Kaplan–Meier survival analysis and Cox regression analyses regarding right ventricular septal pacing: Data from Japanese pacemaker cohort

AbstractThe presented data were obtained from 982 consecutive patients receiving their first pacemaker implantation with right ventricular (RV) lead placement between January 2008 and December 2013 at two centers in Japan. Patients were divided into RV apical and septal pacing groups. Data of Kaplan–Meier survival analysis and Cox regression analysis are presented. Refer to the research article “Implications of right ventricular septal pacing for medium-term prognosis: propensity-matched analysis” (Mizukami et al., in press) [1] for further interpretation and discussion

Fibrosis, Connexin-43, and Conduction Abnormalities in the Brugada Syndrome.

BACKGROUND: The right ventricular outflow tract (RVOT) is acknowledged to be responsible for arrhythmogenesis in Brugada syndrome (BrS), but the pathophysiology remains controversial. OBJECTIVES: This study assessed the substrate underlying BrS at post-mortem and in vivo, and the role for open thoracotomy ablation. METHODS: Six whole hearts from male post-mortem cases of unexplained sudden death (mean age 23.2 years) with negative specialist cardiac autopsy and familial BrS were used and matched to 6 homograft control hearts by sex and age (within 3 years) by random risk set sampling. Cardiac autopsy sections from cases and control hearts were stained with picrosirius red for collagen. The RVOT was evaluated in detail, including immunofluorescent stain for connexin-43 (Cx43). Collagen and Cx43 were quantified digitally and compared. An in vivo study was undertaken on 6 consecutive BrS patients (mean age 39.8 years, all men) during epicardial RVOT ablation for arrhythmia via thoracotomy. Abnormal late and fractionated potentials indicative of slowed conduction were identified, and biopsies were taken before ablation. RESULTS: Collagen was increased in BrS autopsy cases compared with control hearts (odds ratio [OR]: 1.42; p = 0.026). Fibrosis was greatest in the RVOT (OR: 1.98; p = 0.003) and the epicardium (OR: 2.00; p = 0.001). The Cx43 signal was reduced in BrS RVOT (OR: 0.59; p = 0.001). Autopsy and in vivo RVOT samples identified epicardial and interstitial fibrosis. This was collocated with abnormal potentials in vivo that, when ablated, abolished the type 1 Brugada electrocardiogram without ventricular arrhythmia over 24.6 ± 9.7 months. CONCLUSIONS: BrS is associated with epicardial surface and interstitial fibrosis and reduced gap junction expression in the RVOT. This collocates to abnormal potentials, and their ablation abolishes the BrS phenotype and life-threatening arrhythmias. BrS is also associated with increased collagen throughout the heart. Abnormal myocardial structure and conduction are therefore responsible for BrS

Electrophysiological features of repetitive focal Purkinje ventricular arrhythmias originating from the proximal cardiac conduction system

Abstract Background Focal Purkinje ventricular arrhythmias (VAs) might originate from the vicinity of the proximal portion of the cardiac conducting system. This study aimed to clarify the features associated with focal Purkinje VAs originating from the proximal conduction system. Methods A total of 18 patients with focal Purkinje VAs undergoing radiofrequency catheter ablation (RFCA) were retrospectively examined and divided into the proximal type or the non‐proximal type. The proximal type was defined as having the origin at the proximal half of the interventricular septum, or the proximal half and the septal side of the anterior wall. The 12‐lead electrocardiogram and electrophysiological findings were investigated. Results Seven patients met criteria for proximal type of focal Purkinje VA. Out of the 7, 4 patients with proximal VAs had multiple QRS morphologies of VAs clinically, whereas out of 11 patients with non‐proximal VAs, only 1 had multiple morphologies (p = .047). VA QRS duration was shorter in the proximal type than in the non‐proximal type (111.2 ± 19.8 ms vs. 135.7 ± 17.7 ms; p = .003). The absolute axis difference between sinus rhythm and VA was smaller in the proximal type (80.4 ± 46.1°vs. 138.8 ± 59.6°; p = .014). The absolute axis difference ≤134° was useful in distinguishing the two types. Recurrence of VA was recorded in 3 proximal type patients and 3 non‐proximal type patients. No procedure‐related conduction block was observed. Conclusion A VA of absolute axis difference ≤134°, and multiple QRS morphologies of clinical VAs indicate a proximal origin. Focal Purkinje VAs from proximal origins can be suppressed by RFCA without severe conduction disturbance

Spontaneous Localized Persistent Atrial Fibrillation with an Exit Block Mimicking Atrial Tachycardia at the Left Posterior Wall

We describe a 37-year-old man with spontaneous localized atrial fibrillation (AF) with an exit block at the posterior wall of the left atrium (LA). The 12-lead ECG exhibited an atrial tachycardia-like pattern, with distinctive P waves and an isoelectric baseline between the P waves. The cycle length of the P waves ranged from 320 to 500 msec. While the fractionated and rapid deflections were recorded from the posterior wall of the LA, the rest of the atria and the coronary sinus exhibited discrete atrial potentials with irregular intervals. Radiofrequency energy applications to the surrounding tissue created complete isolation of the localized AF area, and the AF was terminated. Fibrillatory activation in the posterior wall of the LA can act as a driver as well as an initiator of atrial fibrillation

A Case with no Hemodynamic Benefit from Right Ventricular Anodal Capture during Biventricular Pacing

This case report describes a patient with a biventricular pacing system in whom right ventricular anodal capture had no hemodynamic benefit. While controlling the ventricular output, three morphologies of the paced QRS complex were obtained: right ventricular stimulation, biventricular stimulation, and biventricular pacing with additional stimulation from the anodal electrode in the right ventricle. While the QRS duration was 5 ms longer, the left ventricular systolic pressure and dP/dtmax during biventricular pacing without anodal capture of the right ventricle were greater than that during biventricular pacing with anodal capture. To avoid useless high output settings, the hemodynamic and clinical data should be compared with and without right ventricular anodal capture in each individual patient