An a-fib/flutter episode that wasn't.

I'm over two years post successful ablation.

I woke up at 0400 with a relatively high and very irregular heart rate (around 100 bpm) combined with many irregularly spaced strong thumps. I got up, took about 2 gms of potassium, wired myself up to the Holter, and went back to bed. My heart settled into what seemed like NSR after about 40 minutes.

When I got up this morning I examined the four hours of Holter recording. There was no a-fib and there was no a-flutter and there were only seven PVCs during the four hours of data (most of which occurred after my heart rate steadied) and there were only three PACs (most of which occurred after my heart rate steadied).

There was a highly irregular NSR heart beat which faded into a steady normal heart rate after some 40 minutes, but the perceived symptoms perfectly mimiced the very familiar symptoms of a-fib/flutter combined with numerous strong PVCs.

I've reported on this before. My data is still consistent with having a normally dormant pacing node located near the AV node. That normally dormant node occasionally comes to life and competes with the AV node for control of heart rate for a while, before becoming dormant again. The result perfectly mimics an a-fib/flutter episode.

At one pole we have "silent a-fib". At the other pole we have "imaginary a-fib".

I wish more of you had some serious ECG instrumentation.

Wil,

Is it possible that Afib occurred before you were able to get your monitor hooked up?

Marian

Well, Wil - this is certainly interesting.

I, too, wish I had your ECG equipment or something similarly reliable. I've had 4 incidents and it certainly feels like 'good ole afib' to me. In fact, I'd call it unmistakable. I tracked my pulse on and off during the hour as I waited for the PIP to take effect, and it was a rhythm pattern which which I am unfortunately all too familiar. I would be stunned to learn that it was only PVCs... and I certainly don't have the courage to wait it out with nothing and risk missing the window where it might convert. I'm just too chicken.

As you say, yours mimicked an afib pattern so I am now really thinking hard about my own events.

In any event, you normalized and all is well. That's the good news.

Jackie

The a-fibby symptoms were unchanged during the period of time after I woke up, took the K, wired up the Holter, and went back to bed. The symptoms continued unchanged until about 30, or so, minutes after returning to bed. The last ten, or so, minutes in bed before returning to normal NSR were less a-fibby, perhaps because the alternate pacing node was losing strength, possibly because the plasma K level was increasing.

I seem able to sense when the plasma K level is rising. There is the appearance of a very slight sense of impending nausea and a slight feeling of chilling. In this case NSR resumed well before those symptoms peaked. The symptoms usually peak about an hour after I injest K.

There were essentially no real PVCs present, Jackie. The wildly irregular heart pacing caused my brain to perceive the presence of lots of PVC thumps, but I was aware of only the brain's perception of PVCs being present. There were essentially no real PVCs recorded. Just highly irregular NSR.

Wil, i went back and read your posts on this same subject of 9/6/07. Very interesting thread. Between you and Kagey, very educational thread concerning 2 coexisting pacemaker nodes following ablations.

[www.afibbers.org]

PeggyM

Wil is this just a post ablation issue for you??.

Also I gather from your posts in the past that your PVC'S not very symptomatic so that could be the reason you confused your irregular NSR with them.

Just as a matter of interest if I was to grade my PACS at 100 my PVCS would be graded at 5% nevertheless they are still unpleasant.

Regards

Mark

Prior to the first ablation I was 24/7 a-fib for over four years. After the first-ablation-post-medication I was 24/7 a-flutter for two months. After the second-ablation I have been 100% NSR except for one recorded a-flutter episode of less than 1 hour, plus two recorded episodes of imaginary a-fib/flutter of less than one hour, plus two or three other short episodes of undetermined nature because I was away from home and didn't have the Holter with me to measure what was actually happening.

The perception of the PVCs (real, or perceived but unreal) amounts to a distinct jar in the chest (like someone giving my chest a distinct quick jerk), often accompanied by a sense of being out of breath for an instant, plus an obvious pause before the following beat.

"I, too, wish I had your ECG equipment or something similarly reliable."

On page 6 of the PDF for CR 52 [www.afibbers.org], I describe a home ECG that I put together for about ~$200 US from high school science equipment.

Unlike Wil's nice Holter, 1) you have to remain hooked up near your computer, 2) you can't record day's or many hours of data, 3) you have to interpret the data yourself and 4) you only get to look at one lead placement at a time since it only has +,- and ground not 5, 7 or more leads.

However it is more affordable and will give you a valid look at the data that you can interpret with regards to afib (or not afib). There is an example screen print of a PVC on p 32 of the PDF.

I would not recommend this option if you are really tech phobic.

George

Hi Wil, was it the software that said no AF or can you manually verify it by reading the plot? If it was software I'd check to see if there is a newer version. I'd also be tempted to stick it under the nose of an EP that does ablations. Interpreting ECGs is often tricky, interpreting ECGs from a heart with ablation scars further complicates the issue and I'm guessing most of the software in these devices are not that capable.
I've lost count of the number of times that an experienced cardiologist has disagreed with a machines interpretation of my readings.

Something was going on in the first 40 minutes to cause your beat to be irregular (isn't an ectopic near and above the AV node still a PAC??).
Sick sinus, AV block and AV re-entrant rhythms are all high on the list for producing irregularities. No doubt there are others - has anyone given a name for leaking ablation scar?

There's a time when a 12 point ECG becomes useful in trying to figure out what is going on - perhaps this is one of those occasions?

All the best
--
James D

Thanks, George. I recall toying with the idea of doing your system, but as Wil's event occurred at 4 am - apparently my breakthroughs are prone to happening in the early morning as well and I'm wondering how practical it is to rise from sleep - fire up the computer and get hooked up.

I'll think about it a bit longer and if it becomes more of an issue, I may consider this version.....but I'm not handy with electronics so it could be way over my head.

Jackie

Perhaps I made it sound worse than it is. The ECG device just plugs into a USB interface which plugs into the computer. I describe how to set up the software to get a rolling display.

The main issues I've had are when I sample for a long time. An ECG measures electrical potential in millvolts (mv) between the leads. I ran it for 40 minutes one time. I set it to sample the mv potential 100 times a second so this equals 40x60x100 or 240,000 data points. This kind of overwhelms the software & it is not too happy. It is really built to handle easily say 40,000 points, which would be 5 minutes.

You could also sample less frequently 100 times/sec may be overkill. The issue is how much resolution you need to interpret the data. In my experience in the Cardio's office. They usually sampled for 30 seconds or a minute. In this range, the software would work well. It did work for the larger data set, it just took forever to bring up an old file for reveiw.

