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Arrhythmia
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THE ROLE OF MEDICAL THERAPY IN IDIOPATHIC VENTRICULAR FIBRILLATION

Published Online: December 6th 2019 European Journal of Arrhythmia &
Electrophysiology. 2019;5(2):87–91 DOI:
https://doi.org/10.17925/EJAE.2019.5.2.87
Authors: Chiara Scrocco, Bode Ensam, Elijah R Behr
Quick Links:
Abstract
Article
Article Information

ABSTRACT:

OVERVIEW

Idiopathic ventricular fibrillation (VF) is a diagnosis of exclusion following a
resuscitated cardiac arrest which remain unexplained after comprehensive
cardiac, respiratory, metabolic and toxicological evaluation. However,
idiopathic VF patients may share electrophysiological and clinical features.
Polymorphic ventricular tachycardia, rapidly degenerating in VF, is often
triggered by short-coupled premature ventricular contractions originating from
the Purkinje system or localised areas of the inferior left or right ventricular
wall. Secondary prevention with an automated implantable cardiac defibrillator
is a cornerstone in idiopathic VF treatment. Ablation strategies may also play a
role where a substrate is identified. The role of medical therapy in idiopathic
VF is, however, poorly defined, mainly due to the lack of exploratory studies
and the absence of randomised clinical trials. Use of IV calcium channel
antagonists and isoprenaline for the acute management of VF has proven effective
in idiopathic VF associated with short-coupled Torsades de Pointes and early
repolarisation, respectively. Despite the lack of large-scale data, long-term
prophylaxis with quinidine seems to be effective in suppressing VF recurrence,
regardless of the associated electrocardiogram phenotype. Further understanding
of the underlying mechanisms of idiopathic VF, including genetic studies, will
play a role in the development of targeted pharmacological therapies.

KEYWORDS

Idiopathic ventricular fibrillation, sudden death, cardiac arrest, ventricular
tachycardia, quinidine, isoproterenol

ARTICLE:

A survivor of cardiac arrest due to ventricular fibrillation (VF), without a
cardiac, respiratory, metabolic, or toxicological explanation, is diagnosed with
idiopathic VF.1 Idiopathic VF is estimated to account for approximately 5–7% of
all out-of-hospital cardiac arrest cases.2,3 Furthermore, the Cardiac Arrest
Survivors With Preserved Ejection Fraction Registry (CASPER) showed that 44% of
out-of-hospital cardiac arrests without a clear presenting cause remained
unexplained despite extensive investigations of the patient and their family
members.4 CASPER also emphasised that the re-evaluation of patients with
idiopathic VF, over time, may lead to a diagnosis in up to 20% of cases.5 More
recent European data on 717 cardiac arrest survivors highlighted that a complete
workup, including pharmacological provocation tests, identified diagnoses in
most of the cases, with 6.8% labelled as idiopathic VF.6 These findings reflect
the importance of comprehensive cardiac evaluation of cardiac arrest victims and
family members for accurate diagnosis.

IDIOPATHIC VENTRICULAR FIBRILLATION

The term “idiopathic VF” is a diagnosis of exclusion; however, patients with
idiopathic VF often share typical electrophysiological and clinical features.
The first use of the term dates back to 1987, with the report by Belhassen of
five cardiac arrest survivors (three men and two women, aged from 24–52 years)
in whom myocardial ischaemia, metabolic or electrolyte disturbances, drug
toxicity, pre-excitation, or prolonged QT interval had been excluded. In all
subjects, a rapid poorly tolerated polymorphic ventricular tachycardia (VT) was
induced by programmed ventricular stimulation, and in one case, a spontaneous
polymorphic VT rapidly degenerating to VF was documented.7

In 1990, Leenhardt et al. described the mode of onset of spontaneous arrhythmias
in 14 subjects with no structural heart disease and unexplained syncope, which
consisted of a single premature ventricular contraction (PVC) with extremely
short coupling interval (R-on-T phenomenon). The PVC occurred during a
vulnerable period and therefore triggered a rapid polymorphic VT or VF. The
electrocardiogram (ECG) pattern was termed “short-coupled Torsades de Pointe”
(TdP) to highlight variable electrical activation of the arrhythmia with
progressive changes in QRS morphology, amplitude, and polarity.8 These findings
were confirmed by Viskin et al. in a cohort of unexplained cardiac arrest
survivors; in 22 VF episodes recorded in nine subjects, the PVC initiating a
rapid polymorphic VT had a coupling interval of 300 ± 52 ms. The episodes were
not preceded by long–short RR sequences.9

