Impact of Changing Activation Sequence on Bipolar Electrogram Amplitude for Voltage Mapping of Left Ventricular Infarcts Causing Ventricular Tachycardia

Introduction: Wavefront direction is a determinant of bipolar electrogram amplitude that could influence identification of low amplitude regions indicating infarction or scar. Methods: To assess the importance of activation sequence on electrogram amplitude 11 patients with prior infarction and ventricular tachycardia were studied. At 819 left ventricular sites bipolar electrograms were recorded during atrial pacing and ventricular pacing, followed by unipolar pacing with a stimulus of 10 mA at 2 ms. Sites with a pacing threshold > 10 mA were designated electrically unexcitable scar. Results: Areas of low voltage (≤1.5 mV) were present in all patients. Atrial paced and ventricular paced electrogram amplitudes were strongly correlated (r = 0.77; P 50% change in electrogram amplitude at 28% of sites and a > 100% change at 10% of sites, but only 8% of sites had an electrogram amplitude classified as abnormal (≦1.5 mV) with one activation sequence and normal (> 1.5 mV) with the other activation sequence. Electrically unexcitable scar (6% of sites) was associated with lower electrogram amplitude but could not be reliably identified based on electrogram amplitude alone for either activation sequence. Conclusion: Voltage maps created with bipolar recordings using these methods should be relatively robust depictions of abnormal ventricular regions despite variable catheter orientation and activation sequences that might be produced by different rhythm

2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias: Executive summary

Ventricular arrhythmias are an important cause of morbidity and mortality and come in a variety of forms, from single premature ventricular complexes to sustained ventricular tachycardia and fibrillation. Rapid developments have taken place over the past decade in our understanding of these arrhythmias and in our ability to diagnose and treat them. The field of catheter ablation has progressed with the development of new methods and tools, and with the publication of large clinical trials. Therefore, global cardiac electrophysiology professional societies undertook to outline recommendations and best practices for these procedures in a document that will update and replace the 2009 EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias. An expert writing group, after reviewing and discussing the literature, including a systematic review and meta-analysis published in conjunction with this document, and drawing on their own experience, drafted and voted on recommendations and summarized current knowledge and practice in the field. Each recommendation is presented in knowledge byte format and is accompanied by supportive text and references. Further sections provide a practical synopsis of the various techniques and of the specific ventricular arrhythmia sites and substrates encountered in the electrophysiology lab. The purpose of this document is to help electrophysiologists around the world to appropriately select patients for catheter ablation, to perform procedures in a safe and efficacious manner, and to provide follow-up and adjunctive care in order to obtain the best possible outcomes for patients with ventricular arrhythmias

Predictors of implantation failure in left bundle branch area pacing using a lumenless lead in patients with bradycardia

Abstract Background Left bundle branch area pacing (LBBAP) is a novel conduction system pacing technique. In this multicenter study, we aimed to evaluate the procedural success, safety, and preoperative predictors of procedural failure of LBBAP. Methods LBBAP was attempted in 285 patients with pacemaker indications for bradyarrhythmia, which were mainly atrioventricular block (AVB) (68.1%) and sick sinus syndrome (26.7%). Procedural success and electrophysiological and echocardiographic parameters were evaluated. Results LBBAP was successful in 247 (86.7%) patients. Left bundle branch (LBB) capture was confirmed in 54.7% of the population. The primary reasons for procedural failure were the inability of the pacemaker lead to penetrate deep into the septum (76.3%) and failure to achieve shortening of stimulus to left ventricular (LV) activation time in lead V6 (18.4%). Thickened interventricular septum (odds ratio [OR], 2.48; 95% confidence interval [CI], 1.15–5.35), severe tricuspid regurgitation (OR, 8.84; 95% CI, 1.22–64.06), and intraventricular conduction delay (OR, 8.16; 95% CI, 2.32–28.75) were preoperative predictors of procedural failure. The capture threshold and ventricular amplitude remained stable, and no major complications occurred throughout the 2‐year follow‐up. In patients with ventricular pacing burden >40%, the LV ejection fraction remained high regardless of LBB capture. Conclusions Successful LBBAP was affected by abnormal cardiac anatomy and intraventricular conduction. LBBAP is feasible and safe as a primary strategy for patients with AVB, depending on ventricular pacing

Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome

Objectives.We examined the modulatory effects of autonomic nervous system and antiarrhythmic drugs on the ST segment in patients with Brugada syndrome to gain an insight into the mechanism of ST segment elevation.Background.Right bundle branch block, ST segment elevation and ventricular tachyarrhythmias define a distinct clinical and electrocardiographic (ECG) syndrome (Brugada syndrome). However, the mechanism of ST segment elevation and the causes of this syndrome are unknown.Methods.The study included four patients in whom structural heart or coronary artery disease was excluded by noninvasive and invasive tests. High take-off ST segment elevation of either the coved or saddle-back type in precordial leads V1, V2and V3was seen in all patients. Three patients experienced recurrent episodes of syncope or aborted sudden cardiac death, and the remaining patient had palpitation. Autonomic receptor stimulation and blockade and intravenous administration of antiarrhythmic drugs were performed during sinus rhythm while the 12-lead ECG was recorded. Metaiodobenzylguanidine (MIBG) scanning and Holter monitoring were also performed.Results.Beta-adrenoceptor stimulation by intravenous isoproterenol consistently reduced (≥0.1 mV) ST segment elevation at or 80 ms after the J point in all four patients. Selective alphaadrenoceptor stimulation by intravenous norepinephrine in the presence of propranolol or by intravenous methoxamine consistently augmented, whereas alpha-adrenoceptor blockade reduced, ST segment elevation in three patients. Intracoronary acetylcholine or intravenous edrophonium or neostigmine augmented ST segment elevation without inducing coronary spasm in three of four patients. Class IA antiarrhythmic drugs also consistently augmented (three patients), whereas class IB drugs had no effect on (two patients) ST segment elevation. No abnormality was found on MIBG imaging or heart rate variability in three patients, suggesting that autonomic dysfunction is not a primary disease process. Class IA drugs had no effect on ST segment in three control patients, suggesting that the ST segment elevation seen in patients with Brugada syndrome in response to the drugs is not a nonspecific response.Conclusions.ST segment elevation in patients with Brugada syndrome was augmented by selective stimulation of alphaadrenoceptors or muscarinic receptors or by class IA drugs but was mitigated by beta-adrenoceptor stimulation or alphaadrenoceptor blockade. These responses might be explained by postulating the presence of an area of early repolarization or a local “depolarized” area in the ventricle causing ST segment elevation in this syndrome. Because only a small number of patients were studied, these possibilities need further evaluation