I am reading that afib could be caused by heartburn. Have you known any patients that had their afib stopped by treating their heartburn? How does heartburn cause afib - assuming this relationship exists at all. Your opinion?
Also, when afib episodes happen on a regular schedule, as if were, what insights does this set pattern tell you about possible causes and potential treatment?
p.s. My father is 53 and I'm trying to learn all I can to help him with this.
Our knowledge of atrial fibrillation is growing rapidily, but there is still a lot to learn. For example, we are just starting large studies on the genetics of a. fib, we are following the long term out comes of patients after a. fib ablations.
There is a subset of people that have a. fib triggered by swallowing. I have heard anecdotes of people with a. fib related to heart burn, but haven't read any papers or seen research in this area. A. fib related to swalling is thought to be from increased vagal tone related to swallowing.
Most physicians manage a. fib conservatively with medications, although most people should at least try cardioversion early in their a fib to try to prevent it from becoming a life long event. There is a subpopulation of people with a fib that are severely affected by the arrhythmia and choose an invasive therapy called PVI (pulmonary vein ablation) or a. fib ablation. This is proving to be very effective but the long term results are not known yet -- we have only been doing them for a few years now.
It never hurts to see a cardiologist or electrophysiologist for advice regarding the management.
I believe that acid reflux is connected to A-Fib and other arrhythmias. The connection is the Vagus nerve which runs near the esophagus and the heart. Irritating the esophagus can trigger the vagus nerve which sends weird signals to the heart's electrical system. This is what my doctor told me.
Hello. A few weeks back I asked a question along those lines. I started having severe GERD in December and my pvc's started in force. I've started a daily exercise program and take acid-reducing drugs and the pvc's are almost gone. My cardiologist denies the link, but when she left the room her nurse said absolutely they are connected. I also had an ED doctor tell me they are connected. It makes sense to me! Good luck.
It amazes me how ill-informed the medical world can be. I saw a high profile arrythmia center and mentioned that certain foods (garlic, spices, etc) triggered my arrythmias and I was told they had never heard of such triggers. I also find that when I get sick (even a minor cold) that my arrythmias get much worse (no, I do not take any medication for it), but again a cardiologist said there is no such known link. I will bet there are many people in this forum that will agree with me that what I have identified above are without question triggers.
No doubt about it - heartburn can trigger heart arrythmias and I am a living example of it!! When my gullet gets inflamed I know I'm in for a lot of palpitations until it subsides.
Heartburn I developed after taking a rather strong anti-biotic resulted in me having an extra heartbeat every two minutes for two days.
So - (in my opinion) heartburn/indigestion is not a cause of a-fib but definitely a trigger.
Very similiar to yours PVCs, PACs, fluttering , thumps, strange heartbeats in general, structurally normal heart, no evidence of coronary heartdisease, no family history, just palpitations in general that trigger anxiety and worry for no apparent reason, sometimes triggers are foods that have in onions, garlic , pizza and spicy foods.Alcohol and indegestion are definite trigger,being very hungry or overeating. I don't drink alcohol anymore, never did smoke, basically otherwise fairly healthy. This has been happening well over 20+ years.
I'm with you. I really noticed a connection with arrhythmia and being sick with flu (fever, cough) this winter... I wound up in the er and it took a lot of meds to get me out of a flutter or sinus tachy or whatever it was exactly, maybe both, into nsr again. Flu shot next year! :)
I was 46 when I first experienced AFIB. I'm now 49. I had been suffering from PAC's for about 8 years, and it turned into AFIB. I tried two different meds, but they didn't work in the long run. Finally had a Pulmonary Vein abalation at Mayo about a year ago which was very successful.
Heartburn is probably not the cause of the AFIB. I have heartburn as well, but heartburn is something that occurs with age as does AFIB. So sometimes people associate the two directly. I'm not saying that heartburn cannot percipitate PVC's, but I went to a very good EP and he didn't even ask the question about heartburn. And Mayo is at the cutting edge of research on this subject. After all AFIB is the most common arrythmia out there.
There are a number of theories about AFIB. One that the EP believed was true in my case is that AFIB is clearly seen in people who have been highly trained athletes. I ran college track and have been a runner through most of my life. They have found that track athletes, basketball players, and hockey players have a high incidence of AFIB. The theory is that the pulomonary veins get stretched and larger causing irritation points for electrical impulses. A great deal of AFIB comes from the pulomonary vein areas.
Another theory is that it is hereditary. In my case my Mom had it (she passed away) and my sister has it. So I wouldn't be surprised that it is hereditary.
You also need to rule out heart disease. Heart disease can be a cause of AFIB.
I would encourage your Father not to ignore AFIB. It does get worse if untreated. If he isn't in AFIB all the time, and it converts on its own there is a good chance that meds will help. Many people can control it through meds quite well. He should also be on a blood thinner because clearly the biggest problem with AFIB is stroke and heart attacks from clotting.
Second of all I would seriously consider an ablation if meds don't work. Most doctors will not consider an ablation unless meds fail, and that's because it is definitely and invasive procedure and not without some risk. But if he is highly symptomatic and meds don't work then it's worth considering. But go to a really really good hospital. Make sure your insurance will cover it because it isn't cheap. Mine cost $55,000.
The big thing is to try and stay in rythmn as much as possible. If he is having frequent episodes then that isn't really acceptable.
I know this can be really frustrating for your Dad. But perservere in getting it treated. Do not settle for anything less than regular heart rythmn. I am so glad my cardiologist settled for nothing less.
I strongly believe there are a subset of people for whom GERD is a potent AF trigger. A number of them (who like me also frequent Hans Larsen's excellent Lone AF forum) have experienced total relief from AF for 2 or more years further to taking PPIs (such as omeprazole) for GERD.
