Flecainide monotherapy is an option for selected patients with β-blockade-intolerant catecholaminergic polymorphic ventricular tachycardia (2023)


Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare genetic disease characterized by malignant exercise-induced ventricular arrhythmias and is an important cause of sudden cardiac death (SCD) in young, healthy patients. Beta-blockers reduce ventricular arrhythmias in CPTV1and is indicated in all patients for symptom relief and prevention of SCD.2, 3

Unfortunately, treatment failure is not uncommon, and side effects associated with β-blockade can lead to drug discontinuation or subtherapeutic dosing by approx. 25% of patients.4Flecainide reduces exercise-induced arrhythmia in patients with PVT, and although the use of flecainide as monotherapy has been described,1, 5 data on flecainide in PVT is largely limited to combined therapy with β-blockers. We present a series of patients with CPVT secondary to mutations in the ryanodine receptor 2 (RyR2) gene, successfully maintained on flecainide monotherapy without β-blockade. This case series indicates that flecainide may have potential as a monotherapy in the treatment of PCT and emphasizes that β-blockers may be poorly tolerated in young and active patients.

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Patients were seen by clinics specializing in hereditary arrhythmia based in 2 tertiary referral centers: Vancouver, Canada and Amsterdam, Netherlands. All 8 patients were free of structural heart disease and had different pathogenic RyR2 mutations (Table 1). Four patients had a history of exertional syncope, and 2 of them were cardiac arrest survivors. The remaining 4 patients were clinically asymptomatic for ventricular arrhythmia. One of the patients refused any form of β-blocker


We describe our initial experience with RyR2-positive CPVT patients successfully treated with flecainide monotherapy due to β-blocker intolerance. None of the patients experienced severe arrhythmia during follow-up, although β-blocker therapy was resumed in one patient after stress testing revealed NSVT. Flecainide was generally better tolerated and was associated with a trend toward increased heart rate and exercise capacity. Clinical trials are needed to determine whether

Study restrictions

This case series is small and only includes patients with clear RyR2 mutations. There are few clinical events and therefore we cannot draw definitive conclusions about the safety of flecainide as a monotherapy for CPVT. In addition, exercise test results can be variable, and a negative test result can be falsely reassuring, as a reduction in exercise-induced arrhythmias during exercise testing does not necessarily equate to a reduction in clinical events (sensitivity 0, 62;


β-blockade remains the first-line therapy in CPVT; however, it may be poorly tolerated in a minority of patients. Flecainide is generally better tolerated than β-blockers, and flecainide monotherapy may be considered in selected patients with CPVT who are truly β-blockade intolerant. Larger case series or clinical trials are still needed to determine the efficacy of flecainide as a monotherapy for CPVT.


We thank Dr. John Imrie for the use of his clinical data and Mr. Dean Giustini, Biomedical Librarian, for his assistance. We are grateful for support from the Dutch Cardiovascular Research Initiative: Dutch Heart Foundation, Dutch Federation of University Medical Centers, Dutch Organization for Health Research and Development and Royal Netherlands Academy of Sciences. CVON FORECAST 2010-12.

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    Of note, adequate β-blocker therapy is considered to be safe during pregnancy and effective in minimizing cardiac events during pregnancy.59 Flecainide is an effective adjunct in patients who experience escape events or continue to have complex ventricular arrhythmias during pregnancy. exercise test despite optimal β-blocker therapy.42,60-64 In a small randomized control study, Kannankeril et al65 showed that combined therapy with flecainide and β-blocker was more effective than β-blocker alone in reduction of exercise-induced ventricular arrhythmias, indicating a possible role for early combination pharmacotherapy.

