Pacemaker-induced ventricular tachycardia in patients with acute inferior myocardial infarction

We analysed a group of 35 consecutive patients with acute myocardial infarction—23 of the inferior, 12 of the anterior wall—who needed temporary pacing for bradycardiac arrhythmias. We observed in three patients ventricular tachycardias induced by pacemaker stimuli falling onto the vulnerable part of the cardiac cycle due to improper sensing. All three had an inferior myocardial infarction involving the right ventricle. Because the pacemaker electrode in this condition lies in the vicinity of the infarcted myocardium sensing problems occur more frequently and re-entry tachy-cardias can be triggered more easily. It represents a possible risk of pacemaker treatment in this group of patients who, on the other hand, often need cardiac pacing in the acute phase following the development of transient AV-block.     

Discrete systolic potentials during ventricular tachycardia in patients with prior myocardial infarction

INTRODUCTION: Isolated diastolic potentials have been found to be helpful in identifying critical sites for ablation of ventricular tachycardia (VT) in patients with coronary artery disease. However, discrete potentials that occur during systole have not been previously described. The purpose of this study was to determine the significance of discrete systolic potentials during VT in patients with coronary artery disease. METHODS AND RESULTS: Twenty-seven patients with a mean age of 66 +/- 12 years ( +/- standard deviation) who had coronary artery disease underwent radiofrequency catheter ablation of 42 VTs that had a mean cycle length of 486 +/- 78 msec. The only criterion used to select target sites for ablation was concealed entrainment, which was present at 92 sites. Thirty-five of the 42 VTs (83%) were successfully ablated. A discrete systolic potential was recorded during 7 of the 42 VTs (17%). In all cases, the interval between the discrete systolic potential and the next QRS complex was equal to the stimulus-QRS interval during concealed entrainment. At all seven sites where a discrete systolic potential was recorded, delivery of radiofrequency energy resulted in successful ablation of the VT. CONCLUSION: Discrete systolic potentials may be present in patients with coronary artery disease in approximately 17% of VTs in which there is concealed entrainment. If the interval between the discrete systolic potential and the next QRS complex matches the stimulus-QRS interval during concealed entrainment, delivery of radiofrequency energy is likely to result in successful ablation of the VT.     

急性下壁心肌梗死伴右室梗死的临床表现和预后分析

目的探讨急性下壁心肌梗死(心梗)不伴或伴右室心梗患者的临床特征、治疗和预后。方法回顾既往6年住我院的103例急性下壁心梗患者,比较下壁心梗不伴右室心梗(65例)和伴右室心梗(38例)两组患者的临床特征和院内死亡率。结果发生低血压、心源性休克、快速心律失常(阵发性心房颤动,非持续性室性心动过速)、缓慢心律失常(包括窦性心动过缓,Ⅲ度房室传导阻滞)在下壁伴右室心梗组高于下壁心梗组,两组比较有显著性差异(P<0.05)。两组左心室射血分数(LVEF)及经皮冠脉介入(PCI)治疗患者的院内病死率比较无显著差异(P>0.05)。结论血流动力学障碍和心律失常是右室心梗住院并发症高的主要因素,右室心梗是独立于左室功能损害的危险因素,早期介入治疗能改善住院死亡率。     

Type II bidirectional ventricular tachycardia in a patient with myocardial infarction

A 84-year-old man presented to the emergency department complaining of chest pain and palpitations. He had no history of coronary artery disease. The 12-lead electrocardiography showed bidirectional ventricular tachycardia (BVT). Coronary angiography revealed severe mid left anterior descending and mid left circumflex lesions. The BVT, in this case, was most likely due to myocardial ischema. The ethiology of published BVT cases are most commonly digitalis toxicity and rarely herbal aconitine poisoning, hypokalemic periodic paralysis, cathecolaminergic VT, myocarditis, and Anderson-Tawil syndrome. The patient had neither of these underlying conditions. To the best of our knowledge and research in the literature, there was no report of bidirectional VT in the patients with myocardial infarction.     

