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Frequent premature ventricular contractions (PVCs) can lead to cardiomyopathy; it is unclear if there are abnormal myocardial mechanics operative in the PVC and non-PVC beats.The aim of this study was to investigate regional and global myocardial mechanics, including dyssynchrony, in patients with frequent PVCs.Fifty-six consecutive patients referred for PVC ablation were prospectively studied. During sinus rhythm (SR) and PVC beats, left ventricular (LV) global longitudinal strain (GLS), LV dyssynchrony (measured as the SD of time to peak GLS), and dyssynergy (measured as maximum regional strain minus minimum regional strain at aortic valve closure) were quantified using 2-dimensional strain echocardiography. GLS, dyssynchrony, and dyssynergy were compared in remote SR, pre-PVC SR, PVC, and post-PVC SR beats.In SR beats remote from the PVC, GLS was -17.3% ± 4%, dyssynchrony was 49 ± 14 ms, and dyssynergy was 22% ± 9%. Myocardial mechanics were significantly abnormal during PVCs compared with remote SR beats (GLS -7.7% ± 3% [P 0.001], dyssynchrony 115 ± 37 milliseconds [P 0.001], and dyssynergy 26% ± 10% [P 0.001]). There were significant mechanical abnormalities in the SR beat preceding the PVC, which demonstrated significantly lower LV strain (pre-PVC SR, -13% ± 4%; P 0.001) and more dyssynchrony (pre-PVC SR, 63 ± 19 milliseconds; P 0.001) compared with remote SR beats. Dyssynergy was significantly higher for pre-PVC SR and PVC beats compared with remote SR (pre-PVC SR, 25% ± 8% [P 0.001]; PVC, 26% ± 10% [P 0.001]).In patients with frequent PVCs, the SR beat preceding the PVC demonstrates significant mechanical abnormalities. This finding suggests that perturbations in cellular physiological processes such as excitation-contraction coupling may underlie the generation of frequent PVCs.

Pulsed field ablation (PFA) leads to cell death by irreversible electroporation. There are limited data about PFA lesion characteristics in the ventricle, particularly in the presence of myocardial scar.This study sought to evaluate the lesion characteristics of PFA and radiofrequency energy (RFA) in healthy and infarcted left ventricular (LV) myocardium in swine.Swine (n = 10) underwent either: 1) 120-minute left anterior descending coronary artery balloon occlusion myocardial infarction and survived for 6 to 8 weeks (n = 8); or 2) served as healthy control subjects (n = 2). PFA or RFA was delivered to the LV endocardium in regions of healthy myocardium or scar identified with electroanatomical mapping. Bipolar, biphasic PFA was delivered for 2.5 seconds × 4 applications/site using 2 different catheters: linear quadripolar (FOCAL) or multispline 8-pole catheter (BASKET). Gross and histologic measurements of lesion size were performed.In the PFA group, 21 lesions were delivered to healthy LV and 20 to areas of scar. Overall, there was no significant difference in lesion depth between catheter groups (FOCAL linear vs BASKET; P = 0.740), whereas lesion width was greater for BASKET (10.6 ± 2.4 mm vs 13.3 ± 3.3 mm; P = 0.007). In myocardial scar, lesion depth was not significantly different between PFA catheters (P = 0.235). However, lesion depth for PFA was greater than for RFA (PFA vs RFA; 6.1 ± 1.7 mm vs 3.8 ± 1.7 mm; P = 0.005).PFA allows rapid, safe, and effective ablation of surviving islands of myocardium within and around infarcted LV substrate. This technology holds promise for treating infarct-related ventricular tachycardia in humans.

