Catheter Ablation of the Mitral Isthmus for Ventricular Tachycardia Associated With Inferior Infarction

705-2 Catheter Ablation of the Mitral Isthmus for Ventricular Tachycardia Associated with Inferior Infarction

Atrial flutter following ethanol infusion in the vein of Marshall

Ventricular tachycardia reentry circuits in chronic infarct scars can contain slow conduction zones, which are difficult to distinguish from bystander areas adjacent to the circuit during catheter mapping. This study developed criteria for identifying reentry circuit sites using computer simulations. These criteria then were tested during catheter mapping in humans to predict sites at which radiofrequency current application terminated ventricular tachycardia. In computer simulations, effects of single stimuli and stimulus trains at sites in and adjacent to reentry circuits were analyzed. Entrainment with concealed fusion, defined as ventricular tachycardia entrainment with no change in QRS morphology, could occur during stimulation in reentry circuit common pathways and adjacent bystander sites. Pacing at reentry circuit common pathway sites, the stimulus to QRS (S-QRS) interval equals the electrogram to QRS interval (EG-QRS) during tachycardia. The postpacing interval from the last stimulus to the following electrogram equals the tachycardia cycle length. Pacing at bystander sites the S-QRS exceeds the EG-QRS interval when the conduction time from the bystander site to the circuit is short but may be less than or equal to the EG-QRS interval when the conduction time to the circuit is long. The postpacing interval, however, always exceeds the tachycardia cycle length. When conduction in the circuit slows during pacing, the S-QRS and postpacing intervals increase and the slowest stimulus train most closely reflects conduction times during tachycardia. Endocardial catheter mapping and radiofrequency ablation were performed during 31 monomorphic ventricular tachycardias in 15 patients with drug refractory ventricular tachycardia late after myocardial infarction. During ventricular tachycardia, trains of electrical stimuli or scanning single stimuli were evaluated before application of radiofrequency current at the same site. Radiofrequency current terminated ventricular tachycardia at 24 of 241 sites (10%) in 12 of 15 patients (80%). Ventricular tachycardia termination occurred more frequently at sites with entrainment with concealed fusion (odds ratio, 3.4; 95% confidence interval [CI], 1.4 to 8.3), a postpacing interval approximating the ventricular tachycardia cycle length (odds ratio, 4.6; 95% CI, 1.6 to 12.9) and an S-QRS interval during entrainment of more than 60 milliseconds and less than 70% of the ventricular tachycardia cycle length (odds ratio, 4.9; 95% CI, 1.4 to 17.1). Ventricular tachycardia termination was also predicted by the presence of isolated diastolic potentials or continuous electrical activity (odds ratio, 5.2; 95% CI, 1.8 to 15.5), but these electrograms were infrequent (8% of all sites). Combinations of entrainment with concealed fusion, postpacing interval, S-QRS intervals, and isolated diastolic potentials or continuous electrical activity predicted a more than 35% incidence of ventricular tachycardia termination during radiofrequency current application versus a 4% incidence when none suggested that the site was in the reentry circuit. Analysis of the postpacing interval and S-QRS interval suggested that 25% of the sites with entrainment with concealed fusion were in bystander areas not within the reentry circuit. At restudy 5 to 7 days later, 6 patients had no monomorphic ventricular tachycardia inducible, and inducible ventricular tachycardias were modified in 4 patients. None of these 10 patients have suffered arrhythmia recurrences during a follow-up of 316 +/- 199 days, although 4 continue to receive previously ineffective medications. Regions giving rise to reentry after myocardial infarction are complex and can include bystander areas, slow conduction zones, and isthmuses for impulse propagation at which radiofrequency current lesions can interrupt reentry.

Verapamil-sensitive left ventricular tachycardia (VT) with a right bundle branch block (RBBB) configuration and left-axis deviation has been demonstrated to arise from the left posterior fascicle, and can be cured by catheter ablation guided by Purkinje potentials. Verapamil-sensitive VT with an RBBB configuration and right-axis deviation is rare, and may originate in the left anterior fascicle. Six patients (five men and one woman, mean age 54+/-15 years) with a history of sustained VT with an RBBB configuration and right-axis deviation underwent electrophysiologic study and radiofrequency (RF) ablation. VT was slowed and terminated by intravenous administration of verapamil in all six patients. Left ventricular endocardial mapping during VT identified the earliest ventricular activation in the anterolateral wall of the left ventricle in all patients. RF current delivered to this site suppressed the VT in three patients (ablation at the VT exit). The fused Purkinje potential was recorded at that site, and preceded the QRS complex by 35, 30, and 20 msec, with pace mapping showing an optimal match between the paced rhythm and the clinical VT. In the remaining three patients, RF catheter ablation at the site of the earliest ventricular activation was unsuccessful. In these three patients, Purkinje potential was recorded in the diastolic phase during VT at the mid-anterior left ventricular septum. The Purkinje potential preceded the QRS during VT by 66, 56, and 63 msec, and catheter ablation at these sites was successful (ablation at the zone of slow conduction). During 19 to 46 months of follow-up (mean 32+/-9 months), one patient in the group of ablation at the VT exit had sustained VT with a left bundle branch block configuration and an inferior axis, and one patient in the group of ablation at the zone of slow conduction experienced typical idiopathic VT with an RBBB configuration and left-axis deviation. Verapamil-sensitive VT with an RBBB configuration and right-axis deviation originates close to the anterior fascicle. RF catheter ablation can be performed successfully from the VT exit site or the zone of slow conduction where the Purkinje potential was recorded in the diastolic phase.

