Very frequent PAC's

Hi all,

Long time lurker first time poster. In the mid 1980's, when i was 12 years old, i had my first rapid heartbeat. I think it was atrial flutter by all the info i have researched about it but I never got it officially diagnosed. My pop used to say it was normal and that he used to get something similar every once in a while. However, they were pretty frequent in those days, happening mainly when i exercised in the heat. The flutter would last from like 5 min to as much as an hour sometimes but my heart would eventually convert back to NSR on it's own with some rest. I had my first episode of afib when i was 21 after drinking a few to many coffees one night in college. That sent me to the hospital for the first time and it lasted for 4 hours before converting on its own eventually.

Unfortunately for me i feel afib and it feels absolutely dreadful (fish flopping in my chest sensation). So for almost 20 years i kept afib at bay by moderating physical activity in hot weather and avoiding caffeine entirely. Unfortunately, in october of 2018 i ended up waking up in the middle of the night with afib. It was sleep apnea that most likely triggered it. I spent 72 hours in the hospital that time waiting for it to stop. Again, my heart converted back to NSR eventually without having to do a cardioversion. However, after that episode i was absolutely determined to get an ablation done. There is absolutely no way i can live with afib. So in the spring of 2019 i had a RF smart touch catheter ablation. Thankfully that has curbed afib for the last 3 years.

The issue that i am having now is similar to the issues i had leading up to the Oct 2018 afib episode. For whatever reason in the summer of 17 i started noticing that i would get more frequent PAC's when i exercised. PAC's always preceded atrial flutter for me. It has always been my early warning system to take it easy and cool off.

I dont know why all of a sudden the PAC's started becoming significantly more frequent with exercise. I had had an upper endoscopy in 2017 to fix a stricture in my esophagus. Doc noticed i had a hiatal hernia which i have been taking PPI's for the last 5 years. One of my thoughts is that the endoscopy changed something in the esophagus near the vagal nerve and is the root cause of the new onset of frequent PAC's.

From that standpoint it was only a matter of time before the PAC's triggered the October 18 afib episode. I had hoped that the ablation would fix the PAC's too but it had no effect on them. Now, three years later the PAC's are worse than ever. When i exercise i get a PAC every 3-4 heart beats. It feels uncomfortable, almost like im in afib. I measure using my kardiaband with my apple watch to verify its not afib. There are some months its better and some months its worse. I have shown my kardia readings to my electro and he says its just PAC's but if want to try different meds to control them its up to me.

I only take 25mg metoprolol to fix some unsual ectopics i get when i stand up to quickly. It really does nothing for PAC's. In the last two weeks the PAC's have been every single time i get up and walk around or right after i eat. Its very annoying. FYI - My pop now has permanent afib but is fortunate that he does not feel it. I am very worried that my fate is inevitably linked to his and that the new frequency of PAC's is the tides beginning to turn

Is it possible the vagal nerve was aggravated with the endoscopy? If so, is there any way to fix this? I really am fearful of trying new more powerful drugs to control PAC's as i have read they can be toxic to the body.

Thanks all.



Edited 1 time(s). Last edit at 01/01/2022 07:04PM by sisyphus222.

It's really unlikely that an irritated vagus nerve is still irritated 4 years later. Nerves heal slowly, but damage severe enough to take 4 years to heal would have had immediately obvious symptoms at the time. I think you're barking up the wrong tree on that one.

There are several antiarrhythmic drugs, and only two of them have any serious toxicity concerns (amiodarone and digoxin). I think if I were you I would ask your doc about trying Multaq. It's a very safe drug with few side effects and it's generally considered the "mildest" of all the antiarrhythmics. In fact, it's often too mild to control full-blown afib, but it can be good at controlling ectopics. There are also supplements and lifestyle modifications that might help. This forum is full of discussions of them.

You wrote you have ectopics when exercising, but... How do they come? At the start or later?
Have you tried starting very gently? Since ablation, I'm dealing with ectopics at rest and after meal. I have ectopics when exercising, but only if I don't care making things gradually. When "warmed", I'm OK.
I'd advice too against PIPs. They're good to deal with some temporary acid reflux issues, but bad on the long run. They reduce your stomach acidity to a point where you've not enough acid to digest normally, nor enough acid to make your LES close efficiently. You'd not feel heartburn any more, but have more reflux; and stomach reflux can irritate the vagus nerve.

Are you sure they are PAC’s and not PVC’s or even a mixture?

Quote
Pompon
You wrote you have ectopics when exercising, but... How do they come? At the start or later?
Have you tried starting very gently? Since ablation, I'm dealing with ectopics at rest and after meal. I have ectopics when exercising, but only if I don't care making things gradually. When "warmed", I'm OK.
I'd advice too against PIPs. They're good to deal with some temporary acid reflux issues, but bad on the long run. They reduce your stomach acidity to a point where you've not enough acid to digest normally, nor enough acid to make your LES close efficiently. You'd not feel heartburn any more, but have more reflux; and stomach reflux can irritate the vagus nerve.

