Postinfarction Ventricular Tachycardia Research Articles

Trans-septal catheterization for radiofrequency catheter ablation of cardiac arrhythmias. Results and safety of a simplified method.

This study reports on the results and safety of a simplified method of trans-septal catheterization for radiofrequency catheter ablation of cardiac arrhythmias. Over 5 years, 411 patients underwent trans-septal catheterization for radiofrequency catheter ablation: 388 patients had a left-sided accessory pathway, 19 a left-sided focal atrial tachycardia, two atrial fibrillation and two post-infarction ventricular tachycardia. All but one patient with ventricular tachycardia underwent elective trans-septal catheterization. In the absence of a patent foramen ovale, puncture of the atrial septum was performed by using an 8F Mullins sheath and a Brockenbrough needle, according to the simplified method described in this paper. Trans-septal catheterization was accomplished in 383/388 patients (98.7%); in 41 patients a second trans-septal catheterization and radiofrequency catheter ablation was performed for initial failure or recurrence. Radiofrequency catheter ablation was successful in 96% of accessory pathway patients, 90% of atrial tachycardia patients, in both patients with atrial fibrillation and in both patients with ventricular tachycardia. No complication related to trans-septal catheterization was observed. In experienced hands and according to the method described in this paper, the elective use of transseptal catheterization for radiofrequency catheter ablation in a large cohort of patients with cardiac arrhythmias is feasible, safe and allows successful ablation in the vast majority of the patients.

Time to termination of post-infarct ventricular tachycardia by radiofrequency catheter ablation suggests superficial endocardial reentry

Time to termination of post-infarct ventricular tachycardia by radiofrequency catheter ablation suggests superficial endocardial reentry

Time to Termination of Post-infarct Ventricular Tachycardia by Radiofrequency Catheter Ablation Suggests Superficial Endocardial Reentry

Time to Termination of Post-infarct Ventricular Tachycardia by Radiofrequency Catheter Ablation Suggests Superficial Endocardial Reentry

Radiofrequency catheter ablation of postinfarction ventricular tachycardia: long-term success and the significance of inducible nonclinical arrhythmias.

Radiofrequency (RF) catheter ablation is effective therapy for monomorphic ventricular tachycardia (VT) in patients without structural heart disease. In patients with postinfarction VT; however, this procedure has been used predominantly as adjunctive therapy, targeting only the patient's clinically documented arrhythmia. By targeting all inducible, sustained VT morphologies, we sought to determine the utility of RF catheter ablation as a primary cure in patients who present with hemodynamically tolerated VT. RF ablation was attempted in 35 patients with a previous myocardial infarction and recurrent, hemodynamically tolerated VT. A mean of 3.9+/-2.7 VTs were induced per patient (range, 1 to 10). The clinically documented arrhythmia was successfully ablated in 30 of 35 patients (86%), and on follow-up electrophysiological testing, 11 patients had no inducible VT and were discharged without other therapy. Nineteen patients had inducible "nonclinical" arrhythmias on follow-up testing, and the majority underwent cardiac defibrillator implantation. Freedom from recurrent arrhythmias, including sudden death, was 91% in patients without inducible VT and 53% in patients with persistently inducible "nonclinical" arrhythmias (P<.05; mean follow-up, 17+/-12 and 12+/-11 months, respectively). In patients with well-tolerated VT, RF catheter ablation may be useful as a primary cure if no other ventricular arrhythmias are inducible on follow-up testing. Ablation of all hemodynamically tolerated arrhythmias should be attempted in patients with multiple inducible VT morphologies because of the high rate of recurrence of unablated VTs in these patients.

Effect of recording site on postpacing interval measurement during catheter mapping and entrainment of postinfarction ventricular tachycardia.

