Anatomical differences of pulmonary vein entry

Hi Everyone,

Something I have been thinking about since my ablation.

It has been documented that the majority of electrical impulses causing AF originates from the pulmonary veins(ectopic pacemaker cells around the pulmonary veins?). The CCF no longer does mapping because they feel that the majority, if not ALL, impulses finally originate around the pulmonary veins.
Mapping may show a different area of origination, but I believe the CCF feels these areas will eventually lead to the pulmonary veins & thus this is why they have elected to stop mapping procedures altogether.

So, why do the impulses come from the pulmonary veins? Why does AF occur in some individuals and not others? A big question. Could it simply be because
of different anatomical positions of the pulmonary veins & how(or where) they enter the left atrium? Veins, arteries, nerves, muscle insertions, etc are not always located exactly in the same positions throughout the population.

If the pulmonary veins were different anatomically somehow in nature, could a certain turbulence be caused from blood flowing in a somewhat abnormal way that it might effect the pacemaker cells around the pul veins which would possibly lead to AF?

We all agree that stress leads to AF, but obviously not most people. Stress causes vasoconstriction which would possibly lead to greater turbulence in the pul veins. What about bending over suddenly, or lying on your left side? Taking a cold drink suddenly could lead to slight constriction and sudden turbulence.

I would appreciate comments before I go any further. Thanks.

Jim

Hi Jim, you may be interest in this...

Nonpulmonary vein foci: do they exist?
[www.ncbi.nlm.nih.gov]

my own opinion as to why the PVs are a major headache is a combination of.
a. they're quite a long way from the SA node so, I assume, are one of the the last cells to fire under normal circumstances
b. they're at the boundary where cells that fire join cells that don't - it's important that all the cells fire each beat otherwise the chances of automaticity taking over and producing an ectopic is increased - I see this as a hard problem at the boundaries.
c. the veins are an ideal site to induce a 'rotor' - activation can chase it's tail simply by spinning round the vein.
d. Myocardial extensions are often longer and thicker in the upper PVs in AFers which just adds to the problem.

I've always seen it as an electrical problem and can't say I've thought much about blood flow (apart from the high oxidative stress leading to damage around the PVs which has been mentioned a few time on this board)

just my view.

all the best
--
James D

The literature suggess that most but not all triggers come from the PVs. Some come from other areas of the heart.
In any event, does anyone know the reasons why the CCF, Pappone et al are not successful 100% of the time.
i.e. What is it about those specific patients, or those specific procedures that doesn't work?

During my consult with Dr. Natale and on the topic of a touch up ablation that is sometimes required, he commented that sometimes the burn or area of scar tissue that is laid down is not enough - that is the scar is not thick enough or doesn't go deep enough. He said some people have a very thick heart wall and that those people frequently need to have a second burn in that area to stop the impulses.

We know that caution is practiced with the amount of burning because of stenosis... so undoubtedly they err on the side of caution to prevent stenosis.

One of the cardiologists there told me....and I've posted this before - that they watch for the microscopic bubbles that begin to form at the burn area and back off when they start to see this because it indicates that it is "cooking" the tissue... and they take care not to burn too much or too deeply. Here is where the skill and expertise factor comes into play. Too much and you have stenosis - too little and you have a touchup.

Dr. Natale also mentioned there is no way to judge the thickness of the heart muscle.

Jackie

Hi James,

Concerning:

a.) If the cells around the pul veins are some of the "last" to fire, what if they are somehow interrupted due to turbulence within the veins, and this interruption goes back to the SA node (kind of like the wavelet theory), & in turn disrupts the SA node resulting in AF?
b.) This would be the result of a.(the above)?
c.) not sure I understand this
d.) Assuming the myocardial extensions are longer and thicker in the pulmonary veins, it would seem most possible that erratic turbulence could possibly interfere with normal electrical impulses.

Maybe my thinking is all wet here. What is going on around the veins, or in the veins that causes ectopics resulting in AF?? Just trying to understand why isolating the veins electrically stops AF. If scar tissue is formed and a "barrier" is produced so whatever is happening around the veins can no longer get through-no more(or simply not enough) abnormal electrical impulses-the heart continues to beat normally. I believe this is why many people have a lot of ectopic beats & AF during the "healing" period after an ablation, but go on to be "cured" after the scar tissue is fully developed providing an adequate "barrier".