Once you've practiced with it a few times, it probably would not take any longer than hooking up a holter and getting it going. The main issue may be thinking clearly at 4 AM, but with a little practice, you easily know where to put the leads, how to connect to them & start the software.

George

The software doesn't have any meaningful capability to identify a-fib or a-flutter explicitly. I scan the data minute by minute, though many minutes are displayed on the screen at one time. I usually initially limit myself to the equivalent of the V1 waveform, to cover more time per screen. That is where a-fib and a-flutter are seen most clearly. If I find anything suspicious in the V1 waveform I can switch the display to see all three waveforms to obtain a better evaluation of what is happening.

In this case the PQRST signature was continuously present during the entire record. That precludes any possibility of either a-fib or a-flutter being present.

The software analysis capability is irrelevant when doing this kind of analysis.

Wil,

I had a similar experience with seeming afllutter/afib at night after my recent ablation. It did not show up on any of the monitor readings, however.

Both my EP and Internist suggested independently that the mind can create a version or sense of afib, especially when it has been traumatized as after an ablation.

Interesting. Ghost afib.

Carol

Carol, if Wil had ghost afib, what made those traces on his equipment? That is more mind influence than even Sarno can explain.
PeggyM, laughing

Wil,

I was also plagued with hard hitting PACs, which unlike the phantom flutter did show up on the monitor readins.

Carol

There are several steps going from dependence on the medical community for ECG data up to a personal Holter.

The first is single channel fixed location recording with an instrument which is relatively sensitive to physical movement. As George says, this allows the a-fibber to determine if a-fib or a-flutter is present, and the limitations are obvious.

The second is a used medical ECG. This gives what is called 12 lead capability, though there are only ten leads. The twelve waveforms displayed are derived from the electrical signals obtained from different combinations of the ten leads. Unless you have additional serious heart electrical problems beyond a-fib or a-flutter only three waveforms are needed to evaluate heart behavior. The medical ECG units usually give two display capablilities: (1) a few seconds of data, displayed as the 12 conventional waveforms; and (2) selecting one or two waveforms which can be recorded for a longer time, as long as 30 minutes if you sacrifice resolution. The medical units are more resistant to physical movement, give more information, but still require the a-fibber be essentially immobile when gathering data.

The third is a Holter. They come as two waveform and three waveform models. The three waveform models are the best choice, because three waveforms give the best ability to discard meaningless data caused by excessive physical motion during the recording period. Generally, the Holter is relatively immune to recording artifacts caused by physically moving around while recording. I suspect my Holter is typical, and the software flags many supposed PVCs, which are actually just aberrant waveforms caused by physical motion. The software usually flags several hundred supposed PVCs which are not actually PVCs. The user has to examine the waveforms to know which PVCs to remove as meaningless. This is easy to do. The Holter is very accurate at identifying PACs. It almost never makes a mistake identifying PACs.

I went directly to a used medical ECG and learned a lot. When I transitioned to the Holter, for the first 18 or so months, I limited myself to recording only on days I knew I would be relatively inactive and felt normal, to be sure to the data gathered included as few unknowns as possible. Another reason for this was that I didn't want to know what might be happening to my heart when I was involved in more stressful activities. When I did start recording on more controversial days I did see some interesting electrical behavior, most of which I've reported on here.

The biggest advantage of the Holter is that it only takes a few minutes to get wired up whenever the heart acts up, and then you go on with life unimpeded. After the heart returns to normal the waveforms can be analyzed to find out what was happening.

Reading ECGs, in most cases, is not difficult to do. The problem is that an a-fibber starts out with essentially zero knowledge about the electrical behavior of the heart and ECGs. It is like entering kindergarten as a five year old with little beyond a basic ability to learn. You have to approach it as a self education project and it takes some time (many months) to acquire all the information and skills needed. As with most self education projects this involves choosing to go down numerous paths, not all of which prove productive, and requires a large amount of determination and initiative.

If you analysis is correct Wil then we are left with the question of what caused 40 minutes of very irregular tachycardia that can't be detected by a holter monitor?

Which still leads me to the conclusion you should verify your analysis with an expert and if they agree with you it's time to get 12 point ECG. (Your previous AF doesn't preclude you from having a new heart problem)

Take care.
--
James D

You seem to be confused over terminology. Tachycardia is a general term used to denote heart rates over some agreed upon rate, usually 120 bpm. There are many possible reasons for such high heart rates: exercise being one; a-fib being another.

Your term "irregular tachycardia" has no meaning in the context of what I reported, because at no time was my heart rate above 120 bpm. I experienced a higher than average normal sinus rhythm resting heart rate, and that heart rate was not constant. The heart rate was irregular.

I do have a 12 lead ECG (which is actually ten leads). Were I to have wired myself up to it, it would have provided the same information the Holter did; perfectly normal sinus rhythm waveforms. But, using it would have precluded getting any more sleep that night, and would only provided a few seconds of data. The Holter provided a far more comprehensive look at what was happening, by gathering data for the entire four hours, about 40 minutes of which was the episode I reported on.

There is nothing to verify with an expert. The waveforms are perfectly normal sinus rhythm waveforms, albeit with a variable time between beats.

I offered an explanation for the forty minutes of irregular rhythm in the first message above. Kagey, in the September thread referenced by PeggyM, experienced something similar and related that Dr. Natale confirmed the validity of the concept of two nearly adjacent pacing nodes. Carol A reported a similar experience to mine, of perceived a-fib/flutter, which did not appear on her monitor's electrical waveforms as a-fib/flutter. She invented the term "ghost a-fib", which is a truly clever idea. We can have a lot of fun with that name.

"Tachycardia is a form of cardiac arrhythmia which refers to a rapid beating of the heart. By convention the term refers to heart rates greater than 100 beats per minute in the adult patient."

or
"Definition of Tachycardia. A rapid heart rate, usually defined as greater than 100 beats per minute."

(all definitions of tachycardia I've ever read put it at over 100 bpm but I'm happy to read any references you can point to that say otherwise.)


You were NOT in NSR if your beats were very irregular. "irregular tachycardia" was the nearest I could get from what you wrote.

1:1 flutter from a leaking PVI is one of several ideas I had that may explain what was going on but I'm well into the realms of speculation. (The list of other possibilities is long and beyond my knowledge)

My concern is that you seem overly confident about your ability to read this new situation. It of of course entirely up to you went to consult an expert, please don't leave it to long.

--
James D

Apologies for the copious miss typing in my last post - I just had a quick browse on my computer before going to bed and am obviously a little tired

--
James D

"You were not in NSR if your beats were very irregular. "

James,
I couldn't have said it better. Normal sinus rhythm is just that - normal. The beats are sinus in origin and regular. An irregular rhythm is a horse of a different gallop!