During entrainment of reentrant ventricular tachycardia (VT), the difference between the postpacing interval (PPI) and the VT cycle length (VTCL) measured at the pacing site is an indication of the conduction time from the pacing site to the reentry circuit. The difference is usually < or = 30 msec at successful ablation sites. However, electrical noise during pacing sometimes obscures the electrograms recorded directly from the pacing site. The objective of this study is to determine if the PPI-VTCL difference measured at the mapping catheter electrodes proximal to the stimulating electrode accurately predicts the PPI-VTCL difference at the stimulating electrode. Endocardial catheter mapping was performed in 26 patients with infarct-related VT. At 191 sites during 56 VTs, unipolar pacing from the distal electrode entrained VT and electrograms recorded from the mapping catheter were discernable following pacing in both the bipolar recordings from the distal electrode pair (BI 1-2) and the electrode pair 6 mm proximal to the distal electrode (BI 3-4). The PPI-VTCL difference at BI 1-2 correlated well with that measured at BI 3-4 (r = 0.88, P = 0.001). A PPI-VTCL difference at BI 3-4 < or = 30 msec predicted a PPI-VTCL difference at BI 1-2 < or = 30 msec with a sensitivity of 95%, specificity of 87 %, and predictive accuracy of 91%. Measurement of the PPI from electrodes proximal to the stimulating electrode is a reasonable alternative when the PPI cannot be assessed from the pacing electrode.

Laser photoablation of experimental post-infarction ventricular tachycardia guided by three dimensional activation mapping.

The purpose of this study was to evaluate the efficacy of epicardially delivered laser energy to ablate induced ventricular tachycardia in a post-infarction canine model. In 13 canines, the left anterior wall myocardial infarction was created. Five days later, 240 plunged electrodes were inserted into the heart. Three-dimensional ventricular activation sequences were analyzed on line by a computerized mapping system. Sixteen sustained monomorphic ventricular tachycardias were reproducibly induced in 10 canines. Epicardially contacted Nd:YAG laser irradiated the areas of the final pathway in macro-reentrant activation and the impulse origin in focal excitation. Linear photocoagulation lesions (11-16 x 50-72 mm) were created. Seven macro-reentrant circuits and six of nine focal origins were eliminated (success rate 81%). Pathology showed that laser photocoagulation involved all surviving subepicardial and intramural fibers. Epicardially delivered laser energy in conjunction with electrical activation mapping has a high probability of ablating post-infarction ventricular tachycardia.

Continuation of antiarrhythmic drugs, or arrhythmia surgery after multiple drug failures: A randomized trial in the treatment of postinfarction ventricular tachycardia

In patients with postinfarction sustained ventricular tachycardia showing one or more antiarrhythmic drug failures, the question is how long to proceed with new drug trials before deciding to perform map-guided arrhythmia surgery. Although the techniques of this surgery developed rapidly in the early 1980s, this therapy may be offset by damage to residual left ventricular function. However, surgery has been shown to be very effective in selected groups of patients. A randomized study was carried out in patients with postinfarction ventricular tachycardia and eligible for arrhythmia surgery based on residual left ventricular function. Therapy failure was defined by the occurrence of the following events: spontaneous recurrence of ventricular tachycardia or ventricular fibrillation, sudden cardiac death, inducibility of sustained ventricular tachycardia or ventricular fibrillation with programmed stimulation of the heart, symptomatic non-sustained ventricular tachycardia requiring therapy or side-effects of antiarrhythmic drugs requiring withdrawal. In the drug limb, failure of the first antiarrhythmic drug was accepted but failure of a second and different drug was regarded as true therapy failure. After randomization, antiarrhythmic drug therapy was administered in 33 patients, and 30 patients underwent surgery. Neither group differed in baseline characteristics, and the mean number of drug failures before randomization was 2.7. The Kaplan-Meier therapeutic failure of antiarrhythmic drugs was 39 +/- 11%, 42 +/- 11% and 51 +/- 18% at 0.5-, 1- and 4-year follow-up, respectively, whereas the therapeutic failure of cardiac surgery was 37 +/- 11%, 37 +/- 11% and 50 +/- 20% at 0.5, 1 and 4 years, respectively, showing no statistical difference. The 1- and 4-year Kaplan-Meier survival of the antiarrhythmic drug-treated group was 91 +/- 6% and 78 +/- 15%, respectively, and of the surgical group 92 +/- 6% and 59 +/- 20%, respectively, and did not differ between either group. However, the relative risk for total cardiac death was higher in the surgical limb than in the drug limb (relative risk 2.2, CI 0.68-7.48). This study demonstrated no difference between the therapeutic result of continuation of two different antiarrhythmic drugs and that of arrhythmia surgery. Despite the small number of patients studied, it is recommended that drug therapy should continue as long as this regimen is tolerated by the patient. When true drug refractoriness or side-effects of drugs arise, arrhythmia surgery offers a valuable alternative. However, when additional reasons for cardiac surgery exist, arrhythmia surgery should be undertaken earlier and may become the first choice of treatment of postinfarction ventricular tachycardia.