Impact of mitral isthmus anatomy on the likelihood of achieving linear block in patients undergoing catheter ablation of persistent atrial fibrillation

Although direct ventricular tachycardia (VT) surgery has been shown to be effective for treatment of inferior myocardial infarction (MI), the differences in the arrhythmia substrates compared to anterior MI have not been systematically delineated. We sought to compare operative procedures and VT substrates between anterior and inferior MI locations. Computerized mapping was performed in 30 patients with a 128-electrode system using epicardial sock and transatrial left ventricular endocardial balloon arrays, followed by combined endocardial resection and cryoablation. At surgery, there were 51 and 34 different VTs in 18 patients with anterior MI and 12 patients with inferior MI, respectively. The proportion of aneurysms was lower in inferior MI (25% vs 78%, P = 0.008). Total activation times accounted for 65% +/- 23% and 50% +/- 22% of the VT cycle length in anterior and inferior infarcts, respectively (P = 0.005). Complete superficial reentry was identified in 12 VTs related to anterior infarcts and in only two VTs associated with inferior infarction (P = 0.038). Involvement of papillary muscles occurred in two patients with inferior MI. Patients with inferior infarcts received more cryolesions and required epicardial cryolesions or mitral valve replacement more frequently, and their operative mortality was greater (2/12 vs 0/18). Noninducibility rate (89.3%) and 2-year survival (76% +/- 8%) did not differ according to infarct location. VT associated with inferior MI can be ablated successfully; however, the substrate is more complex, with frequent participation of intramural layers rendering the ablative procedure more difficult.

The Wolff-Parkinson-White (WPW) syndrome was initially described in 1930 as a clinical syndrome of paroxysmal tachycardias in healthy young people that demonstrated “bundle-branch block and short P-R interval”. These tachycardias were eventually determined to be macro-reentrant arrhythmias utilizing accessory pathways. Surgical approaches for transecting these accessory pathways were being developed as early as the 1960s. Since 1984, catheter ablation has developed into a safe and highly effective therapy option, and the treatment of choice for WPW syndrome today. We present a unique case of a patient with previous surgically treated WPW syndrome that serves as a reminder of treatments past and caution for current therapies. A 54-year-old man with a remote history of WPW syndrome, treated in 1989 with surgical cryoablation of a left ventricular free wall accessory pathway, now presented with an hour of sustained palpitations after a triathlon practice session. He was found to have ventricular tachycardia at a rate of 180 bpm on EKG requiring external cardioversion. The troponin I level peaked at 2.59 ng/mL. Left heart catheterization revealed a peculiar truncated 100% occlusion of the proximal circumflex artery with extensive bridging collaterals to the mid circumflex artery, and also confirmed an infero-basal aneurysm. The cause of the ventricular tachycardia (VT) was deemed non-ischemic and he was referred for electrophysiology study. 3D electroanatomic mapping of the left ventricular (LV) endocardial surface was performed, revealing a discrete posterior wall scar. Reentrant VT was repeatedly induced utilizing a zone of slow conduction along the border zone of the scar. Radiofrequency ablation of Purkinje potentials on the LV septum, running alongside the scar border zone, eliminated the VT. The entire endocardial surface of the postero-basal scar was electrically silenced to prevent further VT events. Typically, during the surgical approach of WPW, a wide endocardial (rarely an epicardial) incision was made along the atrial surface of the mitral valve annulus, dissecting deeply and caudally until ventricular myocardium was exposed. Despite the close proximity of the circumflex artery to the epicardial incision line during these surgeries, there are only rare reports of coronary artery complications, generally considered to be either catheter-induced dissections or embolic events. The development of a network of extensive bridging collaterals in our patient supports progressive stenosis of the left circumflex artery from cryoablation thermic injury, leading to scar formation and VT years later. In conclusion, this case reminds us that current ablative therapies are still relatively new, and long-term follow-ups for delayed complications remain a necessity. J Med Cases. 2016;7(6):216-219 doi: http://dx.doi.org/10.14740/jmc2488w

Identification and catheter ablation of a zone of slow conduction in the reentrant circuit of ventricular tachycardia in humans