Also, as you implied, 12 lead EKGs are very useful in the differential diagnosis of cardiac arrhythmias.

Wil,
I know you don't like people to disagree with you, but we will just have to agree to disagree on these issues.

Marian

James - FYI

After cardioversion post-ablation, I was left with little runs of what Dr. Natale diagnosed from a two-week Holteras 'sinus tachycardia.' I never have enough to calculate how many per minute - there are only about 5 to 8 really fast beats and then NSR. It's an odd feeling and entirely different from what afib feels like.

If I had them for a minute or more at a time, definitely, they would be over 100 in a minute.

Jackie

Let's take these issues one at a time.

Tachycardia: I stated the heart rate, above which tachycardia exists, is defined arbitrarily. My Holter default tachycardia rate is set at 120 bpm. If you want to choose a default rate, above which tachycardia exists, at 100 bpm, then I was above that rate a small percentage of the 40 minute episode. This is not relevant to our discussion about the episode I reported. If you can explain to me why it is relevant to our discussion, I'd be willing to examine your argument.

Sinus Rhythm: I think we all agree that sinus rhythm consists of the presence of a standard PQRST waveform. My data continuously showed such a standard waveform during the entire four hours of Holter data.

Normal Sinus Rhythm: I think we all agree that normal sinus rhythm never occurs at a truly constant rate, because all normal sinus rhythm is irregular to some degree, with one exception; truly constant sinus rhythm is often a sign of impending death. To my knowledge there is no agreed upon degree of irregularity above which sinus rhythm is no longer considered normal. If you want to define normal as being less irregular than my data showed, I see no harm in you substituting the phrase "sinus rhythm" every place I used the phrase "normal sinus rhythm" in my messages. This too, is not relevant to our discussion about the episode I reported. Again, if you can explain to me why it is relevant to our discussion, I'd be willing to examine your argument.

Our discussion is about my report that the presence of highly irregular sinus rhythm, documented by Holter data, was perceived as a combination of a-fib/flutter and PVCs. We also have Kagey's report of alternating sinus rhythm rates, also documented with ECG data and confirmed by Dr. Natale, which adds credibility to the concept of two atrial pacing nodes located close together being perceived as producing pseudo a-fib during the transitions between nodes. We also have Carol A's report of perceived a-fib/flutter, which did not show up on the ECG, combined with the presence of actual PACs which did show up on the ECG.

I am reporting that my irregular sinus rhythm episode was perceived, by this very experienced a-fibber, as the seemingly real presence of a-fib/flutter and PVCs.

Hi Wil,

In my ignorance, I'm confused.

"The result perfectly mimics an a-fib/flutter episode."

But with "perfectly normal sinus rhythm waveforms" I assume.

If so ...

"My data is still consistent with having a normally dormant pacing node located near the AV node. That normally dormant node occasionally comes to life and competes with the AV node for control of heart rate for a while, before becoming dormant again.

What I'm having a hard time understanding is how you can have another (normally dormant) pacing node - are you saying this node is generating the signals versus passing them through, which the AV node does, with a slight delay.

Or, are you saying the normally dormant pacing node has its own pathway from the atria?

If the extra pacing node is generating the signal, I would think you would not get an NSR waveform, but a disassociation of the atrial part of the waveform from the ventricular part.

Perhaps you could explain in more detail. This is interesting to me.

Thanks!

George

Well, you caught me with a serious typo. The AV node designation should have been SA node, in both cases.

The second pacing node would be tissue near the SA node, and capable of automaticity at a rate somewhere around 100 bpm. But that tissue remains more or less dormant most of the time.

I have been experiencing irregular rhythm since immediately after the successful ablation. For a short period, about four months post-ablation, I experienced sufficient irregular rhythm time (designated as such by the Holter) to cause the Holter to report eight hours of it per day. I have no idea how irregular the periods have to be to get so designated by my Holter, though the waveforms clearly showed the periods between beats to be irregular. The Holter designated irregular rhythm time has been averaging about 30 minutes per day for the last year of so, but this latest episode was both more irregular and at a higher average heart rate than has been "typical" (I'd use the word normal, but it might get me into trouble).

Hi Wil,

Thanks for the clarification. IMHO, I would suppose that if you are getting a normal NSR waveform, which would be indicative of a normal atrial - ventricular beat sequence, then I can't really see a lot of harm in irregular beat lengths or a somewhat faster rate around 100 BPM.

In my case, my only longer data sets are with the Polar, which only records beat length (or rate depending upon how you display it). Some times I fall asleep in meditation and get a record for several hours. During these times, I've noticed a minute or so of faster beats, ramping up and increasing by 25 or 30 BPM (from 45 to 70 or 50 to 80), then coming back down. This typically only lasts for a minute and is still very regular. It is interesting.

George

Wil wrote:
"I think we all agree that sinus rhythm consists of the presence of a standard PQRST waveform."

Wil, as you know, the P wave represents atrial depolarization. I think you're assuming that because you have one it must be originating at or near the sinus node - this is not the case. Your arrhythmia may not be sinus in origin. (Though you could indeed have sick sinus syndrome)

You can quibble about me using 'irregular tachycardia' (which I still think is accurate) or extract the useful parts out of my post. A 12 lead recording read by an expert may help to pin point the origins and timings of what you are seeing as a normal PQRST wave when what you are describing is clearly not NSR.

I hope you soon have a better diagnosis for what is going on.

--
James D

Not too long after my first PVI, I began having runs of 'irregular tachycardia' as James describes. When I took the Active ECG rhythms strips to my EP, he called it atrial tachycardia, and refused to investigate further, simply saying that it would go away in time. In fact he stated, "Look, there are P waves all over the place." I think he couldn't deal with the fact that his Pappone type PVI had not been successful. Scattered among those runs of atrial tachycardia were clear indications of Afib which were correctly diagnosed by a local cardiologist and then Dr. Pinski of the Cleveland Clinic in Florida.

That led me to have the PVAI by Dr. Pinski in April of this year. So far, so good. No more foolishness.

Wil, I wish you only the best, but I believe that it would behoove you to seek professional advice.

Marian

Marian said, "Is it possible that Afib occurred before you were able to get your monitor hooked up?

Wil notes: This was a valid question. Looking ahead, I'll note that there is some concern implied that me experiencing the symptoms of a-fib/flutter could have resulted from the presence of real a-fib/flutter rather than me perceiving a-fib/flutter when it did not in fact exist.

James said, "...was it the software that said no AF or can you manually verify it by reading the plot? If it was software I'd check to see if there is a newer version."

Wil notes: This was also a valid question.