Relation of pace mapping QRS configuration and conduction delay to ventricular tachycardia reentry circuits in human infarct scars

Objectives. This study sought to determine the relation of the paced QRS configuration and conduction delay during pace mapping to reentry circuit sites in patients with ventricular tachycardia late after myocardial infarction.Background. The QRS configuration produced by ventricular pacing during sinus rhythm (pace mapping) can locate focal idiopathic ventricular tachycardias during catheter mapping, but postinfarction reentry circuits may be relatively large and contain regions of slow conduction. We hypothesized that for postinfarction ventricular tachycardia, 1) pacing during sinus rhythm at reentry circuit sites distant from the exit from the scar would produce a QRS configuration different from the tachycardia; and 2) a stimulus to QRS delay during pace mapping may be a useful guide to reentry circuit slow conduction zones.Methods. Catheter mapping and ablation were performed in 18 consecutive patients with ventricular tachycardia after myocardial infarction. At 85 endocardial sites in 13 patients, 12-lead electrocardiograms (ECGs) were recorded during pace mapping, and participation of each site in a reentry circuit was then evaluated by entrainment techniques during induced ventricular tachycardia or by application of radiofrequency current.Results. Pace maps resembled tachycardia at <30% of likely reentry circuit sites identified by entrainment criteria and at only 1 (9%) of 11 sites where radiofrequency current terminated tachycardia. Analysis of the stimulus to QRS interval during entrainment with concealed fusion showed that the conduction time from the pacing site to the exit from the scar was longer at sites where the pace map did not resemble tachycardia. Evidence of slow conduction during pace mapping, with a stimulus to QRS interval >40 ms was observed at ≥70% of reentry circuit sites.Conclusions. At many sites in postinfarction ventricular reentry circuits, the QRS configuration during pace mapping does not resemble the ventricular tachycardia QRS complex, consistent with relatively large reentry circuits or regions of functional conduction block during ventricular tachycardia. A stimulus to QRS delay during pace mapping is consistent with slow conduction and may aid in targeting endocardial sites for further evaluation during tachycardia.

Value of body surface mapping in localizing the site of origin of ventricular tachycardia in patients with previous myocardial infarction

Objectives. This study examined the performance of the 62-lead body surface electrocardiogram (ECG) in identifying the site of origin of ventricular tachycardia in patients with a previous myocardial infarction.Background. Because the accuracy of ECG localization of ventricular tachycardia using standard 12-lead recordings is restricted to the identification of rather large ventricular areas, application of multiple torso lead recordings may augment the resolving power of the surface ECG and result in more discrete localization of arrhythmogenic foci.Methods. Thirty-two patients were selected for electrophysiologically guided ablative therapy for drug-resistant postinfarction ventricular tachycardia. In these patients, QRS integral maps of distinct monomorphic ventricular tachycardia configurations were correlated with a previously generated infarct-specific reference data base of paced QRS integral maps. Each paced pattern in the data base corresponded with ectopic endocardial impulse formation at 1 of 18 or 22 discrete segments of the left ventricle with a previous anterior or inferior myocardial infarction, respectively. Electrocardiographic localization was compared with the results obtained during intraoperative or catheter endocardial activation sequence mapping.Results. Body surface mapping was performed during 101 distinct ventricular tachycardia configurations. Compared with the activation mapping data that were acquired in 64 of 101 ventricular tachycardias, body surface mapping identified the correct segment of origin in 40 (62%) of 64 tachycardias, a segment adjacent to the segment where the arrhythmia actually originated in 19 (30%) of 64 tachycardias and a segment disparate from the actual segment of origin in 5 (8%) of 64 tachycardias. With respect to infarct location, the segment of origin was correctly identified in 28 (60%) of 47 ventricular tachycardias in patients with anterior, 7 (70%) of 10 tachycardias ia patients with inferior and 5 (71%) of 7 tachycardias in patients with combined anterior and inferior myocardial infarction.Conclusions. This study shows that body surface mapping enables precise localization of the origin of postinfarction ventricular tachycardia in 62% and regional approximation in 30% of tachycardias. The multiple-lead ECG nay be used to guide and shorten catheter-based mapping procedures during ventricular tachycardia and to provide relevant information on the origin of tachycardias that cannot be mapped with conventional single-site mapping techniques because of unfavorable characteristics.