急性心肌梗死非持续和持续室性心动过速的Q—T离散度

为研究急眭心肌梗死伴持续和非持续室性心动过速患者间Q-T离散度和其它心电图参数之间的关系。比较14例急性心肌梗死伴持续室性心动过速和26例伴非持续室性心动过速患者的心室Q-T离散度、Q-T和Q-T_c间期。结果显示持续和非持续室性心动过速患者之间的Q-T离散度以及相邻胸导联Q-T离散度差异有显著意义(110.1±7.80对80.8±4.4,105.9±6.9对67.6±4.0,P<0.01)。我们认为相邻导联Q-T离散度增大极易出现室性心动过速,Q-T离散度大于110ms有发生持续室性心动过速的危险。而Q-T离散度在80—110ms之间有非持续室性心动过速的可能性。     

右室心肌梗死对急性下壁心肌梗死临床特征和预后的影响

目的：分析右室心肌梗死(心梗)对急性下壁心梗临床特征和预后的影响。方法：比较急性单纯性下壁心梗(第一组)和急性下壁心梗合并右室心梗(第二组)两组患的临床特征和院内病死率。结果：共176例患符合入选条件，第一组115例，第二组61例。第一组低血压、快速心律失常(包括阵发性室上性心动过速，阵发性心房颤动，领发室性早搏，室性心动过速，心室纤颤等)、缓慢心律失常(包括窦性心动过缓，房室传导阻滞)、心功能不全的发生率和院内病死率显低于第二组(P＜0．05)。静脉溶栓、急诊PTCA和未行再灌注治疗的院内病死率在第一组的分别为3．23％，3．33％和29．17％，在第二组分别为9．25％，13．04％和82．35％。结论：当急性下壁心梗合并右室心梗时，患的临床表现更为严重，院内病死率增高。积极行溶栓或急诊PTCA治疗，可显降低其院内病死率.     

Verapamil-sensitive left posterior fascicular ventricular tachycardia after myocardial infarction

Verapamil-sensitive fascicular ventricular tachycardia (VT) of right bundle branch block (RBBB) and superior axis pattern is typically seen in young patients with structurally normal hearts and considered “idiopathic”. Recently, involvement of the Purkinje system in post-infarction monomorphic VT that mimics such idiopathic fascicular VT has been described. In this report we describe a case of a patient who following myocardial infarction developed left posterior fascicular Purkinje reentrant VT that was sensitive to verapamil. The VT was successfully treated by radiofrequency ablation guided by three dimensional electroanatomical CARTO™ mapping. Our case highlights that involvement of Purkinje fibers should be considered in post infarction patients with VT of narrow QRS duration, RBBB morphology and superior axis. Recognition of such VT is clinically important, as this arrhythmia is amenable to curative catheter ablation.     

The QRS morphology in post-myocardial infarction ventricular tachycardia. A study of 100 tracings compared with 70 cases of idiopathic ventricular tachycardia

A hundred tracings of ventricular tachycardia (VT) belongingto 85 patients with myocardial infarction (MI) were comparedwith 70 cases of incessant, benign, idiopathic VT. The two groupsof tracings differed in terms of QRS axis, most often normalin idiopathic VT (75%) and outside normality in MIVT (74%).The sum of QRS amplitude in unipolar limb leads was greaterin idiopathic VT (4.3±1.3 mv, mean±S.D.) thanin MIVT (2.6±0.8 mv, P>0.001). The QRS width was alsodifferent: 135±11 ms in idiopathic VT vs. 171±32ms in MIVT (P>0.001). The QRS morphology in MIVT was characterizedby the presence of a QR pattern in leads other than VR, or aQS pattern in V₅–V₆. These two aspects were constantlyabsent in idiopathic VT, and they were present in 89%of MIVT.In only 38 MIVT tracings were the ECG signs of MI observed inthe same leads during sinus rhythm and during VT. In 51 MIVTtracings the location of the MI indicated by the VT tracingdiffered from that displayed in sinus rhythm. Rather than indicatingan extension of the infarcted area not apparent in the tracingsin sinus rhythm, such a discrepancy suggests that the QRS patternduring VT strongly depends on the point of origin of the VT.Conversely, this explains why the morphology of the QRS is anureliable means for localizing the VT origin if the locationof the MI is not taken into account. We conclude that both factorsshould be taken into consideration, and this might theoreticallypermit a better though complex approach to the VT origin incoronary heart disease using surface tracings.     