They come immediately when I start walking around. They stop after I sit. For the last three years it was random. Sometimes I would get up and go for a jog and not feel or have any palpitations. Most of the time they start within 5-10 min of exercise.

What it feels like right now is when I get sick and the pacs happen every time I move around. I wonder if I might be asymptomatic for some virus right now too. Who knows. The thing is there has been a big change in how fast they come on and how frequent they are occurring. I mean I would get 3 a minute just walking around but now it’s like I’m almost almost in afib every time I get up and move based on the frequency.

My cardiologist and electrophysiologist have both scene the ekgs during stress tests and they confirmed they are PACs.

Quote
Carey
It's really unlikely that an irritated vagus nerve is still irritated 4 years later. Nerves heal slowly, but damage severe enough to take 4 years to heal would have had immediately obvious symptoms at the time. I think you're barking up the wrong tree on that one.

There are several antiarrhythmic drugs, and only two of them have any serious toxicity concerns (amiodarone and digoxin). I think if I were you I would ask your doc about trying Multaq. It's a very safe drug with few side effects and it's generally considered the "mildest" of all the antiarrhythmics. In fact, it's often too mild to control full-blown afib, but it can be good at controlling ectopics. There are also supplements and lifestyle modifications that might help. This forum is full of discussions of them.

Interesting. Well if it’s not a result of the endoscopy that would then point to some other aging of the heart related issues. Not what I was hoping.

I happened to be reading up on Sotalol the last while as my cardiologist says this is what he wants me to take while I wait in line for the ablation he wants me to have. I haven't accepted either recommendation for the time being. He tried to minimize any risk associated with Sotalol.

Perhaps the risk is minimal, I don't know. I've noticed that some doctors view the risks associated with AADs more seriously than others.

According to a 2018 European Heart Rhythm Association and European Society of Cardiology position paper entitled: "Antiarrhythmic drugs–clinical use and clinical decision making: a consensus document..." Sotalol can cause torsade de pointe in up to 8% of the patients who start taking it. Several other AADs can also cause this problem, although less frequently. (Table 8, page 732p)

Torsade de pointe can cause sudden death, among other things.

The consensus document states: "Initiation of any AAD implies some risk of adverse event, including proarrhythmic effects" and goes on to explain how cardiologists should screen patients and select an AAD for the particular patient so that there will be less risk.

I haven't studied the whole document. A few other quotes caught my eye recently:

"Antiarrhythmic drugs are drugs with a narrow therapeutic window, and there is a small plasma concentration interval between the lowest effective dose and the first toxic dose, that is, between undertreatment and the toxic or proarrhythmic effect.

"Patient education on the potential symptoms associated with proarrhythmia (severe palpitations, pre-syncope, and syncope) accompanied by a 12-lead ECG for several days after drug initiation is a strategy that can be applied to the majority of patients in order to safely monitor the effects of AADs. These safety rules apply even more strictly in patients with risk factors for torsade de pointe."

They do mention that only patients deemed at high risk are usually hospitalized at the time they first start taking an AAD so that if a severe adverse event occurs there is a good chance of saving the patient, because of economics.

Re: toxicity of AADs. I ran into this cheery article published in JAAC, just before signing off the computer for the night:

"Torsades de pointes secondary to Sotalol: Predictable, but not always preventable"

They start out the article: "Sotalol is an effective antiarrhythmic drug for the maintenance of sinus rhythm in atrial fibrillation. However, its QTc-prolonging effect increases the risk for torsades de pointes (TdP) and sudden cardiac death. Thus, it is typically loaded in the inpatient setting with close cardiac monitoring and serial electrocardiograms. Despite adherence to inpatient loading protocols, sudden cardiac death due to sotalol can still occur."

They then describe a woman who it was thought was at low risk for an adverse event on Sotalol initiation who died.

They conclude: "This case highlights the fact that while inpatient monitoring of QTc during sotalol loading can reduce the risks of sudden cardiac death, it does not completely eliminate this risk. Patients should be well aware of this risk before they agree to start this medication. Female gender, chronic kidney disease, and a history of congestive heart failure are significant risk factors for TdP due to sotalol."

Quote
David_L
I happened to be reading up on Sotalol the last while as my cardiologist says this is what he wants me to take while I wait in line for the ablation he wants me to have. I haven't accepted either recommendation for the time being. He tried to minimize any risk associated with Sotalol.

Perhaps the risk is minimal, I don't know. I've noticed that some doctors view the risks associated with AADs more seriously than others.