Influence of filtering techniques on the time-domain analysis, diagnosis, and clinical use of signal-averaged electrocardiogram.

In order to investigate the effect of different filtering techniques on the time-domain analysis of signal-averaged electrocardiogram (SAECG), recordings of 1,192 subjects were analyzed using Butterworth and Del Mar filters, both set at 40-250 Hz high and low pass frequencies. The recordings were taken from six clinically defined groups: (a) survivors of acute myocardial infarction (n = 553); (b) patients with sustained symptomatic postinfarction ventricular tachycardia (n = 89); (c) patients with hyperthropic cardiomyopathy (n = 219); (d) patients with dilated cardiomyopathy (n = 76); (e) direct relatives of patients with dilated cardiomyopathy (n = 170); and (f) normal healthy volunteers (n = 85). The study investigated differences between the SAECG results reported with both filters in three individual aspects: (1) numerical values of individual time-domain SAECG variables; (2) differences in SAECG findings of patients with postinfarction ventricular tachycardia and pair matched patients with uncomplicated follow-up after acute infarction; and (3) the power of SAECG findings to predict high risk of arrhythmic complication (sudden death and/or sustained ventricular tachycardia) among survivors of acute myocardial infarction. Compared with the Butterworth filter, the Del Mar filter led to a systematic difference of +8% in total QRS duration, was equally powerful in distinguishing between the pair matched patients with and without postinfarction ventricular tachycardia, and was statistically significantly more powerful in identifying those survivors of acute infarction who were at high risk of arrhythmic complications. The study concludes that the use of different filters may produce discordant results of SAECG analysis. Normal and abnormal values for various types of SAECG recording and analysis have to be established individually for different equipment and different software settings. These optimal cut-offs of SAECG variables should also take into account the clinical characteristics of patient groups.

Atlas of paced body surface QRS integral maps for localization of the site of origin of postinfarction ventricular tachycardia

Current mapping during radiofrequency (RF) catheter ablation of postinfarction ventricular tachycardia (VT) is based primarily on the use of single-site mapping techniques. Although such techniques are highly suitable for distinguishing the ultimate site where RF energy is delivered by enabling detailed localization of the exit site or critical component of the VT reentrant circuit, they are time-consuming and inefficient for initial rapid identification of the arrhythmogenic target area. This study features the design and preliminary clinical application of a new noninvasive method that is aimed at speeding up the initial phase of the VT mapping procedure. This method is based on the use of an atlas of 62-lead body surface QRS integral map patterns that was previously developed using left ventricular pace mapping in patients with remote anterior or inferior myocardial infarction. The atlas contains 18 and 22 different paced QRS integral map patterns obtained in patients with previous anterior or inferior myocardial infarction, respectively. Each specific QRS pattern in the atlas provides a unique infarct-specific spatial electrocardiographic representation of the onset of ectopic ventricular activation in a circumscribed endocardial segment of the left ventricle. Localization of the segment of VT origin is obtained by visually or mathematically comparing the QRS integral map recorded during VT with one of the two sets of paced QRS integral maps contained within the atlas with the purpose of selecting the best matching paced QRS integral map pattern. During RF catheter ablation of postinfarction VT, body surface QRS integral mapping offers an efficient clinical tool that can be used as a first-step localization procedure that may guide subsequent catheter pace mapping or activation mapping quickly to the arrhythmogenic target area.

Effect of ventriculotomy on postinfarction ventricular tachycardia in a canine model

The antiarrhythmic efficacy of ventriculotomy without further resection or ablation was evaluated in 15 dogs with reliably inducible ventricular tachycardia after experimental myocardial infarction. The dogs were placed on cardiopulmonary bypass and assigned to one of two treatment groups: (1) cardiopulmonary bypass only (control) — 5 dogs, (2) ventriculotomy through the infarct scar — 10 dogs. The effects on induction of ventricular tachycardia were evaluated 2 and 4 weeks postoperatively and infarct histology was examined at the termination of the experiment. All of the control dogs maintained inducible ventricular tachycardia postoperatively. In contrast, ventriculotomy abolished arrhythmia induction in 6 of 10 dogs ( p<0.05). Ventriculotomy resulted in destruction of the surviving subepicardial myocardium overlying the infarct, which is a feature of arrhythmogenic areas in this model of postinfarction ventricular tachycardia. In conclusion, inducibility of ventricular tachycardia in this canine model of myocardial infarction is unaffected by thoracotomy and cardiopulmonary bypass, and is therefore well suited to investigation of surgical antiarrhythmic interventions. Ventriculotomy results in subepicardial scarring and is significantly antiarrhythmic. This effect should be taken into account when evaluating any adjunctive procedure in this model.

