Increased myocardial native T1 relaxation time in patients with nonischemic dilated cardiomyopathy with complex ventricular arrhythmia.

PURPOSE: To study the relationship between diffuse myocardial fibrosis and complex ventricular arrhythmias (ComVA) in patients with nonischemic dilated cardiomyopathy (NICM). We hypothesized that NICM patients with ComVA would have a higher native myocardial T1 time, suggesting more extensive myocardial diffuse fibrosis. MATERIALS AND METHODS: We prospectively enrolled NICM patients with a history of ComVA (n = 50) and age-matched NICM patients without ComVA (n = 57). Imaging was performed at 1.5T with a protocol that included cine magnetic resonance imaging (MRI) for left ventricular (LV) function, late gadolinium enhancement (LGE) for focal scar, and native T1 mapping for diffuse fibrosis assessment. RESULTS: Global native T1 time was significantly higher in patients with NICM with ComVA when compared to patients with NICM without ComVA (1131 ± 42 vs. 1107 ± 45 msec, P = 0.006), and this finding remained after excluding segments with scar on LGE (1124 ± 36 vs. 1102 ± 44 msec, P = 0.006). Native T1 was similar in NICM patients with and without the presence of LGE (1121 ± 39 vs. 1117 ± 48 msec, P = 0.68) and mildly correlated with LV end-diastolic volume index (r = 0.27, P = 0.005), LV end-systolic volume index (r = 0.24, P = 0.01), and LV ejection fraction (r = -0.28, P = 0.003). Native T1 value for each 10-msec increment was an independent predictor of ComVA (odds ratio 1.14, 95% confidence interval 1.03-1.25; P = 0.008) beyond LV function and LGE. CONCLUSION: NICM patients with ComVA have higher native T1 compared to NICM without any documented ComVA. Native myocardial T1 is independently associated with ComVA, after adjusting for LV function and LGE. LEVEL OF EVIDENCE: 2 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2018;47:779-786. In memoriam: The authors are grateful for Dr. Josephson's inspiring guidance and contributions to this study.

Atrial Substrate and Triggers of Paroxysmal Atrial Fibrillation in Patients With Obstructive Sleep Apnea.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with atrial remodeling, atrial fibrillation (AF), and increased incidence of arrhythmia recurrence after pulmonary vein (PV) isolation. We aimed to characterize the atrial substrate, including AF triggers in patients with paroxysmal AF and OSA. METHODS AND RESULTS: In 86 patients with paroxysmal AF (43 with ≥moderate OSA [apnea-hypopnea index ≥15] and 43 without OSA [apnea-hypopnea index <5]), right atrial and left atrial voltage distribution, conduction velocities, and electrogram characteristics were analyzed during atrial pacing. AF triggers were examined before and after PV isolation and targeted for ablation. Patients with OSA had lower atrial voltage amplitude (right atrial, P=0.0005; left atrial, P=0.0001), slower conduction velocities (right atrial, P=0.02; left atrial, P=0.0002), and higher prevalence of electrogram fractionation (P=0.0001). The areas of atrial abnormality were consistent among patients, most commonly involving the left atrial septum (32/43; 74.4%). At baseline, the PVs were the most frequent triggers for AF in both groups; however, after PV isolation patients with OSA had increased incidence of additional extra-PV triggers (41.8% versus 11.6%; P=0.003). The 1-year arrhythmia-free survival was similar between patients with and without OSA (83.7% and 81.4%, respectively; P=0.59). In comparison, control patients with paroxysmal AF and OSA who underwent PV isolation alone without ablation on extra-PV triggers had increased risk of arrhythmia recurrence (83.7% versus 64.0%; P=0.003). CONCLUSIONS: OSA is associated with structural and functional atrial remodeling and increased incidence of extra-PV triggers. Elimination of these triggers resulted in improved arrhythmia-free survival.

Paroxysmal atrioventricular block: Electrophysiological mechanism of phase 4 conduction block in the His-Purkinje system: A comparison with phase 3 block.

