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A Rare Case Report of Flecainide-Induced Left Bundle Branch Block (LBBB) and Transient Cardiomyopathy

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Abstract

Flecainide is an antiarrhythmic agent that has been reported to have numerous cardiotoxic effects, including the development of arrhythmias and the reduction of left ventricular ejection fraction (LVEF). However, it is not commonly reported as a cause for left bundle branch block and cardiomyopathy. In this case report, we present the case of a 67-year-old female patient who developed transient cardiomyopathy and left bundle branch block (LBBB) secondary to flecainide therapy. The patient's condition improved upon cessation of flecainide.
Review began 03/12/2023
Review ended 03/18/2023
Published 04/05/2023
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A Rare Case Report of Flecainide-Induced Left
Bundle Branch Block (LBBB) and Transient
Cardiomyopathy
Sukhjinder Chauhan , Desiree Morris , Mina Bhatnagar , Pinak Shah , Dhiraj D. Narula
1. Internal Medicine, Mountainview Hospital, Las Vegas, USA 2. Electrophysiology, Mountainview Hospital, Las Vegas,
USA
Corresponding author: Sukhjinder Chauhan, sukhjindermd@gmail.com
Abstract
Flecainide is an antiarrhythmic agent that has been reported to have numerous cardiotoxic effects, including
the development of arrhythmias and the reduction of left ventricular ejection fraction (LVEF). However, it is
not commonly reported as a cause for left bundle branch block and cardiomyopathy.
In this case report, we present the case of a 67-year-old female patient who developed transient
cardiomyopathy and left bundle branch block (LBBB) secondary to flecainide therapy. The patient's
condition improved upon cessation of flecainide.
Categories: Cardiology, Internal Medicine, Medical Education
Keywords: flecainide adverse effects, pacemaker induced cardiomyopathy, congestive heart failure due to flecainide,
chf, left bundle branch block, flecainide possible lbbb, flecainide toxicity, flecainide, transient nonischemic reversible
cardiomyopathy, cardiomyopathy
Introduction
Cardiomyopathies are a heterogeneous group of conditions characterized by muscular and/or electrical
dysfunction of the heart [1]. These conditions are an important cause of progressive heart failure and
cardiovascular death and can be classified as primary (i.e., genetic, acquired, or mixed) or secondary (i.e.,
toxic, inflammatory, or infiltrative). Major types include dilated cardiomyopathy, restrictive
cardiomyopathy, hypertrophic cardiomyopathy (HCM), and arrhythmogenic right ventricular
cardiomyopathy [1,2]. Drug-induced cardiomyopathy is a potentially reversible form of cardiomyopathy,
which may occur due to exposure to several medications such as chemotherapeutic agents (e.g.,
anthracyclines, trastuzumab), antiretroviral drugs, and antipsychotics [3].
In this report, we present a case of transient cardiomyopathy with a left bundle branch block (LBBB) in a 67-
year-old female who was taking flecainide, a commonly used antiarrhythmic agent. Based on the patient’s
presentation and exclusion of all other possible diagnoses, it was concluded that the cardiomyopathy was
caused by flecainide.
Case Presentation
A 67-year-old Caucasian female, with a past medical history of sick sinus syndrome status post a dual
chamber pacemaker implantation about six months ago, paroxysmal atrial fibrillation (PAF), and
hypertension, was brought to the hospital by the emergency medical services (EMS) for pleuritic chest pain.
The pain was substernal, non-radiating, worsened upon exertion, and did not improve with rest. She also
reported orthopnea, paroxysmal nocturnal dyspnea, and bilateral lower extremity edema that had been
gradually worsening. She had been diagnosed with paroxysmal atrial fibrillation (PAF) after the pacemaker
implant and was subsequently started on flecainide 150 mg BID. She denied any past medical history of
coronary artery disease (CAD), congestive heart failure (CHF), and illicit drug abuse. Her other home
medications included cyclobenzaprine, trazodone, buspirone, and ibuprofen.