Neodymium:YAG contact laser photocoagulation of the in vivo canine epicardium: dosimetry, effects of various lasing modes, and histology.

Neodymium:YAG laser photocoagulation (LPC) is an investigational technique for the treatment of drug-resistant postinfarction ventricular tachycardia that requires cardiopulmonary bypass and open heart surgery. The purpose of this experimental study was to evaluate the feasibility of contact epicardial LPC to reach subepicardial, deep myocardial, and subendocardial regions without ventriculotomy and to analyze the dose-response relationships of this new technology. In 24 open-chest, closed heart dogs, a total of 219 epicardial laser lesions were generated under sterile conditions. Laser source was a continuous wave 1064 nm Nd:YAG; the delivery system consisted of a 400 mu bare quartz fiber fed into an 8F electrode catheter in direct contact with the epicardial surface. Laser variables were power at 10-15-20 W; lasing time, 6-12-18-24 s; lasing mode, continuous and pulse-pause; fiber mode, optical fiber tip inside and extending out from the electrode catheter. Hearts were harvested at 1 week. Histologic measurements included lesion surface diameter, internal diameter, and depth. Significant linear correlation was found between the total delivered energy and all measured lesion parameters. Transmural lesions were found at energy levels of 270-480 J. Maximum depth measured up to 1.68 cm; at high energies, it was limited by myocardial thickness only. At constant energy levels, power and lasing time did not independently affect lesion dimensions; lasing mode and fiber mode had statistically significant but minor effects. Laser lesions were homogeneous and sharply demarcated without epicardial crater or endocardial thrombus formation. Endocardial surface cooling by circulating blood and the presence of epicardial vessels resulted in modifications in lesion morphology. In 29 out of 74 grossly transmural lesions, there was a 0.082 +/- 0.127 cm thin surviving subendocardium. Forty-five coagulation lesions were truly transmural with no surviving myocardial strands. In conclusion, contact epicardial LPC can result in deep, transmural myocardial coagulation lesions. Lesion dimensions can be adequately controlled by total delivered energy. Closed heart epicardial Nd:YAG laser photocoagulation could become a new, less invasive surgical technique for the treatment of drug-resistant ventricular tachycardia.

The management and outcome of late post-infarct ventricular tachycardia presenting to a district general hospital

A review was undertaken of late post-infarct ventricular tachycardia in a district hospital cardiac care unit in order to study the clinical course of a total population of such patients from initial presentation to ultimate outcome. Thirty-six patients with this diagnosis were identified over a 3 1 2 - yr period. Twelve were treated by empirically chosen antiarrhythmic drugs. Twenty-four were referred for electrophysiologically guided treatment, of whom 16 were treated by antiarrhythmic drugs, 3 by anti-ischaemic measures alone, and 5 by non-pharmacological antiarrhythmic treatments (antiarrhythmic surgery, percutaneous ablation, defibrillator implantation, cardiac transplantation). Of those treated empirically, 4 died in hospital of their arrhythmia, 1 died suddenly at home, and 2 suffered non-fatal arrhythmia recurrences during mean follow-up of 20 months. There were no arrhythmic deaths in those whose treatment was guided by serial electrophysiology studies, although 4 patients died of cardiac failure or reinfarction, and 3 were hospitalised with a recurrence of ventricular tachycardia during mean follow-up of 16 months. Age, concomitant medical problems and the apparent response to initial antiarrhythmic therapy were the main factors influencing management decisions. The apparent superiority of more intensive management strategies based on electrophysiology studies must be interpreted in the context of the selection processes applied to the total population initially presenting.

