Does Flecainide interact with Bisoprolol?
My opinion as follows:
Welcome and thank you for asking on HCM!
I carefully passed through your question and would explain as follows:
1- Regarding the first alternative (taking Flecainide), I would assure you that though both Flecainide and Bisoprolol may exert negative inotropic effect (depress myocardial contractility), when combined in proper doses, they could yield a beneficial effect in suppressing frequent PVCs.
So, I would agree with your EP doctor on trying first this combination (Flecainide + Bisoprolol) before concluding for cardiac ablation.
Though all anti-arrhythmic drugs may exert pro-arrhythmic effects, in certain conditions, I would prefer better a relatively short acting anti-arrhythmic drug such as Flecainide compared to other more dangerous anti-arrhythmics (such as Amiodarone with a much longer half life, with dangerous tissue-depositing profile and more frequent adverse effects).
Coming to this point, if a decision to go through anti-arrhythmic therapy would be taken, Flecainide seems to be an attractive alternative, because even if any adverse effects would happen (most frequently gastrointestinal disorders), it would be easily managed by promptly stopping the drug.
b- Regarding cardiac ablation, it seems to represent a more definite and reliable option in eradicating the arrhythmogenic focus.
As your PVCs are monomorphic, it is more likely that a localized PVCs generating focus be easily found during electrophysiologic study (which precedes cardiac ablation).
Once this focus is precisely localized and isolated during cardiac ablation, it is very likely after a successful procedure you become completely cured any free of arrhythmia.
Considering possible serious adverse effects during cardiac ablation, my opinion goes first for anti-arrhythmic therapy and if this is not sufficiently effective, then it would be better to proceed with cardiac ablation. In this regard, it is important that this invasive procedure could be performed by highly experienced electrophyiologist with a sufficient expertise on this field.
Hope to have clarified your uncertainties!
Wishing all the best,
Thank you for your very informative reply. Your answer makes sense and it helps to clarify the questions that I had. If I may ask another question: The prescribed dose of bisoprolol is 2.5 mg/day (very low because I have asthma and found that the dosages of Metoprolol and Bystolic were causing shortness of breath and coughing. I am hoping the low dose of bisoprolol will be free of beta 2 adrenergic antagonism and more cardioselective for beta 1. The dose prescribed for Flecainide is the lowest dose of 50 mg/day. Do you think that these doses could be effective in reducing PVCs? I am very much hoping that the medication works well, thus eliminating the need for ablation. However, I noted your positive comments regarding ablation as a "curative". Last question: how painful is the ablation procedure (the burning)?
Thank you very much for your replies,
Former XXXXXXX Director of Safety Pharmacology and Toxicology
Schering-Plough Pharmaceutical (bought out by Merck)
I would explain as follows:
Hello again, dear XXXX,
Your actually prescribed daily doses of Flecainide (50 mg/day) and Bisoprolol (2,5 mg/day) are quite low. So, I don’t believe that any obvious proarrhythmic effects are going to happen.
Though Bisoprolol has a much higher B1 cardio-selective property in comparison to the majority of other beta-blockers (Nebivolol is more selective in this regard), my opinion would be in favor of maintaining the actual low prescribed dose (2.5 mg).
Regarding Flecainide, 50 mg/day is considered a small dose and I am not sure if it would exert sufficient effectiveness in suppressing PVCs.
So, a rationale strategy would be to observe its effects during 3-5 days after starting and after that decide if a daily dose increase is necessary.
A steady-state Flecainide plasma level is achieved after 3-4 days, so it is recommended to perform a resting ECG (checking for QRS widening ≥ 25% as a marker of effectiveness) and measuring plasma trough Flecainide levels (target ranges 0,2-1 mcg/ml).
If Flecainide is well tolerated and a dose increase would be necessary, then 50 mg twice a day should be tried (again checking ECG and trough plasma level in a week).
Unless significant renal or liver dysfunctions are present, the usual Flecainide dose would be 100 mg twice/day.
An ambulatory 24 to 48 hours ECG monitoring (Holter) would be the best approach to evaluate therapy effectiveness (if around 80% of PVCs are suppressed, then the therapy would be considered effective).
From the other side, if the above discussed strategy doesn’t seem to be beneficial, then cardiac ablation should come on the scene.
In this regards, I would explain that with the introduction of novel mapping techniques of high-density electrophysiological study, it is quite easy to properly localize the culprit arrhythmogenic focus inside ventricular myocardium, isolate and destroy it by utilizing small burns of no more than 5 mm diameter.
So, when performed by experienced hands cardiac ablation procedure is quite safe. No obvious perceived pain or unpleasant discomfort would impede this strategy choice. A good pre-medication with tranquilizers is helpful during the procedure.
You shouldn’t be afraid of that as it (a successful cardiac ablation) could obviate the need for prolonged arrhythmic drug therapy.
You need to discuss with your attending cardiologist and EP doctor the above mentioned strategies, always keeping in mind that your actual cardiac disorder (arrhythmia) is quite curable and in a safe manner.
Hope to have been helpful to you!
Wishing you a pleasant weekend!
Thanks again. You have been very helpful and I do appreciate your input. I believe I now have a rationale course of action for my PVC problem.
You are welcome!
I am glad to have been helpful to you!
If you will have any other uncertainties in the future, you can ask me directly at any time on my personal link:
Wishing all the best,
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