Atrioventricular Conduction: Physiology and Autonomic Influences.

Atrioventricular (AV) nodal conduction is decremental and very prone to alterations in autonomic tone. Conduction through the His-Purkinje system (HPS) is via fast channel tissue and typically not that dependent on autonomic perturbations. Applying these principles, when the sinus rate is stable and then heart block suddenly occurs preceded by even a subtle slowing of heart rate, it typically is caused by increased vagal tone, and block occurs in the AV node. Heart block with activity strongly suggests block in the HPS. Enhanced sympathetic tone and reduced vagal tone can facilitate induction of both AV and atrioventricular node reentry.

Electrocardiography of Atrioventricular Block.

Delayed atrioventricular (AV) conduction most commonly occurs in the AV node, resulting from AH prolongation on an intracardiac electrocardiogram and PR prolongation on a surface electrocardiogram. AV conduction may be blocked in a 2:1 manner, with a normal PR interval and wide QRS suggesting infranodal disease, whereas a prolonged PR interval and narrow QRS are more suggestive of AV nodal disease. Block within the His is suspected when there is 2:1 AV block with normal PR and QRS intervals. Complete heart block occurs when the atrial rhythm is totally independent of a junctional or lower escape rhythm.

Ripple mapping in ventricular tachycardia substrate mapping and ablation of nonischemic ventricular tachycardia.

INTRODUCTION: Substrate-based ablation for ventricular tachycardia (VT) using Ripple map (RM) is an effective treatment strategy for patients with ischemic cardiomyopathy but has yet to be evaluated in patients with nonischemic cardiomyopathy (NICMO). The aim of this study is to determine the feasibility and effectiveness of an RM-based ablation for NICMO patients. METHODS AND RESULTS: This was a single-center, retrospective study including all NICMO patients undergoing VT ablation at St Vincent Hospital between January 1, 2018 and January 12, 2019. Retrospective RM analysis was performed on those that had a substrate-based ablation to identify the location and number of Ripple channels as well as their proximity to ablation lesions. Thirty-three patients met the inclusion criteria and had a median age of 65 (58, 73.5) with 15.2% of the population being female, and were followed for a median duration of 451 (217.5, 586.5) days. Of these patients, 23 (69.7%) had a substrate-based ablation with a median procedural duration of 196.4 (186.8, 339) min, 1946 (517, 2750) points collected per map, and 277 (141, 554) points were within the scar. Two (8.6%) procedural complications occurred, and 7 (30.4%) patients had VT recurrence during follow-up. RM analysis revealed an average of two Ripple channels and the patients without VT recurrence had ablation performed closer to the Ripple channels: 0 (0, 4.7) versus 14.3 (0, 23.5) cm; p = .02. CONCLUSION: An RM-based substrate ablation can be performed in NICMO patients and ablation within Ripple channels is a predictor of VT freedom.

Rapid detection of isthmus block and rhythm change using local electrogram changes during complex atrial flutter ablation.

AIMS: Multiple re-entry circuits may operate simultaneously in the atria in the form of dual loop re-entry using a common isthmus, or multiple re-entrant loops without a common isthmus. When two or more re-entrant circuits coexist, ablation of an individual isthmus may lead to a seamless transition (without significant changes in surface electrocardiogram, coronary sinus activation or tachycardia cycle length) to a second rhythm, and the isthmus block can go unnoticed. METHODS AND RESULTS: We hypothesize and subsequently illustrate in three patient cases, methods to rapidly identify a transition in the rhythm and isthmus block using local electrogram changes at the ablation site. CONCLUSION: Local activation sequence changes, electrogram timing, and the behaviour of pre-existing double potentials can reveal isthmus block promptly when rhythm transitions occur during ablation of multiloop re-entry tachycardias.

Diagnostic utility of early premature ventricular complexes in differentiating atrioventricular reentrant and atrioventricular nodal reentrant tachycardias.

BACKGROUND: His-refractory premature ventricular complexes perturbing a supraventricular tachycardia (SVT) establish the presence of an accessory pathway (AP). Earlier premature ventricular complexes (ErPVCs) may perturb SVTs but are considered nondiagnostic. OBJECTIVE: The purpose of this study was to test the hypothesis that an ErPVC will always show a difference >35 ms in its advancement of the next atrial activation during atrioventricular nodal reentrant tachycardia (AVNRT). During atrioventricular reentrant tachycardia (AVRT), a PVC delivered close to the circuit can result in greater advancement of atrial activation due to retrograde conduction via an AP. Thus, an AP response, defined as ErPVC (H1S2) advancing the subsequent atrial activation (A1-A2) more than this minimum difference (A1A2 ≤ H1S2+35 ms), establishes the presence of an AP. METHODS: Sixty-five consecutive patients with SVT were retrospectively evaluated. ErPVCs were defined when the ventricular pacing stimulus was >35 ms ahead of the His during tachycardia. RESULTS: Among the 65 cases, 43 were AVNRT and 22 AVRT. Fourteen AVRT cases had an AP response with a mean H1S2+35 ms of 336 ± 58 ms and A1A2 of 309 ± 51ms. No AVNRT cases had an AP response. The specificity of an AP response to ErPVC in predicting AVRT was 100%. CONCLUSION: An AP response to PVCs (A1A2 ≤ H1S2+35 ms) is 100% specific for the presence of an AP.

