Identification of Human Ventricular Tachycardia Demarcated by Fixed Lines of Conduction Block in a 3-Dimensional Hyperboloid Circuit.

BACKGROUND: The circuit boundaries for reentrant ventricular tachycardia (VT) have been historically conceptualized within a 2-dimensional (2D) construct, with their fixed or functional nature unresolved. This study aimed to examine the correlation between localized lines of conduction block (LOB) evident during baseline rhythm with lateral isthmus boundaries that 3-dimensionally constrain the VT isthmus as a hyperboloid structure. METHODS: A total of 175 VT activation maps were correlated with isochronal late activation maps during baseline rhythm in 106 patients who underwent catheter ablation for scar-related VT from 3 centers (42% nonischemic cardiomyopathy). An overt LOB was defined by a deceleration zone with split potentials (≥20 ms isoelectric segment) during baseline rhythm. A novel application of pacing within deceleration zone (≥600 ms) was implemented to unmask a concealed LOB not evident during baseline rhythm. LOB identified during baseline rhythm or pacing were correlated with isthmus boundaries during VT. RESULTS: Among 202 deceleration zones analyzed during baseline rhythm, an overt LOB was evident in 47%. When differential pacing was performed in 38 deceleration zones without overt LOB, an underlying concealed LOB was exposed in 84%. In 152 VT activation maps (2D=53, 3-dimensional [3D]=99), 69% of lateral boundaries colocalized with an LOB in 2D activation patterns, and the depth boundary during 3D VT colocalized with an LOB in 79%. In VT circuits with isthmus regions that colocalized with a U-shaped LOB (n=28), the boundary invariably served as both lateral boundaries in 2D and 3D. Overall, 74% of isthmus boundaries were identifiable as fixed LOB during baseline rhythm or differential pacing. CONCLUSIONS: The majority of VT circuit boundaries can be identified as fixed LOB from intrinsic or paced activation during sinus rhythm. Analysis of activation while pacing within the scar substrate is a novel technique that may unmask concealed LOB, previously interpreted to be functional in nature. An LOB from the perspective of a myocardial surface is frequently associated with intramural conduction, supporting the existence of a 3D hyperboloid VT circuit structure. Catheter ablation may be simplified to targeting both sides around an identified LOB during sinus rhythm.

Atypical pathogens associated with cardiac implantable electronic device infections.

BACKGROUND: Cardiovascular implantable electronic device (CIED) infections are associated with significant morbidity and mortality making the identification of the causative organism critical. The vast majority of CIED infections are caused by Staphylococcal species. CIED infections associated with atypical pathogens are rare and have not been systematically investigated. The objective of this study is to characterize the clinical course, management and outcome in patients with CIED infection secondary to atypical pathogens. METHODS: Medical records of all patients who underwent CIED system extraction at the University of Chicago Medical Center between January 2010 and November 2020 were retrospectively reviewed to identify patients with CIED infection. Demographic, clinical, infection-related and outcome data were collected. CIED infections were divided into typical and atypical groups based on the pathogens isolated. RESULTS: Among 356 CIED extraction procedures, 130 (37%) were performed for CIED infection. Atypical pathogens were found in 5.4% (n = 7) and included Pantoea species (n = 2), Kocuria species (n = 1), Cutibacterium acnes (n = 1), Corynebacterium tuberculostearicum (n = 1), Corynebacterium striatum (n = 1), Stenotrophomonas maltophilia (n = 1), and Pseudozyma ahidis (n = 1). All patients with atypical CIED infections were successfully treated with total system removal and tailored antibiotic therapy. There were no infection-related deaths. CONCLUSIONS: CIED infections with atypical pathogens were rare and associated with good outcome if diagnosed early and treated with total system removal and tailored antimicrobial therapy. Atypical pathogens cultured from blood, tissue or hardware in patients with CIED infection should be considered pathogens and not contaminants.

Double loop ventricular tachycardia activation patterns with single loop mechanisms: Asymmetric entrainment responses during "pseudo-figure-of-eight" reentry.