    (Video) Estimating and managing risk in LQTS and CPVT

    Hereditary arrhythmia syndromes are a common cause of apparently unexplained cardiac arrest or sudden cardiac death. These include long QT syndrome and Brugada syndrome, with a well-known phenotype in most patients with disease severe enough to lead to cardiac arrest. Less common and typically less obvious conditions that may not be apparent include catecholaminergic polymorphic ventricular tachycardia, short QT syndrome, and early repolarization syndrome. In patients with cardiac arrest whose extensive testing does not reveal an underlying etiology, a diagnosis of idiopathic ventricular fibrillation or short-circuited ventricular fibrillation is made. This review summarizes our current understanding of less common inherited arrhythmia syndromes and provides clinicians with a practical approach to diagnosis and treatment.

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    Long QT syndrome (LQTS), Brugada syndrome (BrS) and catecholaminergic polymorphic ventricular tachycardia (CPVT) are genetic heart diseases caused by mutations in specific cardiac ion channels and characterized by paroxysmal arrhythmias that can progress to ventricular fibrillation. In LQTS3 and BrS, different mutations in the SCN5A gene lead to a gain or loss of function in the Nav1.5 voltage-gated sodium channel, respectively. Although they share the same genetic mutation, these syndromes are characterized by different clinical manifestations and functional disturbances and, in some cases, even have an overlapping clinical phenotype. Several studies have shown that Na+current abnormalities in LQTS3 and BrS can also cause Ca2+- signaling abnormalities in cardiomyocytes (MCs). Abnormal Approx2+Homeostasis is also the main feature of TVPC, which is mainly caused by heterozygous mutations in the RyR2 gene. A large number of disease-causing mutations have been identified in RyR2 and SCN5A, but it is unclear how different variants in the SCN5A gene produce different clinical syndromes and whether in CPVT Ca.2+abnormalities and drug sensitivity vary depending on the site of the RyR2 mutation. These questions can now be addressed using patient-specific in vitro models of these diseases based on induced pluripotent stem cells (iPSCs). In this review, we summarize several insights gained from these models, focusing on electrophysiological disturbances caused by different ion channel mutations, and discuss how this knowledge will help develop better stratification and more effective personalized therapies for these patients.

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    Hereditary arrhythmia syndromes are rare, but together they are one of the main causes of loss of life in healthy young people. Several syndromes have been described, and the pathogenic mechanisms and molecular genetics are increasingly known. Most of them affect ionic currents and are called "channelopathies".

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    Nadolol is used at 1-2 mg/kg per day and propranolol at 3-5 mg/kg per day [52]. If beta-blockers are not tolerated or are insufficient, treatment with verapamil or flecainide may be considered [53-56]. Flecainide has also been shown to suppress arrhythmias in ICD-induced ventricular arrhythmias in a patient with CPVT [57].

    Although implantable cardioverter defibrillators reduce mortality in high-risk groups of patients with ventricular arrhythmias, antiarrhythmic drugs are still needed to reduce the burden of benign and potentially fatal arrhythmias. This review will address the medical treatment available for ventricular arrhythmias in Australia and its use in different clinical situations.

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    Flecainide prevents VT by inhibiting RyR2-mediated calcium release [74,75]. If beta-blockers cannot be tolerated, flecainide can be used alone [76]. It also works in RyR2-negative cases [77].

    Forty percent (40%) of unexpected sudden natural deaths in people under 35 years of age are associated with a negative autopsy, and cardiac ion channelopathies are the main suspect in these cases. Long QT syndrome (LQTS), Brugada syndrome (BrS) and catecholaminergic polymorphic ventricular tachycardia (CPVT) are the most frequently identified with genetic testing. The cellular action potential that drives the cardiac cycle is shaped by a specific series of depolarizing and repolarizing ionic currents mediated by ion channels. Changes in any of these currents and in the availability of intracellular free calcium leave the myocardium vulnerable to polymorphic ventricular tachycardia or ventricular fibrillation. Each channelopathy has its own electrocardiogram (ECG) signature, typical mode of presentation, and the most commonly related gene. Long QT type 1 (gene, KCNQ1) and CPVT (gene, RyR2) commonly occur with cardiac events (ie, syncope or cardiac arrest) during or immediately after exercise in young men; Long QT type 2 (gene, KCNH2) after startle or at night in adult women - especially early postpartum, and long QT type 3 and Brugada syndrome (gene, SCN5A) at night in young adult men. They are commonly misdiagnosed as seizure disorders. Fever-induced cardiac events should also raise the suspicion of BrS. This review summarizes genetics, cellular mechanisms, risk stratification, and treatments. Beta-blockers are the mainstay in the treatment of long QT syndrome and CPVT, and flecainide is remarkably effective in CPVT. Brugada syndrome is a genetically more complex disease than the others, and risk stratification and management are more difficult.