Differences between predictive characteristics of signal-averaged electrocardiographic variables for postinfarction sudden death and ventricular tachycardia

Several studies indicate that the electrophysiologic substrate for sustained ventricular tachycardia differs from that of ventricular fibrillation. This prospective study examined whether there were clinically relevant differences between the predictive values of the standard time-domain signal-averaged (SA) electrocardiographs (ECG) variables for ventricular tachycardia and sudden death after myocardial infarction. Predischarge SA electrocardiograms were recorded in 332 patients after infarction. During a follow-up period of ≥6 months, there were 12 sudden deaths (3.6%), 14 patients (4.2%) developed spontaneous sustained ventricular tachycardia and 20 patients (6%) died of circulatory failure. The sensitivity, specificity and positive predictive accuracy of the numerical values of the time-domain SA electrocardiographic variables for predicting sudden death and ventricular tachycardia were compared. The optimal criteria for predicting ventricular tachycardia required the positivity of ≥2 of the standard time-domain SA variables, whereas the optimal criteria for predicting sudden death required the positivity of all 3 variables. A high specificity was sustained over a wider range of sensitivity for sudden death than it was for ventricular tachycardia and the values of the variables which provided the same sensitivity for sudden death and ventricular tachycardia were different. For a sensitivity of 70%, the positive predictive accuracy was 31% for predicting sudden death and 13% for predicting ventricular tachycardia. The study concludes that differences in the predictive characteristics of variables for ventricular tachycardia and sudden death may be used to refine postinfarction risk stratification.

Functional role of the epicardium in postinfarction ventricular tachycardia. Observations derived from computerized epicardial activation mapping, entrainment, and epicardial laser photoablation.

Conventionally, monomorphic sustained ventricular tachycardia in patients with remote myocardial infarction is believed to originate from the subendocardium. In a previous study, we demonstrated that electrical activation patterns during ventricular tachycardia occasionally suggest a subepicardial rather than subendocardial reentry. This study prospectively evaluated the functional role of the epicardium in postinfarction ventricular tachycardia with complex intraoperative techniques including computerized electrical activation mapping, entrainment, observation of changes in activation pattern during successful epicardial laser photoblation, and histological study. Five of 10 consecutive patients undergoing intraoperative computerized activation mapping had 10 ventricular tachycardia morphologies displaying epicardial diastolic activation These 10 "epicardial" ventricular tachycardias revealed the following global activation patterns: monoregional spread (two), figure-eight activation (five), and circular macroreentry (three). Entrainment of ventricular tachycardia using epicardial stimulation was successfully performed from an area of slow diastolic conduction in four tachycardia morphologies. During entrainment, global activation remained undisturbed with recordings showing a long stimulus to QRS interval, unchanged QRS morphology, and pacing capture of all components of the reentry circuit. Neodymium:yttrium aluminum garnet laser photocoagulation was delivered during ventricular tachycardia to epicardial sites of presumed reentry. Epicardial photoablation terminated five of five figure-eight tachycardias, two of three circular macroreentry tachycardias but not the monoregional tachycardias. Electrophysiological recordings during epicardial laser photocoagulation demonstrated progressive prolongation of ventricular tachycardia cycle length and apparent interruption of the presumed reentrant circuit. Histological evaluation of the reentrant region (three patients) showed a rim of surviving myocardium under the epicardial surface. This study suggests that 1) chronic postinfarction ventricular tachycardia may result from subepicardial macroreentry, 2) slow conduction within the reentry circuit can be localized by computerized mapping and epicardial entrainment, and 3) ventricular tachycardia interruption by laser photocoagulation results from conduction delay and block within critical elements of the reentrant pathway. Viable subepicardial muscle fibers may constitute the underlying pathology.

Surgical Treatment of Postinfarct Ventricular Tachycardia—Seven Years of Experience

The results of surgery for postischemic drug-resistant ventricular arrhythmias (VA) are still controversial. The operative mortality in the literature ranges between 10% and 40% because of selection of patients. The authors reviewed their experience at Freeman Hospital where all patients with drug-refractory ventricular tachycardia (VT) or ventricular fibrillation (VF) underwent surgical treatment regardless of left ventricular function (LVF) and of time from infarction and operation. Between March, 1981, and March, 1988, 65 patients [53 men, 12 women aged thirteen to seventy-five years (mean fifty-four)] underwent surgery. All of them had a previous myocardial infarct (MI). Mean preoperative ejection fraction was 28% ± 11, and 32 % had single-vessel, 44 % double-vessel, and 24% triple-vessel disease. In 16 surgical treatment was undertaken on an emergency basis. All had intraoperative mapping based on activation sequence or, when this was not possible (noninducible VT/VF), on analysis of fragmented potentials. LV endocardial resection was performed in 64 patients. Heart transplant (HTx) was necessary in 1. Associated procedures were aneurysmectomy in 40 patients (62%), multiple cryoablation in 13 (20%), encircling ventriculotomy in 8 (12%), right ventricular endocardial resection in 1, coronary artery bypass grafting in 43 (66%), mitral valve replacement in 5 (8%), and closure of postinfarct ventricular septal defect (VSD) in 2. The operative mortality was 26% (17 patients}. The main cause of death was left ventricular failure, 13 (20%). The mortality was higher in patients with previous anterior MI 15/49 (31%) and in emergency operations 9/16 (56%). The follow-up ranged between four and forty months (mean twenty-two months) with 6 late deaths (2 arrhythmia related). In 11 patients (17%) postoperative arrhythmic episodes were observed, but only in 6 (5 drug controlled, 1 without therapy) was there recurrence of preoperative arrhythmia. Surgery for life-threatening VA allows good long-term results for relief of arrhythmias. Perioperative mortality is still high in unselected patients; it depends mainly on the preoperative LVF. HTx in cases with very depressed LVF is an option, but in the majority of patients in this group it was contraindicated.

