤形成的机制。室壁瘤的形成可导致恶性室性心律失常、室间隔穿孔、心力衰竭、左室附壁血栓等并发症,病死率较无室壁瘤形成者高6倍以上。因此,室壁瘤的预防、逆转及治疗直接关系到患者的预后。     

Immediate reproducibility of clinical and nonclinical forms of induced ventricular tachycardia

This prospective study assessed the immediate reproducibility of clinical and nonclinical forms of ventricular tachycardia (VT) induced by programmed ventricular stimulation. Twenty-three clinical VTs were unimorphic and previously documented and 22 nonclinical VTs (17 polymorphic and 5 unimorphic) were induced in patients with either no documented or suspected history of VT, or documented VT that had a configuration different from that of the induced VT. The stimulation protocol included 1 to 3 ventricular extrastimuli, 2 drive cycle lengths, and 2 right ventricular stimulation sites. Each VT was induced on the first attempt, then the stimulation protocol was repeated twice in the drug-free state. After the first VT induction, 21 of 23 clinical VTs (91%) and 17 of 22 nonclinical VTs (77%) were reinduced on the second attempt. After 2 VT inductions, 21 of 21 clinical VTs (100%) and 15 of 17 nonclinical VTs (88%) were reinduced on the third attempt. The reinduction rates of the clinical and nonclinical VTs were not significantly different. Among the clinical VTs, the reproducibility of the induction technique was 81% after 1 induction and 88% after 2 inductions with the same technique. These results imply that acute drug testing can be reliably performed after 2 inductions but not 1 induction of clinical VT; reproducibility is not helpful in determining whether an induced VT is clinical or nonclinical; and changes in induction technique during drug testing should be interpreted with caution because changes may occur in the absence of drugs.     

Successful catheter ablation of ventricular tachycardia originating from the idiopathic saccular apical left ventricular aneurysm

Left ventricular (LV) aneurysm has been recognized to frequently become a substrate of ventricular tachyarrhythmias. We report a case of a 66-year-old woman with symptomatic sustained monomorphic ventricular tachycardia (SMVT) originating from saccular apical LV aneurysm without definite underlying diseases. We performed catheter ablation using electroanatomical and conventional bipolar potential mapping. During SMVT, we found an area of fragmented potential -40 ms preceding the earliest wide QRS complex in the area of the apical LV aneurysm. Radiofrequency applications were delivered to this area. Since then, SMVT was no longer inducible by programmed electrical stimulation. The patient has remained free of VT recurrences during a subsequent 12-month follow-up period.     

Procainamide induced sustained monomorphic ventricular tachycardia in a patient with benign premature ventricular complexes

A 59-year old female with history of benign ventricular ectopy who developed sustained monomorphic ventricular tachycardia (VT) during therapy with procainamide is reported. The tachycardia occurred 24 hours after institution of procainamide without any other evidence of drug toxicity or QT prolongation. When procainamide was withheld, VT resolved completely and no arrhythmia could be induced by programmed ventricular stimulation. When the patient was rechallenged with procainamide at therapeutic level, sustained monomorphic VT was initiated reproducibly by programmed ventricular stimulation. Without antiarrhythmic therapy, patient has been asymptomatic and free of recurrent VT after a follow-up of 9 months. This case: Demonstrates that procainamide may cause the first emergence of sustained monomorphic VT in a patient with no previous history of VT; and Emphasizes the utility of programmed ventricular stimulation in providing direct evidence for drug mediated exacerbation of the ventricular arrhythmia.     

Novel mechanism of postinfarction ventricular tachycardia originating in surviving left posterior Purkinje fibers