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    This case report presents a 33-year-old woman with premature ventricular contractions (PVCs). Her genetic test was positive for the KCNJ2 missense mutation in chr17:68171832;NM_000891.2. This mutation was compatible with Andersen-Tawil syndrome. We performed an electrophysiological study to determine the origin of the PVCs, but in the endocardial mapping there was no PVC focus and in the epicardial we removed areas of low voltage in the lower segments of both ventricles. She was discharged on flecainide and metoprolol therapy. After 3 months, her PVC load was significantly reduced by Holter monitoring.

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Copyright © 2016 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.


Is flecainide used for ventricular tachycardia? ›

Flecainide is used to prevent or treat irregular heartbeats (arrhythmias) such as paroxysmal supraventricular tachycardia (PSVT) and paroxysmal atrial fibrillation/flutter (PAF). Flecainide is also used to prevent life-threatening sustained ventricular tachycardia (sustained VT).

What is the drug of choice for CPVT? ›

Recent studies have demonstrated that (1) nadolol is the most effective beta blocker in individuals with CPVT; (2) non-selective beta blockers (nadolol and propranolol) are superior to selective beta blockers; (3) a significant burden of life-threatening arrhythmias persists after left cardiac sympathetic denervation; ...

How does flecainide work in CPVT? ›

Flecainide inhibits RyR2 Ca2+ release channels, reduces spontaneous Ca2+ release events and triggered beats and prevents ventricular tachycardia in a CPVT mouse model.

What medication is used for catecholaminergic polymorphic ventricular tachycardia? ›

Medications for CPVT

Beta blockers work by blocking beta-receptors and preventing adrenaline from affecting the heart. This helps slow the heart rate. A common antiarrhythmic medication used for CPVT is flecainide, which works by affecting the sodium and calcium exchange within the cardiac cell.

What is flecainide used to treat? ›

Flecainide is used to prevent certain types of life-threatening irregular heartbeats. Flecainide is in a class of medications called antiarrhythmics. It works by slowing electrical signals in the heart to stabilize the heart rhythm.

Should flecainide be taken with a beta blocker? ›

If you are prescribed flecainide, you may also have to take a beta block or calcium channel blocker. This is to protect the lower chambers of the heart (ventricles) from contracting too quickly.

What are the 3 treatment options for CPVT? ›

Most people with CPVT need treatment with medicine. Some people need an implantable cardioverter defibrillator. Others may need a procedure called an ablation. Other members of your family may need to be checked and watched for CPVT.

What is the best antiarrhythmic for VT? ›

Amiodarone is the drug of choice for the treatment of hemodynamically unstable VT that is refractory to other antiarrhythmic agents.

What is the first line treatment for polymorphic ventricular tachycardia? ›

Anti-arrhythmic medications are the first-line therapy in emergency departments and CCUs, as discussed earlier. Amiodarone is most commonly used, along with lidocaine, and in some cases procainamide.

Can flecainide cause ventricular tachycardia? ›

Abstract. Flecainide acetate has a recognized proarrhythmic effect in patients treated for ventricular tachycardia. Three patients developed severe ventricular arrhythmias while taking flecainide for atrial fibrillation.

