Thank you for question. There are a number of potential medications for atrial fibrillation. If you heart size and function are normal and you have no evidence of coronary artery disease then we can use all of them. If you have coronary artery disease then we can use Ė dronedarone, dofetilide, sotalol, or amiodarone. If you have heart failure, then we typically need to use amiodarone or dofetilide. The newest medication available is dronedarone. It is like amiodarone (an analog). It is not nearly as strong as amiodarone, but it also does not have the same risk of injury to the lungs and liver. It also does not interact with the thyroid gland like amiodarone. Dronedarone is only safe if you have not had any recent episodes of heart failure and your atrial fibrillation is such that it comes and goes. If you have heart failure or are in atrial fibrillation all the time you should avoid it.
I believe we only have part of your question. It appears that your atrial fibrillation is progressing in severity to a more persistent subtype that requires cardioversion. This pattern is not surprising since you have valvular heart disease with both ventricular and atrial remodeling. Although amiodarone is a relatively cardiac safe medication in the setting of valvular heart disease, your age and pulmonary disease to me would be reasons to consider other options. These options include a washout of amiodarone followed by use of a less toxic medication versus catheter or surgical ablation. With you valvular heart disease and moderate-severe left atrial enlargement, if you are interested in a catheter ablation it should be performed by an operator that is experienced not only in pulmonary vein isolation, but also in mapping both micro- and macroreentrant tachycardias that are often seen in those with a surgically modified heart. The operator should take every possible precaution to minimize your exposure to fluoroscopy during the procedure and rely heavily on a 3D mapping system to avoid placing you at risk for various radiation-relative malignancies over your anticipated long life span. I would consider a percutaneous catheter-based approach before surgery since your prior procedure would preclude a minimally invasive approach.
I completely agree with you. Iím not a fan of drugs but when they work, why not using them. We have to keep in mind that the aim is to reduce the impact of AF on quality of life. If rate control doesnít fulfil that goal, AA drugs have to be tried. You can even continue Propafenone at the same dosage. There is no dugs able to cure AF. What we look for is to reduce the number of episodes and their impact on your quality of life. I therefore donít consider the 2 episodes you had as a failure. You can certainly increase the dosage up to 900 mg per day if your kidney function is normal and shift to Flecainide when Propafenone will be inactive. It may or may not work. Ablation is to be considered if at least one drug has failed. In other words, if you consider the present situation not acceptable with Propafenone, you could go for an ablation. I would suggest to wait a little longer with an increased dosage of Propafenone. Donít wait too long as once the AF is permanent, ablation is more difficult and less successful.
Yes, this is frequently observed and is probably due changes in the autonomic nervous system by ablation. The interruption of AA drugs may also explain it partly. But keep exercising and training and it will improve.
This is an interesting observation. However, I donít think it is that simple. I have had many patients with magnesium supplementation with limited efficacyÖ
No link has been established to the best of my knowledge. Having both conditions is rare and this is why it has not been studied.
You could consider reablation as this could suppress both the PACs and the pauses. Some physicians could recommend to implant a PM if the pauses are significant but it would make more sense to me to repeat the ablation procedure.
The impact of smoking is limited on AF and there have been very few studies on that. None on passive smoking.
The values of your ECG parameters have to be validated by a doctor as the automatic measurements by the machine are sometimes wrong. If confirmed, I would suggest to stop Multaq. The change in your arrhythmia is likely to be due to an incomplete effect of the drug that has organized your AF (into atrial flutter) and shortened atrial fibrillation to some episodes that are now not exciding the simplest form: PACs. But this is not improving your quality of life, as frequently observed, AA drugs are not perfect. AMiodarone would be more effective but at 66 years old, you may be too young and the chances for developing significant side effects are high!
Your description is the one of a Tamponnade where the hemodynamics was further impaired by the arrhythmia. What surprise me is that you donít mention drainage?