BACKGROUND: The classical paradigm of scar-related reentrant ventricular tachycardia (VT) features a circuit with a double loop figure-of-eight (F8) activation pattern. OBJECTIVE: The purpose of this study was to interrogate VT circuits with F8 activation patterns by entrainment mapping to differentiate an active loop from a passive loop. METHODS: Sixty VT circuits with >90% of tachycardia cycle length delineated in high resolution were retrospectively analyzed in 55 patients (nonischemic 49%). A pseudo-F8 VT circuit was defined as a double loop activation pattern driven by a single loop mechanism with a passive loop that yields a long postpacing interval (postpacing interval - tachycardia cycle length ≥ 30 ms). RESULTS: Single loop activation patterns were observed in 33% (n = 20). Of 40 circuits with F8 patterns by activation mapping, 20 were studied with entrainment mapping, where a passive loop was identified by a long postpacing interval in 50%. In 6 circuits where entrainment mapping was performed from both outer loop regions, all demonstrated asymmetric responses to entrainment, confirming a single loop mechanism. Entrainment from both lateral margins of the common pathway (n = 7) demonstrated an asymmetric response in 29%. In all pseudo-F8 circuits (n = 10), the shorter loop functioned as the active loop and ablation targeting the active loop side of the isthmus resulted in VT termination with a single radiofrequency application. CONCLUSION: In a selected cohort, single loop mechanisms are more prevalent than double loop reentry in reentrant human VT. Half of VT circuits with double loop activation patterns can be demonstrated to be sustained by a single active loop mechanism by entrainment mapping. Ablation targeting the shorter active loop resulted in rapid termination during radiofrequency application.

Patient Profiles in the Utilization of the CanGaroo® Envelope.

Background The CanGaroo® Envelope (Aziyo Biologics, Silver Spring, MD) is intended to securely hold a cardiovascular implantable electronic device (CIED) to create a stable environment when implanted in the body. Data on the utilization of this newly available product are limited. Objective In this study, our objective was to describe the specific profiles of patients who may benefit from the use of the CanGaroo® Envelope at the time of CIED implantation. Methods  The utilization of the CanGaroo® Envelope was assessed from January 2019 to October 2019 among a series of patients who were either undergoing de-novo CIED implantation or replacement. Results Among a total of 50 patients, the CanGaroo® Envelope was utilized in 15 (30%). Three distinct patient profiles were identified: profile 1: elderly patients with poor tissue turgor at risk of wound dehiscence or erosion; profile 2: patients with a history of previous device infection; and profile 3: patients at high risk of device infection having one or more of the following risk factors - chronic kidney disease, immunocompromised state, or diabetes mellitus. At a mean follow-up of 18 ±3 months, no CIED pocket erosion, dehiscence, or infection was noted. Conclusions Three distinct profiles of patients who could potentially benefit from the use of the CanGaroo® Envelope were identified by the implanting physicians. Long-term follow-up data, including infection and wound dehiscence rates, are necessary to further analyze the optimal utilization of the device.

Spatial and transmural properties of the reentrant ventricular tachycardia circuit in arrhythmogenic right ventricular cardiomyopathy: Simultaneous epicardial and endocardial recordings.

BACKGROUND: While advances in the characterization of the structural substrate in arrhythmogenic right ventricular cardiomyopathy (ARVC) have been made, the ventricular tachycardia (VT) circuit remains incompletely described. OBJECTIVE: The purpose of this study was to delineate the reentrant VT circuit with simultaneous epicardial and endocardial mapping (SEEM) in ARVC. METHODS: Twenty-three consecutive patients with ARVC and VT underwent SEEM at 4 centers between 2014 and 2020. Retrospective analysis was performed on combined isochronal activation maps. RESULTS: Of the 30 VT circuits, 24 were delineated with SEEM (956 [341-1843] endocardial points and 1763 [882-3054] epicardial points). The apex and outflow tract rarely harbored VT circuits, with 50% distributed in the inferior wall and 43% in the free wall. The entire tachycardia cycle length was recorded from the epicardium in 71% of circuits. In all circuits, a large proportion of the tachycardia cycle length was recorded from the epicardium relative to the endocardium. Localized epicardial reentry was observed in 35% of patients (14 mm × 15 mm), which was associated with smaller endocardial low voltage area (39 cm2 vs 104 cm2; P = .002) and preserved right ventricular ejection fraction (35% vs 25%; P = .046) compared with those with larger circuit dimensions. Seventy percent of termination sites were achieved from the epicardium. CONCLUSION: High-resolution recordings from both myocardial surfaces confirm a consistent predominance of epicardial participation during reentry in ARVC. Only the perivalvular inflow region of the "triangle of dysplasia" had a strong propensity to harbor VT circuits, with the greatest proportion located in the inferior wall. Localized epicardial reentry may be a manifestation of earlier stage disease with a relative paucity of endocardial substrate.