Background: Confirming the presence and participation of concealed nodo-ventricular (cNV) or concealed His-ventricular (cHV) pathways in tachyarrhythmias is challenging. We describe novel observations to aid in diagnosing cNV or cHV pathways. Methods: We present 7 cases of cNV and cHV pathway-mediated arrhythmias and focus on several laboratory observations: (1) differential ventricular overdrive pacing (VOD) from the base versus apex, (2) response to His refractory premature ventricular complexes, (3) paradoxical atriohisian response (shorter atriohisian interval during tachycardia than that during sinus rhythm) in long RP tachycardia, and (4) the role of adenosine to aid in the diagnosis. Results: Three cases underwent differential VOD during tachycardia. All demonstrated a shorter postpacing interval minus tachycardia cycle length during basal pacing than apical pacing with one case exhibiting apical VOD results compatible with atrioventricular nodal reentrant tachycardia. Basal VOD was useful for localizing the ventricular connection in a case with cHV pathway. In 3 cases, His refractory premature ventricular complexes reset the tachycardia without conduction to the atrium, which excluded the involvement of an atrioventricular pathway or atrial tachycardia, or atrioventricular nodal reentrant tachycardia alone. One case had His refractory premature ventricular complexes followed by subsequent constant AA interval and then tachycardia termination, suggesting a bystander cNV pathway involvement. Two cNV pathway cases presented with long RP tachycardia had paradoxical atriohisian shortening of >15 ms, suggesting parallel activation of the atrium and the atrioventricular node. Adenosine terminated the tachycardia with retrograde block in 2 cases with cNV pathways but had no response on a cHV pathway. Conclusions: cNV and cHV pathways mediated tachyarrhythmias can present with variable clinical presentations. We emphasize the important role of differential VOD sites, His refractory premature ventricular complexes that reset or terminate the tachycardia without conduction to the atrium, paradoxical atriohisian response in long RP tachycardia, and the use of adenosine for diagnosing cNV and cHV pathways.

Iatrogenic atrioventricular (AV) block can occur in the context of cardiac surgery, percutaneous transcatheter, or electrophysiologic procedures. In cardiac surgery, patients undergoing aortic and/or mitral valve surgery are at the highest risk for developing perioperative AV block requiring permanent pacemaker implantation. Similarly, patients undergoing transcatheter aortic valve replacement are also at increased risk for developing AV block. Electrophysiologic procedures, including catheter ablation of AV nodal re-entrant tachycardia, septal accessory pathways, para-Hisian atrial tachycardia, or premature ventricular complexes, are also associated with risk of AV conduction system injury. In this article, we summarize the common causes for iatrogenic AV block, predictors for AV block, and general management considerations.

BACKGROUND Patients' self-reports suggest that acute alcohol consumption may trigger a discrete atrial fibrillation (AF) event. OBJECTIVE To objectively ascertain whether alcohol consumption heightens risk for an AF episode. DESIGN A prospective, case-crossover analysis. SETTING Ambulatory persons in their natural environments. PARTICIPANTS Consenting patients with paroxysmal AF. MEASUREMENTS Participants were fitted with a continuous electrocardiogram (ECG) monitor and an ankle-worn transdermal ethanol sensor for 4 weeks. Real-time documentation of each alcoholic drink consumed was self-recorded using a button on the ECG recording device. Fingerstick blood tests for phosphatidylethanol (PEth) were used to corroborate ascertainments of drinking events. RESULTS Of 100 participants (mean age, 64 years [SD, 15]; 79% male; 85% White), 56 had at least 1 episode of AF. Results of PEth testing correlated with the number of real-time recorded drinks and with events detected by the transdermal alcohol sensor. An AF episode was associated with 2-fold higher odds of 1 alcoholic drink (odds ratio [OR], 2.02 [95% CI, 1.38 to 3.17]) and greater than 3-fold higher odds of at least 2 drinks (OR, 3.58 [CI, 1.63 to 7.89]) in the preceding 4 hours. Episodes of AF were also associated with higher odds of peak blood alcohol concentration (OR, 1.38 [CI, 1.04 to 1.83] per 0.1% increase in blood alcohol concentration) and the total area under the curve of alcohol exposure (OR, 1.14 [CI, 1.06 to 1.22] per 4.7% increase in alcohol exposure) inferred from the transdermal ethanol sensor in the preceding 12 hours. LIMITATION Confounding by other time-varying exposures that may accompany alcohol consumption cannot be excluded, and the findings from the current study of patients with AF consuming alcohol may not apply to the general population. CONCLUSION Individual AF episodes were associated with higher odds of recent alcohol consumption, providing objective evidence that a modifiable behavior may influence the probability that a discrete AF event will occur. PRIMARY FUNDING SOURCE National Institute on Alcohol Abuse and Alcoholism.

