A 51-year-old female with no past medical history presented to the emergency department with complaints of midsternal, non-exertional chest heaviness and intermittent palpitations. She had no significant family history and denied drug use, excessive caffeine, or supplement intake. The ED workup discovered occasional premature ventricular contractions (PVCs) on telemetry, but otherwise, her evaluation was negative. She was referred to cardiology as an outpatient, and was seen in clinic two weeks later. Her exam and vital signs were noted to be normal, although her EKG showed sinus tachycardia. The cardiologist determined that her atypical chest pain was likely musculoskeletal and that she was experiencing symptomatic PVCs, but that no further workup was needed. She was not currently taking any medications, and none were prescribed after this office visit.
However, her symptoms of intermittent palpitations persisted with the development of several episodes of near syncope, prompting a repeat appearance in the emergency department. This time, frequent intermittent runs of monomorphic nonsustained ventricular tachycardia (VT) and bigeminy were seen on telemetry. The longest was a nine-beat run up to 200 beats per minute (Figure 1). Interestingly, the patient did not feel symptomatic during these episodes while in the ED. Her blood pressure trends were elevated. EKG demonstrated 118 beats per minute, sinus tachycardia with bigeminy, and three beats of nonsustained ventricular tachycardia (Figure 2). QTc was not prolonged. Potassium was 4.3 and magnesium 2.1. All other labs were normal, including troponin. Her physical exam was notable only for an occasional irregular rhythm. Echocardiogram demonstrated a structurally normal heart. Since she was not hemodynamically compromised, the ED physician treated her with an amiodarone 150 mg intravenous bolus followed by an infusion of 1 mg/min.
Since this patient was relatively young and healthy, the case and further treatment options were brought to the attention of the staff electrophysiologist as well. An EP study was arranged for the following morning. Amiodarone was stopped to avoid PVC suppression and non-inducibility of VT.1 The patient had no symptomatic VT overnight, and her vital signs remained stable.
EKG characteristics can be examined to predict the underlying area of VT focus.2 In her case, the anterior chest leads had a left bundle branch morphology indicating that the right ventricle had been activated first, suggesting that the focus was in the right ventricle. Positive QRS complexes in the inferior leads frequently indicate VT from the outflow tract.2 The electrophysiologist felt that this patient was a good candidate for ablation, with a high likelihood of success.
A complete electrophysiology study with 3D mapping was performed, and the PVC/VT focus was identified without catecholamine stimulation at the junction of the septum and free wall of the right ventricular outflow tract. RF ablation was performed, with resolution of the PVCs. After ~45 minutes of waiting time, isoproterenol was given, with no recurrence of PVCs. The patient had no post-procedural complications, and was discharged with no medications. Eight days later, she again had several hours of fast heart palpitations that she noticed when awakening from sleep.
During this ED visit, she had a similar EKG with normal sinus rhythm and bigeminy with similar morphology. She had not described any recent chest pain, lightheadedness, or dizzy spells. She was admitted overnight for observation. Echocardiogram and labs were normal. She had frequent monomorphic PVCs and bigeminy overnight, but no ventricular tachycardia. This time, she was sent home on metoprolol 25 mg twice a day. Since she was admitted over a weekend, follow-up was arranged as an outpatient. Four days later, she had another EP study with repeat RF ablation “touchup” to the same PVC/VT focus. She was discharged on metoprolol 25 mg BID and a 48-hour Holter monitor.
One month later, she was seen in the EP clinic and was noted to be doing well. There was no recurrence of palpitations, chest pain, or lightheadedness. The 48-hour monitor worn after the second ablation revealed no PVCs or ventricular tachycardia. Her next clinic visit was scheduled with general cardiology for 6 months.
This case study is a reminder to listen attentively to our patients and to consider early non-invasive testing. While it’s easy to review the case in hindsight, it can be difficult to predict the underlying diagnosis in short clinic visits. Underlying ventricular tachycardia was uncovered as the cause of symptoms after multiple visits to various providers, including a cardiologist. A strategy to improve the diagnostic yield could have been to pursue treadmill stress testing to look for an inducible arrhythmia or underlying coronary artery ischemia, and with Holter monitoring to quantify PVC burden. Holter monitoring or a mobile heart monitoring device could also have been discussed. EKGs demonstrating PVC bigeminy suggested that the PVC focus was amenable to catheter ablation. A PVC with steep inferior axis and full transition by V3 in the precordial leads may localize to the RVOT; however, LVOT focus is also as likely, while the possibility of origination with the great cardiac vein (GCV) should not be excluded. Mapping within the LVOT is frequently advisable when an index ablation procedure fails to provide durable suppression. In this case, repeat ablation within the RVOT proved to be successful. ICD implantation was avoided in a young and healthy patient with highly symptomatic VT. Additionally, many of our patients with less concerning symptoms prefer catheter ablation over long-term use of medications, which encourages us to refer for EP consultation and ablation candidacy.
Disclosure: The author has no conflicts of interest to report regarding the content herein.
- Therapy for Cardiac Arrhythmias. In: Mann DL, Zipes D, Libbry P, Bonow R (eds). Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. Philadelphia, PA: Elsevier/Saunders, 2015.
- Sekiguchi Y, Aonuma K, Takahashi A, et al. Electrocardiographic and electrophysiologic characteristics of ventricular tachycardia originating within the pulmonary artery. J Am Coll Cardiol. 2005;45(6):887-895.