James said, "I'd also be tempted to stick it under the nose of an EP that does ablations. Interpreting ECGs is often tricky, interpreting ECGs from a heart with ablation scars further complicates the issue and I'm guessing most of the software in these devices are not that capable.
I've lost count of the number of times that an experienced cardiologist has disagreed with a machines interpretation of my readings.

Something was going on in the first 40 minutes to cause your beat to be irregular (isn't an ectopic near and above the AV node still a PAC??).
Sick sinus, AV block and AV re-entrant rhythms are all high on the list for producing irregularities. No doubt there are others - has anyone given a name for leaking ablation scar?

There's a time when a 12 point ECG becomes useful in trying to figure out what is going on - perhaps this is one of those occasions?"

Wil notes: These are some valid musings. Some erroneous suggestions begin to appear though: the described symptoms are not consistent with sick sinus syndrome; the described symptoms are not consistent with AV block; and the described symptoms are not consistent with AV re-entrant rhythms. The erroneous associations imply an interest in exaggerating the medical seriousness of my situation. The introduction of the possible need for a 12 [lead] ECG could be seen as supporting the exaggerated seriousness of my situation.

James then said:, "If you[r] analysis is correct Wil then we are left with the question of what caused 40 minutes of very irregular tachycardia that can't be detected by a holter monitor?

Wil notes: The irregular rhythm was recorded by the Holter. My report consisted of noting the contrast between the perceived symptoms of a-fib/flutter and the contrasting physical reality of only an irregular sinus rhythm recorded by the Holter.

James said: "Which still leads me to the conclusion you should verify your analysis with an expert and if they agree with you it's time to get 12 point ECG. (Your previous AF doesn't preclude you from having a new heart problem)"

Wil notes: This is a variation of a logical fallacy known as appeal to authority (James notes no data which supports James' conclusion), combined with a further exaggeration of the medical seriousness of my situation (having a new heart problem).

James quibbled: "(all definitions of tachycardia I've ever read put it at over 100 bpm but I'm happy to read any references you can point to that say otherwise.)"

Wil notes: This too is a variation on the appeal to authority fallacy. I had previous stated the heart rate at which tachycardia begins was arbitrarily chosen.

James stated: "You were NOT in NSR if your beats were very irregular. "irregular tachycardia" was the nearest I could get from what you wrote.

1:1 flutter from a leaking PVI is one of several ideas I had that may explain what was going on but I'm well into the realms of speculation. (The list of other possibilities is long and beyond my knowledge)"

Wil notes: The 1:1 flutter idea is not consistent with the ECG data. James continues to expand on the possible seriousness of my situation, but without noting any specific data supporting his concerns. Why is he doing this?

James stated: "My concern is that you seem overly confident about your ability to read this new situation. It of of course entirely up to you w[hen] to consult an expert, please don't leave it to[o] long."

Wil notes: Aha! We begin to get some insight into James' real concern (overly confident), combined with a further escallation of fear about my situation.

Marian then chimed in: "James, I couldn't have said it better. Normal sinus rhythm is just that - normal. The beats are sinus in origin and regular. An irregular rhythm is a horse of a different gallop!

Also, as you implied, 12 lead EKGs are very useful in the differential diagnosis of cardiac arrhythmias."

Wil notes: These comments taken in isolation would be valid observations. Taken in the context of James' prior comments suggests Marion approves of and supports James' assessment of the seriousness of my situation and my inability to correctly assess it, even though neither of them points to any data indicating my situation might be serious.

Marian continued: "Wil, I know you don't like people to disagree with you, but we will just have to agree to disagree on these issues."

Wil notes: Another Aha moment! The first comment is an example of the logical fallacy known as ad hominem (discrediting the person rather than directly addressing the merit of the argument), but in a form that clearly makes no sense. I can't think of anyone on this web site who more enjoys promoting disagreement than I do. The second comment continues to escalate the seriousness of my situation both Marian and James allege exists, but still without pointing to any data which justifies their concern.

James continued: "Wil, as you know, the P wave represents atrial depolarization. I think you're assuming that because you have one it must be originating at or near the sinus node - this is not the case. Your arrhythmia may not be sinus in origin. (Though you could indeed have sick sinus syndrome)"

Wil notes: What James notes is true, but if the depolarization does not begin at or near the sinus node the shape of the P wave will change. But, I repeatedly noted the shape of the PQRST wave was normal. James' second comment continues to suggest that my situation is serious, again offering an assessment which is not supported by any data (you could indeed have sick sinus syndrome). Again, why?

James continued: "You can quibble about me using 'irregular tachycardia' (which I still think is accurate) or extract the useful parts out of my post. A 12 lead recording read by an expert may help to pin point the origins and timings of what you are seeing as a normal PQRST wave when what you are describing is clearly not NSR."

Wil notes: James continues to promote the seriousness of my situation without pointing to any specific error in my analysis of my data, but he only returns to the semantic issue of the definition of NSR. Why?

James concluded: "I hope you soon have a better diagnosis for what is going on."

Wil notes: Here again is the reassertion of James' conclusion that my situation is serious; and I need to understand I am unable to properly interpret my ECG data; and I should consult an expert; all without any specific reference to data that supports James' conclusion. Why?

Marian then chimed in with a description of how the EP for her first PVI misinterpreted her ECG data which were subsequently correctly interpreted by Dr. Pinski which "led me to have the PVAI by Dr. Pinski in April of this year. So far, so good. No more foolishness."

Marion continued: "Wil, I wish you only the best, but I believe that it would behoove you to seek professional advice." Again, Marion is suggesting I am incapable of correctly interpreting my ECG data and should consult a competent professional, with the implication that to do otherwise would be foolish.

Wil's conclusion is that James and Marion are paternalistic toward Wil and are convinced Wil is unable to interpret his ECG data correctly. Why?

The most likely explanation is that James and Marion are not confident of their ability to assess their own medical situation, and are projecting their lack of competence onto Wil.

The heart behavior I described, in the first message above, was present (in a modified form) after the first ablation and, in its present form, from the moment I became conscious after the successful second ablation, at which time Dr. Natale also noted it. The same heart behavior was present at the three month post ablation examination by Dr. Natale. The same heart behavior has been present in each of the subsequent complete ECGs I've sent to Dr. Natale every three months, to take advantage of the opportunity offered by my ownership of a Holter, to obtain some long term monitoring data of a successful ablatee. The same heart behavior has been present, in a greater or lesser percentage of every day, on the weekly ECGs I've gathered during the two years of NSR since the successful ablation.

