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.     

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.     

Correlation of exit sites of inducible ventricular tachycardia post-ST elevation myocardial infarction on electrophysiology study,with region of infarct

Background

Ventricular arrhythmia (VA) is the most common cause of sudden cardiac death post-ST elevation myocardial infarction (STEMI). Ventricular tachycardia (VT) may be inducible in electrophysiology studies (EPS) early (<40 days) post-STEMI. Whether it originates from the infarct site remains unknown. We examined the correlation between inducible VT and infarct location post-STEMI.

Aims

To investigate the correlation between inducible VT and infarct location post-STEMI.

Methods

We retrospectively analysed 46 patients from 2005 to 2017 with STEMI who underwent early programmed ventricular stimulation through EPS (>48 h post-STEMI and <40 days from admission). Gated heart pool scans were used to visualise infarct scar regions, and VT exit sites were derived from induction 12-lead electrocardiography. Patients were followed up for primary outcomes of recurrent VA and all-cause mortality.

Results

Forty-six patients were included for analysis, with 50 uniquely induced VT exit sites. Mean left ventricular ejection fraction was 30 ± 8.7% and 22% had impaired right ventricular ejection fraction. Mean time from presentation to EPS was 16 ± 31.3 days. Of the induced VT, 44 (88%) were from within scar and scar-border regions, whereas 6 (12%) of the induced VT were found to be remote to imaging-derived scar. Over a median follow-up period of 75 months, 6 (13%) patients died, and 7 (15%) patients had recurrent VA. No deaths occurred in patients with remote VT.

Conclusion

The majority of early inducible post-infarct VT arises from acute myocardial scar; however, a small portion arises from sites remote from scars with a possible focal aetiology.     

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。     

Heparin and infarct coronary artery patency after streptokinase in acute myocardial infarction

Anticoagulant therapy is frequently used after thrombolytic agents in the treatment of acute myocardial infarction (AMI) although it is unclear that such therapy will prevent subsequent infarct vessel reocclusion. The role of duration of heparin therapy in maintaining infarct artery patency was studied retrospectively in 53 consecutive AMI patients who received streptokinase therapy and underwent coronary angiography acutely and at 14 +/- 1 days. Of the 39 patients with initial infarct vessel patency, patency at follow-up angiography was observed in 100% (22 of 22) of those who received greater than or equal to 4 days of intravenous heparin but in only 59% (10 of 17) of those patients who received less than 4 days of heparin (p less than 0.05). Of the 14 patients not initially recanalized after streptokinase, patent infarct-related arteries at follow-up angiography were found in 3 of 8 (38%) treated with greater than or equal to 4 days of heparin therapy but in none of the 6 patients treated for less than 4 days (difference not significant). No significant difference in hemorrhagic complications was noted between the short- and long-term heparin treatment groups. Thus, greater than or equal to 4 days of intravenous heparin therapy after successful streptokinase therapy in AMI is more effective in maintaining short-term infarct vessel patency than a shorter duration of therapy and it may maintain the short-term patency of the infarct vessel in those patients who later spontaneously recanalize.     

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.     

Histopathologic correlates of inducible ventricular tachycardia in two experimental canine models of myocardial infarction

Ventricular tachyarrhythmias are the leading cause of sudden cardiac death. Determination of the substrates conducive to the initiation of ventricular tachyarrhythmias remains an important clinical goal. The purpose of this study was to correlate electrophysiologic and histopathologic parameters conducive to the initiation of sustained ventricular tachycardia using programmed electrical stimulation in two canine models of myocardial infarction. Histopathologic correlates included: infarct pattern (heterogeneous vs. homogeneous morphology), distribution (viable epicardial or endocardial rim), and size. Twenty-one adult dogs were randomly divided into two groups: (1) 12 dogs underwent two-stage, 2-hour occlusion of the proximal left anterior descending coronary artery (LAD); and (2) nine animals had permanent, complete occlusion of the LAD with latex embolization. Using programmed ventricular pacing with two premature ventricular extrastimuli, initiation of ventricular tachycardia was attempted at both 1 and 2 weeks after infarction with the chest closed and opened each time. Electrophysiologic evaluation of the infarct type correlated significantly with the histologic morphology of the infarction (p less than 0.001), the presence of a viable epicardial rim was an extremely important discriminating variable for ability to induce sustained ventricular tachycardia (p = 0.04). The presence of an endocardial rim was not significant (p = 1.0). Infarct size alone was only marginally related to ventricular tachycardia inducibility (p = 0.08). Non-uniform infarcts were more conducive to the initiation of sustained ventricular tachycardia than homogeneous infarcts (p = 0.025). The presence of a large, non-uniform infarct was the best overall discrimination variable for inducibility (p = 0.0002). Thus, in these experimental models, specific infarct morphologies correlate significantly with susceptibility to inducible sustained ventricular tachyarrhythmias.     