Comments welcome,

Jim

James D.,

I was unable to get the internet address that you referred to on my computer. What was their conclusion?

Newman

Newman,

Here's the study.

Nonpulmonary vein foci: do they exist?

Shah D, Haissaguerre M, Jais P, Hocini M.

Division of Cardiology, Hopital Cantonal de Geneve, Geneva, Switzerland.

Though the majority of foci triggering atrial fibrillation (AF) have been mapped to the pulmonary veins (PV), recurrence of paroxysmal AF after isolation of all four pulmonary veins indicates the presence of other foci. In a series of 160 consecutive patients who underwent PV ablation, endocardial mapping of AF and ectopy recurring after PV isolation was performed. Thirty-six patients (24%) had a total of 85 non-PV foci; 39 were mapped to the ostia of ablated PVs, 30 to the posterior left atrium (LA), 5 to other parts of the LA, 5 to the right atrium (RA), 4 to the coronary sinus (CS), and 3 to the superior vena cava (SVC) (including one persistent left SVC). Mapping was confirmed by successful ablation. At least 16 foci could not be localized and after a follow-up of 8 +/- 6 months, 68% of patients were free of AF without any antiarrhythmic treatment. The occurrence of non-PV foci correlated with recurrence of AF, perhaps as a correlate of insufficient ostial ablation. These data reinforce the requirement for more proximal disconnection of the PVs by performing ablation within the LA. In patients with non-PV foci that are difficult to map conventionally, the use of surface ECG data, or multielectrode contact or noncontact mapping arrays, or substrate modifying/excluding ablation may be helpful in ablating these foci and therefore eliminating AF.

Jim W.,

It is my understanding that the CCF EPs (and Dr. Natale) still do some mapping during ablations. Since they have had so much success with PVIs, they have now decreased the time spent mapping on the first ablation. In my case, I am pretty sure that Dr. Natale found some other "hot" areas away from the pulmonary veins, and he ablated those areas. It is also my understanding that he does a lot of mapping during touchup (or second) ablations. I think I am correct, but am not absolutely certain. Your statement that the CCF no longer does mapping really surprised me. Are you sure?

Newman

Newman,

I should of said they no longer did mapping on the first ablation. Yes, I understand they do use mapping if a second procedure is necessary. I thought I understood Dr. Natale to say that usually foci in other areas of the left atrium usually still originate around the pulmonary veins, but they are sometimes more difficult to ablate, possibly due to different anatomical situtations. Mapping is used to comfirm these other areas & they are ablated. As I understand it, the burns around the PVs are ofter not deep enough(as Jackie said), or not continuous, and impulses are allowed to get through.

The study in Switzerland, to some degree, supports what I understood Dr. Natale to say.

Jim

Hi Jim, you wrote:
>a.) If the cells around the pul veins are some of the "last" to fire,
>what if they are somehow interrupted due to turbulence within the
>veins, and this interruption goes back to the SA node (kind of like the
>wavelet theory), & in turn disrupts the SA node resulting in AF?

I'm struggling to see how blood flow within the heart (even if it is turbulent) is going to affect the firing of the cells. I'm also struggling to see why such disturbance has to get back to the SA node before there's a problem the SA node can be functioning normally and AF can still arise due to ectopic activity in the PVs.


>b.) This would be the result of a.(the above)?
not sure I understand this

>c.) not sure I understand this
I wrote
"the veins are an ideal site to induce a 'rotor' - activation can chase it's tail simply by spinning round the vein."
I don't know if this is actually happens -I'm only guessing that the veins are large enough for this to happen...
Imagine a cylinder of heart cells - a cell fires on one side of the cylinder and only manages to cascade the excitement in one direction (let's say clockwise around the cylinder for arguments sake) by the time the excitement travels round the cylinder the original cell may be ready to fire again so the activity caries on circling the cylinder -that's a rotor in my book (as I say I'm not actually sure if this is what happens in the PVS but see it as a possibility)


>d.) Assuming the myocardial extensions are longer and thicker in the
>pulmonary veins, it would seem most possible that erratic turbulence
>could possibly interfere with normal electrical impulses.
are you suggesting that blood in contact with the heart wall is somehow managing to induce heart cell activation? I think we are in trouble if this is the case - what's to stop it triggering any other part of the heart?