Afib/pacs/pvcs are largely caused by cardiac foci, which we are all born with (ergo the inherited connection). In many folks the locations of these foci (islands of electrical cardiac cells) are of no consequence since their constant signalling can't communicate with the normal electrical pathways in the heart. For some folks this is not true. Athletes can develop "stretched" areas of muscular cardiac tissue, typically in the PV ostia where foci are known to live, and channels develop through which ions can be pulsed from the foci leading to, bingo, arrhythmia.
For many folks, these foci are close to normal signalling channels, but need an assist to get their ion pulses through...the assist comes in the way of the nervous system ennervating the cardiac tissue, typically, vagal. When something happens to change the state of your nervous system, like hormonal surges, drugs, foods, posture, heartburn, you-name-it, then the focal signalling can travel easier.
There's really no mystery to it. It's both genetic (since we all have them from birth) and physical (athletic "stretch" and disease). What confuses the situation is that partially hidden foci (that are not normally causing a lot of havoc) can result in all sorts of arrhythmia given the so-called triggers mentioned above which affect the nervous system surrounding the heart.
The foci - nervous system connection is only mentioned tangentially in text and/or papers. One-on-one discussions with EP specialists with academic experience (ie, research), have pointed to this universal theory. Everything I have experienced, and others have complained about on this forum and other forums, is consistent with this hypothesis.
The facts as I understand them:
(1) foci are electrical cardiac cells which represent one of the two types that make up the heart: (electrical and structural or specialized muscle)...they are not created and seldom disappear on their own (pretty much figure that they last as long as the rest of your heart).
(2) foci continuously depolarize (at their own pace, pretty much governed by their size and shape)
(3) the ability of focal signalling (the ion pulses generated by depolarization) to affect the heart's normal pacemaker systems (made up of the same electrical cells) is contingent upon how close the foci are to such systems and how easy the ion pulse can travel.
(4) Ion pulses (from depolarizations) travel in a way that is modulated by the normal nervous sytems ennervating cardiac tissue (of course, this includes the vagal system)
(5) foods, drugs, postural changes, anxiety, exertion, digestion, indigestion, pain, GERD, and changes in temperature all affect this nervous system and generally will make it easier for focal signalling to travel...interestingly, even slight the changes in this autonomic nervous tone can be significant, for example, inhalation/exhalation will engender different effects as well as, excuse the French, farting...which has a calming effect on the autonomic system and can actually halt the production of simple arrhthymia such as PACs.
(6) current thinking on athletes and their prediliction towards arrhythmias such as PACs and PAF, is based on the previously-mentioned "stretched" PV ostia mentioned previously, as that's one of the areas of the heart which tend to be affected by a lifetime of exercise...presumably, the strething effect leaves behind more channels in the tissue for focal signalling to travel through.
As I said, the source for this information is from current textbooks (medical library), recent papers (PubMed on the Web and many other pay-for services), and discussions with scientists. By and large, the Web itself tends of offer up anecdotal evidence for all kinds of theories, and leads you to forums such as these...which of course I would never depend upon for factual information (quite the enigma).
Thanks. The theory seems to explain well a few personal observations and is relevant to solving a real problem having to do with some planning for risk I must do.
With WPW pathway supposedly ablated now, I wonder if I could be like many others with WPW who also have afib (via PV ostia). What appears as short run VT may not be regular, but two EPs have been very very confident that the signature is that of VT.
The theory does't preclude the development of channels in the ventricle caused by ablation does it?
From what I understand, rf ablation would not produce new channels. The theory appears to be that the removal of one particular type of arrhythmia (presumably due to a focus/channel combo) by blocking the channel (isolating the focus) or by toasting the focus itself, may result in other previously existing but less obvious foci/channels to become evident. That is, the first arrhythmia was dominant, and simply did not allow others to surface. The net effect would feel as if a new focus/channel was created by ablation.
I believe this is consistent with the current view held by the majority of EPs.
I did see an article (freebee on the web someplace, maybe in Circulation) on regenerated nerve growth in cardiac scar tissue. Based on microscopic inspection of cardiac tissue harvested from the hearts of people with heart disease, the authors showed how dendrites of nerve regenerate and grow haphazardly (against the grain) in tissue surrounding cardiac scar, presumably explaininig one possible way to connect heart disease with VT.
I am going to have to admit that I was only able to skim the article, and study the pictures - a real understanding is beyond me really. It made me wonder though whether new nerve growth might occur near scar caused by heart disease, then why not in the scar near an ablation site, particularly if that site was difficult to access (eg mitral annulus) such that an electrode could not be placed squarely?
As I understand it, nerves do not conduct the cardiac impulses, ie, the depolarization process. Depolarization is a process much like a when a capacitor discharges its stored electrons. The foci generate a load of ions which eventually either disperse or find a conduit. The presence of a nervous system and its activity around that conduit changes the ease with which that ion pulse travels. So, when nerves reappear in and around scar tissue, it shouldn't really make a big difference... however, like you, I am no expert in these matters.
Presumably, rf ablation toasts the cardiac tissue in such a way as to close up those conduits. But just like toast, the scarred tissue may have it's own set of new conduits, however, it seems that this doesn't happen too often based on the success rates in shutting down the targetted arrhythmia.
the best i can think of what might cause your symptoms after ablation , presuming your ablation was a success is that the ablation simply unmasked the foci for an arrhythmia that was already present, the arrhythmia that was causing your initial problem probably suppressed the dormant arrhythmia, now with the main arrhythmia gone , this one has had time to show its dirty face, this is what happens after some ablation as i understand especially those with concealed accessory pathways.
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