What is the best predictor of spontaneous ventricular tachycardia and sudden death after myocardial infarction?

BACKGROUND. Death during the first year after myocardial infarction is most commonly due to spontaneous ventricular tachycardia (VT) or fibrillation (VF). The purpose of this study was to compare, in a single cohort of patients, the values of inducible VT, delayed ventricular activation, low left ventricular ejection fraction, high-grade ventricular ectopy, and ST segment displacement on exercise in predicting electrical events (witnessed instantaneous death and spontaneous VT or VF) during the first year after myocardial infarction. METHODS AND RESULTS. Three hundred sixty one patients aged less than 71 years underwent electrophysiological study, signal-averaged electrocardiogram, gated blood-pool scan, 24 hour ambulatory electrocardiographic monitoring, and exercise testing 1-2 weeks after myocardial infarction and were then followed up for at least 1 year. There were 34 deaths (eight witnessed instantaneous, 26 other), and nine patients survived one or more episodes of spontaneous VF or VT. Patients with inducible VT were 15.2 times more likely to suffer electrical events than patients without inducible VT. No proportional-hazards model excluding inducible VT was as good a predictor of electrical events as was inducible VT alone. CONCLUSIONS. Inducible VT at electrophysiological study was the single best predictor of spontaneous VT and sudden death after myocardial infarction.     

Non-arrhythmic therapy of ventricular tachyarrhythmias and sudden cardiac death after acute myocardial infarction

The management of ventricular tachyarrhythmias and prevention of sudden cardiac death after acute myocardial infarction (AMI) underwent important evolution. In the CAST study, encanaide and other antiarrhythmic drugs were not only ineffective but also increased mortality after myocardial infarction. Amiodarone had some beneficial effect on arrhythmic events without improving survival, and ICDs failed to improve outcome early after AMI. In comparison, short and long term survival benefits of beta blockers, angiotensine converting enzyme inhibitors and aldosterone antagonists after AMI is well established. This review discusses the role of non-arrhythmic therapy in the prevention of ventricular tachyarrhythmia's and sudden cardiac death after AMI.     

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.     

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。     

Prodromata of myocardial infarction and sudden death.

A sample of 160 hospitalized, acute myocardial infarction patients and 138 individuals who died prior to hospitalization from acute coronary heart disease were studied to determine the incidence and duration of prodromal symptoms and action taken to cope with the symptoms. Seventy percent of the in-hospital subsample (IHS) and 64% of the out-hospital subsample (OHS) reported prodromata. The OHS reported a significantly longer median duration of symptoms than the IHS (29 versus 10.5 days). Sixty-seven percent of the IHS reported new or accelerated anginal symptoms as the most frequently occurring symptom, in contrast to 35% for the OHS. Twenty-seven percent of the IHS and 36% of the OHS consulted a physician about symptoms. Individuals in both subgroups, especially chronically diseased patients, considered their symptoms manageable. Likewise, when contacted, their physicians may have viewed these symptoms as manageable. Patients with a high risk of myocardial infarction and sudden death were significantly more likely to have consulted physicians during the prodromal phase than low-risk patients. A clearly delineated prodromal syndrome is needed so that both lay and medical communities can effectively respond to and intervene during the prodromal phase of acute myocardial infarction and sudden cardiac death.     

Emergency treatment of chronic ventricular tachycardia after myocardial infarction by endocavitary fulguration

Endocavitary catheter ablation consists of delivering an impulse of 160 to 240 joules via a catheter used for electrophysiological investigation resulting in an electrical discharge which, in addition to its thermal effects may alter the arrhythmogenic substrate mechanically. This method was used in 2 patients with resistant and recurrent VT after myocardial infarction complicated by ventricular aneurysm. Two sessions of catheter ablation were necessary in both patients, but in the second one a single shock was successful in critically ill patients with VT. The first patient has been followed up for 20 months and the second for 13 months. Under prophylactic antiarrhythmic therapy, neither patient has had recurrence of the ventricular arrhythmias which had previously led to their hospitalisation. Catheter ablation is therefore presented as a technique which may be performed in the electro-physiological laboratory and repeated in cases of incomplete efficacy. This method may be used successfully in the treatment of chronic VT after myocardial infarction complicated by ventricular aneurysm.     

Mapping and ablation of polymorphic ventricular tachycardia after myocardial infarction

