Download Management of Aborted Sudden Cardiac Arrest with J Wave

CASE
International Journal of Arrhythmia 2016;17(1):60-63
REPORTS
doi: http://dx.doi.org/10.18501/arrhythmia.2016.010
Management of Aborted
Sudden Cardiac Arrest with
J Wave Syndrome
Ki Hong Lee, MD; Hyung Wook
Park, MD, PhD
The Heart Research center of Chonnam National University
Hospital, Cardiovascular Research Institute of Chonnam
National University, Gwangju, Korea
Received: November 16, 2015
Accepted: March 28, 2016
Correspondence: Hyung Wook Park, MD, PhD
Associate Professor, Cardiovascular Medicine,
Chief of Cardiovascular Medicine,
The Heart Center of Chonnam National University
Hospital, 42 Jaebongro, Dong-gu, Gwangju,
Republic of Korea, 501-757
Tel: 82-62-220-6572 Fax: 82-62-223-3105
E-mail: [email protected]
Copyright © 2016 The Official Journal of Korean Heart
Rhythm Society Editorial Board & MMK Co., Ltd.
ABSTRACT
We report the case of a 19-year-old male who successfully recovered from sudden cardiac arrest. Careful evaluation did not reveal
any electrical or structural abnormalities. He underwent implantable cardioverter defibrillator (ICD) implantation, with a diagnosis
of idiopathic ventricular fibrillation (VF). Three months later, VF
recurred and was successfully terminated by ICD shock. Electrocardiogram (ECG) revealed a slurred type J point elevation at the
inferolateral leads with a horizontal/descending ST segment change,
which was not present during the initial hospitalization. Cilostazol
was prescribed to prevent further lethal ventricular arrhythmias.
Subsequently, no arrhythmic events were reported, and the J wave
disappeared at the follow-up ECG. However, recurrent VF episodes
with an interval of 1–2 weeks occurred 1 year later, and were terminated by ICD shock. Simultaneous ECG revealed a J point elevation at the inferolateral leads. Cilostazol was replaced by quinidine.
Subsequently, no arrhythmic event recurred for over 12 months. Serial follow-up ECG is needed to identify masked inherited primary
arrhythmic syndromes in sudden cardiac arrest survivors diagnosed
with idiopathic VF. Cilostazol and quinidine might be good therapeutic options to prevent further lethal events in cases where the J
wave syndrome is present with recurrent ventricular arrhythmias.
Key Words: ■Heart Arrest ■Arrhythmias, Cardiac
■Anti-Arrhythmia Agents
Introduction
majority of survivors. IPAS is often revealed during serial followup examinations because electrocardiographic abnormalities of
Lethal ventricular arrhythmias can occur even in the absence of
IPAS tend to change spontaneously. The J wave syndrome is a
structural heart disease. Inherited primary arrhythmia syndrome
recently discovered form of IPAS and is an important cause of
(IPAS) is a rare condition, but is often associated with high
SCA in relatively young patients. We report the case of a 19-year-
mortality rates. Despite meticulous evaluation, the underlying
old male who survived SCA and a diagnosis of J wave syndrome
cause of sudden cardiac arrest (SCA) remains idiopathic in a
was made subsequently.
60
Management of J Wave Syndrome
Case
horizontal/descending ST segment change (Figure 2). Cilostazol
was prescribed to prevent further lethal ventricular arrhythmias.
A 19-year-old male was transferred to the emergency
Nevertheless, recurrent VF episodes with an interval of 1 to 2
department with aborted sudden cardiac arrest. He had no
weeks occurred 1 year later, and were terminated by ICD shock
previous history of hypertension, diabetes mellitus, dyslipidemia,
(Figure 3). At that time, ECG also demonstrated a J point
or other cardiac problems. He was a student with ordinary activity
elevation at the inferolateral lead, which was not apparent during
levels. Cardiac arrest developed during sleep. When the
the ‘no-event’ period. To minimize shock therapy, cilostazol was
emergency team arrived, an automated external defibrillator
switched with quinidine, as class Ic anti-arrhythmic agents directly
demonstrated ventricular fibrillation (VF), which was terminated
inhibit Ito, thereby decreasing the J point elevation resulting in
by three rounds of defibrillation. After the successful recovery of
decreased the transmural dispersion of repolarization and
spontaneous circulation, the patient underwent hypothermia
refractoriness. No arrhythmic events were reported subsequently
treatment. Subsequently, careful evaluation was performed to
and ECG revealed no J wave.
identify the cause of sudden cardiac arrest. None of the
examinations performed, including electrocardiogram (ECG),
Discussion
holter monitoring, coronary angiogram, brain computer
tomography, and flecainide or epinephrine drug challenge test,
The early repolarization pattern in ECG, known as the J wave,
revealed any abnormalities. Electrophysiological studies did not
is considered to be benign. Recent studies, however, have reported
induce any ventricular tachycardia. Finally, a diagnosis of
that the J wave may be associated with an increased risk of death.1,2
idiopathic VF was made and the patient underwent implantable
Additionally, early repolarization has been reported to be
cardioverter-defibrillator (ICD) implantation to protect him
associated with recurrent VF in cardiac arrest survivors.3 Rosso et
from further lethal ventricular arrhythmias.
al. have termed early repolarization with a horizontal/descending
The patient had an uneventful recovery after being discharged
ST segment as “malignant”, because it was more strongly
from the hospital. However, 3 months later, an ICD shock
correlated with idiopathic ventricular fibrillation among all types
occurred, which was revealed to be a VF event at ICD
of early repolarization.4 In the present case report, a horizontal/
interrogation (Figure 1). At that time, a simultaneous ECG
descending type of early repolarization pattern was documented
demonstrated the presence of a newly developed J point elevation
in the ECG. This abnormal pattern, which exhibited dynamic
at the inferolateral lead, which was of the slurred type with a
changes with time, might cause recurrent VF episodes.
