Bundle Branch Block Inferior Axis Research Articles

Risk Stratification of Patients With Apparently Idiopathic Premature Ventricular Contractions: A Multicenter International CMRRegistry.

This study investigated the prevalence and prognostic significance of concealed myocardial abnormalities identified by cardiac magnetic resonance (CMR) imaging in patients with apparently idiopathic premature ventricular contractions (PVCs). The role of CMR imaging in patients with frequent PVCs and otherwise negative diagnostic workup is uncertain. This was a multicenter, international study that included 518 patients (age 44 ± 15 years; 57% men) with frequent (>1,000/24 h) PVCs and negative routine diagnostic workup. Patients underwent a comprehensive CMR protocol including late gadolinium enhancement imaging for detection of necrosis and/or fibrosis. The study endpoint was a composite of sudden cardiac death, resuscitated cardiac arrest, and nonfatal episodes of ventricular fibrillation or sustained ventricular tachycardia that required appropriate implantable cardioverter-defibrillator therapy. Myocardial abnormalities were found in 85 (16%) patients. Male gender (odds ratio [OR]: 4.28; 95% confidence interval [CI]: 2.06 to 8.93; p=0.01), family history of sudden cardiac death and/or cardiomyopathy (OR: 3.61; 95%CI: 1.33 to 9.82; p=0.01), multifocal PVCs (OR: 11.12; 95%CI: 4.35 to 28.46; p<0.01), and non-left bundle branch block inferior axis morphology (OR: 14.11; 95%CI: 7.35 to 27.07; p<0.01) were all significantly related to the presence of myocardial abnormalities. After a median follow-up of 67months, the composite endpoint occurred in 26 (5%) patients. Subjects with myocardial abnormalities on CMR had a higher incidence of the composite outcome (n=25; 29%) compared with those without abnormalities (n = 1; 0.2%; p<0.01). CMR can identify concealed myocardial abnormalities in 16% of patients with apparently idiopathicfrequent PVCs. Presence of myocardial abnormalities on CMR predict worse clinical outcomes.

Mechanism, diagnosis, and treatment of outflow tract tachycardia.

Idiopathic ventricular arrhythmia is a generic term for a spectrum of arrhythmias that occur in the absence of structural heart disease or ion channelopathy. These arrhythmias include monomorphic premature ventricular contractions (PVCs), nonsustained monomorphic ventricular tachycardia (VT), and sustained VT. Most idiopathic ventricular arrhythmias originate from the right and left ventricular outflow tracts and include sites accessed from the aortic sinuses of Valsalva. Outflow tract arrhythmia is identified by an electrocardiographic pattern consistent with a left bundle branch block inferior axis morphology. Characteristically, outflow tract VT is caused by cAMP-mediated triggered activity, and is terminated by administration of adenosine. Outflow tract arrhythmias are focal and, therefore, are readily amenable to definitive treatment with catheter-based radiofrequency ablation. Although arrhythmia might be associated with reversible PVC-mediated cardiomyopathy, and infrequently with PVC-induced polymorphic VT or ventricular fibrillation, prognosis is generally favourable.

Ubiquitous myocardial extensions into the pulmonary artery demonstrated by integrated intracardiac echocardiography and electroanatomic mapping: changing the paradigm of idiopathic right ventricular outflow tract arrhythmias.

Idiopathic ventricular arrhythmias of left bundle branch block inferior axis morphology are usually localized to the right ventricular outflow tract (RVOT), presumably below the pulmonic valve (PV). However, the PV location is usually not confirmed by direct visualization. Intracardiac echocardiography was used to visualize and tag the PV annulus, which was then integrated with 3-dimensional voltage maps of the RVOT. Distances were measured from the furthest extent of myocardial signal (bipolar voltage ≥1.5 mV) to the PV annulus. This was performed in 24 control patients and 24 prospective patients with RVOT arrhythmias. Myocardial signal beyond the PV was found in 92% of controls and 88% of RVOT arrhythmia patients (P=1.000). Average myocardial extension was further on the septal side than on the free wall side for control patients (5.6 mm; interquartile range [IQR], 3.6-7.7, versus 1.7 mm; IQR (-)0.1 to (+)4.0; P=0.002) and RVOT arrhythmia patients (5.7 mm; IQR, 2.7-7.7, versus 1.4 mm; IQR, (-)0.8 to (+)4.8; P=0.004). Eleven (46%) RVOT arrhythmia foci were localized beyond the valve in the pulmonary artery (median 8.2 mm above PV; IQR, 6.6-10.3 mm); these locations were confirmed as supravalvular by direct intracardiac echocardiography visualization. Myocardial voltage extension into the pulmonary artery in humans is ubiquitous and can be demonstrated in vivo using 3-dimensional integrated intracardiac echocardiography to localize the PV. These extensions frequently serve as origins of presumed RVOT arrhythmias; intracardiac echocardiography localization of the PV allows reclassification of these as pulmonary arterial arrhythmias.

Catheter Ablation for Right Ventricular Outflow Tract Ventricular Tachycardia Induced by Fever in a 7-Year-Old Girl

We report a 7-year old girl with ventricular tachycardia exacerbated by fever. She experienced her first symptom of palpitations during an influenza infection, and electrocardiogram showed wide QRS tachycardia of a left bundle branch block inferior axis pattern. We performed an electrophysiological study (EPS) for diagnosis, but the wide QRS tachycardia could not be induced. The wide QRS tachycardia recurred during upper respiratory tract infection with fever and ceased with lidocaine administration. Wide QRS tachycardia is characteristic of ventricular tachycardia (VT) exacerbated by fever. VT was not able to be induced at a normal temperature on EPS; however, when her temperature exceeded 38 degrees C, VT was easily induced and was accompanied by decreased blood pressure. Radiofrequency catheter ablation was performed in the right ventricular outflow tract (RVOT) just under the pulmonic valve, with a fractionated potential 29 ms before onset of V1 QRS. VT was terminated approximately 4 s after RF application, and then VT could not be induced with or without high fever. This is the first report of successful ablation treatment in RVOT VT exacerbated by fever in a young child.

Arrhythmogenic right ventricular dysplasia presenting as right ventricular outflow tract tachycardia

A case of a 51-year old male is presented. A left bundle branch block inferior axis tachycardia was manifest. At electrophysiological study this tachycardia was inducible and was ablated in the septal right ventricular outflow tract (RVOT). Two other tachycardias were identified both with right bundle branch block (RBBB) morphology raising the suspicion of diffuse pathology. Arrythmogenic right ventricular dysplasia (ARVD) was confirmed by right ventricular angiography and magnetic resonance imaging (MRI). An implantable cardioverter defibrillator (ICD) was implanted and an appropriate shock was later delivered.