How well does flecainide work? ›

Flecainide is also moderately effective and, with the exception of amiodarone, equivalent to other AADs for the chronic suppression of paroxysmal and persistent AF.

Can flecainide restore heart rhythm? ›

Intravenous or oral flecainide may promptly restore normal sinus rhythm in patients with recent-onset atrial fibrillation.

What is the best drug used to treat ventricular premature beats and ventricular tachycardia? ›

Beta blockers — The first-line therapy to reduce PVC burden is beta blockers. An exception may be those with heart failure who may proceed directly to catheter ablation. Commonly used beta blockers to treat PVCs include metoprolol and carvedilol.

Is catecholaminergic polymorphic ventricular tachycardia fatal? ›

If CPVT is not recognized and treated, an episode of ventricular tachycardia may cause the heart to stop beating (cardiac arrest), leading to sudden death. Researchers suspect that CPVT may be a significant cause of sudden death in children and young adults without recognized heart abnormalities.

What are new treatments for ventricular tachycardia? ›

  • Epicardial catheter ablation. ...
  • Intramyocardial infusion-needle catheter ablation. ...
  • Bipolar ablation. ...
  • Cardiac sympathetic denervation. ...
  • Renal sympathetic denervation. ...
  • Stereotactic radioablative therapies. ...
  • Cryoablation. ...
  • Surgical therapy for VT.
Jul 26, 2018

When should you not use flecainide? ›

Please note that flecainide is not recommended for use in patients with chronic atrial fibrillation.

Who should not take flecainide? ›

You should not take flecainide if you have certain other medical conditions, particularly other heart conditions. Your healthcare provider may advise against flecainide if you have conditions such as: Bundle branch block, a delay or blockage in electrical impulses as they travel through your heart to make it beat.

Is flecainide a high risk drug? ›

FDA warning for heart attack and irregular heart rate

If you've had a heart attack within the past two years, flecainide may raise your risk of having another heart attack, which can be fatal. This drug should only be used if you have a life-threatening irregular heart rate.

Can flecainide be taken alone? ›

This medicine may be taken with or without food. This medicine works best when there is a constant amount in the blood. To help keep this amount constant, do not miss any doses. Also, it is best to take the doses 12 hours apart, in the morning and at night, unless otherwise directed by your doctor.

Does flecainide need to be taken with metoprolol? ›

Flecainide–metoprolol combination therapy improves effectiveness of rhythm control in persistent symptomatic AF and increases tolerability, with a concomitant reduction of side effects and a better compliance.

How fast does flecainide work? ›

It will typically take up to 5 days for you to see the full effect after starting flecainide or after each dose change.

What is the first line medication for treatment of ventricular tachycardia without a pulse? ›

Medical treatment of pulseless VT usually is carried out along with defibrillation and includes intravenous vasopressors and antiarrhythmic drugs. 1 mg of epinephrine IV should be given every 3 to 5 minutes. Epinephrine can be replaced by vasopressin given 40 units IV once.

What age is catecholaminergic polymorphic ventricular tachycardia? ›

Typical age of onset of CPVT is between 7 and 15 years of age. Exercise- or emotion-induced syncopal spells are frequently the first symptom. In a subset of patients (10-20%), the disease is clinically silent, presenting only in the event of sudden death.

What is the best beta blocker for CPVT? ›

Nadolol is the beta-blocker of choice in a high dosage, 1–2 mg/kg.

What is the best medicine for tachycardia? ›


They help to slow down the heart rate and are approved by the Food and Drug Administration (FDA) to treat tachycardia and cardiac arrhythmias. Beta-blockers also help lower blood pressure, reducing the risk of heart attacks.

What is the difference between V Tach and V fib? ›

Although both are types of life-threatening arrhythmia, ventricular tachycardia (V-tach) differs from ventricular fibrillation (V-fib) in that the heart beats quickly in a more organized pattern rather than in an irregular rhythm. However, episodes of V-tach can lead to V-fib or cardiac arrest.