Background: Data on atrial fibrillation (AF) ablation and outcomes are limited in patients with congenital heart disease (CHD). We aimed to investigate the characteristics of patients with CHD presenting for AF ablation and their outcomes. Methods: A multicenter, retrospective analysis was performed of patients with CHD undergoing AF ablation between 2004 and 2020 at 13 participating centers. The severity of CHD was classified using 2014 Pediatric and Congenital Electrophysiology Society/Heart Rhythm Society guidelines. Clinical data were collected. One-year complete procedural success was defined as freedom from atrial tachycardia or AF in the absence of antiarrhythmic drugs or including previously failed antiarrhythmic drugs (partial success). Results: Of 240 patients, 127 (53.4%) had persistent AF, 62.5% were male, and mean age was 55.2±13.3 years. CHD complexity categories included 147 (61.3%) simple, 68 (28.3%) intermediate, and 25 (10.4%) severe. The most common CHD type was atrial septal defect (n=78). More complex CHD conditions included transposition of the great arteries (n=14), anomalous pulmonary veins (n=13), tetralogy of Fallot (n=8), cor triatriatum (n=7), single ventricle physiology (n=2), among others. The majority (71.3%) of patients had trialed at least one antiarrhythmic drug. Forty-six patients (22.1%) had reduced systemic ventricular ejection fraction Conclusions: AF ablation in CHD was safe and resulted in AF control in a majority of patients, regardless of complexity. Future work should address the most appropriate ablation targets in this challenging population.

Objectives This study describes a series of cases best explained by invoking the left septal fascicle (LSF) as a critical component of the arrhythmia circuit. Background Numerous anatomic studies have shown evidence of the LSF, but its precise role in the onset of arrhythmia is unclear. Methods This paper presents 5 cases that implicated the LSF as a critical component of arrhythmogenesis. Results The first case had ventricular fibrillation repeatedly documented after a single premature atrial complex, produced left-sided conduction delay and simultaneous earliest activation of the left anterior fascicle (LAF) and left posterior fascicle (LPF). The LSF was ablated, resulting in an arrhythmia cure. The second case showed narrow QRS morphology during fascicular re-entrant tachycardia. The earliest mid-septal diastolic potentials had distal-to-proximal activation suggesting an LSF as a retrograde common pathway. The third case, with multiple ectopic Purkinje-related premature complexes exhibited earliest Purkinje potentials in the mid-septum, with subsequent anterograde activation of the LAF and LPF. Ablation of the LSF eliminated the premature ventricular complexes (PVCs). The fourth case demonstrated LPF and LAF PVCs. The His-left bundle activation showed earliest potentials at the proximal insertion of the left bundle during LPF PVCs, as well as a distal-to-proximal activation pattern during LAF PVC, suggestive of LSF involvement. The fifth case had focal non–re-entrant fascicular beats successfully ablated over the LSF. Conclusions Involvement of the LSF is suspected with presentation of multiform fascicular and narrow QRS complex ventricular episodes of arrhythmia. Diagnoses and ablation require detailed mapping of the entire left sided conduction system.

INTRODUCTION Some patients have late recurrence after acutely successful radiofrequency catheter ablation (RFCA) of premature ventricular complexes (PVCs). The aim of this study was to evaluate predictors of long-term success following acutely successful PVC RFCA. METHODS We identified consecutive patients at our institution with frequent PVCs undergoing RFCA and reviewed procedural data and medical records. Acute success was defined as elimination of targeted PVCs for at least 30-min after RFCA. Long-term success was defined as absence of targeted PVCs during all follow-up visits and PVC-burden

This case report discusses a diagnosis of scimitar syndrome in a woman aged 79 years who presented with worsening dyspnea on exertion and new-onset atrial fibrillation.

Objectives This study sought to characterize the presentations, electrophysiological features and diagnostic maneuvers for a series of unique arrhythmias involving the HPS. Background By v...

