Mechanism, diagnosis, and treatment of outflow tract tachycardia

Abstract

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.

Comparison of patients with early-phase arrhythmogenic right ventricular cardiomyopathy and right ventricular outflow tract ventricular tachycardia

“…Furthermore, early-phase ARVC patients had less frequent PVC and arrhythmias, with <2%PVC in early-phase ARVC compared with 18%PVC in RVOT-VT patients and less frequent nsVT. The relatively low number of PVC in early-phase ARVC and the frequent origin of PVC in the lateral free wall have also been reported by others 9,13,21,22 and emphasize that RVOT-VT is most likely in patients with very frequent monomorphic PVC originating from the septal part of the RVOT. Importantly, severe arrhythmias were more prevalent in ARVC compared with RVOT-VT, and all aborted cardiac arrests occurred only in ARVC patients, highlighting the different prognosis of these conditions.…”

“…In contrast, monomorphic origin of PVC and VT in RVOT-VT is thought to be a result of triggered activity. 9,10 …”

Electrocardiographic differentiation of idiopathic right ventricular outflow tract ectopy from early arrhythmogenic right ventricular cardiomyopathy

“…unrelated to structural heart disease) and carry a benign prognosis, 1 but in a minority of cases, they can be the expression of an underlying ARVC, a genetically determined cardiomyopathy characterized by desmosomal-protein dysfunction leading to progressive fibrofatty infiltration, ECG abnormalities, VAs, and regional and/or global ventricular dysfunction. 2,3,15 Although in the ‘overt’ phase of ARVC, differentiation with idiopathic RVOT-VT is usually straightforward; as ECG and echocardiographic abnormalities are prominent, desmosomal-gene mutation carriers with early ARVC phenotypic expression may show VEBs with a left bundle branch block/inferior axis configuration as the only feature of the disease, thus mimicking idiopathic RVOT arrhythmias.…”

“…The site of origin is also different in the two conditions: idiopathic RVOT VEBs usually arise from the endocardial and septal portions of the RVOT, whereas the source of ARVC-related VEBs is typically the epicardial layer of the anterior wall. 1,2,22,23 …”

“…1 In a minority of cases, however, those VEBs may be the expression of an underlying arrhythmogenic right ventricular cardiomyopathy (ARVC), a genetically determined heart muscle disease predisposing to ventricular arrhythmias (VA) and sudden death. 2,3 …”