What is another name for polymorphic ventricular tachycardia? ›

Polymorphic ventricular tachycardia with an alternating QRS morphology is often associated with prolongation of the QT interval during sinus rhythm, in which case it is known as torsades de pointes.

What is the first line treatment for unstable tachycardia? ›

Patients with unstable tachycardia should be treated immediately with synchronized cardioversion. If a pulseless tachycardia is present patients should be treated using the cardiac arrest algorithm. The AHA no longer provides specific shock dose recommendations for synchronized cardioversion.

Can flecainide make SVT worse? ›

Flecainide may cause or exacerbate arrhythmias in 1% of patients with preexisting paroxysmal supraventricular tachycardia and in 7% of patients with paroxysmal atrial fibrillation.

What should I avoid while taking flecainide? ›

What may interact with this medication?
  • Amoxapine.
  • Arsenic trioxide.
  • Certain antibiotics like clarithromycin, erythromycin, gatifloxacin, gemifloxacin, levofloxacin, moxifloxacin, sparfloxacin, or troleandomycin.
  • Certain antidepressants called tricyclic antidepressants like amitriptyline, imipramine, or nortriptyline.

What are the long term effects of flecainide? ›

The results of CAST deterred physicians from using flecainide, even in patients without any demonstrable cardiovascular disease. One of the most difficult issues is that patients may develop coronary disease, ischaemia and/or structural heart disease while receiving chronic flecainide.

What is the success rate of flecainide? ›

Flecainide was the most effective drug, with a primary response rate of 95% (see Figure 5).

Which is better amiodarone or flecainide? ›

Amiodarone slowed the ventricular response, an effect that was not seen with flecainide or placebo. Although flecainide was less effective for rate control, it was associated with earlier reversion to sinus rhythm than amiodarone or placebo. Note that the time scale is nonlinear.

What happens if you suddenly stop taking flecainide? ›

If you suddenly stop taking flecainide you will not get withdrawal symptoms. However, the cardiac arrhythmia will no longer be being controlled as intended. So never stop using it without your doctor knowing. Like all medicines, this medicine can cause side effects, although not everybody gets them.

Can flecainide worsen heart failure? ›

There is a chance that flecainide may cause new or make worse existing heart rhythm problems when it is used. Since it has been shown to cause severe problems in some patients, it is only used to treat serious heart rhythm problems. Discuss this possible effect with your doctor.

Does flecainide stop PVCs? ›

Eighty-five percent (100 of 118) of flecainide patients had at least 80% suppression of PVCs, compared with 57% (63 of 110) of quinidine patients (p < 0.0001). (Although complete [100%] suppression of PVCs was unusual, it occurred significantly more often [p < 0.001] with flecainide than with quinidine, 16% vs 3%.)

Can flecainide treat atrial flutter? ›

Flecainide is indicated for patients with atrial flutter, paroxysmal supraventricular tachycardia, and the prevention of documented life-threatening ventricular arrhythmias.

How safe is ablation for PVCs? ›

The potential risks from a PVC ablation depend on the region it is coming from but in general the risk of a potentially serious complication such as bleeding around the heart, heart attack or stroke (PVCs from the left side of the heart only) is ≤1% and the risk of bleeding or injury in the groin where the catheters ...

What is the drug of choice for a stable client with ventricular tachycardia? ›

IV amiodarone is the drug of choice. Vasopressors can include epinephrine 1 mg IV given every 3-5 minutes or, in lieu of epinephrine, vasopressin 40 units IV as a 1-time dose.

What is the best treatment for polymorphic ventricular tachycardia? ›

Polymorphic ventricular tachycardia (a.k.a. Torsades de Pointes) is best treated with intravenous magnesium. Patients with a prolonged QT interval have a higher risk of developing polymorphic VT. Remove offending drugs that prolong the QT interval and correct potassium or calcium imbalances as well.

