Calcified myocardial scar seen via cardiac imaging correlating with ventricular tachycardia focus.

A 74-year-old man presented with presyncope and non-sustained monomorphic ventricular tachycardia in the setting of acute coronary syndrome. On coronary angiogram, a calcified myocardial scar was revealed, which was later identified as the ventricular tachycardia focus via electrophysiological study.

A case report of unusually long episodes of asystole in a severe COVID-19 patient treated with a leadless pacemaker.

BACKGROUND: Experience has been emerging about cardiac manifestations of COVID-19-positive patients. The full cardiac spectrum is still unknown, and management of these patients is challenging. CASE SUMMARY: We report a COVID-19 patient who developed unusually long asystolic pauses associated with atriventricular block (AV) block and atrial fibrillation who underwent leadless pacemaker implantation. DISCUSSION: Asystole may be a manifestation of COVID-19 infection. A leadless pacemaker is a secure remedy, with limited requirements for follow-up, close interactions, and number of procedures in a COVID-19 patient.

Transesophageal Echocardiography-Guided Epicardial Left Ventricular Lead Placement by Video-Assisted Thoracoscopic Surgery in Nonresponders to Biventricular Pacing and Previous Chest Surgery.

OBJECTIVE: The aim of the study was to study the feasibility, safety, and efficacy of transesophageal echocardiography-guided intraoperative left ventricular lead placement via a video-assisted thoracoscopic surgery approach in patients with failed conventional biventricular pacing. METHODS: Twelve patients who could not have the left ventricular lead placed conventionally underwent epicardial left ventricular lead placement by video-assisted thoracoscopic surgery. Eight patients had previous chest surgery (66%). Operative positioning was a modified far lateral supine exposure with 30-degree bed tilt, allowing for groin and sternal access. To determine the optimal left ventricular location for lead placement, the left ventricular surface was divided arbitrarily into nine segments. These segments were transpericardially paced using a hand-held malleable pacing probe identifying the optimal site verified by transesophageal echocardiography. The pacing leads were screwed into position via a limited pericardiotomy. RESULTS: The video-assisted thoracoscopic surgery approach was successful in all patients. Biventricular pacing was achieved in all patients and all reported symptomatic benefit with reduction in New York Heart Association class from III to I-II (P = 0.016). Baseline ejection fraction was 23 ± 3%; within 1-year follow-up, the ejection fraction increased to 32 ± 10% (P = 0.05). The mean follow-up was 566 days. The median length of hospital stay was 7 days with chest tube removal between postoperative days 2 and 5. CONCLUSIONS: In patients who are nonresponders to conventional biventricular pacing, intraoperative left ventricular lead placement using anatomical and functional characteristics via a video-assisted thoracoscopic surgery approach is effective in improving heart failure symptoms. This optimized left ventricular lead placement is feasible and safe. Previous chest surgery is no longer an exclusion criterion for a video-assisted thoracoscopic surgery approach.

Identification and electrophysiological characterization of early left atrial structural remodeling as a predictor for atrial fibrillation recurrence after pulmonary vein isolation.

BACKGROUND: Voltage-guided substrate ablation following pulmonary vein isolation (PVI) improves atrial fibrillation (AF) ablation outcomes. However, by setting an upper voltage cutoff of 0.5 mV during sinus rhythm (SR) to guided substrate ablation using electroanatomic voltage mapping (EAVM), mildly affected low-voltage area (maLVA) may be undetected. We sought to determine the optimal bipolar voltage cutoff to identify maLVA, its electrogram complexity, and the implication on ablation outcome. METHODS AND RESULTS: Left atrial (LA) EAVMs were obtained in patients without AF and structural heart disease (control) to devise a voltage cutoff to identify maLVA. Subsequently, we investigated 100 patients without low-voltage area (LVA) of < 0.5 mV who underwent PVI alone. In our 6 control cohorts, 95% of LA regional bipolar voltage was > 1.17 mV. maLVA, defined as <1.1 mV, was present in 43% of AF patients, associated with higher prevalence of abnormal electrograms (44.1% vs. 4.4%, P < 0.001). During a median of 2.4 years, patients with maLVA had higher recurrence rate (Log-rank P < 0.001), and maLVA was an independent predictor for recurrence in a multivariate analysis (hazard ratio [HR] 3.944; 95% confidence interval [CI] 1.292-12.042; P = 0.016). CONCLUSIONS: A control-derived LA voltage cutoff of <1.1 mV for EAVM in SR reveals maLVA, harboring abnormal electrograms, as an independent predictor for recurrences after PVI alone in patients without LVA (< 0.5 mV). Adjunctive maLVA-guided substrate ablation targeting mildly remodeled and potentially arrhythmogenic LA substrate may further improve the long-term outcome of AF ablation.