BACKGROUND: Other than bundle branch reentry and interfascicular reentry, monomorphic postmyocardial infarction (post-MI) reentrant ventricular tachycardia (VT) including the His-Purkinje system has not been reported. Verapamil-sensitive idiopathic left VT includes the left posterior Purkinje fibers but develops in patients without structural heart disease. OBJECTIVES: The purpose of this study was to describe a novel mechanism of reentrant VT arising from the left posterior Purkinje fibers in patients with a prior MI. METHODS: The study consisted of four patients with a prior MI and symptomatic heart failure who underwent electrophysiologic study and catheter ablation for VT showing right bundle branch block (n = 3) or atypical left bundle branch block (n = 1) morphology with superior axis. In two patients, the VT frequently emerged during the acute phase of MI and required emergency catheter ablation. RESULTS: Clinical VT was reproducibly induced by programmed stimulation. In three patients, both diastolic and presystolic Purkinje potentials were sequentially recorded along the left ventricular posterior septum during the VT, whereas in the fourth patient, only presystolic Purkinje potentials were observed. During entrainment pacing from the right atrium, diastolic Purkinje potentials were captured orthodromically and demonstrated decremental conduction properties, whereas presystolic Purkinje potentials were captured antidromically and appeared between the His and QRS complex. Radiofrequency energy delivered at the site exhibiting a Purkinje-QRS interval of 58 +/- 26 ms successfully eliminated the VTs without provoking any conduction disturbances. CONCLUSION: Reentrant monomorphic VT originating from the left posterior Purkinje fibers, which is analogous to idiopathic left VT, can develop in the acute or chronic phase of MI. Catheter ablation is highly effective in eliminating this VT without affecting left ventricular conduction.     

Ventricular tachycardia late after repair of congenital heart disease: efficacy of combination therapy with radiofrequency catheter ablation and class III antiarrhythmic agents and long-term outcome

OBJECTIVE: This study investigated the treatment of ventricular tachycardia (VT) after repair of tetralogy of Fallot or double outlet of the right ventricle. BACKGROUND: The ideal antiarrhythmic therapy for VT in patients after repair of congenital heart disease, especially without left ventricular dysfunction, has not yet been established. METHODS: Seven consecutive patients (2 women and 5 men) with stable monomorphic sustained VT were investigated. The mean age was 25 +/- 7 years (range, 16-35 years). Four patients had undergone surgical repair of tetralogy of Fallot, and 3 had surgical correction of double outlet of the right ventricle at the mean age of 18 +/- 7 years (range, 9-27 years) before documentation of the arrhythmia. RESULTS: The mean ejection fraction of the left ventricle was 60% +/- 8% (range, 50-72). Fourteen sustained monomorphic VTs were induced in 7 patients using programmed electrical stimulation. The mean cycle length of tachycardia was 346 +/- 77 milliseconds (range, 260-480 seconds). The site of the surgical correction of the right ventricle was associated with the origin of VT in all patients. Radiofrequency catheter ablation was attempted in 8 VTs in 7 patients: 7 clinical and 1 nonclinical VTs. In 6 patients, class III antarrhythmic agents were added because VT remained inducible after ablation. During a follow-up of 61 +/- 29 months (range, 15-110 months), there were no recurrences of VT. CONCLUSION: In patients with drug-refractory VT originating from the right ventricle late after congenital heart disease, and when their left ventricular function do not deteriorate, combined therapy for radiofrequency catheter ablation with class III antiarrhythmic agents might effective and should be considered as a therapeutic option.     

Programmed electrical stimulation in healed myocardial infarction using a standardized ventricular stimulation protocol

The diagnostic accuracy of programmed electrical stimulation was prospectively assessed in 111 patients with myocardial infarction (MI) with or without a history of spontaneous ventricular arrhythmias. In 29 patients neither ventricular tachycardia (VT) nor episodes of 10 premature ventricular depolarizations per hour was documented. Fifty patients had documented nonsustained VT and 32 had sustained monomorphic VT. One and 2 extrastimuli (twice diastolic threshold, 2 ms in duration) were given during sinus rhythm and ventricular pacing at 100, 120 and 140 beats/min in the right ventricular apex (part I). When this protocol failed to induce a sustained monomorphic VT, a third extrastimulus was introduced (part II). Repetitive ventricular responses were induced in all patients, and in 15 (14%) polymorphic ventricular arrhythmias requiring DC shock were induced. Incidence of initiation of sustained monomorphic VT and polymorphic ventricular arrhythmias requiring DC shock was related to the clinical arrhythmia and the stimulation protocol. In patients with documented sustained monomorphic VT, a third extrastimulus only increased the incidence of sustained monomorphic VT (68% to 94%), whereas in patients with documented nonsustained VT and without VT the incidence of both polymorphic and monomorphic arrhythmias increased by 7 to 12%. Sustained monomorphic VTs induced in patients without such a history were faster (p less than 0.01), depended on site of MI (p less than 0.05) and were more often preceded by nonsustained polymorphic VT (p less than 0.01) than in patients with documented sustained monomorphic VT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of catheter ablation of ventricular tachycardia associated with structural heart disease