On admission, the patient was afebrile. She had a blood pressure of 164/70 mmHg and was hypoxic,
requiring supplemental oxygen. Complete blood count (CBC) was unremarkable. Comprehensive metabolic
panel (CMP) was significant for a serum potassium level of 5.6 mEq/L, blood urea nitrogen (BUN) of 19
mg/dL, creatinine of 1.35 mg/dL, N-terminal pro-b-type natriuretic peptide (NT-proBNP) of 8,767 pg/mL,
and high sensitivity troponin levels of 38 ng/mL. The 12-lead electrocardiogram (EKG) shown in Figure
1 demonstrated a new LBBB with left axis deviation and a wide QRS complex of 194 milliseconds.
1 1 1 1 2
Open Access Case
Report DOI: 10.7759/cureus.37184
How to cite this article
Chauhan S, Morris D, Bhatnagar M, et al. (April 05, 2023) A Rare Case Report of Flecainide-Induced Left Bundle Branch Block (LBBB) and
Transient Cardiomyopathy. Cureus 15(4): e37184. DOI 10.7759/cureus.37184
FIGURE 1: 12-lead EKG demonstrated a new left bundle branch block
(LBBB) with left axis deviation and a wide QRS complex of 194
milliseconds on admission.
EKG: Electrocardiogram, LBBB: Left bundle branch block
A prior EKG from 2013 (Figure 2) was unremarkable and did not show LBBB.
FIGURE 2: EKG from 2013 was unremarkable and did not show LBBB
EKG: Electrocardiogram, LBBB: Left bundle branch block
Chest radiography demonstrated bilateral diffuse interstitial opacities and interstitial pulmonary edema
with central pulmonary vascular engorgement, cardiomegaly, and a dual-chamber pacemaker (Figure 3).
2023 Chauhan et al. Cureus 15(4): e37184. DOI 10.7759/cureus.37184 2 of 7
FIGURE 3: Chest radiography demonstrated bilateral diffuse interstitial
opacities and interstitial pulmonary edema with central pulmonary
vascular engorgement, cardiomegaly, and a dual-chamber pacemaker.
CXR: Chest X-ray
Computed tomography pulmonary angiography (CTPA) was negative for pulmonary embolism.
Transthoracic echocardiography (TTE) demonstrated a left ventricular ejection fraction (LVEF) of 35-40%
with multiple wall motion abnormalities, including apical wall dyskinesis and akinesis of the apical anterior,
mid anteroseptal, and apical septal walls, along with grade 2 diastolic dysfunction (Video 1).
VIDEO 1: TTE demonstrated an LVEF of 35-40% with multiple wall
motion abnormalities, including apical wall dyskinesis and akinesis of
the apical anterior, mid anteroseptal, and apical septal walls, along with
grade 2 diastolic dysfunction
TTE: Transthoracic echocardiography, LVEF: Left ventricular ejection fraction
View video here: https://youtu.be/6Pnxex4TNvE
The patient was admitted to the intensive care unit (ICU), was placed on bilevel-positive airway pressure
(BiPAP), and was treated with diuretics for pulmonary edema. The patient responded well to diuretics and
was successfully weaned off from BiPAP to a low-flow nasal cannula. A heparin drip was initiated for possible
non-ST elevation myocardial infarction (N-STEMI) ischemic cardiomyopathy and paroxysmal atrial
fibrillation (PAF). During this hospitalization, the patient's home medication, flecainide, was withheld due to
2023 Chauhan et al. Cureus 15(4): e37184. DOI 10.7759/cureus.37184 3 of 7
a suspected flecainide-induced new-onset left bundle branch block and transient cardiomyopathy, indicated
by the initial EKG, which demonstrated a prolonged QRS of 194 milliseconds. Follow-up electrocardiograms
were conducted at 24, 42, and 72 hours after cessation of flecainide. EKGs showed a gradual improvement in
QRS duration from 194 milliseconds to 152 milliseconds after 24 hours (Figure 4), 142 milliseconds after 40
hours (Figure 5), and 122 milliseconds after 72 hours (Figure 6).
FIGURE 4: 12-Lead EKG showing QRS complex duration improved from
194 milliseconds to 150 milliseconds after 24 hours following flecainide
cessation
EKG: Electrocardiogram
FIGURE 5: 12-Lead EKG showing QRS complex duration improved from
150 milliseconds to 142 milliseconds after 42 hours following flecainide
cessation.