The relation of global and regional right and left ventricular function during the acute phase after a first myocardial infarction was assessed by first pass radionuclide angiography in 20 patients (10 after anterior and 10 after inferior myocardial infarction). The right ventricular ejection fraction did not differ significantly between the groups, but left ventricular ejection fraction was significantly depressed after anterior myocardial infarction. There was evidence of right ventricular dilatation and impaired transit in the group with inferior infarction. Five patients with anterior infarction and six with inferior infarction had abnormal right ventricular ejection fractions. Right ventricular wall motion abnormalities affected the septal wall in the group with anterior infarction and the free wall in the group with inferior infarction. The relation between right and left ventricular ejection fractions was markedly different in the two groups. In the group with anterior infarction there was a significant linear relation between right and left ventricular ejection fraction, whereas in the group with inferior infarction there was not. Thus right ventricular dysfunction commonly occurs after both anterior and inferior myocardial infarction. Right and left ventricular impairment are related after anterior myocardial infarction, but are independent after inferior myocardial infarction. Finally, the different effects of anterior and inferior myocardial infarction on right ventricular function may be explained by differences in septal and free wall involvement.

Results of signal-averaged electrocardiography and electrophysiologic study in patients with nonsustained ventricular tachycardia after healing of acute myocardial infarction

Demonstration of diastolic and presystolic purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia

Clinical Case: A 53-year-old male patient was referred to our center for the management of severe electrical storm (ES). The patient experienced 76 appropriate shocks within 30 minutes delivered from his implantable cardioverter-defibrillator as a result of recurrent ventricular tachycardia (VT) occurring just after retiring to his hotel room at the end of an uneventful business meeting. The implantable cardioverter-defibrillator was implanted 16 years ago when the patient presented with syncope and had inducible VT at an electrophysiological study. Coronary artery disease was ruled out at that time with coronary angiography. However, the systolic function of the left ventricle was moderately impaired, with an ejection fraction of 38% measured by echocardiography, which also revealed regional wall motion abnormalities. This nonischemic cardiomyopathy was attributed to remote myocarditis. When presenting with ES, the patient was admitted at first to the intensive care unit of the local university hospital. A 12-lead ECG showed monomorphic VT of 188 bpm (Figure 1A). Ventricular tachyarrhythmia was stabilized acutely by sequential drug application of β-blockers, amiodarone, and lidocaine as well as sedation followed by endotracheal intubation under general anesthesia. After the initial cooling-down phase, the patient was transferred to our center for further management. To prevent more episodes of ES and to avoid long-term use of amiodarone with the risk of potentially severe adverse effects, catheter ablation was performed. Figure 1. A , Twelve-lead ECG showing a monomorphic ventricular tachycardia (VT) with inferior axis, Q wave present in lead I and absent in lead aVF, right bundle-branch block pattern with positive QRS complex in V1 through V3 and negative in V4 through V6, and with a pseudo δ-wave and late intrinsicoid deflection, suggesting a left lateral midventricular epicardial origin. B , Stepwise management of electrical storm. Application of different steps should be individualized for …

Mechanism of higher incidence of ischemic mitral regurgitation in patients with inferior myocardial infarction: Quantitative analysis of left ventricular and mitral valve geometry in 103 patients with prior myocardial infarction

A REMINDER OF TREATMENTS PAST

Reentrant ventricular tachycardia is dependent on an area of myofibers, embedded in scar tissue, which exhibit slow conduction. Late potentials recorded by signal-averaged electrocardiography appear to correspond to these zones of slow conduction and frequently are present in patients with VT. We hypothesized that elimination of inducible VT by catheter-mediated ablation of critical areas of slow conduction would alter late potentials. Four patients underwent catheter ablation in which radiofrequency current was delivered to zones of slow conduction exhibiting isolated mid-diastolic potentials that could not be dissociated from the tachycardia. The four patients had developed VT (cycle length 382 +/- 50 msec; mean +/- SEM) 13-180 months after inferior myocardial infarction. Late potentials were present in each patient before catheter ablation was attempted. Although VT was not inducible in any patient immediately after ablation, late potentials were still present in all four patients and there was no significant difference in the QRS duration (136.5 +/- 4.0 msec postablation; 135.7 +/- 4.5 msec preablation), root mean square voltage in the terminal 40 msec of the QRS (10.0 +/- 1.0 microV postablation; 5.9 +/- 0.4 microV preablation), or in the duration of the low amplitude signal (69.2 +/- 2.0 msec postablation; 62.7 +/- 3.4 msec preablation). At follow-up electrophysiology study performed 14 +/- 7 days after ablation, one of the four patients had inducible VT. In conclusion, late potentials persist even after successful radiofrequency catheter ablation and do not appear to be useful for predicting results of follow-up electrophysiology study.