Sustained ventricular tachycardia as a marker of inadequate myocardial perfusion during the acute phase of myocardial infarction

BACKGROUND: Sustained ventricular tachycardia (VT) complicating the acute phase of myocardial infarction (AMI) is a quite rare event but with short-term unfavorable prognosis. The clinical characteristics as well as the therapeutic implications have not yet been well defined. HYPOTHESIS: This paper attempts to prove that VT may be considered a marker of inadequate myocardial perfusion after thrombolysis. METHODS: To assess the clinic-electroangiographic characteristics and prognosis of patients with VT occurring within the first 4 days of an AMI, a case-control study was carried out in 23 patients from a total of 1,100 patients (1.9%) hospitalized with AMI between March 1993 and July 1997. These patients were compared with a control group of 131 patients hospitalized consecutively. A statistical analysis was made using the chi-square test, t-test, and logistic regression. RESULTS: There were no differences among groups with regard to age, gender, and area of necrosis. Average time for the onset of VT was 26 h (range 0-92 h). Sixteen patients underwent coronary angiography: 4 patients had left main coronary artery disease, 2 had single-vessel disease, 8 had lesions in two vessels, and 2 had triple-vessel disease. Univariate analysis showed that patients with VT had a higher incidence of creatine phosphokinase (CPK)-MB peak > 300 UI/l (61 vs. 30%; p<0.001), more frequent occurrence of previous AMI (48 vs. 17%; p<0.001), and acute intraventricular conduction disorders (26 vs. 4%; p<0.001). Furthermore, these patients suffered ischemia previous to VT more frequently (65 vs. 11%; p<0.0001), and had a greater mortality rate than that in the control group (35 vs. 4%; p<0.0001). In the multivariant analysis, the variables related to the occurrence of VT were CPK-MB peak > 300 IU/l (OR 5.9; 95% CI 1.6-21), acute intraventricular conduction disorders (OR 9.02; 95% CI 1.7-48), and ischemia immediately prior to VT (odds ratio [OR] 19.64; 95% confidence interval [CI] 5.3-73). CONCLUSIONS: Ventricular tachycardia may be considered a marker of inadequate myocardial perfusion after thrombolysis; therefore, a more aggressive revascularization treatment in these patients would be advisable. The profile of patients with AMI, hospitalized in the coronary care unit, who will likely suffer from VT is previous AMI, CPK-MB peak > 300, acute intraventricular conduction disorders, Killip > I, and ischemia previous to VT.     

Induction of transient third degree atrioventricular block during radiofrequency catheter ablation in a patient with ventricular tachycardia and remote myocardial infarction

