Outflow tract ventricular tachycardias (OTVT) are the most common cause of idiopathic ventricular tachycardias followed by fascicular tachycardias
Structural heart disease must be ruled out as OTVT tachycardias can manifest in patients with underlying heart disease such as myocardial infarction, arrhythmogenic cardiomyopathy or sarcoidosis
In the absence of structural heart disease the prognosis is good
Management of OTVT differs in RVOT and LVOT tachycardias
The region of outflow tracts is anatomically complex and many structures can give rise to arrhythmias and precise determination of the origin may be possible only during electrophysiological study
two types of OTVT can be distinguished: - Paroxysmal OTVT is typically triggered by exercise or stress - Repetitive monomorphic OTVT usually occurs at rest and presents with runs of nonsustained VTs interrupted by sinus beats
Right Ventricular Outflow Tract VT/PVC
RVOT is the most common origin of idiopathic VT, it represents approximately 70% of VTs in patients with structurally normal hearts and 10% of all VTs
RVOT VT typically presents in patients 20-50 years old and affects more frequently women
RVOT VT can also occur in patients with arrhythmogenic cardiomyopathy as the right ventricle is the most common localisation (ARVC arrhythmias do not terminate with adenosine)
Clinical presentation can vary and it can be asymptomatic or present with palpitations or syncope. RVOT VT presents with syncope more often than LVOT VT
Localising RVOT VT may be difficult due to the proximity of several structures acting as potential origin of outflow tract VTs (RVOT, LVOT, cusps of aortic valve, great cardiac veins, epicardial myocardium, aortomitral continuity and rarely pulmonary artery)
Apart from typical features of a VT, the following ECG features are used to localise RVOT VT/PVCs: - LBBB morphology - Inferior axis - Anterior sites in the RVOT show a dominant Q-wave or a qR complex in lead I and a QS complex in aVL. Pacing at the posterior sites produces a dominant R-wave in lead I, QS or R-wave in aVL and an early precordial transition (R/S = 1 by V3) - Precordial transition in V3 or later and shorter R wave duration in V1 and V2 (distinguishes RVOT origin from LVOT)
If multiple morphologies are present, scar related VT as in arrhythmogenic cardiomyopathy should be suspected
Outflow tract VT can usually be terminated by either vagal manoeuvres, adenosine or verapamil
In symptomatic patients with RVOT VT or PVCs, catheter ablation can be highly effective and is a recommended treatment (targeting the earliest high-frequency Purkinje potential during VT)
Patients with moderate symptoms can be treated with oral verapamil (120 mg/day to 480 mg/day)
runs of non sustained VT from RVOT with interposed sinus beats
inferior axis (positive QRS complex in II, III and aVF)
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