BACKGROUND: Paroxysmal atrioventricular (A-V) block is relatively rare, and due to its transient nature, it is often under recognized. It is often triggered by atrial, junctional, or ventricular premature beats, and occurs in the presence of a diseased His-Purkinje system (HPS). Here, we present a 45-year-old white male who was admitted for observation due to recurrent syncope and near-syncope, who had paroxysmal A-V block. The likely cellular electrophysiological mechanisms(s) of paroxysmal A-V block and its differential diagnosis and management are discussed. METHODS: Continuous electrocardiographic monitoring was done while the patient was in the cardiac unit. RESULTS: Multiple episodes of paroxysmal A-V block were documented in this case. All episodes were initiated and terminated with atrial/junctional premature beats. The patient underwent permanent pacemaker implantation and has remained asymptomatic since then. CONCLUSIONS: Paroxysmal A-V block is rare and often causes syncope or near-syncope. Permanent pacemaker implantation is indicated according to the current guidelines. Paroxysmal A-V block occurs in the setting of diseased HPS and is bradycardia-dependent. The detailed electrophysiological mechanisms, which involve phase 4 diastolic depolarization, and differential diagnosis are discussed.

Interlead heterogeneity of R- and T-wave morphology in standard 12-lead ECGs predicts sustained ventricular tachycardia/fibrillation and arrhythmic death in patients with cardiomyopathy.

INTRODUCTION: Nonuniformities in depolarization and repolarization morphology are critical factors in ventricular arrhythmogenesis. METHODS AND RESULTS: We assessed interlead R-wave heterogeneity (RWH) and T-wave heterogeneity (TWH) in standard 12-lead electrocardiograms (ECGs) using second central moment analysis. This technique quantifies variance about the mean morphology of beats in adjoining precordial leads, V4 , V5 , and V6 in this study. The study was conducted in 120 consecutive patients without an apparent reversible trigger for ventricular tachycardia (VT), recent myocardial infarction, or active ischemia, who presented for electrophysiologic study, implantable cardioverter defibrillator (ICD) placement, or generator change at our institution from 2008 to 2011. Primary outcome was sustained VT/ventricular fibrillation (VF) or appropriate ICD therapies. Secondary outcome was arrhythmic death or resuscitated cardiac arrest. Cutpoints for elevated RWH (>160 µV) and TWH (>80 µV) identified 67% of primary outcome cases and 85% of secondary outcome cases. Cardiomyopathy patients who met the primary outcome (n = 42) had significantly higher TWH than those who did not (n = 28) (TWH: 95 ± 11 µV vs. 44 ± 9 µV, P < 0.002). Likewise, cardiomyopathy patients who met secondary outcome (N = 13) had VT/VF during follow-up and also had significantly higher TWH than survivors (N = 57) (TWH: 105 ± 24 µV vs. 67 ± 8 µV, P < 0.002). Kaplan-Meier analysis revealed significant differences in arrhythmia-free survival (P = 0.012) and total survival (P = 0.011) among cardiomyopathy patients with (n = 37) compared to without (n = 33) elevated RWH and/or TWH independent of age, sex, and left ventricular ejection fraction (LVEF). CONCLUSION: Interlead RWH and TWH in 12-lead ECGs predict sustained ventricular arrhythmia, appropriate ICD therapies, and arrhythmic death or cardiac arrest in cardiomyopathy patients independent of LVEF and other standard variables.

Electrophysiological Testing for the Investigation of Bradycardias.

In this article we review the role of electrophysiological testing in patients presenting with bradycardia due to sinus node or atrioventricular node disease. In sinus bradycardia the role of electrophysiology studies is not established. In AV conduction disturbances, an electrophysiology study may be necessary both for the establishment of atrioventricular block as the main cause of symptoms, and for identification of the anatomic site of block that may dictate the potential need of permanent pacing.

Mahaim Accessory Pathways.