INTRODUCTION: Radiofrequency catheter ablation has been demonstrated to bean effective and safe therapy in patients with so-called idiopathicventricular tachycardia, whereas the benefit/risk profile forablation of ventricular tachycardia in patients with chronicmyocardial infarction and severely compromised left ventricularfunction still needs to be determined. The present report describesthe unintended induction of transient third-degree atrioventricularblock in a patient with remote myocardial infarction who underwentradiofrequency catheter ablation of ventricular tachycardia. METHODS AND RESULTS: Endocardial catheter mapping and radiofrequency ablation wereperformed in a 57-year-old patient with chronic recurrent ventriculartachycardia, who had previously suffered from anterior and posteriorwall myocardial infarction. Additionally, the patient presentedwith complete right bundle branch block during sinus rhythm.Radiofrequency energy applied to a critical site of the reentranttachycardia at the left ventricular basal septum during sinusrhythm induced third-degree atrioventricular block after 20s of current delivery, which lasted for 24 h. At this site,a presumable left bundle branch potential was recorded duringsinus rhythm. CONCLUSIONS: Radiofrequency current application for ablation of ventriculartachycardia may induce third-degree atrioventricular block inpatients with remote myocardial infarction. When current isdelivered to target sites at the left ventricular basal septum,radiofrequency energy should be applied during sinus rhythmto allow continuous monitoring of atrioventricular conduction.Special caution should be given to patients with right bundlebranch block during sinus rhythm.     

Non-contact mapping in the treatment of ventricular tachycardia after myocardial infarction

The treatment of ventricular tachycardia (VT) in patients with underlying ischaemic heart disease (IHD) remains a challenge. Ablation of these arrhythmias may have a significant impact on quality of life for patients. For those patients with haemodynamically unstable VT, ablation success rates have been improved by the use of non-contact mapping. Care has to be taken in the analysis and interpretation of non-contact mapping studies, as chamber size and filter settings have a large effect on the appearance of the activation maps produced. Despite this limitation the majority of VT exit sites and part of the diastolic pathway can be identified with non-contact mapping techniques.     

Catheter ablation of ventricular tachycardia by intramyocardial injection of ethanol in an animal model of chronic myocardial infarction

INTRODUCTION: Direct injection of ethanol into myocardium has been shown to create large, well-demarcated lesions with transmural necrosis in normal ventricular myocardium and in regions of healed myocardial infarction. The aim of this study was to investigate the effects of direct ethanol injection on the inducibility of ventricular tachycardia (VT) in an animal model of chronic myocardial infarction. METHODS AND RESULTS: Eight sheep with reproducibly inducible VT underwent an electrophysiologic study 139 +/- 65 days after myocardial infarction. Noncontact mapping was used to analyze induced VT. Fifteen different VTs were targeted for catheter ablation. Ablation was achieved by catheter-based intramyocardial injection of a mixture of 96% ethanol, glycerine, and iopromide (ratio 3:1:1). Direct intramyocardial ethanol injection resulted in noninducibility of any VT 20 minutes after ablation in 7 of 8 animals. Four of 5 animals with initially successful ablation remained noninducible for any VT at follow-up study at least 2 days after the ablation procedure. Microscopic examination revealed homogeneous lesions with interstitial edema, intramural hemorrhage, and myofibrillar degeneration at the lesion border. The lesions were well demarcated from the surrounding tissue by a border zone of neutrophilic infiltration. CONCLUSION: Catheter ablation of VT by direct intramyocardial injection of ethanol during the chronic phase of myocardial infarction is feasible. It may be a useful tool for catheter ablation when the area of interest is located deep intramyocardially or subepicardially or when a more regional approach requires ablation of larger amounts of tissue.     

Human histopathology of electroanatomic mapping after cooled-tip radiofrequency ablation to treat ventricular tachycardia in remote myocardial infarction

