Idiopathic monomorphic ventricular tachycardia and premature ventricular complexes (PVCs) commonly arise from the right and left ventricular outflow tracts (VOT). Their mechanism is most commonly triggered activity from delayed after-depolarizations and successful ablation is performed at the site of earliest endocardial activation. Re-entrant mechanisms have been rarely described. We report a case of an otherwise healthy patient who ultimately underwent six electro-physiology studies (EPS) and suffered numerous implantable cardiac defibrillator (ICD) discharges prior to the successful radiofrequency ablation (RFA) of two idiopathic VOT tachycardias. During the sixth EPS, a proximal aortogram demonstrated a left aortic sinus of valsalva (LASV) aneurysm. Subsequntly, a novel and successful RFA strategy of aneurysm isolation was undertaken. The presence of multiple clinical or inducible VT morphologies and the characterization of a VT as re-entrant should raise concerns that a complex arrhythmogenic substrate is present and defining the anatomy with angiography or an alternative imaging modality is essential in achieving a successful ablation strategy.
Sustained monomorphic ventricular tachycardia (SMMVT) is an arrhythmia that occurs almost exclusively in adolescents and young adults without structural heart disease. The mechanism of this arrhythmia has classically been attributed to triggered activity originating from the ventricular outflow tracts and management with radiofrequency ablation targeting the site of earliest endocardial activation is first line therapy [
A 34 years old male presented to an outlying emergency room in October 1995 with palpitations, dyspnea, and lightheadedness. An ECG revealed sustained monomorphic ventricular tachycardia at 230 beats/min with a left bundle branch block (LBBB) morphology, inferior axis, R wave transition in V3, and negative QRS complexes in lead 1, AVL and AVR (VT1,
After suffering an ICD discharge in April 2004, the patient elected to undergo a repeat EPS at an outside hospital. Programmed stimulation induced a 300 msec cycle length SMMVT with a left bundle branch block morphology, inferior axis, R wave transition in V4, positive QRS complexes in lead 1 and AVL, and a negative QRS complexes in AVR (VT2,
In February 2006, the patient returned to the emergency department with palpitations and a 12 lead ECG demonstrating sustained VT1. After cardioversion the patient was taken to the EP lab for his fifth EP study with the intent to map and ablate VT1. Decremental pacing from the RV apex while on isoproterenol induced VT1. Activation mapping with the CARTO electroanatomic mapping system (Biosense Webster, Diamond Bar, CA) demonstrated a broad area of early activation (35 msec prior to QRS onset) 0.5 cm - 1 cm below the aortic valve along the aorto-mitral continuity. The RVOT, coronary sinus, and aortic sinuses did not demonstrate early activation. Bipolar pacing from the RVOT and LVOT did not fulfill criteria for manifest entrainment. The arrhythmia could not be terminated with burst pacing.
Twelve mg and 18 mg boluses of adenosine transiently lengthened the underlying atrial cycle length but had no effect on the VT cycle length. RFA lesions delivered at the earliest site of endocardial activation along the aorto-mitral continuity as described above (12 lesions for a total of 2 minutes and 37 seconds via a Biosense Webster 4 mm tip, non-irrigated, D-curve, 60 degree Celsius temperature limited ablation catheter at 50 watts) had no effect on the tachycardia. The patient was subsequently sedated and cardioverted with a 200 joule synchronized shock. Bipolar pace mapping in the area of earliest endocardial activation was performed with no match in QRS morphology. At this point, while still on an isoproterenol drip, spontaneous VT1 recurred, requiring a second 200 joule shock. After discussing the results of the EP study with the patient once awake, it was decided to give a trial of more aggressive beta blocker therapy.
Within months, the patient experienced a recurrence of VT1 requiring cardioversion at an outside hospital. During a sixth EPS, the aortic sinuses were more thoroughly mapped. In this study, a 4 mm tip, non-irrigated, 60 degree Celsius temperature limited ablation catheter was advanced deep into the left aortic sinus of valsalva (LASV). Fractionated electrograms extending into early diastole were noted during sinus rhythm (
application on 3 separate occasions. However, decremental pacing was able to re-induce both VT1 and VT2. Subsequently, a limited proximal aortogram was performed using the Judkins left catheter revealing a small LASV aneurysm (
The mechanism of the majority of outflow tract ventricular tachycardias is due to increased intracellular cAMP levels and abnormal calcium handling, resulting in delayed after-depolarizations and consequent triggered activity [
LBBB, inferior axis VT a second VT with right bundle branch block (RBBB) and inferior axis was noted clinically and induced by programed stimulation. Activation mapping of the RVOT during the LBBB tachycardia revealed a mid-diastolic potential and pacing from this site revealed concealed entrainment with a stimulus to QRS of 100 - 150 msec. After ablation at this site, neither the LBBB nor the RBBB, inferior axis ventricular tachycardia could be induced. Yamada et al. described a patient with an inferior axis, LBBB VT that was induced via programmed stimulation [
underlying tachycardia mechanism is unclear.
Although outflow tract VT is commonly referred to as “normal heart ventricular tachycardia” because of the uniformly preserved biventricular size and function, subtle structural abnormalities such as congenital outflow tract, basal LV, or aortic sinus of valsalva aneurysms have been described and implicated in arrhythmia pathogenesis [
Our case is the first to describe ventricular tachycardia originating from an aortic sinus cusp aneurysm successfully treated with aneurysm isolation by RFA. The mechanism of the ventricular tachycardia was likely re-entrant with VT1 and VT2 representing either multiple exit sites from a common isthmus, two distinct isolated isthmuses, or bi-directional propagation across a common isthmus. The tachycardia was induced with decremental pacing and fractionated electrograms were recorded within the aneurysm extending into early diastole during sinus rhythm and throughout diastole during ventricular tachycardia. Adenosine was ineffective in terminating the arrhythmia or prolonging the tachycardia cycle length. Manifest entrainment could not be demonstrated from the RV apex or the RV outflow tract. However, this is not surprising considering the presumably small re-entrant circuit and isolated isthmus within the left aortic sinus cusp aneurysm. The case is novel and clinically important for two reasons. First, although rare, outflow tract VT can be associated with subtle structural abnormalities. The presence of multiple VT morphologies (either seen clinically or induced in the EP lab) or characterization as a re-entrant mechanism should raise concern that a complex arrhythmogenic substrate is present and technical difficulty with RFA will be more likely. In this setting, defining the local anatomy with angiography or an alternative imaging modality is essential in performing a successful ablation. In our case, it was only with the 6th EP study that the proximal aortogram was taken and the left aortic sinus cusp aneurysm was identified. Secondly, this case demonstrates the novel use of arrhythmogenic substrate isolation in treating outflow tract VT. Such a methodology has potential application whenever catheter accessibility is limited or where direct RF application is deemed too risky. In our case, a continuous line of RF ablation lesions was placed around the orifice of the left aortic sinus cusp aneurysm. The focal origin of the VT or the VT’s isolated isthmus, in the case of a re-entrant mechanism, was electrically isolated within the aneurysm. Our patient has remained arrhythmia free for the last 7 years without anti-arrhythmic or beta-blocker therapy.