Sotalol is usually effective in suppressing AF or reducing episodes, and the electrophysiological effects of Sotalol on heart cells – prolongation of effective refractory period – is opposite to the changes that are seen in patients who develop AF. However, conceivably the heart-rate slowing effect of Sotalol may permit more time for APCs/premature beats to develop between heart beats and these APCs are often triggers for AF. Also this may be compounded by increased “vagal” tone which occurs during sleep that also promotes AF occurrences. Hence pacing people at a heart rate just faster than their own rate has been shown in some studies to reduce AF occurrences.
The development of AF is a long road with many different directions and final destinations – some people don’t feel it and others feel every single beat. The ability to control AF differs from patient to patient because everybody’s AF is different, depending on their specific medical condition(s), lifestyle, and general habits. Believe it or not, some people who are “too healthy”, that is competitive athletes or people with athletic physical conditioning have a different neurohormonal makeup than the general public – they often have lower resting heart rates related to elevated “vagal” tone from being in peak physical shape. Vagal tone is increased also at night, and we do see that in some people elevated vagal tone provokes AF. Sometimes a degree of “deconditioning” is required to reduce vagal tone. This does not relegate one to a sedentary life, but it may be different than the physical activity level and lifestyle you describe. Amiodarone is the strongest of antiarrhythmics available but if that is not effective in maintaining sinus rhythm after cardioversion, there are less potent antiarrhythmics that your particular physical make-up may still respond to better, such as Dronedarone (Multaq) – there may be some evidence that Multaq works better in people with vagally-mediated AF. If medications are unsuccessful, then an ablation is likely the next best step to prevent or at least reduce your AF burden.
First it should be understood that not all people with AF progress require ablation. In fact ablation is just another treatment option - people who are symptomatic from AF and intolerant to or failing medical therapy are candidates for ablation, but ablation is not mandatory. There are other options including pacemaker implantation with AV junction ablation that can be done in most countries. Medical tourism exists and our particular institution participates. You can find more information at: http://www.onlinemedicaltourism.com/Aurora-St-Lukes-Medical-Center.html
In people with a low risk profile including younger age, aspirin 162 mg may be beneficial and adequate to prevent strokes. Stomach lining erosion with gastritis, ulcers and acid reflux can be an important side effect of aspirin and aspirin should be used with caution in this setting as it may provoke serious acute gastrointestinal bleeding, the risks of which may far outweigh the potential for stroke, particularly in younger patients with an otherwise low-risk profile.
Lone atrial fibrillation is AF that develops without significant risk factors or heart disease, and therefore the risk of stroke is generally low, particularly in patients under 65 years, and Aspirin (or even nothing) is generally adequate to prevent strokes even for people who are in truly lone AF all the time. Since your heart rate is not too fast in AF, stopping diltiazem should be fine because it is not intended to prevent AF episodes, rather only to control the heart rate in AF. However it may be that the diltiazem maintains your heart rate in a reasonable range during AF episodes and that stopping diltiazem may allow your heart rate to become faster. Ablation is usually reserved for people who are symptomatic from AF AND who have failed medicines including antiarrhythmic agents. Daily antiarrhythmics or “pill in a pocket” approach in which antiarrhythmic agents are used only during episodes of AF may be a reasonable next step, and if that does not adequately suppress AF, THEN you may be a candidate for an ablation. Rarely AF may be considered in people who wish to avoid medications. It is very difficult to identify people who are likely to progress to more persistent forms of AF but currently you describe yourself as having paroxysmal AF; your low risk profile and absence of heart disease are in your favor.
PVCs can in some cases induce other arrhythmias, including SVTs. However it sounds like the kind of arrhythmia you were having is atrial flutter which is not classified as a PSVT. While this arrhythmia is generally unrelated to PVCs, it is commonly seen in association with AF. (In many ablations may be truly curative, but sometimes the same rhythm may recur, and at other times a similar heart rhythm – not necessarily the original rhythm that was ablated – may develop over time. PVCs can arise from many different areas of the heart, and an ablation to target PVCs from one area of the heart does not guarantee that PVCs from another area will not manifest. Frequent PVCs are not dangerous themselves but it may reflect an irritability of the cardiac electrical system due to blockages in the arteries of the heart (coronary artery disease), weakening of the heart muscle (cardiomyopathy), or just excessive sensitivity of a specific location to produce extra beats (i.e. PVCs) particularly in response to stress or anxiety or any source of excess adrenaline release. Depending on the underlying condition, ventricular tachycardia can develop.)
BP is difficult to measure in AF because of the irregularity of the systolic and diastolic phases that are required to obtain accurate BP measurements. However, if BP is reproducibly found to be elevated then it may be related to the following: AF decreases the cardiac output and may provoke a compensatory increase in vascular tone and thereby increase blood pressure, sometimes not just back to baseline but overshooting baseline. Further the anxiety provoked by AF can be enough to increase BP.
Shortness of breath in someone with mitral valve repair, and AF requiring cardioversion and Amiodarone, should be considered as either related to 1) the quality of the valve repair and degree of residual mitral regurgitation, 2) due to Amiodarone from pulmonary toxicity/pneumonitis/fibrosis, or 3) due to other causes unrelated to the AF or its treatment. Also in people with recent open heart surgery, they can develop fluid collections around the heart (pericardial effusion) or lungs (pleural effusion) that can cause shortness of breath. Pulmonary congestion related to progressive weakening of the heart muscle (cardiomyopathy) can also provoke shortness of breath, and finally blood clots that travel to the lungs can also cause shortness of breath – this option is less likely if chronic anticoagulation is continued with ability INR maintained between 2.0 and 3.0. Finally confirm that your shortness of breath is not in fact related to a recurrence of AF.
AV node ablation does not control AF, it only controls the ventricular rate the AF produces so you would still require coumadin. AV node ablation itself is usually associated with success rates >98-99%, however it results in complete heart block and therefore requires permanent pacing.
While the “pill in a pocket” approach is effective and is not just for emergencies, every patient and their AF should be individualized. While one patient may tolerate this approach, another patient may require daily antiarrhythmics to maintain adequate suppression of AF. Consult you physician regarding this possible treatment method.
Yes flecainide can increase risk of conduction block. Most antiarrhythmics do affect the conduction system in a manner that inhibits conduction of arrhythmias, but the normal rhythm can be affected as well.
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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