We present a novel case of a 42-year-old male with an unusual substrate for right ventricular outflow tract (RVOT) tachycardia – post-cardiac surgery-associated RVOT sternal adhesion (confirmed on cardiovascular MRI [CMR] pre-ablation).
He presented with palpitations and presyncope, which correlated with ventricular tachycardia (VT). His medical history included percutaneous closure of an ostium secundum atrial septal defect (ASD) 11 years prior. This was complicated by device erosion requiring open-heart surgical device extraction and ASD repair 3 weeks later. His pre-operative 12-lead electrocardiogram (ECG) was normal (Figure 1A). His post-surgery sinus rhythm (SR) ECG demonstrated T-wave inversion across the precordial and inferior leads (Figure 1B).
Two years following this, he developed presyncope with non-sustained VT and was started on amiodarone. Subsequent amiodarone-induced thyroid dysfunction necessitated discontinuation of amiodarone 8 years later. His drug history included bisoprolol (2.5 mg) and levothyroxine (125 µg).
He presented with sustained VT this year, with the VT morphology suggestive of RVOT origin (left bundle branch block and inferior QRS axis, Figure 2 and 3A).
His cardiovascular MRI (CMR, Figure 3B) demonstrated no myocardial infiltration, infarction, or fibrosis, and was not consistent with arrhythmogenic right ventricular cardiomyopathy (ARVC) by the modified Task Force criteria.1
However, the entire RVOT (30 mm in length) and RV anterior wall were thickened and adhered to the sternum (Figure 3B and Videos 1, 2, and 3) with associated akinesia and moderate RV systolic impairment (left ventricular systolic function was normal). He was transferred to the coronary care unit and underwent RVOT VT ablation.
The procedure was performed under conscious sedation with the EnSite Precision Cardiac Mapping System (Abbott). High-density endocardial mapping of the RV was performed with the Advisor HD Grid Mapping Catheter, Sensor Enabled (Abbott). Epicardial mapping was not performed in view of his sternotomy from previous cardiac surgery.
Frequent ventricular arrhythmias of RVOT origin were easily inducible with isoprenaline. Interestingly, the RV substrate map in SR (Figure 3C and Videos 1, 2, and 3) showed no evidence of endocardial (bipolar voltage 1.5-0.1 mV) or epicardial (5.5-2.0 mV) scar. However, very late potentials (LP) at 138 ms post-QRS were identified at the anterior mid-RVOT (Figure 3C), which overlaid with the VT activation map localizing the VT site of origin (SOO) at 114 ms pre-QRS (Figure 3A and Videos 1-3). Pace mapping from the VT SOO yielded a 95% clinical VT morphology match.
Catheter ablation was performed with the TactiCath DF catheter (Abbott) at 30W targeting the entire LP region. A post-ablation SR substrate map confirmed elimination of all LPs, and VT was no longer inducible with isoprenaline. The patient made a good recovery and was discharged without complication. He remained free of symptoms or recurrence of his arrhythmia at 6-month follow-up.
Our case highlights the crucial interplay of multimodality cardiovascular imaging and electroanatomical mapping in guiding the treatment of our patient. This case was unusual as despite no evidence of scar (neither CMR nor electroanatomical mapping) at the tethered RVOT region, the same focal region was a source of very late potentials. Furthermore, the activation map demonstrated early signals >100 ms pre-QRS akin to mid-diastolic potentials observed in scar-dependent reentrant VT. Both of these electrophysiological observations are highly unusual for benign normal heart RVOT and are more in keeping with a reentrant VT circuit. However, the induction of VT secondary to isoprenaline suggested triggered activity as a mechanism (similar to that of benign RVOT VT),2 although this is not specific since isoprenaline can also facilitate re-entrant VT.
Putting all of his CMR and electroanatomical findings together, it is unlikely for the patient to have 2 separate diagnoses, RVOT VT and RVOT adhesion. Therefore, it was more likely that the substrate of our young patient’s RVOT VT was post-cardiac surgery RVOT adhesion. While post-operative RV adhesion has been proposed as a mechanism for RV dysfunction,3 our case suggests that post-cardiac surgery-associated RVOT adhesion can be detected on CMR and act as a focus of arrhythmogenesis that can be effectively treated by catheter ablation.
Disclosures: The authors have no conflicts of interest to report regarding the content herein.
- Marcus FI, McKenna WJ, Sherill D, et al. Diagnoss of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of Task Force criteria. Eur Heart J. 2010;31(7):806-814.
- Prystowsky EN, Padanilam BJ, Joshi S, Fogel RI. Ventricular arrhythmias in the absence of structural heart disease. J Am Coll Cardiol. 2012;59(20):1733-1744.
- Schuuring MJ, Bolmers PPM, Mulder BJM, et al. Right ventricular function declines after cardiac surgery in adult patients with congenital heart disease. Int J Cardiovasc Imaging. 2012;28(4):755-762.