Long-Term Outcome of Left Atrial Voltage-Guided Substrate Ablation During Atrial Fibrillation: A Novel Adjunctive Ablation Strategy.

INTRODUCTION: Left atrium (LA) low voltage area (LVA) on 3-D electroanatomic bipolar voltage mapping (EAVM), as a surrogate for scar, is associated with poor AF ablation outcome. We evaluated the long-term outcome of an LVA-guided atrial fibrillation (AF) substrate modification strategy as an adjunct to pulmonary vein isolation (PVI). METHODS AND RESULTS: Two hundred and one consecutive patients with AF (82% persistent/Non-PAF, age 65 years), who underwent EAVM during AF prior to PVI, were divided into 2 groups according to the presence or absence of LVA outside the PV antra, defined as bipolar voltage of <0.5 mV. LVA-guided substrate modification was performed after PVI in patients with LVA. LVA was found in 159 patients (79%). Non-PAF (OR 3.851, P = 0.002) and CHA2 DS2 -VASc score (OR 1.815, P < 0.001) were independent predictors for the LVA. After the index procedure, 144 patients (72%) were free from AF at 12 months. With multiple procedures, 148 patients (74%) during a median follow-up of 3.1 years were free from the recurrence. There was no difference in the recurrence (log-rank P = 0.746), and complications (0% vs. 7%, P = 0.125) between the groups. Neither LVA nor Non-PAF was an independent predictor for the recurrence in a multivariate analysis. CONCLUSIONS: Patients with LVA had an equally favorable long-term ablation outcome compared to those without. As an adjunct to PVI, voltage-guided substrate modification may be an important ablation strategy in patients with LA structural remodeling.

Correlation of Left Atrial Voltage Distribution Between Sinus Rhythm and Atrial Fibrillation: Identifying Structural Remodeling by 3-D Electroanatomic Mapping Irrespective of the Rhythm.

INTRODUCTION: Left atrial (LA) electroanatomical voltage mapping (EAVM) correlates with scar on LGE-MRI and has been used to guide ablation of low voltage area (LVA) in sinus rhythm (SR). We compared EAVM in SR and AF in a cohort of AF patients, and in SR between patients with AF and without AF or structural heart disease (control). METHODS AND RESULTS: Twenty-seven AF patients, 9 with paroxysmal AF (PAF), underwent point-by-point EAVM during SR and AF using same Carto3 geometry. Only adjacent SR-AF points (≤ 5 mm apart) were compared. In addition, 6 control patients were evaluated. There was a linear bipolar voltage correlation between SR and AF (r = 0.707, P < 0.001, Y = 1.515X + 0.786). LA bipolar voltage in patients with PAF was higher than those with Non-PAF in SR (2.24 ± 1.51 vs. 1.56 ± 1.53 mV) and AF (0.81 ± 0.60 vs. 0.58 ± 0.62 mV, both for P < 0.001). The pulmonary vein antra voltage was significantly lower than other LA regions in PAF (1.28 ± 0.79 vs. 2.54 ± 1.50 mV, P < 0.001) and Non-PAF patients (1.13 ± 1.04 vs. 1.86 ± 1.72 mV, P < 0.001), while no voltage differences was found in the control group (P = 0.998). CONCLUSION: There was a linear voltage correlation between SR and AF, suggesting a similar extent of LA fibrotic substrate can be identified on EAVM by adjusting the voltage cutoff. Structural remodeling starts in the PV antra and may progress to other LA regions.

Long-Term Evaluation of Biotronik Linox and Linox(smart) Implantable Cardioverter Defibrillator Leads.