INTRODUCTION: Catheter ablation of ventricular tachycardia (VT) in remote myocardial infarction (MI) often requires excessive mapping procedures. Documentation of the electrical substrate via electrogram amplitude may help to identify regions of altered myocardium resembling exit areas of reentrant VTs. METHODS AND RESULTS: A patient with multiple symptomatic monomorphic VTs (biventricular ICD, remote MI) underwent electroanatomic substrate mapping (CARTOtrade mark) for VT ablation. Regions of scar (bipolar electrogram amplitudes or=1.5 mV), and "altered" myocardium (0.5-1.5 mV) were identified. Ablation was directed to regions with "altered" myocardium based on pace map correlation. After ablation the clinical VT did not reoccur. The patient died due to worsening of heart failure 7 days afterward. During postmortal evaluation specified sites of electroanatomic mapping were correlated to histopathological findings. Annotated scar areas were documented to consist of areas with massive fibrosis (>or=80% of mural composition). Ablations were found to span through regions with intermediate fibrosis (21-79%) mapped as "altered" myocardium. Ablation produced transmural coagulation necrosis of mesh-like fibrotic tissue with interspersed remnants of myocardial cells up to a maximum depth of 7.0 mm. Subendocardial intramural bleedings were universal findings 7 days after ablation. CONCLUSIONS: Electroanatomic substrate mapping for VT ablation sufficiently identified regions of scar and normal myocardium. Regions with bipolar electrogram amplitudes between 0.5 and 1.5 mV were found to correlate to areas of "intermediate" fibrosis (21-79%) with only remnant strands of myocardial cells and were identified as target region for ablation. Cooled-tip endocardial radiofrequency ablation lead to transmural coagulation necrosis up to a depth of 7.0 mm.     

伴右心室出口的左心室起源缺血性室性心动过速的标测和消融

目的折返性的缺血性室性心动过速（VT）绝大多数发生于左心室并表现为右束支阻滞（RBBB）图形。本文报道1组VT折返环位于左心室但出口在右心室且表现为左束支阻滞（LBBB）的病例。方法32例因陈旧性心肌梗死伴VT而接受电生理检查和射频消融的患者,其中4例临床有LBBB形态的VT。使用非接触等电位和虚拟单极标测判断VT起源,结合舒张中期电位（MDP）和拖带标测确定折返关键通路和消融靶点。用盐水冲洗电极导管在折返环的关键峡部行线性消融。结果全部32例患者中,4例临床有LBBB型VT者均成功被诱发,其中1例有两种LBBB型VT,1例同时有RBBB型VT但周长与LBBB型相同;另有1例共有6种形态的VT,包括RBBB和LBBB型。在右心室内的非接触式等电位标测可迅速确定VT在右心室的传出部位,该处的虚拟单极标测显示rS型提示左心室起源。3例在左心室成功拖带并消融成功,靶点均紧邻左心室间隔,其中1例位于下壁,1例在前壁,1例两种LBBB型VT分别在前壁和下壁间隔旁消融成功。随访1～4．2年,未服抗心律失常药无VT发作。而1例诱发出6种单形（包括RBBB和LBBB型）VT患者因巨大室壁瘤及心功能障碍不能耐受而中途放弃消融。结论紧邻室间隔的前壁和下壁心肌梗死后的左心室起源VT可能因在右心室有出口而表现为LBBB型,需要在标测和消融时予以注意。     

Sustained monomorphic ventricular tachycardia ablation from the aortic sinus of valsalva

INTRODUCTION: The aim of this study was to delineate the electrophysiologic mechanisms of a novel type of ventricular tachycardia (VT) originating from the aortic sinus of Valsalva. METHODS AND RESULTS: Endocardial mapping was performed in four patients with symptomatic VT originating from the aortic sinus of Valsalva. Two patients suffered from dilative cardiomyopathy; the other two patients had no structural heart disease. Five VTs could be induced and terminated by programmed ventricular stimulation. Successful ablation was performed in the noncoronary sinus of Valsalva in three VTs and in the left aortic sinus in two. Abnormal (diastolic or presystolic) potentials were recorded during sinus rhythm (mean interval from the end of QRS complex to the potential 121+/-98 msec) and during VT (mean interval from the potential to QRS complex 64+/-45 msec) at effective sites in the aortic sinuses of Valsalva. Concealed entrainment was demonstrated at all successful sites. VT recurred in one patient after 1 month, whereas no recurrences were observed during follow-up of 8+/-6 months in the other three patients. CONCLUSION: Reentry constitutes one mechanism of VT originating from the aortic sinus of Valsalva. Entrainment mapping is useful to characterize the reentrant circuit of these VTs and to guide ablation.     

