Ablation of Ventricular Tachycardia in a Patient with Traumatic Ventricular Septal Defect

Todd J. Cohen, MD, Alexandru Mitrache, PA, Ilyssa Scheinbach Winthrop-University Hospital Mineola, New York

Todd J. Cohen, MD, Alexandru Mitrache, PA, Ilyssa Scheinbach Winthrop-University Hospital Mineola, New York

Abstract Ventricular tachycardia (VT) was mapped and ablated in a 34-year-old man with a history of a traumatic ventricular septal defect. Nonfluoroscopic three-dimensional (3D) mapping was used to guide the VT ablation. Case Report The patient is a 34-year-old man with symptomatic palpitations and nonsustained ventricular tachycardia. He had a traumatic ventricular septal defect that had been clinically stable via two-dimensional echocardiogram and cardiac catheterization, with QP:QS ratio of 1:2, and a left ventricular ejection fraction of 40 percent. Cardiac MRI demonstrated the presence of a small muscular ventricular septal defect measuring 4 to 5 mm at the base with left to right flow. The apical septum is thinned and akinetic. The left ventricle is mildly dilated with mild to moderate global systolic dysfunction (ejection fraction of 42 percent). More recently he developed symptoms of New York Heart Association Class II congestive heart failure. The patient was referred for an electrophysiology study with nonfluoroscopic 3D mapping and ablation of the ventricular tachycardia focus. The patient’s medications included metoprolol succinate 25 mg orally once daily and ramipril 2.5 mg once daily. The patient also was taking aspirin 325 mg once daily, fish oil 1000 mg once daily, and simvastatin 20 mg once daily for hypercholesterolemia. The patient had normal coronary arteries at cardiac catheterization.  The patient underwent an electrophysiologic study with radiofrequency (RF) catheter ablation and nonfluoroscopic three-dimensional mapping using the EnSite NavX navigation and visualization technology (St. Jude Medical, St. Paul, Minnesota). We performed mapping of the left ventricle via the retrograde aortic approach from the right femoral arterial approach. Spontaneous premature ventricular contractions (PVCs) consistent with the patient’s nonsustained VT were mapped and localized to the left ventricular apical septum (near akinetic region). The patient was anticoagulated with heparin throughout the procedure to achieve an ACT between 250 and 350 seconds. Nine RF applications were given to the location of the earliest activation site as well as the site of the lowest voltage. This site also approximated a pacemapping match to the clinical premature ventricular contractions (Figures 1A and 1B). Radiofrequency energy was delivered at 100 watts of power set for a temperature of 60 degrees for a total of 60 seconds. Figure 2 shows color images of nonfluoroscopic 3D mapping of the left ventricle with localization of the VT to a left ventricular septal apical location. The red dots indicate the RF applications performed. After the second radiofrequency application, the PVCs disappeared. The additional seven applications were given to “carpet bomb” the area. Some premature ventricular contractions were observed in follow-up (but were asymptomatic), so additional monitoring is necessary in order to determine if the patient will have a clinical recurrence.  Discussion Traumatic ventricular septal defect can occur as a result of blunt or sharp chest trauma.1 Ventricular tachycardia is not uncommon in patients with ischemic and nonischemic cardiomyopathies. Ventricular tachycardia has been reported in patients following surgical repair of a ventricular septal defect and in fact, one of the authors reported such a case in a patient who had repair of tetralogy of Fallot.2 The question of whether to ablate PVCs alone has been debated.3 However, the literature is scant with respect to VT following traumatic ventricular septal defect without repair. In addition, ventricular tachycardia ablation has been well described in patients with ischemic and nonischemic cardiomyopathies as well as those with idiopathic ventricular tachycardias.4,5 Ventricular tachycardia and ablation in a patient with a history of traumatic ventricular tachycardia to our knowledge has not previously been reported. Presumably, a periventricular septal defect scar and/or septal injury/infarction resulted and may have contributed to this patient’s left ventricular dysfunction. The mechanism of this patient’s ventricular tachycardia appeared to be reentrant. Catheter ablation may prove useful in management. Additional follow-up is necessary to determine the long-term outcome from this procedure.