Circuit Determinants of Ventricular Tachycardia Cycle Length: Characterization of Fast and Unstable Human Ventricular Tachycardia.

BACKGROUND: Fast ventricular tachycardias (VTs) have historically been attributed to shorter path lengths with smaller reentrant circuit dimensions in animal models. The relationship between the dimensions of the reentrant VT circuit and tachycardia cycle length (TCL) has not been examined in humans. This study aimed to analyze the determinants of the rate of human VT with comparison of circuit dimensions and conduction velocity (CV) across a wide range of both stable and unstable VTs delineated by high-resolution mapping. METHODS: Fifty-four VTs with complete circuit delineation (>90% TCL) by high-resolution multielectrode mapping were analyzed in 49 patients (men, 88%; age, 65 years [58-71 years]; nonischemic, 47%). Fast VT was defined as TCL <333 milliseconds (rate >180 bpm). Unstable VT was defined by hemodynamic deterioration with an intrinsic mean arterial pressure <60 mm Hg during a sustained episode. RESULTS: The median TCL of VT was 365 milliseconds (306-443 milliseconds), and 24 fast VTs were characterized. A wide range of CVs was observed within the entrance (0.03-0.55 m/s), common pathway (0.03-0.77 m/s), exit (0.03-0.53 m/s), and outer loop (0.17-1.13 m/s). There were no significant differences in the median dimensions of the isthmus and path length between fast and slow VTs and between unstable and stable VTs. The outer loop CV was the only circuit component that correlated with TCL in both ischemic cardiomyopathy (r=-0.5, P=0.006) and nonischemic cardiomyopathy (r=-0.45, P=0.028). The duration of the longest diastolic electrogram was inversely correlated with the dimensions of common pathway (length: r=-0.46, P=0.001, width: r=-0.3, P=0.047) and predictive of rapid VT termination by a single radiofrequency application (r=-0.41, P=0.023). CONCLUSIONS: Because of a wide spectrum of CV observed within the reentrant path during human VT, the dimensions of the circuit were not predictive of VT cycle length. For the first time, we demonstrate that the CV of the outer loop, rather than isthmus, is the principal determinant of the rate of VT. The size of the circuit was similar between fast and slow VTs and between unstable and stable VTs. Long, continuous electrograms were indicative of spatially confined isthmus dimensions, confirmed by rapid termination of VT during radiofrequency delivery.

Late presentation of recurrent syncope after permanent pacemaker implantation due to Lead-Header malapposition.

Permanent pacemaker (PPM) malfunction due to electrical connection problems such as a loose set screw or lead-header malapposition is extremely rare. We present a patient with complete heart block (CHB) who had PPM malfunction and recurrent syncope, late (14 months) after initial implantation, which was caused by the ventricular lead pin disengagement from the header resulting in oversensing due to noise, pacing inhibition and recurrent syncope. PPM due to lead-header malapposition this late after device implantation has previously not been reported.

Indirect and Direct Evidence for 3-D Activation During Left Atrial Flutter: Anatomy of Epicardial Bridging.

OBJECTIVES: This study sought to describe arrhythmia characteristics using ultra-high density (UHD) mapping of macro-re-entrant left atrial flutter (LAFL) which propagate via epicardial bridging (EB), and highlight regional anatomy that poses challenges to ablation. BACKGROUND: Three-dimensional propagation via EB may contribute to the maintenance and complexity of LAFL. METHODS: UHD activation maps of macro-re-entrant LAFL created with a mini-electrode basket catheter were analyzed between June 2015 and March 2020. EB was defined as a region of wave front discontinuity with focal activation distal to an activation gap. Regions of EB were correlated with anatomic structures known to have specialized epicardial bundles. Direct evidence of EB was obtained via percutaneous epicardial access (n = 22) with simultaneous epicardial recordings during endocardial activation gaps. RESULTS: Among 159 patients who underwent LA endocardial procedures with UHD mapping, 43 patients with 47 macro-re-entrant LAFLs were included in this analysis. Evidence of EB was present in 38% of LAFLs. Four anatomic areas of EB were observed: coronary sinus (17%), vein of Marshall (28%), Bachmann's region (33%), and region of the septopulmonary bundle (22%). All 47 LAFLs were successfully ablated. Percutaneous epicardial mapping yielded direct evidence for EB in 9 patients with LAFL (41%). At 23 ± 13 months, 70% remained free from recurrent LAFL. CONCLUSIONS: In a selected population, UHD mapping demonstrates evidence of EB in 38% of cases of LAFL involving 4 distinct epicardial anatomic regions. Identification of discontinuous 3-dimensional activation patterns with attention to correlative regional LA anatomy may reduce the incidence of ablation failures for complex re-entry.