Objectives: This study sought to prospectively study the development and then regression of premature ventricular contraction (PVC)-induced cardiomyopathy, with the hypothesis that structural left ventricular (LV) changes that are of potential clinical significance may endure beyond the period of exposure to PVCs. Background: Recovery of LV function after eradication of PVCs in PVC-induced cardiomyopathy is incompletely defined. Methods: Fifteen swine were exposed to: 1) 50% paced PVCs from the LV lateral epicardium for 12 weeks (LV PVC, n = 5); 2) no pacing for 12 weeks (Control, n = 5); or 3) 50% paced LV PVCs for 12 weeks followed by pacing cessation for 4 weeks (Recovery, n = 5). LV function was quantified biweekly in sinus rhythm with echocardiography. Dyssynchrony was measured from pressure-volume loops at baseline and terminal studies. LV fibrosis was quantified after sacrifice. Results: LV ejection fraction during sinus rhythm fell between baseline and terminal studies in the LV PVC group (65.8 ± 3.0 to 39.3 ± 3.2; p < 0.05), whereas there was no significant change in the Control group (69.6 ± 3.0 to 72.2 ± 3.0; p = NS) or after Recovery (64.5 ± 3.4% to 61.4 ± 3.4%; p = NS) groups. There was a significant increase in LV dyssynchrony measured during sinus rhythm between baseline and terminal studies in the LV PVC group (4.0 ± 1.5% to 9.0 ± 1.5%; p < 0.05); there was a similar increase in dyssynchrony that persisted 4 weeks after PVC cessation in the Recovery group (4.4 ± 1.7% to 12.8 ± 1.7%; p < 0.05). After sacrifice, percent fibrosis was higher in the LV PVC group compared with Control (5.7 ± 0.3% vs. 3.0 ± 0.3%; p < 0.05) and remained elevated in Recovery (4.1 ± 0.3% vs. 3.0 ± 0.3%; p < 0.05) despite return to baseline LV ejection fraction. Conclusions: In a swine model of PVC-induced cardiomyopathy, cessation of PVCs for 4 weeks leads to normalization of LV systolic function but significant changes in myocardial fibrosis and LV dyssynchrony during sinus rhythm persist.

This study sought to define the extent and spatial distribution of endocardial-epicardial dissociation (EED) in a swine model.The mechanisms underlying persistent atrial fibrillation (AF) remain unclear.Sixteen swine underwent simultaneous endocardial and epicardial mapping using 32-electrode grid catheters. This included 6 swine with rapid atrial pacing-induced atrial remodeling. Three right atrial (RA) and 3 left atrial (LA) regions were mapped during sinus rhythm, atrial pacing, acute or persistent AF, and AF in the presence of pericardial acetylcholine. Unipolar electrogram recordings over 10-s epochs underwent offline phase analysis using customized software. Regional activation patterns on paired surfaces and the instantaneous phase at each matched electrode location were analyzed. EED was defined as paired electrodes out of phase by ≥20 ms.The mean distance between matched endocardial-epicardial electrode pairs was 4.4 ± 1.8 mm. During episodes of AF, rotational activations with ≥3 full rotations were not seen. EED was seen during 34.4 ± 16.4% of mapped time periods: LARA, persistentacute AF in the LA, and acetylcholine-inducedacute AF in both atria (p 0.05 for each). Most marked EED in persistent AF was in the LA appendage (47.2 ± 3.7%) and the LA posterior wall (50.3 ± 4.7%).Marked EED was seen in a swine model of AF, particularly during persistent AF. There was significantly more EED in the LA than the RA and, particularly, in the LA PW and LAA. Mapping approaches limited to the endocardium may not sufficiently characterize the complexity of AF.

Background No independently validated score currently exists for risk stratification of patients with frequent premature ventricular complexes (PVCs). Objectives The purpose of this study was to develop a risk score to predict adverse events in patients with frequent PVCs. Methods We analyzed consecutive patients between 2012 and 2017 undergoing 14-day continuous monitoring with frequent PVCs (>5%) and concurrent echocardiography. We performed binary logistic regression to determine multivariate predictors of adverse left ventricular remodeling (left ventricular ejection fraction [LVEF] 75 mL/m2). A risk score was created using the log(odds ratio (OR)) of these predictors and validated prospectively to determine the risk of future adverse events in those with baseline LVEF >45%. An adverse event was defined as LVEF decline by 10%, heart failure hospitalization, or cardiovascular mortality. Two validation cohorts were used: follow-up from the original derivation cohort (cohort 1) and an independent Korean PVC registry (cohort 2). Results The derivation cohort comprised 206 patients with a mean PVC burden of 11.6% ± 6.2% and considerable daily fluctuation (minimum burden 7.3% ± 6.2% vs maximum 17.9% ± 8.0%). Independent predictors of adverse remodeling were as follows: superiorly directed PVC axis (OR 2.7; 1 point), PVC burden 10%–20% (OR 3.5; 2 points) and >20% (OR 4.4; 3 points), PVC coupling interval >500 ms (OR 4.7; 4 points), nonsustained ventricular tachycardia (OR 5.3; 4 points), which form the ABC-VT risk score. This score predicted future adverse events in both validation cohorts: cohort 1, hazard ratio 1.43; 95% confidence interval 1.19–1.73; P Conclusion The ABC-VT score is a simple tool that predicts adverse left ventricular remodeling and future clinical deterioration in patients with frequent PVCs.