>Maybe my thinking is all wet here. What is going on around the veins,
>or in the veins that causes ectopics resulting in AF??
I'm not sure you should be thinking of them as veins at this point - rather think of them as heart muscle that is extending up the openings. These cells are still excitable but many are connected to cells that aren't excitable - this makes passing on the activation from cell to cell a harder job. (I've read somewhere that heart cells on average are in contact with around 11 other heart cells - I suspect this number drops quite a bit at the boundaries - which may reduce the chance of successful propergation and increase the chance of ectopic activity?)


>Just trying to understand why isolating the veins electrically stops >AF.
I think it just stops excitement in the PVs from triggering AF. The heart is still capable of sustaining AF if it's receives a trigger from a location away from the PVs.

>If scar tissue is formed and a "barrier" is produced so whatever is
>happening around the veins can no longer get through-no more(or simply
>not enough) abnormal electrical impulses-the heart continues to beat
>normally.
>I believe this is why many people have a lot of ectopic beats & AF
>during the "healing" period after an ablation, but go on to be "cured"
>after the scar tissue is fully developed providing an adequate
>"barrier".
I think you're right.

It may also be worth considering the new boundary that appears as a result of an ablation. I assume that the nice thing to happen is that every cell at the atrial side of the scar should fire every time the heart fires but this may not always be the case. (It does appear to improve the situation considerably though

--
James D

James,

You said, "are you suggesting that blood in contact with the heart wall is somehow managing to induce heart cell activation? I think we are in trouble if this is the case - what's to stop it triggering any other part of the heart?"

Yes, I am speculating. Maybe I just do not understand enough about heart cell activity, but other parts of the heart wouldn't be triggered simply because of the area where the pulmonary veins enter. They certainly do not enter around the SA node or the ventricles. If ectopics originate around the pul veins, why? If there was an erratic "bumping" on the heart cells coming from the veins, would it not be possible this could lead to ectopics leading to AF? The "bumping" being caused by erratic turbulence.

Just my simple mind,

Jim

FWIW, here's my, not so educated, take on the possibility of what is going on. Based on my own testings that I had done, I know I'm low in glutathione (GSH) and all sulfur containing amino acids. As you well know, the pulmonary vein is the pathway of the blood returning from the lungs, after being oxygenated. In breathing of oxygen, our lungs are constantly assaulted by foreign agents, such as pollution, bacteria, or other forms of free radicals. The lungs are supposed to be a rich source of glutathione for protection of these invaders, and to donate an electron to the free radicals, which calms them down, as you will read. It has been reported that AFers have more myocardial tissue reaching beyond the heart into the pulmonary vein, which may make us more susceptible to these electron seeking, free radical invaders. In regards to problems with the baroflex receptor, this may indicate further damage by free radicals, however I believe this is due to suppression or deficiency of epinephrine or norepinephrine. The reason I say this, is because when I was taking beta blockers, which inhibit epinephrine, this caused me to have the same problems with the baroflex that others have here, that I did NOT have before. Other tests indicated that I was, indeed, already low in these catecholamines, so betas further insulted my problem. S-adenosyl methionine, a breakdown of methionine and another sulfur amino that I was also low in, is critical to this pathway. Another problem several of us are known to have, is noticeable AF/flutter upon eating MSG or free glutamate. Excess glutamate blocks the uptake of cystine (sulfur amino) in the endothelial cells, and excessive exercise further exacerbates this problem, and causes tissue degradation. In other reading that I have done, I am also finding some bacteria to use our methionine stores for their own survival. So I still maintain, that the all encompassing sulfur amino, methionine, and its by products, are constantly being assaulted by invaders of our environment, and our stores are at subnormal levels, which can cause a multitude of cascading events. If interested, go to the link provided, to read this research in its entirety. One other questions still remains. If we see our situation as a defect or polymorphism, then how have some here (Fran and Erling) basically cured themselves, or others seen improvement by certain supplements?