The fact that I am comfortable being in control of my assessment of my medical condition is not bad. Nor have James and Marion offered any reason to think I am incapable of correctly assessing my medical condition. As a Culture, I hope we still celebrate self-sufficiency.

Regardless, I will again state my observation. The presence of irregular sinus rhythm (confirmed by ECG data) created the perception of a-fib/flutter with accompanying PVCs in an unemotional and experienced a-fibber. That is an interesting observation, especially for those experiencing short term episodes of what seems like a-fib/flutter after a successful ablation.

Hi Wil,
Dick has an interested notice on his site:PULMONARY VEIN ARRHYTHMIA SITES
It is interesting that you can see the origin of the contraction in a 12 lead EKG. Perhaps you can get hold of the article and find an answer to the origin for your dual heart rates.

I looked at the Morady link, describing how the form of the P wave can help determine the source of the atrial wave source. My P wave, seen on the Holter lead approximately equivalent to the V1 signal, is a nice clean symmetric positive wave of normal amplitude and occurs before the R wave by the correct amount of time, as it should if the source of the atrial wave is located at or near the SA node.

I continue to be puzzled by all the distractions created by concerns about my interpretation of an irregular sinus rhythm. The waveform was definitely not a-fib and was definitely not a-flutter. Doubts about my analysis do not affect, in any way, the validity of my observation: The presence of an irregular sinus rhythm (confirmed by ECG data) created the perception of a-fib/flutter with accompanying PVCs in an unemotional and experienced a-fibber. That is an interesting observation, especially for those experiencing short term episodes of what seems like a-fib/flutter after a successful ablation.

Is it possible that the underlying goal of the distractions could be to avoid discussing the possibility of "ghost a-fib"?

There seems to be a plethora of extremely clever people writing on this thread, hence I jump in with a question:

Am I correct in thinking that AF is (sort of) when the atria beat (usually chaotically) to a different rhythm to the beat of the ventricles which are manfully trying to continue their usual 70 bpm and the atria are fooling around all over the place?

Kate

Kate,

I'm not sure I'm part of the plethora, but here is a shot at answering your question.

In simple terms, normally, the SA node [en.wikipedia.org] fires and the atria contract. The signal continues on to the AV node [en.wikipedia.org] which delays the signal for ~0.1 seconds, then sends it on to the ventricles. "An important property that is unique to the AV node is decremental conduction, in which the more frequently the node is stimulated, the slower it conducts. This is the property of the AV node that prevents rapid conduction to the ventricle in cases of rapid atrial rhythms, such as atrial fibrillation or atrial flutter."

In afib, there are reentrant wavelets and the atria are contracting at 300 BPM or more. Therefore there is a shower of signals to the AV node. Because of the aforementioned "decrimental conduction", not all the signals get passed on to the ventricles. Because the number of signals that get passed on are somewhat random, there is a lot of variability in the afib ventricular beat.

In aflutter it is similar however, there is very little variability. Hence, assume the atria are beating at 300 BPM in aflutter. If you have 4:1 conduction, the ventricles will beat 1 time for every for atrial beats or 75 BPM. 3:1 conduction, you get 100 BPM. 2:1 conduction, you get 150 BPM.

I don't know why aflutter has very little variablity and afib has a lot. In both cases, the atria are beating at a very high rate (perhaps one of the plethora can answer this question).

Cheers,

George

I'd always assumed the AV node failed to transmit all the atrial waves down to the ventricle (delayed as you noted, via the HIS bundle) because the AV node became refractory (non-conducting) for a fixed time after successfully passing the atrial wave down to the ventricle.

Subsequent to that fixed time after the AV node passed the signal down to the ventricle and became refractory, the AV node returned to its non-refractory state, and then after some random time (caused by the randomness of the atrial waves) the next passing atrial wave would again trigger the AV node, and the cycle repeated.

According to this explanation the irregularity of the a-fib ventricular rate is caused primarily by the random time between when the AV node become non-refractory and the passage of the next atrial wave.

Also, according to this explanation, the more-or-less regularity of the a-flutter ventricular rate results from the regularity of the atrial wave removing (or reducing) the randomness of the time between when the AV node becomes non-refractory and the arrival of an atrial wave.

What do you think, Boss?

According to the following, the ventricular beat randomness or lack thereof in afib and aflutter, respectively are because of the randomness or lack thereof in the atria.

[en.wikipedia.org]

"In atrial fibrillation, the regular impulses produced by the sinus node to provide rhythmic contraction of the heart are overwhelmed by the rapid randomly generated electrical discharges produced by larger areas of atrial tissue, often localized to the pulmonary veins. It can be distinguished from atrial flutter, which is a more organized electrical circuit usually in the right atrium that produces characteristic saw-toothed p-waves on the electrocardiogram; in atrial flutter, the discharges circulate rapidly (at a rate of 300 beats per minute) around the atrium; in AF, there is no regularity of this kind at all."

I suppose that either "decrimental conduction" or refractory of the AV node would then be responsible for the conduction ratio (i.e. 4:1, 3:1, 2:1 & etc.). Perhaps "decrimental conduction" and refractory of the AV node are saying the same thing. Tonight when I looked this up was the first time I ran into the term "decrimental conduction."

George

Thanks boys! Imagine how much and how quickly we could all exchange information and experience if we met up for a afibbers conference!!

I wonder, based on one of the above posts regarding transmission of signal, if my AF has something to do with fourteen years later "scar tissue" from my original WPW ablation. It was done in 1993 and was therefore very "early". My EP said, four years ago, that he is finding a number of his WPW patients are developing AF about ten years later.

I wonder if I have some "bad cells" which are messing things up. Oh well. Thanks for your answers boys, although I will have to read them several times before I can take the information in properly.

Kate

A number of us ablatees are interested, both publicly on this web site and sometimes privately, about the long term prognosis of ablation.

A few months ago I did a pseudo-analysis here and came up with a guess that, on average, our a-fib would return about five years after a successful ablation.

I assume that your ablation in '93 addressed pre-existing a-fib, in addition to the auxiliary pathways from the atrium to the ventricle. Is this true?

I, and I'm sure others here, would be interested in when and how your a-fib re-appeared after the successful ablation in '93?

To George and the others who use wikipedia as a reference resource.

Just a question - I'm not sure of the answer other than what is on their home page (below).

How reliable is the science provided in wikipedia answers? Is wikipedia the best resource to quote or should it be something out of one of the medical websites, heart institution websites, Gray's anatomy or other scientific reference? I've seen criticism of facts not always being accurate from wikipedia.

Comments?