Periaortic ventricular tachycardia in structural heart disease: Evidence of localized reentrant mechanisms.

BACKGROUND: The mechanisms for scar-related ventricular tachycardia (VT) originating from the periaortic region remain incompletely characterized. OBJECTIVE: The purpose of this study was to map the circuits responsible for periaortic VT in high resolution. METHODS: Cases with periaortic VT (2016-2020) were analyzed to characterize the substrate and mechanisms with multielectrode mapping. Periaortic VT was defined as low-voltage and/or deceleration zones within 2 cm of the left ventriculoaortic junction with a corresponding critical site during VT. RESULTS: Forty-nine periaortic monomorphic VTs were analyzed in 30 patients (25% of all patients with nonischemic cardiomyopathy). Isolated periaortic substrate was observed in 27% of patients, with 73% having concomitant scar, most commonly in the mid-septum (47%). Deceleration zones were equally prevalent on the septal and lateral portions of the periaortic region (87% vs 73%; P = .19). During activation mapping of VT (tachycardia cycle length 392 ± 105 ms), localized reentrant patterns of activation (14 mm [10-17 mm] × 10 mm [7-14 mm]) were demonstrated in 63% and 37% of VTs showed centrifugal activation, consistent with a focal breakout pattern. Ninety-three percent of VTs fulfilled criteria for a reentrant mechanism. Sixty-five percent of reentrant circuits had endocardial activation gaps within the tachycardia cycle length (3-dimensional circuitry), which were associated with higher rates of recurrence as compared with 2-dimensional complete circuits at 1 year (73% vs 37%; P = .028). CONCLUSION: Periaortic VTs were observed in 25% of patients with nonischemic cardiomyopathy and scar-related VT. For the first time, localized reentry confined to this anatomically challenging region was demonstrated as the predominant mechanism by high-resolution circuit activation mapping.

Simultaneous Endocardial and Epicardial Delineation of 3D Reentrant Ventricular Tachycardia.

BACKGROUND: Mechanisms of scar-related ventricular tachycardia (VT) are largely based on computational and animal models that portray a 2-dimensional view. OBJECTIVES: The authors sought to delineate the human VT circuit with a 3-dimensional perspective from recordings obtained by simultaneous endocardial and epicardial mapping. METHODS: High-resolution mapping was performed during 97 procedures in 89 patients with structural heart disease. Circuits were characterized by systematic isochronal analysis to estimate the dimensions of the isthmus and extent of the exit region recorded on both myocardial surfaces. RESULTS: A total of 151 VT morphologies were mapped, of which 83 underwent simultaneous endocardial and epicardial mapping; 17% of circuits activated in a 2-dimensional plane, restricted to 1 myocardial surface. Three-dimensional activation patterns with nonuniform transmural propagation were observed in 61% of circuits with only 4% showing transmurally uniform activation, and 18% exhibiting focal activation patterns consistent with mid-myocardial reentry. The dimensions of the central isthmus were 17 mm (12 to 28 mm) × 10 mm (9 to 19 mm) with 55% exhibiting a minimal dimension of <1.5 cm. QRS activation was transmural in 63% and located 43 mm (34 to 52 mm) from the central isthmus. On the basis of 6 proposed definitions for epicardial VT, the prevalence of an epicardial circuit ranged from 21% to 80% in ischemic cardiomyopathy and 28% to 77% in nonischemic cardiomyopathy. CONCLUSIONS: A 2D perspective oversimplifies the electrophysiological circuit responsible for reentrant human VT and simultaneous endocardial and epicardial mapping facilitates inferences about mid-myocardial activation. Intricate activation patterns are frequently observed on both myocardial surfaces, and the epicardium is functionally involved in the majority of circuits. Human reentry may exist within isthmus dimensions smaller than 1 cm, whereas QRS activation is often transmural and remote from the critical isthmus target. A 3-dimensional perspective of the VT circuit may enhance the precision of ablative therapy and may support a greater role for adjunctive strategies and technology to address arrhythmogenic tissue harbored in the mid-myocardium and subepicardium.