EKG: Electrocardiograms
2023 Chauhan et al. Cureus 15(4): e37184. DOI 10.7759/cureus.37184 4 of 7
FIGURE 6: 12-lead EKG showing QRS complex duration improved from
142 milliseconds to 122 milliseconds after more than 72 hours following
flecainide cessation
EKG: Electrocardiogram
With an improvement in the respiratory status, cardiac catheterization was performed on day 3, which
showed no evidence of coronary artery disease. Data from the pacemaker interrogation revealed that the
dual-chamber pacemaker was 81% atrial paced and 25% ventricular paced with no significant atrial
fibrillation, and the longest episode of arrhythmia was noted to be 8 seconds long. Transthoracic
echocardiography (TTE) was repeated on the 4th day shown in Video 2, demonstrating an improvement in
the LVEF from 35% to 50%.
VIDEO 2: Transthoracic echocardiography (TTE) was repeated on the
fourth day, which showed an improvement in LVEF from 35% to 50%
TTE: Transthoracic echocardiography, LVEF: Left ventricular ejection fraction
View video here: https://youtu.be/yFtxb1oU840
The cardiac electrophysiology (EPS) team was consulted for further management. The pacemaker was
reprogrammed to a longer atrioventricular (AV) delay of 280/250 milliseconds with prolongation up to 400
milliseconds, to allow intrinsic AV conduction. The patient's home medication, flecainide, which was
initially held, was discontinued before discharge due to a suspected flecainide-induced new-onset left
bundle branch block and transient cardiomyopathy.
On discharge, guideline-directed medical therapy (GDMT) for HF with improved ejection fraction was
initiated with low-dose lisinopril 2.5 mg daily, and apixaban 5.0 mg BID was prescribed for
thromboembolism prevention in the setting of PAF. The patient was advised to follow up with outpatient
cardiology and the electrophysiologist within one week for further management.
Discussion
Flecainide is an oral class Ic antiarrhythmic agent, which is used for the prevention and treatment of
supraventricular arrhythmias such as atrial fibrillation (AF), atrioventricular reentrant tachycardia (AVRT),
atrioventricular nodal re-entrant tachycardia (AVNRT), and Wolff-Parkinson-White (WPW) syndrome. It
may also be used for the treatment of life-threatening ventricular arrhythmias, refractory to other treatment
options [4,5].
2023 Chauhan et al. Cureus 15(4): e37184. DOI 10.7759/cureus.37184 5 of 7
Flecainide works by blocking the open-state fast inward sodium channels, thus markedly depressing phase 0
of the action potential. It also inhibits IKr channels, delaying the potassium rectifier current. This results in
the prolongation of the duration of action potential in both ventricular and atrial muscle fibers. The drug
also inhibits ryanodine receptor 2 (RyR2), which reduces calcium release from the sarcoplasmic reticulum,
thus decreasing arrhythmogenic calcium current. In addition, flecainide decreases the inflow of sodium and
calcium ions in myocardial cells. This causes a negative inotropic effect, thus reducing the cardiac output
and stroke volume [4,6]. Flecainide is absorbed almost completely from the gastrointestinal tract and
reaches peak serum concentration in one to three hours. It is hepatically metabolized via the CYP450 system
and then excreted in the urine. Its half-life ranges from 12-27 hours but may be prolonged in patients with
heart failure, liver disease, or renal disease [6].
Flecainide has a narrow therapeutic index (0.2-1.0 mcg/mL). Therefore, small differences in dose or blood
concentration can result in life-threatening adverse drug reactions. Flecainide toxicity can cause an excess
blockade of the cardiac sodium channels, which can lead to delayed conduction, negative inotropy, and fatal
arrhythmias, such as ventricular tachycardia and ventricular fibrillation [7]. Toxicity may be precipitated in
patients with liver and/or renal failure secondary to decreased drug metabolization and clearance.