INTRODUCTION: Expert consensus holds that post-market, systematic surveillance of ICD leads is essential to ensure confirmation of adequate lead performance. GALAXY (NCT00836589) and CELESTIAL (NCT00810264) are ongoing multicenter, prospective, non-randomized registries conducted to confirm the long-term safety and reliability of Biotronik leads. METHODS AND RESULTS: ICD and CRT-D patients are followed for Linox and Linox(smart) ICD lead performance and safety for 5 years post-implant. All procedural and system-related adverse events (AEs) were assessed at each follow-up, along with lead electrical parameters. An independent CEC of EPs adjudicated AEs to determine AE category and lead relatedness. The analysis used categories of lead observations per ISO 5841-2 (Third edition). A total of 3,933 leads were implanted in 3,840 patients (73.0% male, mean age 67.0 ± 12.2 years) at 146 US centers. The estimated cumulative survival probability was 96.3% at 5 years after implant for Linox leads and 96.6% at 4 years after implant for Linox(smart) leads. A comparison of the Linox and Linox(smart) survival functions did not find evidence of a difference (P = 0.2155). The most common AEs were oversensing (23, 0.58%), conductor fracture (14, 0.36%), failure to capture (13, 0.33%), lead dislodgement (12, 0.31%), insulation breach (10, 0.25%), and abnormal pacing impedance (8, 0.20%). CONCLUSIONS: Linox and Linox(smart) ICD leads are safe, reliable and infrequently associated with lead-related AEs. Additionally, estimated cumulative survival probability is clinically acceptable and well within industry standards. Ongoing data collection will confirm the longer-term safety and performance of the Linox family of ICD leads.

Simultaneous Biatrial High-Density (510-512 Electrodes) Epicardial Mapping of Persistent and Long-Standing Persistent Atrial Fibrillation in Patients: New Insights Into the Mechanism of Its Maintenance.

BACKGROUND: The mechanism(s) of persistent and long-standing persistent (LSP) atrial fibrillation (AF) is/are poorly understood. We performed high-density, simultaneous, biatrial, epicardial mapping of persistent and LSP AF in patients undergoing open heart surgery (1) to test the hypothesis that persistent and LSP AF are due to ≥ 1 drivers, either focal or reentrant, and (2) to characterize associated atrial activation. METHODS AND RESULTS: Twelve patients with persistent and LSP AF (1 month to 9 years duration) were studied at open heart surgery. During AF, electrograms were recorded from both atria simultaneously for 1 to 5 minutes from 510 to 512 epicardial electrodes with ECG lead II. Thirty-two consecutive seconds of activation sequence maps were produced per patient. During AF, multiple foci (QS unipolar atrial electrograms) of different cycle lengths (mean, 175 ± 18 ms) were present in both atria in 11 of 12 patients. Foci (2-4 per patient, duration 5-32 s) were either sustained or intermittent, were predominantly found in the lateral left atrial free wall, and likely acted as drivers. Random and nonrandom breakthrough activation sites (initial r or R in unipolar atrial electrograms) were also found. In 1 of 12 patients, only breakthrough sites were found. All wave fronts emanated from foci and breakthrough sites, and largely either collided or merged with each other at variable sites. Repetitive focal QS activation occasionally generated repetitive wannabe reentrant activation in 5 of 12 patients. No actual reentry was found. CONCLUSIONS: During persistent and LSP AF in 12 patients, wave fronts emanating from foci and breakthrough sites maintained AF. No reentry was demonstrated.

Insights into new-onset atrial fibrillation following open heart surgery and implications for type II atrial flutter.

AIMS: Postoperative atrial fibrillation (POAF), new-onset AF after open heart surgery (OHS), is thought to be related to pericarditis. Based on AF studies in the canine sterile pericarditis model, we hypothesized that POAF in patients after OHS may be associated with a rapid, regular rhythm in the left atrium (LA), suggestive of an LA driver maintaining AF. The aim of this study was to test the hypothesis that in patients with POAF, atrial electrograms (AEGs) recorded from at least one of the two carefully selected LA sites would manifest a rapid, regular rhythm with AEGs of short cycle length (CL) and constant morphology, but a selected right atrial (RA) site would manifest AEGs with irregular CLs and variable morphology. METHODS AND RESULTS: In 44 patients undergoing OHS, AEGs recorded from the epicardial surface of the RA, the LA portion of Bachmann's bundle, and the posterior LA during sustained AF were analysed for regularity of CL and morphology. Sustained AF occurred in 15 of 44 patients. Atrial electrograms were recorded in 11 of 15 patients; 8 of 11 had rapid, regular activation with constant morphology recorded from at least one LA site; no regular AEG sites were present in 3 of 11 patients. CONCLUSIONS: Atrial electrograms recorded during sustained POAF frequently demonstrated rapid, regular activation in at least one LA site, consistent with a driver maintaining AF.