The term Mahaim conduction is conventionally used to describe decrementally conducting connections between the right atrium or the AV node and the right ventricle in or close to the right bundle branch. Although such pathways are rare, their unique properties make their diagnosis and treatment cumbersome. In this article we review the published evidence, and discuss the electrocardiographic and electrophysiological characteristics as well as the anatomy and origin of these fibres.

Catheter ablation vs. antiarrhythmic drug therapy in patients with symptomatic atrioventricular nodal re-entrant tachycardia: a randomized, controlled trial.

AIMS: To conduct a randomized trial in order to guide the optimum therapy of symptomatic atrioventricular nodal re-entrant tachycardia (AVNRT). METHODS AND RESULTS: Patients with at least one symptomatic episode of tachycardia per month and an electrophysiologic diagnosis of AVNRT were randomly assigned to catheter ablation or chronic antiarrhythmic drug (AAD) therapy with bisoprolol (5 mg od) and/or diltiazem (120-300 mg od). All patients were properly educated to treat subsequent tachycardia episodes with autonomic manoeuvres or a 'pill in the pocket' approach. The primary endpoint of the study was hospital admission for persistent tachycardia cardioversion, during a follow-up period of 5 years. Sixty-one patients were included in the study. In the ablation group, 1 patient was lost to follow-up, and 29 were free of arrhythmia or conduction disturbances at a 5-year follow-up. In the AAD group, three patients were lost to follow-up. Of the remainder, 10 patients (35.7%) continued with initial therapy, 11 patients (39.2%) remained on diltiazem alone, and 7 patients (25%) interrupted their therapy within the first 3 months following randomization, and subsequently developed an episode requiring cardioversion. During a follow-up of 5 years, 21 patients in the AAD group required hospital admission for cardioversion. Survival free from the study endpoint was significantly higher in the ablation group compared with the AAD group (log-rank test, P < 0.001). CONCLUSIONS: Catheter ablation is the therapy of choice for symptomatic AVNRT. Antiarrhythmic drug therapy is ineffective and not well tolerated.

Catheter Ablation of Atypical Atrioventricular Nodal Reentrant Tachycardia.

BACKGROUND: Because of its low prevalence, data on atypical atrioventricular nodal reentrant tachycardia (AVNRT) are scarce, and the optimal ablation method has not been established. Our study aimed at assessing the efficacy and safety of conventional slow pathway ablation, as applied for typical cases, in atypical AVNRT. METHODS: We studied 2079 patients with AVNRT subjected to slow pathway ablation. In 113 patients, mean age 48.5±18.1 years, 68 female, atypical AVNRT or coexistent atypical and typical AVNRT without other concomitant arrhythmia was diagnosed. Ablation data and outcomes were compared with a group of age- and sex-matched control patients with typical AVNRT. RESULTS: Fluoroscopy and radiofrequency current delivery times were not different in the atypical and typical groups, 20.3±12.2 versus 20.8±12.9 minutes (P=0.730) and 5.9±5.0 versus 5.5±4.5 minutes (P=0.650), respectively. Slow pathway ablation was accomplished from the right septum in 110 patients, and from the left septum in 3 patients, in the atypical group. There was no need for additional ablation lesions at other anatomic sites, and no cases of atrioventricular block were encountered. Recurrence rates of the arrhythmia were 5.6% in the atypical (6/108 patients) and 1.8% in the typical (2/111 patients) groups in the next 3 months following ablation (P=0.167). CONCLUSIONS: Conventional ablation at the anatomic area of the slow pathway is the therapy of choice for symptomatic AVNRT, regardless of whether the typical or atypical form is present.

Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia.

Atrioventricular nodal reentrant tachycardia (AVNRT) should be classified as typical or atypical. The term 'fast-slow AVNRT' is rather misleading. Retrograde atrial activation during tachycardia should not be relied upon as a diagnostic criterion. Both typical and atypical atrioventricular nodal reentrant tachycardia are compatible with varying retrograde atrial activation patterns. Attempts at establishing the presence of a 'lower common pathway' are probably of no practical significance. When the diagnosis of AVNRT is established, ablation should be only directed towards the anatomic position of the slow pathway. If right septal attempts are unsuccessful, the left septal side should be tried. Ablation targeting earliest atrial activation sites during typical atrioventricular nodal reentrant tachycardia or the fast pathway in general for any kind of typical or atypical atrioventricular nodal reentrant tachycardia, are not justified. In this review we discuss current concepts about the tachycardia circuit, electrophysiologic diagnosis, and ablation of this arrhythmia.