Electrolyte abnormalities, such as hyponatremia, may contribute to cardiac toxicity by enhancing the
inhibitory effect of flecainide on cardiac sodium channels [8,9] . Other non-cardiac adverse effects may
include dizziness, visual disturbances, abdominal pain, and constipation [4]. Due to its negative inotropic
effects, the drug is contraindicated in patients with congestive heart failure, coronary artery disease,
cardiomyopathy, and left ventricular ejection fraction (LVEF) of less than 30%. In this patient population, it
has been shown to cause a significant reduction in the stroke volume index and LVEF, while increasing the
right atrial pressure and pulmonary capillary wedge pressure (PCWP) [9,10].
Finally, flecainide has been associated with a proarrhythmic effect, which can lead to the development of
atrial flutter or ventricular tachyarrhythmia. For instance, it has the potential to convert atrial fibrillation to
atrial flutter with 1:1 atrioventricular (AV) conduction, resulting in rapid tachycardia and a heart rate of
more than 200 beats per minute. Drugs that block the AV node, such as beta-blockers and calcium channel
blockers, should be used concurrently to lower this risk [4,10]. In the Cardiac Arrhythmia Suppression Trial
(CAST), an increased rate of mortality and nonfatal cardiac arrest was observed in patients with a history of
myocardial infarction. Based on the results of this study, the apparent proarrhythmic effect of flecainide is
believed to be caused by its use in patients with structural abnormalities of the heart. Therefore, flecainide is
contraindicated in patients with structural heart disease [11,12].
Our patient presented with CHF and new-onset LBBB. The differential diagnosis included ischemic
cardiomyopathy (based on the new finding of LBBB with elevated serum troponin levels), arrhythmia-
induced cardiomyopathy (given the patient’s history of sick sinus syndrome and atrial fibrillation), pacing-
induced cardiomyopathy (due to the patient’s recent history of pacemaker implantation), and drug-induced
cardiomyopathy (based on the patient’s use of flecainide). Ischemic cardiomyopathy was ruled out, as
cardiac catheterization showed no signs of coronary artery disease in our patient. Arrhythmia-induced
cardiomyopathy was excluded, as the data retrieved upon pacemaker interrogation demonstrated that the
longest arrhythmia episode was only eight seconds long and that there were no episodes of atrial fibrillation.
Next, the possibility of pacing-induced cardiomyopathy (PICM) was considered. PICM is a rare complication
of pacemaker therapy that is characterized by a reduction in LVEF and an increase in the end-systolic
volume and wall stress, mainly due to ventricular dyssynchrony where the ventricles beat out of rhythm with
each other [13,14]. A study on right ventricle (RV) pacing-induced LBBB has reported that when the
ventricular lead is positioned in the apical region of the RV, it may result in an Intraventricular conduction
delay (IVCD) that presents electrocardiographically as an LBBB pattern [15]. Treatment of PICM may involve
adjusting the pacemaker settings or switching to a different type of device. However, it is generally
recommended to minimize right ventricular pacing as much as possible and to use atrial pacing instead, as
this type of pacing is less likely to cause pacemaker-induced cardiomyopathy [13,16]. PICM was excluded in
our patient upon pacemaker interrogation, as it demonstrated a normal functioning pacemaker with 81%
atrial pacing and 25% ventricular pacing.
As previously mentioned, flecainide toxicity can cause a widening of the QRS interval as an adverse effect.
This is due to the drug's ability to slow down the conduction velocity of electrical signals in the ventricles,
which can lead to a prolonged QRS complex on an EKG. A widened QRS interval of more than 122
milliseconds is typically observed [6]. The half-life of flecainide ranges from 12 to 27 hours, and in patients
with heart failure, it can last up to 70 hours [6]. In our patient's case, there was a gradual improvement in
QRS duration from 194 milliseconds on the initial EKG to 122 milliseconds on the EKG obtained after 72
hours of flecainide cessation. This suggests that the prolonged QRS duration was likely due to flecainide
toxicity. While volume optimization could have aided in the improvement of ejection fraction (EF), the
patient's LVEF improvement from 35% to 50%, however, in combination with the gradual improvement in
QRS duration after flecainide discontinuation, without any significant alterations in pacemaker settings,
provides additional evidence for the diagnosis of flecainide-induced transient cardiomyopathy.