The home page of wikipedia says:

Visitors do not need specialised qualifications to contribute, since their primary role is to write articles that cover existing knowledge; this means that people of all ages and cultural and social background can write Wikipedia articles. With rare exceptions, articles can be edited by anyone with access to the Internet, simply by clicking the edit this page link. Anyone is welcome to add information, cross-references or citations, as long as they do so within Wikipedia's editing policies and to an appropriate standard. For example, if you add information to an article, be sure to include your references, as unreferenced facts are subject to removal.

Jackie

Jackie,

It is like any source - you have to use discrimination. On many technical subjects, I've found it to be pretty good. One guy who analyzed a number of Wiki pages said he found it generally to be at the level of a grad student knowlege - not necessarily at the level of the best authority in the field. If the answer really mattered, I'd certainly check the footnotes and other references. Many Wiki pages are referenced.

It is kind of like the information off this board - anybody can post and you have to use your brain (and possibly other sources) to determine if it makes sense.

I certainly have no problem using it for providing backup to an answer like the above. The Wiki author(s) is/are probably much more of an authority than I am.

When my daughter was in high school and would ask me questions on AP calculus, AP chemistry, physics & etc. (topics I've generally not thought about for more than 30 years), I found the Wiki answers did a nice job of explaining things and were accurate.

I've thought that the Wiki format might be nice for some of the information we try to present here, as it is editable as opposed to our posts which are static. Of course if I edited one of Peggy's posts, she might not take kindly to it (just kidding Peggy).

The idea is that the knowledge of the group is collectively pretty good and better than any individual. For an interesting read on this topic I recommend: "Wikinomics: How Mass Collaboration Changes Everything" by Don Tapscott and Anthony D. Williams.

In summary, I wouldn't trust anyone piece of information, if it really mattered, without backup, but collectively it is a good reference.

George

Wil, my ablation in 1993 only addressed the WPW. I have something called Wenkebach and a second degree heart block as well, Mobitz type 2 or something like that - (I have no idea what they are and have never asked) all this was diagnosed when I was 19 years old and not asking questions. My EP at that time has since died (of cancer).

To my knowledge, there was no AF back in 1993, that has only developed the past four years, which is approximately ten years after the WPW was knocked out. The WPW has never returned, thankfully.

Kate

The WPW is a much simpler ablation, has much higher probability of success and would generally not address any afib.

My understanding of WPW is that in WPW there are two pathways to the AV node. A fast and a slow one. You can end up with a circular conduction - down the fast and back up the slow. The WPW ablation kills the extra pathway.

Afib can occur after heart or lung operations (i.e. trauma to the heart). I'm wondering if this might be the reason for WPW patients getting afib. Pure speculation.

George

When you chose a medical problem, you really picked a rare and unusual one.

You are correct that there was a partial variable AV block, in multiple variations.

"Second degree A-V block type II (Mobitz)" ... "Type II (Mobitz) second degree A-V block results from prolongation of the absolute refractory period of the A-V node or of both bundle branches" ... "Long ventricular pauses may allow idionodal or idioventricular rhythms to escape; the arrhythmia may then mimic complete A-V block."

The latter means the ventricle could possibly fire on it own, independent of the atrial electrical activity, because the ventricle fired spontaneously before the atrial signal arrived.

But, in genera,l the firing sequence of the ventricle will be related to the atrial electrical activity as (atrial waves to ventricular waves) 2:1, or 3:2, or 4:3, or 5:4, or ..., or in any sequence of these ratios. Your heart rate would mimic a-fib's irregular rhythm, but the average ventricular heart rate would be lower than the atrial rate because of lost atrial signals.

Wenckebach, Type II, and Mobitz all seem to refer to minor variations of the same problem.

"Wolff-Parkinson-White syndrome (WPW)" ... "Ventricular pre-excitation occurs when sinus impulses activate some part of the ventricles through an accessory pathway, earlier than through the normal conduction pathways. The Wolff-Parkinson-White (WPW) syndrome consists of ventricular pre-excitation associated with paroxysmal supraventricular tachycardias." ... "The paroxysmal tachycardias of the WPW syndrome are usually supraventricular and include atrial tachycardia, A-V nodal tachycardia, atrial flutter (rare), and atrial fibrillation."

It would seem that you may have had: (1) some kind of atrial problem like a-fib or atrial tachycardia; and (2) prolonged conduction delay along the normal pathway from the atrium to the ventricle; and (3) an auxilliary direct pathway from the atrium to the ventricle.

So, the odds are that your ablation involved both blocking the direct pathway between the atrium and ventricle, and eliminating whatever atrial misbehavior (most likely either tachycardia or a-fib) was present.

My texts do not mention any fix for the prolongation of the atrial signal passage. Do you still have a somewhat irregular heart rhythm?

i monitor many pt's post ablation, all i want to say is that university of penn is the best. there is 1 dr. from NY that does ablations (dont want to mention name at this time) & almost everyone of those pt's go back in a-fib.

Wil, I have an irregular heart rhythm at the best of times.

Kate

kate you should look into taking a basic ekg course at your local community college, you dont need to know 12 leads but you will learn & understand wenkebach, second degree type2 ect. then you may be able to find a portable ekg machine in e-bay or wherever & check yourself out.

just a thought

inthebiz: I sympathize with your advice, and I personally followed it, but after five years of advancing the idea here it seems clear that advocating that idea is an exercise in futility.

I failed to express my question precisely enough.

During the period after your ablation and before the appearance of a-fib did you have a somewhat irregular heart rhythm?

What is the history of your a-fib symptoms, and what data has been gathered about your a-fib?

Wil,

I would agree that for someone such as Kate, personal 12 lead or holter monitoring makes sense. However, I'm not sure the cost and hassle of a personal holter is justified in "run of the mill" lone afib cases. I do value simple monitoring.

Here are the questions I try to answer with my monitoring:

- what is my heart rate in or out of afib
- am I in afib
- am I in aflutter
- what are my PAC and PVC counts per hour

I can answer all of these with a relatively simple beat to beat heart rate monitor. I have mentioned that I do have my own ECG monitor. However I use it rarely as it generally does not give more information, for the above questions, than the recording HR monitor (Polar S810).

In addition, for several years I've had access to a friend's holter that I can use whenever I please. I have used it a number of times, but again do not find it worth the extra bother. It always confirms my Polar recordings.

This is not to criticize your monitoring, as I'm sure it has great value to you. In fact, I would venture that more holter data exists for you than for any other single individual.

I eagerly await your rebuttal.

Cheers,

George

Sorry Boss, I agree with you.

Two years ago, after the successful ablation, I recognized that the ECG: (1) required immobility; and (2) was limited to short data gathering periods. Those limitations were unacceptable to me then.