In patients with structural heart disease, ventricular tachycardia (VT) worsens the clinical condition and may severely affect the shortand long-term prognosis. Several therapeutic options can be considered for the management of this arrhythmia. Among others, catheter ablation, a closed-chest therapy, can prevent arrhythmia recurrences by abolishing the arrhythmogenic substrate. Over the last two decades, different techniques have been developed for an effective approach to both tolerated and untolerated VTs. The clinical outcome of patients undergoing ablation has been evaluated in multiple studies. This editorial gives an overview of the role, methodology, clinical outcome and innovative approaches in catheter ablation of VT.     

Identifying patients at risk of sudden death after myocardial infarction: Value of the response to programmed stimulation, degree of ventricular ectopic activity and severity of left ventricular dysfunction

The ability of programmed ventricular stimulation to identify risk of sudden death after acute myocardial infarction (MI) was compared with 24-hour electrocardiographic assessment of ventricular ectopic activity and determination of left ventricular (LV) dysfunction. Forty-six patients underwent programmed stimulation 8 to 60 days (mean 22) after documented MI. Programmed stimulation consisted of single and double extrastimuli from the right ventricular apex at 2 times diastolic threshold during ventricular pacing and normal sinus rhythm. Of the 46 patients, 44 underwent electrocardiographic monitoring at least 6 days after MI. In 43 of the 46 patients, LV ejection fraction (EF) and the presence of LV aneurysm were determined. In response to programmed ventricular stimulation, 5 patients had sustained ventricular tachycardia (VT), 5 had nonsustained VT (≥4 beats), 13 had intraventricular reentrant repetitive responses, and 23 had either bundle branch reentrant repetitive responses or no extra responses to programmed ventricular stimulation (negative study).

During a mean follow-up of 18 months, 10 patients died, 6 suddenly. One of the 10 patients with sustained or nonsustained VT died suddenly, compared with 3 of 13 patients with intraventricular reentrant responses and 2 of 23 patients with a negative study (difference not significant). Of 25 patients with Grade 0 to 2 ventricular ectopic activity, 3 died suddenly after MI, compared with 3 of 19 patients with Grade 3 or 4 activity (difference not significant). By comparison, the frequency of sudden death was greater in patients with an LVEF of <40% (5 of 16 versus 1 of 27 patients) or an LV aneurysm (5 of 13 versus 1 of 30 patients).

Thus, using the described protocol, the response to programmed ventricular stimulation is not helpful in identifying patients at risk for sudden death after MI. The presence of an LV aneurysm or EF of <40% appears to provide the greatest prognostic information with respect to risk for sudden cardiac death.     

心肌梗死后室壁瘤形成与室性心动过速的关系探讨

目的 探讨心肌梗死（MI）后室壁瘤形成大小、左室大小、左心功能与室性心动过速的关系.方法 回顾性分析114例心肌梗死后室壁瘤形成患者的临床资料,根据动态心电图、心电监护证实并发室性心动过速21例归为室速组,其余为非室速组,分析比较两组患者的病史特点、左房直径、左室舒张末期直径、左室收缩末期直径、左室舒张期室间隔厚度、左室舒张期后壁厚度、室壁瘤大小及左室射血分数.结果 两组间左房直径[（4.49±0.47）cm比（4.07±0.62）cm,P=0.040]、左室舒张末期直径[（6.34±0.80）cm比（5.77±0.76）cm,P=0.029]和左室收缩末期直径[（5.18±1.01）cm比（4.33±0.94）cm,P=0.008]比较,差异有统计学意义,左房直径、左室舒张期后壁厚度、室壁瘤基底直径、室壁瘤膨出直径、左室射血分数两组间比较差异无统计学意义（P〉0.05）.结论 心肌梗死后室壁瘤形成,其左室大小与室性心动过速有一定关系,而与室壁瘤大小无关.