Noninvasive diagnostic mapping of supraventricular arrhythmias (Wolf-Parkinson-White syndrome and atrial arrhythmias).

The 12-lead electrocardiogram has limited value in precisely identifying the origin of focal or critical component of reentrant arrhythmias during supraventricular arrhythmias, as well as precisely locating accessory atrioventricular conduction pathways. Because of these limitations, efforts have been made to reconstruct epicardial activation sequences from body surface measurements obtained noninvasively. The last decade has registered significant progress in obtaining clinically useful data from the attempts to noninvasively map the epicardial electrical activity. This article summarizes the recent advances made in this area, specifically addressing the clinical outcomes of such efforts relating to atrial arrhythmias and Wolf-Parkinson-White syndrome.

Variable clinical features and ablation of manifest nodofascicular/ventricular pathways.

BACKGROUND: Manifest nodofascicular/ventricular (NFV) pathways are rare. METHODS AND RESULTS: From 2008 to 2013, 4 cases were identified with manifest NFV pathways from 3 centers. The clinical findings and ablation sites are reported. All 4 cases presented with a wide complex tachycardia but with different QRS morphologies. Case 1 showed a left bundle branch block/superior axis, case 2 showed a right bundle branch block/inferior axis, case 3 showed a left bundle branch block/inferior axis, and case 4 showed a narrow QRS tachycardia and a wide complex tachycardia with a left bundle branch block/inferior axis. Three of the 4 tachycardias had atrioventricular dissociation ruling out extranodal accessory pathways, including atriofascicular pathways. Programmed extrastimuli showed evidence of a decremental accessory pathway in 3 of the 4 cases. Coexisting tachycardia mechanisms were seen in 3 of the 4 cases (atrioventricular nodal reentry tachycardia [2] and atrioventricular reentrant tachycardia [1]). Ablation in the slow pathway region eliminated the NFV pathway in 3 (transient in 1) with the other responding to surgical closure of a large atrial septal defect. The NFV pathway was a critical part of the tachycardia circuit in 1 and proved to be a bystander in the other 3 cases. CONCLUSIONS: Manifest NFV pathways presented with variable QRS expression dependent on the ventricular insertion site and often coexisted with other tachycardia mechanisms (atrioventricular nodal reentry tachycardia and atrioventricular reentrant tachycardia). In most cases, the atrial insertion of the pathway was in or near the slow pathway region. The NFV pathways were either critical to the tachycardia circuit or served as bystanders.

Validation of novel 3-dimensional electrocardiographic mapping of atrial tachycardias by invasive mapping and ablation: a multicenter study.

OBJECTIVES: This study prospectively evaluated the role of a novel 3-dimensional, noninvasive, beat-by-beat mapping system, Electrocardiographic Mapping (ECM), in facilitating the diagnosis of atrial tachycardias (AT). BACKGROUND: Conventional 12-lead electrocardiogram, a widely used noninvasive tool in clinical arrhythmia practice, has diagnostic limitations. METHODS: Various AT (de novo and post-atrial fibrillation ablation) were mapped using ECM followed by standard-of-care electrophysiological mapping and ablation in 52 patients. The ECM consisted of recording body surface electrograms from a 252-electrode-vest placed on the torso combined with computed tomography-scan-based biatrial anatomy (CardioInsight Inc., Cleveland, Ohio). We evaluated the feasibility of this system in defining the mechanism of AT-macro-re-entrant (perimitral, cavotricuspid isthmus-dependent, and roof-dependent circuits) versus centrifugal (focal-source) activation-and the location of arrhythmia in centrifugal AT. The accuracy of the noninvasive diagnosis and detection of ablation targets was evaluated vis-à-vis subsequent invasive mapping and successful ablation. RESULTS: Comparison between ECM and electrophysiological diagnosis could be accomplished in 48 patients (48 AT) but was not possible in 4 patients where the AT mechanism changed to another AT (n = 1), atrial fibrillation (n = 1), or sinus rhythm (n = 2) during the electrophysiological procedure. ECM correctly diagnosed AT mechanisms in 44 of 48 (92%) AT: macro-re-entry in 23 of 27; and focal-onset with centrifugal activation in 21 of 21. The region of interest for focal AT perfectly matched in 21 of 21 (100%) AT. The 2:1 ventricular conduction and low-amplitude P waves challenged the diagnosis of 4 of 27 macro-re-entrant (perimitral) AT that can be overcome by injecting atrioventricular node blockers and signal averaging, respectively. CONCLUSIONS: This prospective multicenter series shows a high success rate of ECM in accurately diagnosing the mechanism of AT and the location of focal arrhythmia. Intraprocedural use of the system and its application to atrial fibrillation mapping is under way.

