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A subgroup of right bundle branch block (RBBB) patients may exhibit a significant left ventricular (LV) activation delay. We evaluated echocardiography in a non-ischemic heart failure patient whose QRS morphology changed from left bundle branch block (LBBB) to atypical RBBB. The septum to posterior wall motion delay (SPWMD) measured using the M-mode was 196 ms while the patient presented with LBBB but decreased to 32 ms after the morphology changed to RBBB. These changes were also associated with delayed appearance of the septal displacement peak. Speckle tracking longitudinal strain was evaluated using three standard apical views after the morphology changed to RBBB. The LV contraction initially appeared in the basal inferior wall and there was delayed anterior wall contraction. The LV contraction pattern in our patient changed when the QRS morphology changed to atypical RBBB. A specific LV contraction sequence observed in atypical RBBB may reflect a significant LV activation delay between the inferior and anterior wall.

Hideyuki Hara,1 Takako Nagata,2 Hiroshi Ito,1 Shinichi Niwano,2 Junya Ako2 1Division of Cardiology, Numazu City Hospital, Numazu, Japan; 2Department of Cardiovascular Medicine, Kitasato University School of Medicine, Sagamihara, JapanCorrespondence: Hideyuki HaraDivision of Cardiology, Numazu City Hospital, Aza-Harunoki 550, Higashi-Shiiji, Numazu City, Shizuoka Prefecture 410-0302, JapanTel +81-55-924-5100Fax +81-55-924-5133Email hideyuki@med.kitasato-u.ac.jpAbstract: A subgroup of right bundle branch block (RBBB) patients may exhibit a significant left ventricular (LV) activation delay. We evaluated echocardiography in a non-ischemic heart failure patient whose QRS morphology changed from left bundle branch block (LBBB) to atypical RBBB. The septum to posterior wall motion delay (SPWMD) measured using the M-mode was 196 ms while the patient presented with LBBB but decreased to 32 ms after the morphology changed to RBBB. These changes were also associated with delayed appearance of the septal displacement peak. Speckle tracking longitudinal strain was evaluated using three standard apical views after the morphology changed to RBBB. The LV contraction initially appeared in the basal inferior wall and there was delayed anterior wall contraction. The LV contraction pattern in our patient changed when the QRS morphology changed to atypical RBBB. A specific LV contraction sequence observed in atypical RBBB may reflect a significant LV activation delay between the inferior and anterior wall.Keywords: left bundle branch block, right bundle branch block, masquerading bundle branch block, bilateral bundle branch block, activation delay, longitudinal strain

The sites of atrial fibrillation genesis and electrophysiological parameters of the atria were evaluated in 24 patients with Wolff-Parkinson-White (WPW) syndrome with induced atrial fibrillation in an electrophysiologic study. The twenty-four patients, 8 females and 16 males had a mean age of 42± 16 years. Atrial electrogram was recorded at three atrial sites during the initiation of atrial fibrillation: the high right atrium (HRA), the His bundle electrogram recording site (HBE), and the coronary sinus (CS). The site of atrial fibrillation genesis was determined as the recording site that first showed fragmented atrial electrogram at the time atrial fibrillation occurred. Atrial fibrillation was generated from the HRA site in 15/24 patients, the HBE site in 6/24 patients, and the CS site in 3 patients. Atrial effective refractory period (AERP), atrial wave duration at the HRA site (A1), prolongation of atrial wave during premature beat at the HRA site (%A2/A1), prolongation of atrial wave duration at the CS site during retrograde excitation of the atrium (% Cret/Cant), antegrade and retrograde effective refractory period of the accessory pathway (Kant-ERP, KretERP), and wavelength index (WLI) were evaluated in each patient. Only the %A2/A1 and WLI were significantly different among the groups with different sites of atrial fibrillation genesis. Atrial vulnerability of the HRA site was highest in patients with HRA genesis of atrial fibrillation as represented by the largest %A2/A1 and shortest WLI at the HRA recording site. Although different types of atrial fibrillation might occur, the HRA site is considered to play an important role in initiating atrial fibrillation in patients with WPW syndrome.

Implantable cardioverter-defibrillators (ICD) were implanted in 11 patients with drug refractory ventricular tachyarrhythmias. Both ventricular fibrillation (VF) and sustained ventricular tachycardia (VT) were documented in 4 of the 11 patients, and VF or VT was observed in the other 4 and 3 patients, respectively. The mean left ventricular ejection fraction of the 11 patients was 40±22%; underlying heart diseases were observed in 9 patients, old myocardial infarction in 4 patients, and dilated cardiomyopathy in 5 patients. Transvenous ICD was implanted in 10 patients (91%), but because of a high defibrillation threshold, two epicardial patch electrodes were necessary in the remaining one patient. During the operative procedure, no complications were observed except for an episode of vasospastic angina in one patient with normal coronary arteries. In 3 patients with severe left ventricular dysfunction, VT with clinical QRS morphology was frequently observed within a few days after surgery, and additional antiarrhythmic drug therapy and changes in the detection mode of VF were required. Subclavian crash syndrome was noticed 26 months after ICD implantation in one patient. During the follow-up periods of 6 to 54 months (the mean being 28.7 ± 20.6 months), VT and/or VF recurred in 6 of the 11 patients, and these tachycardias were terminated by appropriate ICD treatment. One patient died due to refractory heart failure 7 months after ICD implantation. Transvenous implantation was easier and judged to be the first choice procedure for ICD implantation. ICD is a feasible therapy for drug refractory ventricular tachyarrhythmias, but special management is required to control VT/VF by antiarrhythmic drug or to detect complications.