Atrioventricular Conduction: Physiology and Autonomic Influences.

Atrioventricular (AV) nodal conduction is decremental and very prone to alterations in autonomic tone. Conduction through the His-Purkinje system (HPS) is via fast channel tissue and typically not that dependent on autonomic perturbations. Applying these principles, when the sinus rate is stable and then heart block suddenly occurs preceded by even a subtle slowing of heart rate, it typically is caused by increased vagal tone, and block occurs in the AV node. Heart block with activity strongly suggests block in the HPS. Enhanced sympathetic tone and reduced vagal tone can facilitate induction of both AV and atrioventricular node reentry.

Electrocardiography of Atrioventricular Block.

Delayed atrioventricular (AV) conduction most commonly occurs in the AV node, resulting from AH prolongation on an intracardiac electrocardiogram and PR prolongation on a surface electrocardiogram. AV conduction may be blocked in a 2:1 manner, with a normal PR interval and wide QRS suggesting infranodal disease, whereas a prolonged PR interval and narrow QRS are more suggestive of AV nodal disease. Block within the His is suspected when there is 2:1 AV block with normal PR and QRS intervals. Complete heart block occurs when the atrial rhythm is totally independent of a junctional or lower escape rhythm.

Mechanism and interpretation of two-for-one response to premature atrial complexes during atrioventricular node re-entry tachycardia.

AIMS: The response to premature atrial complexes (PACs) during tachycardia has been shown to differentiate atrioventricular nodal re-entrant tachycardia (AVNRT) from focal junctional tachycardia (JT). His refractory PAC (HrPACs) perturbing the next His (resetting with fusion) is diagnostic of AVNRT and such a late PAC fusing with the native beat cannot reset the focal source of JT. Early PAC advancing the immediate His with continuation of tachycardia suggests JT but can also occur in AVNRT due to simultaneous conduction through the AV nodal fast and slow pathways [two-for-one response (TFOR)]. The objective of this study was to evaluate the incidence and mechanism of TFOR after early premature atrial complexes (ePACs) during AVNRT and to differentiate it from the known response to ePACs during JT. METHODS AND RESULTS: Typical AVNRT cases were diagnosed using standard criteria. We evaluated the responses to scanning PACs delivered during tachycardia in 100 patients undergoing AV node slow pathway modification for AVNRT. The responses to HrPACs and ePACs delivered from coronary sinus os or high right atrium were retrospectively reviewed. In 10 patients, ePACs advanced the immediate His with continuation of tachycardia. In all 10 cases, HrPACs advanced the next His, confirming AVNRT as the mechanism, and indicating a TFOR. CONCLUSION: A TFOR can occur in a small number of patients during AVNRT and is therefore not diagnostic of JT. However, HrPACs always perturbed the next His in these cases, confirming the diagnosis of AVNRT and allowing for differentiation from JT.

Differentiating Atrioventricular Reentry Tachycardia and Atrioventricular Node Reentry Tachycardia Using Premature His Bundle Complexes.

BACKGROUND: Current maneuvers for differentiation of atrioventricular node reentry tachycardia (AVNRT) and atrioventricular reentry tachycardia (AVRT) lack sensitivity and specificity for AVRT circuits located away from the site of pacing. We hypothesized that a premature His complex (PHC) will always perturb AVRT because the His bundle is obligatory to the circuit. Further, AVNRT could not be perturbed by a late PHC (≤20 ms ahead of the His) due to the retrograde His conduction time. Earlier PHCs can advance the AVNRT circuit but only by a quantity less than the prematurity of the PHC. METHODS: High-output pacing at the distal His location delivered PHCs. AVRT was predicted when late PHCs perturbed tachycardia or when earlier PHCs led to atrial advancement by an amount equal or greater than the degree of PHC prematurity. RESULTS: Among the 73 supraventricular tachycardias, the test accurately predicted AVRT (n=29) and AVNRT (n=44) in all cases. Late PHC advanced the circuit in all 29 AVRTs and none of the AVNRTs (sensitivity and specificity, 100%). With earlier PHCs, the degree of atrial advancement was equal or greater than the PHC prematurity in 26/29 AVRTs and none of the AVNRTs (90% sensitivity and 100% specificity). The mean prematurity of the PHC required to perturb AVNRT was 48 ms (range, 28-70 ms) and the advancement less than the prematurity of the PHC (mean, 32 ms; range, 18-54 ms). CONCLUSIONS: The responses to PHCs distinguished AVRT and AVNRT with 100% specificity and sensitivity.