Figure 1. Interrogated intracardiac electrogram from an implantable cardioverter defibrillator (ICD).
Ventricular fibrillation was present and was terminated by ICD shock 36 J.
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International Journal of Arrhythmia 2016;17(1):60-63
Figure 2. Electrocardiogram (ECG) after successful defibrillation from ventricular fibrillation. A newly developed J point elevation at
the inferolateral lead of the slurred type with a horizontal/descending ST segment change was detected by ECG.
Figure 3. Interrogated intracardiac electrogram from an implantable cardioverter defibrillator (ICD). Ventricular fibrillation (VF) was
detected and was terminated by ICD shock 36 J. Recurrent VF episodes occurred at 1-2 week intervals.
The J wave is formed due to an outward shift in the balance of
sodium current (INa). The loss of the action potential dome in the
the membrane ionic currents at the end of the phase 1 and phase 2
epicardium, but not in the endocardium, results in the
action potentials. In these phases, an outward current occurs
development of a marked transmural dispersion of repolarization
mainly due to the activation of the transient outward current (Ito),
and refractoriness. This event is responsible for the development
while the inward current is a result of the activation of an inward
of a vulnerable window during which a premature impulse or
calcium current (ICa) and an inactivating component of an inward
extrasystole can induce a reentrant arrhythmia.5-7
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Management of J Wave Syndrome
Although the primary therapy for VF is ICD implantation,
Cardiovasc Electrophysiol. 2011;22:131-136.
shock reduction and the prevention of recurrent ventricular
4) Rosso R, Glikson E, Belhassen B, Katz A, Halkin A, Steinvil A,
arrhythmia should be considered. A pharmacologic intervention,
Viskin S. Distinguishing "benign" from "malignant early
which either decreases the membrane outward currents, or
repolarization": The value of the ST-segment morphology. Heart
increases the inward currents, prevents the loss of the action
Rhythm. 2012;9:225-229.
potential dome in the right ventricular epicardium. Quinidine has
5) Antzelevitch C, Brugada P, Brugada J, Brugada R, Towbin JA,
been shown to directly inhibit the Ito in addition to a secondary
Nademanee K. Brugada syndrome: 1992-2002: A historical
inhibition due to an increase in the heart rate by a vagolytic
perspective. J Am Coll Cardiol. 2003;41:1665-1671.
action.5,7 Experimental studies have shown quinidine to be
6) Priori SG, Napolitano C, Gasparini M, Pappone C, Della Bella P,
effective in restoring the epicardial action potential dome, thus
Brignole M, Giordano U, Giovannini T, Menozzi C, Bloise R,
normalizing the ST-segment and preventing phase 2 reentry and
Crotti L, Terreni L, Schwartz PJ. Clinical and genetic heterogeneity
polymorphic VT.8 Cilostazol, an oral phosphodiesterase type-III
of right bundle branch block and ST-segment elevation syndrome:
inhibitor has been shown to increase the ICa due to the inhibition
A prospective evaluation of 52 families. Circulation .
of the phosphodiesterase activity in the ventricular myocytes and
decreases the Ito due to an increased heart rate which again is
secondary to an increased ICa in the sinus node.9
In the present case report, the patient underwent ICD
implantation with the initial diagnosis of idiopathic VF. However,
J point elevation occurred during late follow-up, which was related
2000;102:2509-2515.
7) Yan GX, Antzelevitch C. Cellular basis for the brugada syndrome
and other mechanisms of arrhythmogenesis associated with
ST-segment elevation. Circulation. 1999;100:1660-1666.
8) Antzelevitch C. The brugada syndrome: Ionic basis and arrhythmia
mechanisms. J Cardiovasc Electrophysiol. 2001;12:268-272.
with recurrent ventricular arrhythmia, and potential preventive
9) Matsui K, Kiyosue T, Wang JC, Dohi K, Arita M. Effects of
strategies were indicated. Pharmacological therapy with cilostazol
pimobendan on the l-type Ca2+ current and developed tension in
and quinidine successfully suppressed lethal ventricular
guinea-pig ventricular myocytes and papillary muscle: Comparison
arrhythmias. Therefore, careful and serial follow-up evaluation is
essential in patients with idiopathic VF because unrevealed IPAS
with ibmx, milrinone, and cilostazol. Cardiovasc Drugs Ther.
1999;13:105-113.
might be present. Additional therapeutic strategies may be
considered to prevent and minimize the occurrence of further
lethal arrhythmias.
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