The highly malignant nature of this non-pause dependent idiopathic polymorphic
VT (i.e., not influenced by the sympathetic tone or by coronary hyperreactivity)
was described further by Eisenberg et al. in a cohort of 15 idiopathic VF
patients.10 The study showed that shorter PVC coupling intervals correlated with
greater risk of spontaneous polymorphic VT and sudden cardiac death. The advent
of electro-anatomical mapping techniques has allowed accurate identification of
the site of origin of PVCs triggering VF in unexplained cardiac arrest
survivors. Haïssaguerre and colleagues found that the foci are localised in the
specialised Purkinje system in more than 85% of cases. These Purkinje beats,
similar in morphology to fascicular tachycardias from the left ventricle or
right ventricle, usually exhibited a short coupling interval.11,12 An example of
short-coupled PVC triggering non-sustained polymorphic VT is shown in Figure 1.

In the last decade, case-control and epidemiological studies have described the
association between J waves, defined as positive deflections immediately
following the QRS complex and idiopathic VF.13–15 The presence of a J wave in
the inferolateral ECG leads, which may or may be not be followed by ST segment
elevation, is known as early repolarisation pattern. Early repolarisation
pattern is a common ECG finding (estimated incidence 1–13%), usually considered
innocent amongst healthy asymptomatic young individuals.1

Haïssaguerre et al. found that early repolarisation pattern was present in 31%
of 206 case subjects with idiopathic VF cases and 5% of 412 matched subjects
without heart disease; moreover, idiopathic VF subjects with early
repolarisation pattern had a higher incidence of recurrent VF at follow-up
(hazard ratio 2.1).13 The link between early repolarisation pattern and
malignant arrhythmias is supported by the accentuation of the J wave before the
onset of VF, and the observation of triggering PVCs coincident with the J wave
at ECG. J waves are also associated with VF storms, defined as ≥3 VF episodes in
24 hours.13,16,17 The term early repolarisation syndrome has increasingly been
used to identify patients with idiopathic VF and early repolarisation pattern at
ECG (Figure 2A).1

The pathophysiology underlying early repolarisation syndrome is, however, still
debated. According to animal models supported by ECG imaging studies, enhanced
inward ion currents during phase 2 of the action potential (AP) are responsible
for premature myocardial repolarisation.18,19 Increasing evidence supports an
alternative hypothesis, according to which the J point elevation typical of
early repolarisation pattern could be an expression of delayed depolarisation.
High-density mapping studies in some early repolarisation syndrome survivors
showed delayed, fragmented epi- and endocardial ECGs indicating local structural
alterations in the inferior right and/or left ventricular walls coincident with
the J wave.20 Similar findings have also been reported in a study involving 24
patients with no electrocardiographic phenotype. Localised areas of abnormal
depolarisation were identified in 62%, highlighting the increasing role of
depolarisation defects, with or without ECG manifestation, in the
pathophysiology of sudden cardiac death in apparently normal hearts.21

MEDICAL MANAGEMENT OF IDIOPATHIC VENTRICULAR FIBRILLATION

Both guidelines and expert consensus documents agree that implantable cardiac
defibrillator (ICD) implantation is recommended in patients with a diagnosis of
idiopathic VF (class I). Optimal pharmacological treatment is less well defined
due to the low prevalence of the condition and the absence of randomised case
control studies.1,22 Table 1 summarises the current recommendations for medical
therapy in idiopathic VF.1,22 The first drug trial in idiopathic VF was
described by Belhassen and colleagues almost 30 years ago; in two of the first
five described patients with inducible VF at electrophysiology study, electrical
stimulation was repeated after intravenous disopyramide administration. In one
case, disopyramide was effective in suppressing arrhythmias inducibility and
long-term prophylaxis started (600 mg/daily), while in the other subject a
self-terminating VT/VF could still be induced and disopyramide was substituted
with quinidine. Four patients began long-term prophylaxis with oral quinidine
(mean dosage 1,650 mg/daily) alone or, in two cases, combined with amiodarone.
All patients remained asymptomatic during a mean follow-up of 52 months.7 The
long-term efficacy of quinidine was confirmed by the same group over 20 years
later in nine subjects with idiopathic VF or Brugada syndrome with previous
cardiac arrest or syncope. Over a mean follow-up of 15 ± 7 years no recurrences
of arrhythmias were documented and repeat electrophysiological studies failed to
reproduce any sustained arrhythmias.23