According to a 2018 European Heart Rhythm Association and European Society of Cardiology position paper entitled: "Antiarrhythmic drugs–clinical use and clinical decision making: a consensus document..." Sotalol can cause torsade de pointe in up to 8% of the patients who start taking it. Several other AADs can also cause this problem, although less frequently. (Table 8, page 732p)

Torsade de pointe can cause sudden death, among other things.

The consensus document states: "Initiation of any AAD implies some risk of adverse event, including proarrhythmic effects" and goes on to explain how cardiologists should screen patients and select an AAD for the particular patient so that there will be less risk.

I haven't studied the whole document. A few other quotes caught my eye recently:

"Antiarrhythmic drugs are drugs with a narrow therapeutic window, and there is a small plasma concentration interval between the lowest effective dose and the first toxic dose, that is, between undertreatment and the toxic or proarrhythmic effect.

"Patient education on the potential symptoms associated with proarrhythmia (severe palpitations, pre-syncope, and syncope) accompanied by a 12-lead ECG for several days after drug initiation is a strategy that can be applied to the majority of patients in order to safely monitor the effects of AADs. These safety rules apply even more strictly in patients with risk factors for torsade de pointe."

They do mention that only patients deemed at high risk are usually hospitalized at the time they first start taking an AAD so that if a severe adverse event occurs there is a good chance of saving the patient, because of economics.

My gosh! I was given a choice of an AV ablation (final nuke of my AV node) or try Sotalol. I started Sotalol in the hospital during a 226hr because no drugs worked, I was ecv 51 times and I was out of options. Then a week later (4 out of 5 weekends in a row admitted), I was back and they increased my dosage and I had three 12 lead ekgs and spent two days in telemetry and they said I had prolonged AV conduction but I was safe to be discharged with no schedule of getting follow up ekgs. Since then I’m getting 2-3 episodes a day, same166 hr but they self convert.

Now after reading your post I see why an AV ablation was suggested. I was told it was safer than being on sotalol for life. The problem with an AV ablation is one is pacemaker dependent which can possibly lead to pacing induced cardiomyopathy-heart failure…and one may get a pacemaker controlled lower heart rate but they would feel the symptoms of being in afib. The selling points were no more ER visits for tachycardia flutter and no more drugs.

I had a flecainide overdose in 2019 and ended up fighting for my life in icu because I am sensitive to arrhythmia drug increases. So getting an increase dosage of sotalol —cardiologist goal— was chosen to cut down in my weekly hospital visits of being admitted Friday and discharged on Monday or Tuesday, home three days and repeat again the cycle back to the ER. It was the option I was given on my birthday being stuck in a hospital bed for two days in high tachycardia.

Thank you David for your post on the dangers of sotalol.

I figured out why I suddenly may had 5 weeks of hospitalized stays. My cpap machine was malfunctioning I thought because the water canister remained the same level. I thought it was just a temperature control error until I woke up choking last week and the machine had turned itself after 2 hours 40 minutes. Looking back I believe another time I wasn’t sure if I turned it off because was off when I woke up. It makes sense…4-5 days in the hospital I used my functional travel cpap but once I returned home after three days of waking up dozens of times during the night because unknowingly it turned in and off and I would return to the ER.

I’m now using my travel cpap since the past week.

I'm not enthusiastic about AADs, and I'm not enthusiastic about ablation, but I'm not enthusiastic about A-fib either. At this point, I would take ablation over any extended use of AADs, but I haven't gotten in line anywhere at an ablation clinic. If I was experiencing an extended episode of A-fib that would not respond to ECV and I could not get an appointment for an ablation for many months I would certainly consider an AAD.

I'm currently in NSR. I have been in continuous NSR much longer than my cardiologist appeared to believe was going to happen given the A-fib episodes I presented to him with starting in October. I'm optimistic at the moment that my heart will continue in NSR for another long period of time. I've made a number of lifestyle changes aimed at lowering my risk of going into A-fib. I've also gotten more serious about meditation - instead of meditating at a certain time of day I meditate when I feel I'm letting stress affect me. And I'm enjoying acupuncture treatments every week. At least I can dream that I can continue in NSR and never have to make the decision to get an ablation.... I like the idea of somehow staying in NSR long enough they'll approve the Pulsed Field catheters that appear so promising right now.

As I'm retired, I spend most of my time studying A-fib, with an aim to get the best understanding I'm capable of about it, so if or when it comes back I can feel more confident about any decision I make.

Update: Less than 100 PACs a day for the past full month!
Last change that seem to eliminate frequent PACs: Changed time of day for atorvastatin 40mg; now taken at 1pm instead of 8pm.
Continued using raised room temp for sleep to 67 degrees.
Continued the higher level of exercise;
In the past month, I have brought back caffeine-1 mug a day; alcohol (1-2 drinks/day on some days); sweets;
Have some days with fasting glucose in 115 range; other days in the 80s.
Still monitoring glucose and ECG.

I see my cardiologist next week.