Directional Influences of Ventricular Activation on Myocardial Scar Characterization: Voltage Mapping With Multiple Wavefronts During Ventricular Tachycardia Ablation.

BACKGROUND: The effects of varying the wavefront of activation on ventricular scar characterization has not been systematically assessed. METHODS AND RESULTS: Patients referred for ablation of scar-related ventricular tachycardia underwent voltage maps during a minimum of 2 wavefronts of activation. The bipolar and unipolar low-voltage areas were compared, and direct electrogram analysis was performed in regions where discrepancies were seen. Concordance between wavefronts was measured by calculating percentage of overlap between maps. Sixty endocardial voltage maps (360±147 points) were performed in 29 patients during 2 distinct wavefronts, with 3 wavefronts in 7 patients. With median bipolar and unipolar low-voltage areas of 37 and 116 cm(2), respectively, 22% and 14% variability in median scar area was observed with a different activation wavefront. Concordance between wavefronts was lower in patients with mixed scar compared to those with dense scar (52% [interquartile range, 29%-70%] versus 84% [interquartile range, 71%-87%]), with septal scars exhibiting the lowest concordance [(27% (interquartile range, 21%-56%)]. Among 16 critical sites for ventricular tachycardia, 3 (18%) were in a discordant region of scar, with one of the wavefronts showing voltage >1.5 mV. CONCLUSIONS: Significant differences in bipolar and unipolar low-voltage characterization of scar were observed with different ventricular activation wavefronts, particularly in septal locations and in patients without dense scar. In patients with a paucity of dense, low-voltage regions identified during substrate mapping, an alternate activation wavefront may increase the sensitivity to detect arrhythmogenic substrate and critical sites for ventricular tachycardia.

High-Resolution Mapping of Postinfarction Reentrant Ventricular Tachycardia: Electrophysiological Characterization of the Circuit.

BACKGROUND: In vivo description of ventricular tachycardia (VT) circuits is limited by insufficient spatiotemporal resolution. We used a novel high-resolution mapping technology to characterize the electrophysiological properties of the postinfarction reentrant VT circuit. METHODS: In 15 swine, myocardial infarction was induced by left anterior descending artery balloon occlusion. Animals were studied 6 to 8 weeks after myocardial infarction. Activation mapping of VTs was performed by using the Rhythmia mapping system. Activation time was based on a combination of bipolar and unipolar electrograms. The response to overdrive pacing from different zones of the circuit was examined. RESULTS: A total of 56 monomorphic VTs were induced (3.8±2.1 per animal). Among these, 21 (37.5%) were hemodynamically stable and allowed mapping of the circuit. Isthmuses were 16.4±7.2 mm long and 7.4±2.8 mm wide. Conduction velocities were slowest at the inward curvature into the isthmus entrance (0.28±0.2 m/s), slightly faster at the outward curvature exit (0.40±0.3 m/s) and nearly normal at the central isthmus (0.62±0.2 m/s). In 3 animals, 2 VT morphologies with opposite axes sharing the same isthmus were mapped. Conduction velocities within the shared isthmus were dependent on the activation vector, consistently slower at the proximal curvature. Overdrive pacing from isthmus sites determined by activation mapping was consistent with entrainment criteria for isthmus. However, dimensions of the isthmus defined by entrainment exceeded dimensions of the isthmus measured by activation mapping by 32±18%. CONCLUSIONS: In postinfarction reentrant VT, conduction velocities are slowest at the proximal and distal curvatures. Entrainment mapping overestimates the true size of the isthmus. High-resolution activation mapping of VT may better guide ablation therapy.