SHORT-COUPLED TORSADES DE POINTE/POLYMORPHIC VENTRICULAR TACHYCARDIA

Only two case series studies, to date, described the response to antiarrhythmic
agents in idiopathic VF cases triggered by short-coupled PVCs. In the study by
Leenhardt et al.8 isoproterenol and atropine had mixed effects on suppressing
short-coupled PVCs. During follow-up, two subjects treated with betablockers and
one treated with verapamil died of sudden cardiac death. Overall, verapamil
suppressed arrhythmia recurrence in seven out of 12 subjects. Verapamil, a slow
calcium channel blocking agent, acts mostly on the sinoatrial (SA) and
atrioventricular (AV) nodes causing depression of automaticity, slowing of
conduction and increase in refractoriness. In addition, calcium-channel blockers
can ameliorate arrhythmias caused by afterdepolarisations, or by localised areas
of slow conduction. The proposed mechanisms for the effectiveness of verapamil
in short-coupled TdP were lengthening of the coupling interval and suppression
of repetitive PCVs. In the cohort described by Eisenberg et al.10 for patients
with spontaneous, short-coupled TdP, treatment included both beta-blockers
and/or calcium channel blockers; although again, these were not effective in the
long term. According to the most recent guidelines, the use of IV calcium
channel blockers should be considered for the acute management of VF storms or
recurrent ICD discharges in subjects with short-coupled TdP (class IIb).22
Importantly, cases of idiopathic VF that responded well to quinidine also seem
to be triggered by short-coupled PVCs.7,23 Thus, whilst not formally mentioned
in the guidelines, quinidine can also be useful in suppression of PVCs.

IDIOPATHIC VENTRICULAR FIBRILLATION ASSOCIATED WITH J WAVES (EARLY
REPOLARISATION SYNDROME)

Haïssaguerre et al. first described the effectiveness of different drug
therapies in early repolarisation syndrome in 2009.24 In 16 subjects with VF
storms, no response was achieved with beta-blockers (tested in 11 subjects),
lidocaine/mexiletine (tested in nine subjects), and verapamil (tested in three
subjects), while amiodarone was effective in one-third of cases. Isoproterenol
infusion (1–5 μg/min) immediately suppressed all arrhythmias in seven patients
when the sinus heart rate was increased above 120 beats/minute.24

Isoproterenol is a beta-1 and beta-2 adrenergic receptor agonist. The effects on
beta-1 adrenergic receptors, primarily concentrated in the heart, include an
increase in intracellular calcium, resulting in a steeper slope of the cardiac
pacemaker AP phase 4; therefore, pacemaker cells reach the threshold at a faster
rate, resulting in the characteristic decrease in basic cycle length. In the
epicardium, this markedly diminishes the spike-and-dome appearance of the AP
plateau and causes marked shortening of AP duration, due to a rate-dependent
reduction of the transient outward current (ITo) secondary to incomplete
recovery from inactivation.

In the endocardium ITo currents are weaker, resulting in little or no change in
AP duration in response to increases in heart rate. Experimental models of early
repolarisation syndrome suggest that cells in the inferior region of ventricular
epicardium possess a higher level of ITo than those in the lateral LV and that
this predisposes the inferior region to develop phase 2 re-entry and VT/VF. It
also suggests that isoproterenol acts by restoring the epicardial AP dome by
causing an inward shift in the balance of current.18

In the same case series, the efficacy of different pharmacological treatments
over a follow-up of 69 ± 58 months was reported.24 Prophylaxis with standard
antiarrhythmic drugs was poor in preventing recurrent VF: beta-blockers were
effective in 2/16 subjects, verapamil in 0/4, mexiletine in 0/4, amiodarone in
1/7, and class Ic drugs in 2/9. Only quinidine/hydroquinidine was successful in
all tested patients (9/9), decreasing recurrent VF from 33 ± 35 episodes to nil.

