A woman in her late 40s with a history of hypertension presented to the emergency department after multiple episodes of palpitations with near syncope. While in the emergency department, she developed monomorphic ventricular tachycardia (VT) with hemodynamic instability and was successfully cardioverted. She continued to have nonsustained monomorphic VT, so intravenous amiodarone and oral metoprolol were initiated. She was admitted for further evaluation. Results of tests of electrolyte levels and coronary angiography were normal. Cardiac magnetic resonance imaging with gadolinium contrast revealed normal-sized cardiac chambers and normal biventricular function without delayed enhancement. The presenting electrocardiogram (ECG) is shown in Figure 1.

1. Wide Complex Tachycardia and Syncope
in a Middle-aged Woman
Laith A. Derbas, MD; Omair K. Yousuf, MD; Faraz Kureshi, MD, MSc
A woman in her late 40s with a history of hypertension presented to the emergency
department after multiple episodes of palpitations with near syncope. While in the
emergency department, she developed monomorphic ventricular tachycardia (VT) with
hemodynamic instability and was successfully cardioverted. She continued to have
nonsustained monomorphic VT, so intravenous amiodarone and oral metoprolol were
initiated. She was admitted for further evaluation. Results of tests of electrolyte levels
and coronary angiography were normal. Cardiac magnetic resonance imaging with
gadolinium contrast revealed normal-sized cardiac chambers and normal biventricular
function without delayed enhancement. The presenting electrocardiogram (ECG)
is shown in Figure 1.
Diagnosis
Outflow tract ventricular tachycardia
What to Do Next
B. Electrophysiology study with possible catheter ablation
Discussion
This patient presented with recurrent symptomatic monomorphic
VT suggestive of an outflow tract (OT) origin. An electrophysiology
(EP) study to anatomically localize the abnormal rhythm and
ablation therapy is the preferred strategy in severely symptomatic
patients. Medical therapy may be considered; owing to limited and
varying efficacy of pharmacologic therapy and its adverse effects,
an EP study with ablation, with its high success rate and low com-
plication rate, is preferred. Outflow tract VT (OTVT) is a monomor-
phic subset of idiopathic VT diagnosed in patients without under-
lying structural heart disease, metabolic abnormalities, or cardiac
channelopathies. Right ventricular OT (RVOT) VT makes up about
I
II
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Figure 1. Patient electrocardiogram at presentation.
WHAT WOULD YOU DO NEXT?
A. Placement of an implantable
cardioverter-defibrillator
B. Electrophysiology study with
possible catheter ablation
C. Discharge with oral
antiarrhythmic therapy
with a class I or III agent
D. Discharge with oral β-blocker or
nondihydropyridine calcium
channel blocker
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2. 80% of OTVT cases, with most originating just inferior to the
pulmonic valve from the anterior and superior septal aspects of
the RVOT. The other 20% are left ventricular OT (LVOT) VT, which
commonly arises from the region of the aortic cusps in the aortic
root.1
A surface ECG with an inferior axis, left bundle branch block
(BBB) morphology, and precordial R-wave transition at V4 or after
suggests RVOT VT, while one with an inferior axis, right or left BBB
morphology, and precordial R-wave transition at V2 or earlier sug-
gests LVOT VT.2
Despite surface ECG findings that may differenti-
ate LVOT from RVOT, definitive localization is via electroanatomic
mapping in an EP study.
Presenting ECGs (Figure 1) showed runs of a monomorphic
wide complex tachycardia interceded by normal sinus rhythm
(with a normal axis and narrow QRS complexes). As the wide com-
plex monomorphic tachycardia rhythm developed, a new left BBB
morphology with an inferior axis (positive QRS deflections in infe-
rior leads II, III, and aVF) and a precordial R-wave transition (a ratio
R-wave to S-wave amplitude of Ն1) at lead V3 were observed
(Figure 2).
Management of OTVT is dictated by symptom frequency and
severity and can include medical therapy and/or catheter ablation.
Acute termination can be achieved by vagal maneuvers and abor-
tive drugs (eg, adenosine, β-blockers, verapamil). Preventive
medications include class IA, IC, and III antiarrhythmic drugs;
β-blockers; and verapamil. Radiofrequency catheter ablation
can be used early in management (with success rates >90%
and recurrence of 5% in the first year in RVOT3,4
); indications
include severe symptoms or ones refractory to medical therapy,
cardiomyopathy, or younger age and desire to avoid long-term
medical therapy.5
Idiopathic VT has a favorable prognosis,6
but symptoms can decrease quality of life, and patients may be
at risk for cardiomyopathy if premature ventricular contraction
(PVC) burden is high.7
Patient Outcome
ThepatienthadsufficientPVCsforactivationmappingwithaCARTO
3advanced3-dimensionalmappingsystem(Biosense-Webster).The
origin was localized to the LVOT at the junction between the right
and noncoronary cusps of the aortic root. Catheter ablation with
radiofrequency energy was performed successfully; VT was nonin-
ducible at the end of the EP study, and the patient had no recur-
rence of VT or PVCs in the next 24 hours per telemetry.
ARTICLE INFORMATION
Author Affiliations: Division of Medicine,
University of Missouri, Kansas City (Derbas);
Division of Cardiology, Saint Luke’s Mid America
Heart Institute, Kansas City, Missouri (Yousuf);
Advanced Cardiovascular Imaging Laboratory,
Cardiovascular and Pulmonary Branch, National
Heart, Lung, and Blood Institute, National Institutes
of Health, Bethesda, Maryland (Kureshi).
Corresponding Author: Laith A. Derbas, MD,
Division of Medicine, University of Missouri,
Kansas City, 2301 Holmes St, Kansas City, MO 64111
(derbasl@umkc.edu).
Published Online: November 7, 2018.
doi:10.1001/jamacardio.2018.3687
Conflict of Interest Disclosures: All authors have
completed and submitted the ICMJE Form for
Disclosure of Potential Conflicts of Interest.
Dr Yousuf reports receiving honoraria from
Medtronic and Boston Scientific as a part of their
speakers’ bureaus and Abbott and Biosense
Webster as a consultant. No other disclosures
were reported.
Additional Contributions: We thank Alan P.
Wimmer, MD, Saint Luke’s Health System, for his
manuscript review. He was not compensated.
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I
II
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Figure 2. Patient electrocardiogram on development of a wide complex
monomorphic tachycardia rhythm. Note positive QRS deflections in the inferior
leads II, III, and aVF, indicating a new left branch bundle block morphology
with an inferior axis and a precordial R-wave transition at lead V3.
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