Functional role of the epicardium in postinfarction ventricular tachycardia: Observations derived from global epicardial activation mapping, entrainment, and epicardial laser photoablation

Functional role of the epicardium in postinfarction ventricular tachycardia: Observations derived from global epicardial activation mapping, entrainment, and epicardial laser photoablation

Termination of ventricular tachycardia with epicardial laser photocoagulation: A clinical comparison with patients undergoing successful endocardial photocoagulation alone

Electrical activation-guided laser photocoagulation was used intraoperatively to terminate ventricular tachycardia in patients with ischemic heart disease. During ventricular tachycardia, laser irradiation was delivered to mapped sites with local diastolic activation. In 30 long-term survivors, 85 ventricular tachycardia configurations were terminated by ablation; 72 (84.7%) were terminated by endocardial photocoagulation. Thirteen (15.3%) required epicardial photocoagulation; however, these 13 ventricular tachycardias occurred in 10 (33%) of the 30 patients. An aneurysm was present in 70% of patients with successful endocardial photocoagulation, but in only 10% of patients requiring epicardial photocoagulation for at least one ventricular tachycardia configuration; 90% of all patients requiring epicardial laser photocoagulation had no aneurysm and had either a right or a left circumflex coronary artery-related infarction.In this group, epicardial activation data were similar to those described for ventricular tachycardia with an “endocardial” origin and included 1) delayed potentials during sinus rhythm, 2) presystolic or pandiastolic activation sequences during ventricular tachycardia, and 3) regions of block near the presumed region of reentry during ventricular tachycardia. This study suggests that the critical anatomic substrates supporting reentry in postinfarction ventricular tachycardia may occur at intramural or epicardial sites, particularly in patients with right or circumflex coronary artery-related infarction and no aneurysm.

Left ventricular segmental wall motion score as a criterion for selecting patients for direct surgery in the treatment of postinfarction ventricular tachycardia.

No indisputable criteria for selecting candidates for direct surgery in postinfarction ventricular tachycardia are yet available. We prospectively tested the result of surgery in patients showing normokinesia or slight hypokinesia in at least 3 of 9 segments of the left ventricle as determined on two oblique projections of the left ventricular angiogram. Sixty consecutive patients with recurrent symptomatic ventricular tachycardia were stratified on the basis of this criterion; 50 candidates were thus eligible for surgery. Direct surgery (endocardial resection and/or cryoablation) was performed in 23 patients (after a mean of 4.1 antiarrhythmic drug trials), while 27 patients were maintained on drug treatment (at discharge, a mean of 3.7 drug trials). Surgery was map-guided in 19 patients and non-map-guided in four emergency cases. No patients died in the immediate postoperative phase, but two (9%) died during follow-up. The actuarial survival at 12 months was 93%; the surgery-alone cure rate for ventricular tachycardia was 78%. Of the 27 non-operated surgical candidates, two died during in-hospital drug testing and five after discharge (total 26%). Actuarial survival at 12 months was 78% and did not differ significantly from that of the operated patients. After discharge, 80% of the non-operated surgical candidates still using the drug at discharge remained free of recurrence. In the 10 drug-treated non-surgical candidates (at discharge, a mean of 3.8 drug trials), survival and the number of arrhythmia-free patients were markedly lower than in surgical candidates. This study shows that the segmental wall motion score is of great clinical value and can be applied for stratification of patients with ventricular tachycardia after myocardial infarction for either surgery or medical therapy.