Similar results were obtained in another case study of 10 patients with
idiopathic VF and VF storms: isoproterenol was effective in suppressing the
arrhythmias and reducing the J waves amplitude at ECG (from 0.493 ± 0.198 mV
prior to VF recurrence to 0.091 ± 0.101 mV [p<0.0001]), while trials with
procainamide, lidocaine, verapamil, amiodarone, nifekalant, dofetilide,
beta-blockers, and magnesium sulphate were unsuccessful.16 Quinidine was also
effective, but was tested in only three subjects. Thus, quinidine may be useful,
in addition to an ICD, for secondary prevention of VF in patients with a
diagnosis of early repolarisation syndrome (class IIb).1

MECHANISM OF QUINIDINE

The anti-arrhythmic effects of quinidine are thought, in part, to be due to
inhibition of ITo and IKr currents causing a prolongation of both AP duration
and refractory periods. Quinidine also blocks the fast sodium channel, therefore
slowing the phase 0 of the AP and depressing spontaneous phase 4 diastolic
depolarisations. Its effects are seen in both atrial and ventricular tissue, and
the added anti-vagal action causes acceleration of AV nodal conduction.
Quinidine appears effective across idiopathic VF with no definite ECG phenotype,
short-coupled TdP, or associated with J waves. Its efficacy in short-coupled TdP
could arguably be attributed to its negative dromotropic effect (reduction of
conduction velocity) and the prolongation of the refractory period, making
myocytes unexcitable by short-coupled PVCs and suppressing automaticity in
Purkinje fibres.

There are different theories on the impact of quinidine on the mechanisms of
arrhythmogenesis in early repolarisation syndrome. According to the
repolarisation theory, a transmural heterogeneity of the AP phase 2 duration,
mediated by ITo currents, leads to a net increase of repolarisation current in
the epicardium relative to endocardium, resulting in local re-entry and
polymorphic ventricular arrhythmias, providing both the trigger and substrate of
VF.25 The ITo blocking effect of quinidine would restore the phase 2 dome and
suppress this vulnerability. The depolarisation theory suggests that slow
conduction areas, secondary to fibrosis and discontinuities in conduction, plays
a primary role in the development of the ECG and arrhythmic manifestations.
Changes in ionic currents (loss of function in INa and l-type ICa and gain of
function of ITo; Figure 3) reduce the safety of conduction at high-resistance
junctions, such as regions of extensive fibrosis or Purkinje fibre ventricular
myocyte junctions, by altering the AP morphology during phase 2 as described
above. Experimental studies in rabbits showed that ITo inhibition significantly
enhances conduction between ventricular myocytes, suggesting that ITo current
plays a major functional role in rate-dependent conduction abnormalities.26
Moreover, coupling-induced spontaneous activity in the Purkinje can trigger
acute arrhythmias by increased gap junctional resistance at the
Purkinje–ventricular interface.27 In this scenario, the block of ITo currents
and the consequent restoration of a normal AP phase 2 dome would be a key factor
for the suppression of arrhythmias by quinidine and the reduction of the J wave
amplitude at ECG (Figure 2B).

Interestingly, both isoproterenol and quinidine are also effective in the acute
management and long-term prophylaxis of arrhythmias in the Brugada and short QT
syndromes.28–31 Further insights into the mechanisms of these genetically
mediated ion channel diseases could help shed some light on the mechanism
underlying early repolarisation syndrome.

SUMMARY

The pharmacological treatment of idiopathic VF is poorly defined, mainly due to
the lack of exploratory drug studies and the absence of randomised clinical
trials and large-scale data. However, relatively robust evidence justifies the
use of calcium channel antagonists and isoprenaline for the acute management of
VF triggered by short-coupled TdP and associated with early repolarisation,
respectively. Long-term prophylaxis with quinidine appears to be safe and
effective in suppressing VF recurrence, regardless of the associated ECG
phenotype. Further understandings on the underlying mechanisms of idiopathic VF,
including genetic studies, will undoubtedly play a role in the development of
targeted pharmacological therapies.

ARTICLE INFORMATION:

DISCLOSURE

Chiara Scrocco, Bode Ensam and Elijah R Behr have nothing to declare in relation
to this article.

COMPLIANCE WITH ETHICS

This study involves a review of the literature and did not involve any studies
with human or animal subjects performed by any of the authors.

REVIEW PROCESS

Double-blind peer review.

AUTHORSHIP

The named authors meet the International Committee of Medical Journal Editors
(ICMJE) criteria for authorship of this manuscript, take responsibility for the
integrity of the work as a whole, and have given final approval for the version
to be published.

CORRESPONDENCE

Elijah R Behr, Cardiology Clinical Academic Group, St George’s University
Hospitals’ NHS Foundation Trust and Molecular and Clinical Sciences Institute,
St George’s University of London, Cranmer Terrace, London SW17 0RE, UK. E:
ebehr@sgul.ac.uk

SUPPORT

No funding was received in the publication of this article.

RECEIVED

16 August 2019

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