It is true the Holter has been useful for measuring heart misbehavior in more physically and emotionally stressful situations, but while that misbehavior is more extreme than experienced when immobile, I believe the two levels of misbehavior are proportional to the stress level, rather than being different in kind.

I could also argue that the 24 hours of Holter data every week shows how much heart misbehavior varies from week to week and month to month. That tends to provide perspective on days when my heart gets cantankerous.

Wil - You said early on in this thread

The same heart behavior has been present in each of the subsequent complete ECGs I've sent to Dr. Natale every three months

Did Dr. Natale or his staff respond to your sending and if so what were his comments?

Did they support your own conclusions?

It would be helpful to learn what they determined.

Jackie

Wil, my heart beat as steady as a metronome for ten years after the ablation for WPW. I had it very severely and couldn't get up from a chair or turn over in bed or do virtually anything by the time I was ablated. It took quite a long time for the heart to "recover" and I was prone to an amazing racing heart beat where the heart literaly accelerated like a car going from 0 to 60. It just picked up speed speed speed. And then would knock back to 70 bpm ish for no reason with no warning. But after a few months my heart was steady and I was able to be physcialy active and learned to play polo and had a fabulous time for ten years. Such types of activity previously had to be undertaken on medication which stopped me reaching full physical fitness.

After about ten years I started to sense a "chaotic" heart beat and after about another year or so I complained to the EP and was monitored and they found the AF.

The wenkebech and type II stuff was all there 32 years ago when I was diagnosed with WPW.

One of the things that happened about 4 years ago when the AF got going properly was that I had become less physically fit. I was no longer playing polo. My EP had always warned me that because I had always been very fit (as a teenager I was a runner and then always rode horses all my life) I had to be careful as I got older because as I lost my physical fitness the atria would become "floppy". He has told me time and time again that if I could get back to a high level of physical fitness the AF would improve a lot. But it is a Catch 22 situation, and I can't exercise hard enough to get fit enough to improve the strength in the heart muscle and stop the "floppiness".

Kate

I don't see any reason to worry about the forms of misbehavior my heart displays. Certainly some people come out of a successful ablation with no misbehavior experienced at all. But, they are a small minority. The rest of us experience ablation after effects, as various forms of heart quirkiness.

When you go in and kill a lot of tissue, the boundaries of that killed tissue will contain a lot of damaged living tissue. I'm not surprised that some of that damaged tissue would subsequently exhibit abnormal behavior. In my case the symptoms are a mildly irregular rhythm about 30 minutes total per day (as many short bursts of irregular rhythm). Such behavior is consistent with the hypothesis of damaged tissue near the SA node displaying some pacing behavior, which competes with the SA node pacing during about 2% of each day. That, to me, is pretty insignificant.

I'll also not be surprised if the misbehavior of this damaged tissue will either get better or worse with time. Lately, it seems to be very slowly getting better. Six months ago the irregular rhythm time was 4% per day. Before that it was 0% per day for a year. Before that it was 33% per day for most of a month. Before that (post-ablation-medication) it was about 2% per day for two months. So the current amount of irregular rhythm is about the same as experienced post ablation for two months, and the irregular rhythm time per day has been both worse and better in the meantime.

As I said above, the long term Holter data allows for a peaceful tolerance of variations in the amount of heart misbehavior. Over the two years SVT, tachycardia, irregular rhythm, PACs, PVCs, heart rate, and blood pressure have all been varying, sometime dramatically, especially during the first eight months after the ablation. Once I documented that misbehavior comes and goes, and therefore doesn't seem to portend anything serious, and in most cases gets slowly, if erratically, better, then it is relatively easy to remain philosophical about the changes.

Minerva has called a few times after I submitted a three month report, acknowledging its receipt, and to chat about how life is going. But, apparently they also don't see anything which disturbs them enough to comment on it.

As George said, I probably have more long term data on a successful ablatee than has ever been gathered. The fact that I am finding evidence of things that otherwise would have gone unnoticed, should be regarded as interesting, but not necessarily reason to act to fix something that is probably just normal variations in heart misbehavior post-ablation.

Kate: There is no reason to expect the "Type II (Mobitz) second degree A-V block [which] results from prolongation of the absolute refractory period of the A-V node or of both bundle branches" would have gone away post ablation. The fact that your heart rate eventually became steady post-ablation suggests that the second degree A-V block was just a hypothesis that was incorrect.

You probably did have "Wolff-Parkinson-White (WPW) syndrome consist[ing] of ventricular pre-excitation associated with paroxysmal supraventricular tachycardias." ... "The paroxysmal tachycardias of the WPW syndrome are usually supraventricular and include atrial tachycardia, A-V nodal tachycardia, atrial flutter (rare), and atrial fibrillation."

The ablation probably treated the auxilliary pathway and the superventricular arrhythmia (most likely a-fib). A-fib reappeared after ten years, and will have to be treated again. That is consistent with the expectations of the more realistic of us here.

The technology has improved a lot since your ablation. I'd suggest you contact Dr. Natale in California. He clearly has a special knack for eliminating supraventricular (atrial) arrhythmia. He will like your straight forward no-nonsense communication style.

Kate: A number of us here would question the association of peak physical fitness and less a-fib. The heart stress associated with reaching peak physical fitness seems strongly associated with heart changes which promote a-fib.

Wil, I'll do an "experiment of one" and try to work myself up to a reasonable level of peak physical fitness for a 52 year old woman (!) and keep you up to date with how I go on. The "clean" diet isn't controlling my AF at times of mental stress (work and relationship related) at the moment and I am taking propafenone much more often, sometimes twice a day for two days.

I have recently purchased a new horse a little Dutch warmblood mare, only 4 years old and I will be putting in a lot of phsyical work which I haven't been doing for a few years!! I'll see if the AF improves if I can get back to a high level of fitness.

I was not aware, incicentally, that I have a "straight forward no-nonsense communcation style".

I am in the UK so would use my EP from when my WPW was done. He won't "do" me at the moment, I asked him about a year ago, he says I am unusual in that I have 2 rhythms and he is reluctant to go "in". He has promised he will have a go before he retires in a couple of years time. I trust him implicitly, he is a genius, a sort of an English Dr Natale!!

I don't think my insurance would cover me for a US based operation anyway, only the high level hospitals here in the UK are specified on my insurance. There are small, private clinics in London where all the rich Arabs etc. go and that is the place to have this type of work done.

Kate

I started on my "experiment of one" physical fitness regime immediately. I'd started to afib (because of stress) and I would usually take a tablet and then wait an hour or so for the propafenone to knock the AF on the head before I go out and do physical chores with the animals in the fields.