What is the treatment of choice for polymorphic ventricular tachycardia? ›

Tachycardia-dependent torsade de pointes is best treated with high doses of β-blockers (and left cardiac sympathetic blockade if β-blockers fail). On the other hand, shortening the pauses that facilitate pause-dependent torsade with either cardiac pacing or isoproterenol is antiarrhythmic.

Can you live a normal life with CPVT? ›

Without treatment, CPVT can lead to health complications, including cardiac arrest, when your heart suddenly stops beating. Cardiac arrest can be life-threatening. But with treatment, many people with CPVT live a high quality of life.

Can anxiety cause ventricular tachycardia? ›

Stress and anger not only impact ventricular arrhythmias but also atrial arrhythmias.

Does ventricular tachycardia ever go away? ›

Ventricular tachycardia may go away on its own within 30 seconds (nonsustained V-tach ) or last more than 30 seconds (sustained V-tach or VT ). Brief episodes may not cause any symptoms. But sustained VT can cause serious problems, including: Fainting.

Can a pacemaker fix ventricular tachycardia? ›

Overdrive pacing may prevent certain cases of ventricular arrhythmias, and antitachycardia devices may be useful in terminating paroxysmal ventricular tachycardia.

Which drug is used to treat ventricular tachycardia in patients who have a pulse? ›

Typical medical therapy includes beta-blockers, amiodarone, sotalol and mexiletine. All medications do have the risk of side effects, which can be serious and should be prescribed by heart rhythm specialists.

What is used for treatment of ventricular tachycardia and atrial fibrillation? ›

Sotalol is often a safe and effective choice in patients with CS as it treats both atrial and ventricular arrhythmias and avoids the risks of pulmonary and hepatic toxicities that can occur with amiodarone.

What is the first drug of choice for ventricular tachycardia? ›

Mostly class I antiarrhythmic drugs, such as lidocaine or ajmaline, are preferred. In hemodynamically unstable ventricular tachycardia, electrical cardioversion should be applied, in case of recurrences, followed by pharmacological treatment with class I antiarrhythmic drugs or amiodarone.

What is the best antiarrhythmic for ventricular tachycardia? ›

Amiodarone is the drug of choice for the treatment of hemodynamically unstable VT that is refractory to other antiarrhythmic agents. Prehospital studies currently suggest that amiodarone is safe and efficacious for use in out-of-hospital cardiac arrest.

What is the first-line drug to treat ventricular fibrillation? ›

Epinephrine is the first drug given and may be repeated every 3 to 5 minutes. If epinephrine is not effective, the next medication in the algorithm is amiodarone 300 mg.

Which beta blocker is best for ventricular tachycardia? ›

Arrhythmias: bisoprolol and metoprolol succinate are often preferred. Beta-blockers are the first-line treatment for long-term symptomatic rate control in patients with a range of cardiac arrhythmias, including atrial fibrillation and ventricular tachycardia.

What are three antiarrhythmic drugs that can be used to treat a patient in ventricular tachycardia? ›

First-line therapy: Beta-blockers are usually effective to treat idiopathic VT. Beta-blockers should be titrated to maximally tolerated dose. Second-line therapy: Class IV agents (verapamil). Third-line therapy: amiodarone, sotalol, flecainide, mexiletine, or propafenone are available as third-line alternatives.

What is the top priority treatment of ventricular fibrillation? ›

Emergency treatment for ventricular fibrillation includes:
  • Cardiopulmonary resuscitation (CPR). CPR mimics the pumping motion of the heart. It keeps blood flowing through the body. ...
  • Defibrillation. This treatment is also called cardioversion.
Oct 28, 2022

What is the most effective treatment for ventricular tachycardia? ›

If you have ventricular tachycardia, you may be given medications called anti-arrhythmics by mouth or IV to slow the fast heart rate. Other heart medications, such as calcium channel blockers and beta blockers, may be prescribed with anti-arrhythmic drugs.

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