Several studies have also shown that LBBB can be caused by flecainide toxicity secondary to a decrease in
the electrical conduction in the left ventricular myocardium [12,17,18]. Our patient's EKG, shown in Figure 1,
2023 Chauhan et al. Cureus 15(4): e37184. DOI 10.7759/cureus.37184 6 of 7
was remarkable for a QRS duration of 194 milliseconds with a new onset of left bundle branch block, as
shown in Figure 1. All these findings supported the diagnosis of flecainide toxicity in our patient.
Conclusions
Cardiomyopathy due to chronic exposure to medically prescribed drugs with cardiotoxic effects, such as anti-
cancer, antiretroviral, and antipsychotic drugs, is common. However, the diagnosis remains particularly
challenging for other drugs that are not commonly associated with the development of drug-induced
cardiomyopathy.
Flecainide is an antiarrhythmic agent that is not a common cause of cardiomyopathy; however, the
proarrhythmic effects, such as QRS, widening as an adverse effect of this medication are well-documented.
Therefore, physicians should be aware of the potential cardiotoxicity of this drug and perform routine
monitoring with EKG and patients should follow up with cardiology closely for the early identification of any
adverse effects. Discontinuation of flecainide therapy and the use of alternative medications should be
considered.
Additional Information
Disclosures
Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In
compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services
info: All authors have declared that no financial support was received from any organization for the
submitted work. Financial relationships: All authors have declared that they have no financial
relationships at present or within the previous three years with any organizations that might have an
interest in the submitted work. Other relationships: All authors have declared that there are no other
relationships or activities that could appear to have influenced the submitted work.
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2023 Chauhan et al. Cureus 15(4): e37184. DOI 10.7759/cureus.37184 7 of 7
... Given its primary mechanism of action is inhibition of fast-inward sodium channels, flecainide prolongs depolarization within atrial and ventricular myocytes as well as slows conduction within the atrioventricular node and His-Purkinje system, with increased inhibition at faster heart rates. 1 Consequently, 12-lead electrocardiograms (ECGs) are necessary to monitor for significant QRS prolongation after initiation of flecainide, both at rest and with exercise. Although case reports have documented the risk of marked QRS prolongation 2,3 and left bundle branch (LBB) block 4,5 with flecainide, the effect of flecainide on electrophysiologic criteria during conduction system pacing has not been previously assessed. Herein, we present a patient who underwent pacemaker implantation with a conduction system pacing lead in the LBB area in whom LBB capture based on accepted criteria was noted only after discontinuation of flecainide. ...
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Pacing induced cardiomyopathy (PICM) is most commonly defined as a drop in left ventricle ejection fraction (LVEF) in the setting of chronic, high burden right ventricle (RV) pacing. Recent data suggests, however, that some individuals may experience the onset of heart failure symptoms more acutely after pacemaker implantation. Definitions of PICM which emphasize drop in LVEF may underestimate the incidence of deleterious effects from RV pacing. Treatment of PICM has primarily focused on upgrade to cardiac resynchronization therapy (CRT) when LVEF has dropped. However, emerging data suggests that conduction system pacing (CSP) may offer an opportunity to prevent PICM in the first place. This article is protected by copyright. All rights reserved.
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Drug-induced cardiomyopathy (CM) is a potentially reversible form of acquired CM and a common consequence of exposure to numerous medically prescribed drugs. It is particularly a common serious adverse side effect of anticancer and antiretroviral therapies. The two drugs may have significantly improved longevity in cancer and HIV-infected patients respectively but their cardiotoxic effects threaten to undermine their therapeutic efficacy and reduce survival in affected patients. Hospitalization due to drug-induced CM also places a considerable burden on the healthcare system in terms of reduced drug efficacy and patient management. Early detection is clinically important for improve efficacy in the management of drug-induced CM as well as the prevention of the progression into heart failure. Thus, prescribers should be fully aware of drugs with the potential to cause CM and the clinical value of monitoring the cardiotoxic effects of these drugs. Thus, the present paper provides a systematic review of literature and meta-analysis of diagnosis and management methods. The aim is to broaden the understanding of the major causative drugs, pathophysiology, diagnosis and management of drug-induced CM.