Confirmation of novel noninvasive high-density electrocardiographic mapping with electrophysiology study: implications for therapy.

BACKGROUND: Twelve lead ECGs have limited value in precisely identifying atrial and ventricular activation during arrhythmias, including accessory atrioventricular conduction activation. The aim of this study was to report a single center's clinical experience validating a novel, noninvasive, whole heart, beat-by-beat, 3-dimensional mapping technology with invasive electrophysiological studies, including ablation, where applicable. METHODS AND RESULTS: Using an electrocardiographic mapping (ECM) system in 27 patients, 3-dimensional epicardial activation maps were generated from >250 body surface ECGs using heart-torso geometry obtained from computed tomographic images. ECM activation maps were compared with clinical diagnoses, and confirmed with standard invasive electrophysiological studies mapping. (1) In 6 cases of Wolff-Parkinson-White syndrome, ECM accurately identified the ventricular insertion site of an accessory atrioventricular connection. (2) In 10 patients with premature ventricular complexes, ECM accurately identified their ventricular site of origin in 8 patients. In 2 of 10 patients transient premature ventricular complex suppression was observed during ablation at the site predicted by ECM as the earliest. (3) In 10 cases of atrial tachycardia/atrial flutter, ECM accurately identified the chamber of origin in all 10, and distinguished isthmus from nonisthmus dependent atrial flutter. (4) In 1 patient with sustained exercise induced ventricular tachycardia, ECM accurately identified the focal origin in the left ventricular outflow tract. CONCLUSIONS: ECM successfully provided valid activation sequence maps obtained noninvasively in a variety of rhythm disorders that correlated well with invasive electrophysiological studies.

Oral vanoxerine prevents reinduction of atrial tachyarrhythmias: preliminary results.

BACKGROUND: Vanoxerine is a promising, new, investigational antiarrhythmic drug. The purpose of this study was to test the hypothesis that oral dosing of vanoxerine would first terminate induced atrial flutter (AFL) and atrial fibrillation (AF), and then prevent their reinduction. METHODS: In 5 dogs with sterile pericarditis, on the fourth day after creating the pericarditis, we performed electrophysiologic (EP) studies at baseline, measuring atrial excitability, refractoriness (AERP), and conduction time (CT) when pacing from the right atrial appendage, Bachmann's bundle (BB), and the posteroinferior left atrium at cycle lengths (CLs) of 400, 300, and 200 ms. Then, after induction of AFL or AF, all dogs received hourly oral doses of vanoxerine: 90 mg, followed by 180 mg and 270 mg. Blood was obtained to determine plasma vanoxerine concentrations at baseline, every 30 minutes, when neither AFL nor AF were inducible, and, finally, 1 hour after the 270 mg dose. Then we repeated the baseline EP studies. RESULTS: Four dogs had inducible, sustained AFL, and 1 dog only had induced, nonsustained AF. In 4 AFL episodes, oral vanoxerine terminated the AFL and then rendered it noninducible after an average of 111 minutes (range 75-180 minutes) after the first dose was administered. The mean vanoxerine plasma level at the point of noninducibility was 84 ng/mL, with a narrow range of 76-99 ng/mL. In the dog with induced, nonsustained AF, it was no longer inducible at a drug level of 75 ng/mL. Vanoxerine did not significantly (1) prolong the AERP except at BB, and then only at the faster pacing CLs; (2) change atrial excitability thresholds; (3) prolong atrial conduction time, the PR interval, the QRS complex or the QT interval. CONCLUSIONS: Orally administered vanoxerine effectively terminated AFL and rendered it noninducible. It also suppressed inducibility of nonsustained AF. These effects occurred at consistent plasma drug levels. Vanoxerine's insignificant or minimal effects on measured electrophysiologic parameters are consistent with little proarrhythmic risk.