OBJECTIVES: The goal of this study was to describe the mapping and ablation of polymorphic ventricular tachycardia (VT) after myocardial infarction (MI). BACKGROUND: The initiating mechanisms of polymorphic VT after MI have not been reported. METHODS: Five patients (four males; age 61 +/- 7 years) with recurrent episodes of polymorphic VT after anterior MI (left ventricular ejection fraction 32 +/- 7%) despite revascularization and antiarrhythmic drugs were studied. All patients demonstrated frequent ventricular premature beats (PBs) initiating polymorphic VT. Pace mapping and activation mapping were used to identify the earliest site of PB activity. The presence of a Purkinje potential preceding PB defined its origin from the Purkinje network. Electroanatomic voltage mapping was performed to delineate the extent of MI. RESULTS: The PBs were observed in all cases to arise from the Purkinje arborization in the MI border zone. These PBs were right bundle-branch block in all five patients, with morphologic variations in the limb leads in four; one also had a left bundle-branch block morphology. The coupling interval of the PB to the preceding QRS complex demonstrated significant variations (320 to 600 ms). During PB, the Purkinje potential at the same site preceded the QRS complex by 20 to 160 ms and was associated with different morphologies. Repetitive Purkinje activity was documented during polymorphic VT. Splitting of Purkinje activity and Purkinje to muscle conduction block were also observed. Ablation at these sites eliminated all PBs. At 16 +/- 5 months follow-up using defibrillator memory interrogation, no patient has had recurrence of arrhythmia. CONCLUSIONS: The Purkinje arborization along the border-zone of scar has an important role in the mechanism of polymorphic VT in patients after MI. Ablation of the local Purkinje network allows suppression of polymorphic VT.     

Encircling endocardial ventriculotomy in the treatment of recurrent ventricular tachycardia after myocardial infarction

Thirty nine men and two women aged 26 to 76 years old (average 55 years) with ventricular tachycardia (VT) complicating chronic myocardial infarction were operated on between December 1971 and September 1980. Epicardial mapping was performed in sinus rhythm in 25 cases and in VT in 12 cases. The series was divided into two consecutive groups: --The first group comprised 14 patients operated on between December 1971 and November 1975 in which the operative mortality at the 30th day was 36%. There was one death due to recurrent VT in the early post-operative period; two deaths due to arrhythmia were observed between the 11th and 26th postoperative months. VT was successfully prevented in 6 cases with over 2 years' follow-up. --The second group comprised 27 patients operated after November 1975, in which encircling endocardial ventriculotomy (EEV) was the procedure used. The operative mortality fell to 18% with no relation to the arrhythmia. In the first 10 cases of this group, VT recurred in 2 patients in the early postoperative period. These two cases were controlled with antiarrhythmic therapy at doses that had been ineffective preoperatively. Four other recurrences of VT were observed at the 3rd, 34th, 45th, and 56th postoperative months. They were controlled by anti arrhythmic agents in 3 cases. The other patient died. VT was prevented for over 2 years in 7 patients and for over I year in 16 patients. These results suggest that EEV is more effective than the techniques used previously in resistant VT. Its side effects on myocardial contractility are discussed.     

Prediction of sudden death in patients discharged after acute myocardial infarction.

A follow-up was made of 475 patients discharged after an acute myocardial infarction. Sudden death, i.e. death within 2 hours after the onset of the final attack, was more common in patients below 60 years on admission than in the older age groups. Patients succumbing suddenly often had a history of an earlier myocardial infarction. They also had a higher incidence of inferior infarcts and more frequently showed ventricular tachycardia during the early hospital period than those dying more than 24 hours after the onset of the final episode. When comparisons were made with all patients dying after more than 2 hours' duration of the terminal attack no significant differences were noted for these or other parameters. Prediction of sudden death in immediate survivors of acute myocardial infarction thus seems elusive. Further studies of the relations between the incidence of ventricular ectopic activity during the early and late hospital phase of acute myocardial infarction and sudden death after discharge from hospital are implicated.     

Reduction in incidence of inducible ventricular tachycardia after myocardial infarction by treatment with streptokinase during infarct evolution

The aim of this study was to determine whether intravenous streptokinase administered with or without oral aspirin to patients with evolving myocardial infarction reduces the inducibility of ventricular tachycardia at electrophysiologic study and thus the risk of sudden death in infarct survivors. Of 159 patients randomized at Westmead Hospital to the multicenter Second International Study of Infarct Survival (ISIS-2) after streptokinase and aspirin in acute myocardial infarction, 87 underwent electrophysiologic testing 6 to 28 days after infarction to determine their risk of subsequent ventricular arrhythmias (streptokinase 20 patients; aspirin 25 patients; streptokinase and aspirin 21 patients; both placebos 21 patients). Patients who underwent electrophysiologic testing had similar clinical characteristics to those of patients who did not. The stimulation protocol comprised up to and including four extrastimuli applied to the right ventricular apex at twice diastolic threshold. An abnormal result was defined as ventricular tachycardia with a cycle length greater than or equal to 230 ms lasting greater than or equal to 10 s. Ventricular tachycardia was inducible at electrophysiologic study in 8 patients who received placebo streptokinase, but in no patient who received active streptokinase (8 of 46 versus 0 of 41; p = 0.005, Fischer's exact test). Ventricular tachycardia was inducible in 4 patients who received aspirin therapy and 4 who did not (4 of 41 versus 4 of 46; p = NS). During a mean follow-up period of 39 +/- 9 months, there were no spontaneous episodes of ventricular tachycardia, ventricular fibrillation or witnessed sudden death in the streptokinase-treated group compared with three such events in the placebo-treated group (p = 0.13). When compared with placebo therapy, intravenous streptokinase substantially reduced the incidence of inducible ventricular tachycardia in infarct survivors. No similar benefit was attributable to aspirin therapy.