You are entirely correct, we know that the arrhythmias related to atrial fibrillation arise in certain areas of the heart like the pulmonary vein, the posterior wall of the left atrium, superior vena cava, coronary sinus, intreratrial septum and the crista terminalis. What we do not know is why they arise there. We know that by ablating these areas we may decrease the likelihood of a patient having such an arrhtyhmia, but in the process we likely modify the final common pathway of the arrhythmia rather than the causative factor per-se. The most prevalent theory linking these parts of the heart to arrhythmia generation explains this relationship via greater vagal / parasympathetic innervation of the heart in the areas described. The theory then suggests that heightened vagal input to these areas of the heart via local autonomic ganglia leads to arrhythmia initiation and maintenance and some investigators have targeted autonomic ganglia directly. Practically, however, pulmonary veins remain the easiest target for an intervention with reasonable clinical and cost effective outcomes.
Tendonitis does not result from tooth decay and does not predispose to AF.
Your presentation is not unusual. Triggers for AF are quite variable and include exercise, anxiety, caffeine, alcohol, after meals or during sleep. It is believed that people who develop AF with low heart rates (after meals or during sleep) have a vagal component. At this time it may be worthwhile trying an antiarrhythmic drug since you are symptomatic. If the triggers are attributable to vagal events then disopyramide is one option. Obviously before starting any drug, you will have to get an evaluation to r/o any structural and or ischemic heart disease.
Your AF progression is consistent with the natural history of the disease and although antiarrhythmic drugs may initially be able to control the arrhythmia, in half the cases it breaks through. It is unclear how weight loss may help - perhaps by achieving better blood pressure control and / or reducing sleep apnea. At this time, since you are having AF episodes despite sotalol (and tambocor), I agree that AF ablation is an alternative. For patients with self terminating episodes of AF, long term efficacy of single ablation procedure to achieve AF control is ~75%. With additional procedures the success rate is >85%.
No, there is no difference. These agents are typically used to control the ventricular rate during AF episodes and as such should not have any direct bearing on AF itself.
Your presentation is not unusual. Triggers for AF are quite variable and include exercise, anxiety, caffeine, alcohol, after meals or during sleep. It is believed that people who develop AF with low heart rates (after meals or during sleep) have a vagal component. At this time it may be worthwhile trying an antiarrhythmic drug since you are symptomatic. If the triggers are attributable to vagal events then disopyramide is one option. Obviously before starting any drug, you will have to get an evaluation to r/o any structural and or ischemic heart disease. Overall efficacy of antiarrhythmic drug therapy to control AF is about 50% (some people do really well and some people fail the drugs early on). It is however still the recommendation to try drugs first and if AF breaks through then ablation is an option. The choice of antiarrhythmic drug therapy is determined by co-morbidities. Typically patients need an echocardiogram and a stress test to r/o structural and ischemic heart disease before flecainide can be initiated.
Your presentation is not unusual. Triggers for AF are quite variable and include exercise, anxiety, caffeine, alcohol, after meals or during sleep. It is believed that people who develop AF with low heart rates (after meals or during sleep) have a vagal component. At this time it may be worthwhile trying an antiarrhythmic drug since you are symptomatic. If the triggers are attributable to vagal events then disopyramide is one option. Obviously before starting any drug, you will have to get an evaluation to r/o any structural and or ischemic heart disease. As far as where the trigger is located, it would be highly unusual for an extra beat from the lower chamber to initiate AF unless there was an accessory pathway (congenital extra connection between the upper and lower chamber). One way to determine that is by doing an electrophysiologic study which is an invasive procedure. Alternative is to wear an event monitor with auto-trigger ability. This may not be as accurate as an EP study but is non-invasive.
Discontinuing warfarin will put you at a higher risk of stroke. Based on your other co-morbidities, the risk of stroke off warfarin may be low, moderate or high. It is recommended that patients falling in the the latter two categories should be on warfarin. The risk of discontinuing metoprolol is that during AF / Flutter the ventricular rates can get excessively high.
Yes, you can still have an ablation procedure. There is a growing population of patients experiencing AF after maze surgery that have undergone the ablation procedure.
The return of AF following corrective surgery is typically managed in a stepwise fashion involving medical threapy, cardioversion, and percutaneous catheter ablation. Epicardial surgical ablation can be performed in selected patients with previous heart surgery. Appropriate therapy for you can be discussed with your cardiologist.
The indications for pacemaker implantation are very clear. If you meet the criteria then you stand to benefit from a pacemaker. Atrial fibrillation is not a contraindication for a pacemaker. The choice of single versus dual chamber pacer system may be influenced by whether you are in paroxysmal, persistent or permanent AF. Traditional approach to placing wires in the heart transvenously for pacemaker cannot be used if your tricuspid valve has been replaced by a metallic prosthesis. However, since the surgeon has already placed wires in your heart, in your case, this is a not an issue.
Your doctor may be recommending a pacemaker to control the symptoms of atrial fibrillation or another heart rhythm. Patients often have dramatic improvement following this therapy. The wires placed at the time of your last procedure may be located and used in a fairly minimally invasive manner, if needed.
If your husband is in AF and has fast heart rates then his medications need to be adjusted / changed. The propanolol can be adjusted as an outpatient but if for changing the flecainide to another agent, typically that requires monitoring / hospitalization. He may need another cardioversion and may also be a good candidate for AF / flutter ablation.
Some patients do not tolerate atrial fibrillation or atrial flutter and feel poorly. Further visits with your doctor would be helpful regarding management.
Dr. Andrea Natale
Dr. Andrea Natale is a board certified electrophysiology expert and practices at executive medical director of the Texas Cardiac Arrhythmia Institute at St. David's Medical Center in Austin, Texas. Dr. Natale also is the Senior Medical Director at Pacific Atrial Fib and Arrhythmia Center in San Francisco. He visits MetroHealth in Cleveland, and Akron General, Ohio. He has pioneered a new circumferential ultrasound vein-ablation system to correct atrial fibrillation and performed the procedure on the world's first five patients. For further details Please visit :Link
Dr. Dhanunjaya Lakkireddy
Dr. Dhanunjaya Lakkireddy, MD, F.A.C.C, FHRS. is a board certified electrophysiology expert and practices at Mid-America Cardiology and The University of Kansas Hospital Clinics in Kansas City, KS, USA. He has several distinctions in clinical and research career to his credit and serves as an associate editor for Journal of Atrial Fibrillation.For further details Please visit :Link
Dr. Dhanunjay Lakkireddy, MD, F.A.C.C, FHRS, The Kansas City Heart Rhythm Institute (KCHRI), KS, USA.
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