A few excerpts:
Free radicals are molecules that are missing an electron. Usually electrons come in pairs. This creates problems when free radicals bump into the cell's membrane, other proteins or even DNA: their greedy acquisition of electrons results in those tissues being damaged through chain reactions. GSH prevents this by donating an electron. The sulfur atom in the cysteine makes a bridge with a sulfur atom in the other GSH peptide, donating an electron to the errant free radical, calming it down. Or GSH may directly bind to a free radical, creating a mixed disulfide. The chemistry of reduction (acquiring an electron) and oxidation (donating an electron) is a fundamental aspect of the way our bodies function. When this chemistry is significantly and chronically awry, disease may ensue or be worsened.

Where do free radicals come from? Many sources, including smoking, oxygen and some other drug therapies, protein-energy malnutrition, pollution and the ultraviolet (UV) part of sunlight.

Excess plasma glutamate has been shown to block the uptake of cystine by endothelial cells as well (Miura, 1992). Others have found that the excess glutamate blocks cystine uptake into macrophages and peripheral blood mononuclear cells (Eck and Droge, 1989; Gmunder, 1991). This particularly occurs in people with wasting; the muscle tissue doesn't take up the glutamate and convert it into glutamine which is the major amino acid used for creating muscle tissue. Why this system fails is not understood.

In trying to understand the reason for this elevated glutamate, Droge and his colleagues looked also at healthy individuals who underwent "anaerobic" exercise, with or without use of NAC. They noted that even some healthy people were at risk for loss of body cell mass under heavy exercise conditions, and this was correlated to a higher level of glutamate in the venous blood. This is partly due to the excessive exercise overwhelming the body's ability to make sufficient ATP to offset the high rate of glycolytic activity (breakdown of sugars). When this happens, the muscles excrete a fair amount of chemicals called pyruvate and lactate. As they do this, they also take some protons, often derived from local stores of cysteine which otherwise would be used to synthesize glutathione. (Remember, a proton is a hydrogen atom missing an electron). Meanwhile, glutamate builds up in the blood and is blocked from entering into the muscle tissues. Voila: muscle tissues deteriorate (Kinscherf, 1996).

[www.ziawolf.com]

Richard

Richard,

My take is also uneducated, and I have found myself wondering(since my ablation) "what" sets off the first cell to cause a chain of events which leads to AF. I know this has been discussed many times. In my case, most of the time my episodes started from being startled(stressed), bending over, drinking something too cold, sitting down in my car and bumping myself suddenly, somebody slapping me on the back, over eating, etc.

I have read all the theories in the conference room & on this board over the years. They sound reasonable enough, but sometimes my mind works in simple ways. Maybe I'm just a simpleton.

You said, "If we see our situation as a defect or polymorphism, then how have some here (Fran and Erling) basically cured themselves, or others seen improvement by certain supplements?"

The people who have "cured" themselves on this board are in what percentile would you say? 1%, maybe 2%. Anyway, it is a very, very low number. We are all different, and likewise even our anatomy. Magnesium, which seems to "help" so many has been shown to lower blood pressure, and for some a natural Ca channel blocker-never was the case for me & many others-we are all different.

Just looking from a different perspective.

Jim

I think Natale routinely ablates an area around the superior vena cava in addition to the pulmonary veins. At least they tried in me during my PVA, but had to stop because they captured the phrenic nerve.

I think that's why they put that catheter into patients neck's before the PVI--so they can work on the superior vena cava. Correct me if I'm wrong.

njb,

They only ablate the SVC if signals are coming from there. They found nothing on me there so no ablation of the SVC in my case. I'm not sure why the catheter in the patients neck is used, but I had one there.

Newman - I've read so much I can't remember where I heard/read this - or if I was told this, but it is my understanding that on the first ablation, Dr. Natale also checks in the superior vena cava area and if there are rogue impulses there, he ablates there as well. I know I didn't dream this, but I can't give you a reference.

Did you receive a copy of your procedure report? I asked for one twice now and have not received it yet. Another gripe about the CCF.

But, very grateful for Dr. Natale's skill.

Jackie

boring.

Jackie,

I have not requested a copy of my procedure report.

Newman