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.     

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.     

Quantitative analysis of myocardial infarct structure in patients with ventricular tachycardia

To study whether myocardial infarction differs in patients with and without ventricular tachycardia, the hearts of 22 deceased patients with ventricular tachycardia and 21 deceased control patients were analyzed quantitatively. The hearts from the ventricular tachycardia group were heavier and more dilated than those from the control group. Histologic analysis of a representative cross section from each heart showed that the ventricular tachycardia group had larger, more solid infarcts than did the control group. The ventricular tachycardia group also had a greater area of spared subendocardium, more hydropic change of the spared subendocardium, and more "ribbon type" spared subendocardium, which was defined as spared subendocardium of uniform contour 1 mm thick or less. The ventricular tachycardia group was divided into a subacute subgroup (n = 14, dying less than or equal to 10 weeks after infarction) and a chronic subgroup (n = 8, dying greater than 10 weeks after infarction). The infarcts of the subacute ventricular tachycardia group were more solid and had a greater amount of ribbon type spared subendocardium than those of the chronic ventricular tachycardia group. This information can serve as a baseline for the evaluation of animal preparations of tachycardia and, when combined with knowledge of the location of the arrhythmogenic region furnished by intraoperative mapping, should lead to better understanding of the anatomic substrate for ventricular tachycardia.     

Radiofrequency ablation of haemodynamically unstable ventricular tachycardia after myocardial infarction

OBJECTIVE—To determine whether radiofrequency (RF) ablation might have a role in haemodynamically unstable ventricular tachycardia.
METHODS—10 patients with a history of ventricular tachycardia producing haemodynamic collapse in whom drug treatment had failed and device therapy was rejected underwent RF ablation of ventricular tachycardia in sinus rhythm. The arrhythmogenic zone was defined on the basis of abnormal systolic movement, the presence of fragmentation (low amplitude, prolonged multiphasic electrograms), and pace mapping. RF lesions were delivered in power mode in linear fashion within the defined arrhythmogenic zone.
RESULTS—Success (no ventricular tachycardia inducible postablation or at retest) was achieved in six patients, possible success (a different ventricular tachycardia inducible at more aggressive stimulation) in three. In one patient, the procedure was abandoned because of poor catheter stability. There were no clinical events during a mean (SD) follow up period of 23 (10) months in any of the nine patients defined as definite or possible successes.
CONCLUSIONS—RF ablation for addressing haemodynamically unstable ventricular tachycardia opens the door for the wider use of catheter ablation for treating this arrhythmia.


Keywords: tachycardia; catheter ablation; sudden death     

Effects of procainamide and lidocaine on electrically inducible ventricular tachycardia studied with programmed ventricular stimulation in post myocardial infarction

The effects of procainamide and lidocaine, representative of class IA and IB antiarrhythmic agents, on electrically inducible ventricular tachycardia (VT) were studied using programmed ventricular stimulation in 47 post myocardial infarction patients at an average of 1.5 months after the onset. The mean doses of administered procainamide and lidocaine were 1050 mg and 161 mg, and their mean plasma concentrations were 7.5 micrograms/ml and 3.1 micrograms/ml respectively. The induction of sustained VT was suppressed in 15 of 29 patients (52%) by procainamide, but in none by lidocaine. The induction of nonsustained VT was suppressed in 6 of 18 patients (33%) by procainamide, and in 1 of 8 patients (13%) by lidocaine. The efficacy rate of procainamide was significantly higher than that of lidocaine in suppression of VT induction (21/47 vs 1/14 p less than 0.01). Procainamide significantly prolonged the effective refractory period of the right ventricle as well as the HV and QRS interval, however lidocaine did not affect them significantly. On the other hand, the worsening effect which changed nonsustained VT inducible in the baseline into sustained VT inducible post drug administration was demonstrated in 8 of 18 procainamide cases (44%), and in 3 of 8 lidocaine cases (38%). Between the procainamide effective and ineffective or worsening patients, there were no differences found in the electrophysiologic variables either in the baseline or post procainamide administration. We concluded that procainamide was more effective than lidocaine for the prevention of potential life-threatening VT induction in post myocardial infarction patients, although its efficacy was considerably limited, and to confirm the effectiveness and exclude the worsening effects of the class IA and IB antiarrhythmic agents, drug testing using programmed ventricular stimulation appeared to be valuable.     

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.