I decided not to take a tablet and put on my boots and went off to feed the animals, which is strenuous exercise. After about ten minutes I think I had frightened my heart into submission!! I was really surprised. Afib stopped. Back in NSR again. How odd. I shall have to think about this. I have often thought of giving my heart something to fibrillate about when it starts to muck about!!

Now that I am sitting quietly I can feel the heart starting muck about again.

Structurally I suppose the ventricles were thinking " hell she's working hard, we better get beating faster and stronger" which over rode the atria and shut them up. There, that's pretty much as medical-minded as I am!!

Kate

The high intensity athlete's probability of experiencing a-fib is thousands of percent higher than for normal humans. While correlation is not causation, if you are inclined toward being athletic, and you are experiencing a-fib, I'd suggest your belief that exercise will improve your a-fib is misguided.

Another comment is that the effect of exercise on a-fib in the short term is not necessarily indicative of the effect of exercise in the long term. In other words, exercise may have bad effects long term in spite of exercise terminating a-fib short term.

i find it strange that you can have mobitz 2 & then nothing, mobitz 2 is not a prolonged pr interval it just blocks the sa node from going to ventricles, that usually requires meds or a pacemaker at the least. mobitz 1 or wenkebach is a prolonged pr interval that gets so long that it eventually drops a beat (no big deal) but type 2 is 1 step away from complete heartblock.

inthebiz: we are both of the opinion that Kate's initial diagnosis was partly incorrect, because Kate's heart behavior subsequent to her ablation indicates it was incorrect.

I worry that Kate's dedication to her physician may represent justified loyalty, because of what he did for her, but she should consider another physician for her next ablation, partly because her present physician has already indicated some hesitancy about addressing her new problem.

It is also interesting that Kate may be the fourth post-ablatee with "two rhythms", whatever that means.

My boyfriend is insisting that if I am intent on this physical fitness regime that I must visit my EP first. I'll arrange to see him.

My EP is considered to be the best in the UK, one of the best in Europe and lectures all over the world. He is very focussed on passing on knowledge and skill to the next "generation" of EP's. Anyone else who I go to has been taught by him and will not have superior skills or knowledge. Back in the early 90's when ablation for rhythm was very new I was 11th to be done. When I consulted with him I was 7th, he did 3 more the next 3 weeks and I was 11th. Having been inside my heart for three and a half hours (I was awake the whole time, it was fascinating to watch on the screen) and listened to it and studied graphs of my heart for nearly 14 years, he has my total confidence.

I still have the heart block, I don't consider that an irregular rhythm in the same sense that WPW or AF is an irregular rhythm because it doesn't impede my life in any sense at all. I simply have an odd heart beat. When I say my heart beat steadily after the WPW ablation, I mean without WPW.

Incidentally, cardiac arrhythmia (of one kind or another) is currently the number one killer in the UK. A recent UK statistic shows that 25% of patients with AF die within 2 years of diagnosis. That doesn't sound like a benign condition to me!

Kate

kate: i'm no cardiologist but as far as i know heart block is a very serious issue. again there are 4 types, 1st degree av block (no biggie) 2nd degree type1 (no biggie if you are asymptomatic) then 2nd degree type2 & 3rd degree also known as complete heartblock.
if you fall under type2 or complete i would be concerned, im sure its not complete heartblock or you wouldnt be here right now.
pacemakers save soo many lives its amazing. ppl are afraid of the word pacemaker but it is a rather easy procedure.

and for anyone else reading this & you need to have an ablation done you need to see dr. frances marchlinski at university of pennsylvania in philadelphia PA
google him & you'll see what i mean. i have seen his work & he is the best period

Hi Kate,

could you expand on the cardiac arrythmia is currantly the No1 killer in the UK.

I'm guessing that any diseased heart will function improperly/irregulary which will termed an arrythmia so this would not really be relevant to Laffers.

The statement that 25% of patients with AF die within 2 years of diagnosis again goes against the grain when dealing with laffers but its surely a warning against all this stuff about 'learning to live with it'.

For my money try the meds /suppliments for a while and if things don't improve dramatically then get on the ablation route even though there's no guarantee of 100% cure.

Been there, got the tee-shirt.

Don't waste time, you're only here once

Barry

Thanks inthebiz. I'm in the UK and insured in the UK so couldn't use an EP in the US unless I pay and that is probably prohibitive.

Barry - I am hypothyroid and take thyroxin and tertroxin as well as the propafenone and it is the balance between the thryoid medications and the propafenone which has started to "get me down" this year.

Previously, I have taken the propafenone happily for 3 years, until I developed the hypothyroidism as a result of Hashimoto's.

Yes, I have always known heart block is serious and one is susceptible to SDD. Because I have had all this (not the AF though) since I was a teenager I have always taken the attitude of not worrying about it. Nothing can be done about it so I just got on with it. Hence I competed (equestrian) and pushed on as hard as possible, I'd rather have quality than quantity.

Here is the link to the info ref 25% etc. www.bcs.com/pages/page_asc.asp?pageID=255

Thanks for your interest.

Kate

" He won't "do" me at the moment, I asked him about a year ago, he says I am unusual in that I have 2 rhythms and he is reluctant to go "in""

Gee i wish Kagey could hear about this, she feels she is the only one with this 2 rhythm condition.

PeggyM

We now have four successful ablatees that developed some variation of a two rhythm heart behavior; Kate, Kagey, Wil, and one other I can't remember the name of now. In addition, it is possible that a lot of post-ablation arrythmia, which is not verified by an ECG, could be the result of a two rhythm situation similar to the one I seem to have.

Will:

If you remember I had my ablation a couple of months after yours with Natale. I was in 24/7 Afib with slight symptoms and reluctant to have the ablation until reading your research and perspective on the long haul deterioration 'theories' based on what I think is decent research .

I'm merely checking in to say that your mentined monitoring equipment practicalities really may become essential at some period.

After an over stimulation session with caffine (non organic) I went into what I thought for sure was afib. Checked into the ER quickly hoping for the 'non penalty' within 24 hour cardiovert. After 3 ECG's showing perfect NSR in the midst of my pulse jumping all over the place the Er Dr. came in, listened to my heart while watching the monitor and said I was experiencing PVC's (my first known). Now I know about PVC's and how they feel and seem to be Afib.

This post is really about the caution that perhaps there could be some anxiety relieved if we were to include in the ole 'knowledge is power' bank (I could be 100 years late on this) the possibility that for the new one PVC;s are not afib and then of course could be afib and/or a precoursor to it. For the slam bang 200ppm wild pulse its a no brainer but for the slight and subtle yet undeniable symptom it may not be what one thinks it is and maybe only equipment can distinquish the difference.

mike

mike