Objectives The goal of this study was to report a multicenter series of left-sided catheter ablations performed by using intravenous direct thrombin inhibitors (DTIs) as an alternative to heparin. Background Amidst a looming worldwide shortage of heparin, there are insufficient data to guide nonheparin-based peri-procedural anticoagulation in patients undergoing catheter ablation. Methods This study reviewed all catheter ablations at 6 institutions between 2006 and 2019 to assess the safety and efficacy of DTIs for left-sided radiofrequency catheter ablation of atrial fibrillation and ventricular tachycardia. Results In total, 53 patients (age 63.0 ± 9.3 years, 68% male, CHA₂DS₂-VASc [congestive heart failure, hypertension, age ≥75 years, diabetes mellitus, stroke/transient ischemic attack, vascular disease, age 65 to 74 years, sex category] score 2.8 ± 1.6, left ventricular ejection fraction 46 ± 15%) underwent ablation with DTIs (75% bivalirudin, 25% argatroban) due to heparin contraindication(s) (72% heparin-induced thrombocytopenia, 21% heparin allergy, 4% protamine reaction, and 4% religious reasons). The patient’s usual oral anticoagulant was continued without interruption in 69%. Procedures were performed for atrial fibrillation (64%) or ventricular tachycardia/premature ventricular contractions (36%). Transseptal puncture was undertaken in 81%, and a contact force–sensing catheter was used in 70%. Vascular ultrasound was used in 71%, and femoral arterial access was gained in 36%. A bolus followed by infusion was used in all but 4 cases, and activated clotting time was monitored peri-procedurally in 72%, with 32% receiving additional boluses. Procedure duration was 216 ± 116 min, and ablation time was 51 ± 22 min. No major bleeding or embolic complications were observed. Four patients had minor self-limiting bleeding complications, including a small pericardial effusion ( Conclusions In this multicenter series, intravenous DTIs were safely used as an alternative to heparin for left-sided catheter ablation.

Ventricular bipolar voltage values0.5 and1.0/1.5 mV (epi- and endocardium) correlating with dense scar and border zone, respectively, were established using a 3.5-mm tip catheter. Novel microelectrode catheters promise improved mapping resolution; however, whether standard voltage criteria apply to catheters with smaller electrode size and interelectrode distance remains unclear.The purpose of this study was to determine whether traditional bipolar voltage criteria for scar apply during substrate mapping with a microelectrode catheter.Paired bipolar and microbipolar voltage values were acquired from control swine (n = 2) using the microelectrode catheter and assessed for systemic differences. In a postinfarction swine model (n = 6), scar characteristics were compared between the bipolar maps and microbipolar maps using both standard and adjusted voltage criteria derived from the control animals.In control swine, although 5th percentile values for bipolar and microbipolar voltage were similar (1.12 vs 1.22 mV [left ventricular (LV) endo]; 0.88 mV vs 0.98 mV [epi]), median values were significantly greater when acquired by microbipolar electrodes (3.60 vs 6.76 mV, P = .002 [LV endo]; 2.61 vs 2.72 mV, P = .02 [epi]). Microbipolar values were systematically larger by 2.0× and 1.4× in the LV endocardium and epicardium, respectively. Application of standard voltage values to microbipolar maps in postinfarct swine underestimated scar area by approximately 41% in the LV endocardium (13.7 vs 33.4 cmBipolar voltage values acquired from microelectrodes are systemically larger than those acquired from standard catheters. New reference values should be established for these novel catheters.

A 68 year-old man presented with palpitations. A standard 12‑lead ECG was performed and demonstrated significant conduction disease. Using findings on the index and prior ECGs, we review the differential diagnoses for his conduction abnormality. We discuss the possibility of phase III delay, phase IV delay, and “supernormal conduction” to explain the ECG findings. We explore each of these phenomena and review their relative likelihood as it applies to the case presented.