心肌梗塞后室性心动过速的微波消融

目的　比较射频消融与微波消融对心肌梗塞后室性心动过速 (室速 )的疗效。　方法　 2 7只健康成年犬 ,开胸。用 Harris二期阻闭加再灌注法造成心肌梗塞模型 ,用程序电刺激或毒毛旋花子甙 K(毒K)诱发持续性室速。将能诱发出持续性室速存活的 2 0只犬随机分成 2组 : 组为射频消融组 , 组为微波消融组 ,每组各 1 0只。射频消融组与微波消融组能量与放电时间均为 4 0× 1 2 0 Ws。　结果　射频消融组中被诱发出的 4 0次 (2 3次为程序电刺激诱发 ,1 7次为毒 K诱发 )持续性室速中 ,有 1 6次 (1 5次为毒 K诱发 ,1次为程序电刺激诱发 )被射频消融终止 ,分属 4只犬 ,在 3只犬术后未能再诱发出室速 ,成功率 3 0 %。微波消融组诱发出 2 8次 (1 7次为程序电刺激诱发 ,1 1次为毒 K诱发 )持续性室速 ,2 8次均被微波消融终止 ,1 0只犬术后未能再诱发出室速 ,成功率 1 0 0 %。　结论　微波消融比射频消融对心肌梗塞后室速可能具有更好的疗效。     

Antidromic atrioventricular reentrant tachycardia mimicking ventricular tachycardia in the setting of previous myocardial infarction

The differentiation between ventricular tachycardia and broad-complex supraventricular tachycardia can be extremely difficult, particularly in emergency situations. We report a case of hemodynamically compromising broad-complex tachycardia in a 63-year-old man. The patient had previously sustained an anteroseptal myocardial infarction and had subsequently undergone coronary artery bypass surgery because of triple-vessel coronary artery disease. Intravenous treatment with ajmalin terminated the tachycardia and revealed preexcited QRS complexes compatible with the presence of a left-sided atrioventricular accessory pathway. An antidromic atrioventricular reentrant tachycardia (identical to the clinical tachycardia) was induced during an electrophysiologic study. In conclusion, there are several causes of broad-complex tachycardia, even in patients with previous myocardial infarction, and, where doubt exists, electrophysiologic studies should be performed.     

窦性心律下通过三维电压标测心肌梗死后瘢痕性室性心动过速

目的 介绍一种不需行拖带标测,而在窦性心律下可标测和消融心肌梗死后瘢痕性室性心动过速(室速)的方法.方法 两例男性患者,均在心肌梗死和冠状动脉再通治疗后出现室速.经胺碘酮治疗后出现甲状腺功能异常而停药.其中例1为前壁心肌梗死合并心尖部室壁瘤,在发作室速时心功能恶化伴顽固咳嗽;例2为下后壁心肌梗死,其临床室速有两种形态,室性早搏(室早)有多种形态.该两种情况占心肌梗死后室速的大部分,均不太适合常规的拖带标测.首先在窦性心律时在Carto系统指导下建立左心室的三维电解剖图,通过调整瘢痕区电压标准,使梗死边缘区三层结构清楚显示后,沿边缘区行起搏标测,通过特征电位和测量刺激至QRS间距来判定峡部区,然后以峡部区为中心,以垂直于边缘区的方向行连续线性消融,直至室速不能被诱发视为消融终点.结果 两例在消融前均可反复诱发室速,在经过几条垂直线消融后室速均不能被诱发,随访3个月室速也未复发.心功能和生活质量明显改善.但例1出现室壁瘤附壁血栓.结论 对大多数心肌梗死后瘢痕性室速患者,均可在窦性心律下标测到其关键峡部区,并以此为中心点沿着垂直于边缘区方向行线性消融,以室速不能被诱发做为急性期终点同样能得到较好的远期成功率,但术后1个月需保持华法林抗凝.