Idiopathic Ventricular Arrhythmias
Premature ventricular complex (PVC), non-sustained ventricular tachycardia (VT), and sustained ventricular tachycardia (VT) may occur in the absence of structural heart disease.1
Idiopathic ventricular tachycardia in patients with an anatomically normal
heartis a distinct entity whose management and prognosis differs from ventricular tachycardia associated with structural heart disease.2 Idiopathic VT refers to ventricular tachycardia that is not associated with structural heart disease or coronary artery disease.2 It accounts for 10% of VT cases evaluated by electrophysiology centers in the United States and 20% of those in Japan.3
These arrhythmias have certain anatomical locations within the heart and manifest specific electrocardiographic patterns that help to identify their site of origin.2 Right ventricular outflow tract VT (more often seen in women) and left ventricular outflow tract VT (more often seen in men) have distinct electrocardiogram characteristics and account for 80% of idiopathic VT cases.2
Almost 15% of idiopathic ventricular arrhythmias have an epicardial origin.4 Electrocardiogram characteristics can help to differentiate epicardial from endocardial ventricular arrhythmias. The site of origin can be ablated from within the coronary venous system in approximately 70% of patients.4
Our patient is a 52-year-old Asian female who presented to her cardiologist complaining of palpitations. Electrocardiogram showed a sustained ventricular rhythm of 100, QRS 160 ms, 1 to 1 VA conduction, and left bundle branch block. Medical history included hypertension, chest pain of unknown etiology with normal echocardiogram (ejection fraction is 60%), normal cardiac CT angiogram, irregular heartbeat, palpitations, and vertigo. There is no history of drug or alcohol abuse; the patient has also never smoked. She is married with one child. Home medications are aspirin daily and meclizine 25 mg as needed for dizziness. She is transported by ambulance to be seen by electrophysiologist Dr. Khan for electrocardiogram consistent with ventricular tachycardia. She is awake and alert with stable vital signs, in no acute distress. Laboratory data is within normal limits including potassium and magnesium. She is allergic to atenolol and codeine.
Electrophysiology study at baseline showed a slow ventricular rhythm. QRS morphology showed inferior axis with left bundle morphology. The VA interval was 220 ms with a cycle length of 600 ms. Retrograde His electrogram was recorded. There was no variation in cycle length. The QRS was 125 ms. Proximal coronary sinus recording showed earliest ventricular electrogram. Three-dimensional mapping was performed of the right atrium, right ventricle, and coronary sinus ostium. It was found that the arrhythmia was originating from the middle cardiac vein. Coronary sinus venogram was performed to highlight the ostium and venous structures. After careful mapping, radiofrequency energy was applied up to 15 watts. Impedance on the ablation catheter was noted to be greater than 300 ohms, which is consistent with venous flow. This resulted in termination of the tachycardia with resumption of sinus rhythm and sinus bradycardia. The patient had reoccurrence of the arrhythmia spontaneously and with the administration of isoproterenol. After several unsuccessful attempts at ablation, the procedure was terminated. Post-procedure intervals where similar to pre procedure. The patient left the EP lab in the ventricular rhythm.
The patient was started on sotalol 40 mg twice a day; she received one dose and converted to
sinus rhythm in less than 8 hours. She developed bradycardia, long QT (648 ms), and bigeminy with original PVC morphology. Bradycardia and prolonged QT measurements are common side effects of this beta-blocking antiarrhythmic.5 Flecainide 50 mg twice a day was instituted with the patient developing shortness of breath, chest tightness, and swelling of extremities. She was diuresed and flecainide was discontinued. These symptoms are commonly seen with flecainide therapy.6 Both medications were discontinued. The last electrocardiogram in hospital showed sinus rhythm without PVCs. The patient was sent home in stable condition with further follow-up.
Although attempts were made to ablate the arrhythmia, research shows the location of the site of origin determines success.4 The ability to deliver sufficient ablative energy appeared to determine whether or not ablation was effective.4 In this case, the sight of origin proved to a barrier.
Disclosures: The authors have no conflicts of interest to report.
- Ablation of Idiopathic Ventricular Tachycardia. The Journal of Innovations in Cardiac Rhythm Management. Published 2012. Available online at http://www.innovationsincrm.com/cardiac-rhythm-management/2012/fellows-edition-supplement/252-ablation-of-idiopathic-ventricular-tachycardia. Accessed April 30, 2013.
- How to recognise and manage idiopathic ventricular tachycardia. An article from the E-Journal of the ESC Council for Cardiology Practice. Published March 9, 2010. Available online at http://www.escardio.org/communities/councils/ccp/e-journal/volume8/Pages/Idiopathic-Ventricular-Tachycardia-Brugada.aspx#.UYAxhILJCRE. Accessed April 30, 2013.
- Badhwar N, Scheinman MM. Idiopathic ventricular tachycardia: Diagnosis and management. Curr Probl Cardiol. 2007;32(1):7-43.
- Baman TS, Ilg KJ, Gupta SK, et al. Mapping and ablation of epicardial idiopathic ventricular arrhythmias from within the coronary venous system. Circ Arrhythm Electrophysiol. 2010;3(3):274-279. doi: 10.1161/CIRCEP.109.910802. Epub 2010 Apr 17.
- Sotalol. Mayo Clinic. Published November 1, 2012. Available online at http://www.mayoclinic.com/health/drug-information/DR602503. Accessed April 30, 2013.
- Flecainide. Mayo Clinic. Published November 1, 2012. Available online at http://www.mayoclinic.com/health/drug-information/DR600665. Accessed April 30, 2013.