Seeding Hearts

[www.washingtonpost.com]

The above is a very interesting heart article but the mention of electrical problems does not seem to offer much hope to Afibbers. Perhaps the knowledge that there are problems with the electrical signals will lead to a better overall understanding of Afib problems.

It is puzzling that you feel that a-fib problems are not understood.

A-fib is produced after heart tissue deteriorates, either because of aging, poisoning, or disease. This deterioration can take many forms, but in general, deteriorated atrial cells, or mutant atrial like cells in the walls of various blood vessels which enter the atrium, begin firing spontaneiously and continuously. This triggers the nearby functional atrial cells, which leads to the confused set of waves propagating back and forth across the atrium, independent of the timing signals delivered by the SV node. This confused atrial behavior we call atrial fibrillation.

Admittedly, most of us want believe that our hearts are normal and something triggers a-fib in our otherwise healthy heart.

But, we have lots of evidence that should cause us to conclude that that is not true.

For instance, youngsters seldom have a-fib.

For instance, the various medical operations, which help those with a-fib, work by isolating or destroying the deteriorated or mutant cells so their signals cannot travel into the remaining functional atrium and allows the SV node to regain control over the atrium's contractions.

Wil,

There are cases that you could be right, but if the atrial cells are damaged then one must ask themself two questions. If the cells are damaged, then why wouldn't one be in chronic AF? Secondly, if there is damage to the cells, then why have some here permanently alleviated AF via magnesium or avoidance of free glutamate, coupled with a change in diet?

I, as well as others here, have correlated events of AF/flutter to the consumption of MSG/free glutamate, while others have episodes when ingesting caffeine or alcohol.

I agree, that we would all like to believe we have healthy hearts, but in actuality, I'm more concerned about my brain, and if there has been damage there. The heart can be fixed to some extent, but the brain is a whole different story.

Richard

Wil,

To my knowledge, AF is the product of ectopic focii (one or more of which nearly every healthy adult has - typically in the PVs) PLUS (and more importantly from an AF point of view) a shortened EARP + dispersion of said refractoriness (which every healthy adult does NOT have).

I personally consider the main problem for myself and some other AFrs here to be an out-of-balance ANS as opposed to damaged heartcells per se. Do not underestimate the pull/effect of an unbalanced ANS (SNS v. PNS) on an undamaged healthy heart. This is not wishfull thinking on my part - evidence abounds in the medical literature in this regard. And not particularly good news either given the bewildering complexity of the ANS.

Mike F.

There is no area of excitable tissue known as the SV node. The sino-atrial node (SA) node is the normal heart's pacemaker. The SA node is located in the right atrium. It's impulse discharge, and subsequent spread through the atrium causes atrial systole (squeeze). The impulse travels then to the AV (atrio-ventricular) node, whose normal function it is to slow down the impulse, allowing adequate ventricular filling time. The AV node is capable of discharging, or initiating an electrical impulse, but only does so in time of need, or compensatory pacing. This would be a junctional, or nodal rhythm. It only occurs in SA node failure, as compensation, and is capable of rates of 40 to 60. The impulse then travels down the intraventricular septum via a pathway known as the Bundle of His. At the base of the ventricles, the impulse divides and spreads via another pathway called the Perkinje Fibers, across the bases of the right and left ventricles and up the lateral walls, causing ventricular systole (squeeze). The ventricles are also capable of initiating an impulse in times of need at a rate of 20 to 40. That would be a passive ventricular rhythm. Under some circumstances (usually heart muscle disease) the ventricles go into tachycardia (V Tach) and beat at rates of 110 to ? This is usually a lethal arrhythmia.

I would tend to agree with those who think that rogue impulses can arise from healthy heart tissue, and not necessarily diseased or damaged cells.

Pam

Pam,

Good explanation and thankyou for posting it. I would respectfully, however, point out that it is V.Fib which is lethal without rapid medical intervention. V.Tach comes in 2 flavors: either unsustained (<30 secs), or sustained (>30 secs). It is to my knowledge, in and of itself, rarely lethal..... unless it deteriorates into VF..... and I don't think that that happens very often thankfully. Occasional asymptomatic unsustained VT with rates of 200 or less would not normally present a serious threat to a patient. Anything faster and/or longer would, of course, invariably require some treatment.

Mike F.

Mike: There are 2 flavors of V Tach, 1)What is called walking V tach, wich occurs at a slower rate, and does pump some blood. 2) V tach, which, almost always, untreated, rapidly deteriorates into V Fib.

In my 20 years of working in CCUs, I have never seen it not deteriorate into V Fib. The V Tach alone will render a patient unconscous in about 30 seconds . There is very little blood being pumped.

In walking V Tach, and it's usually a young person, they will walk into the ER and usually wind up being electrically cardioverted. Then they almost always wind up with an ICD (intercardiac defibrillator).

V Tach is always life threatening. I might also add that the faster it goes, the worse the prognosis and the less blood (or no blood at all) being pumped.

In 95% of "Code Blues", the code is called for V Tach.

Respectfully,
Pam

Life is a continuous process of deterioration caused by cellular repair errors, poisoning, and disease eventually ending in death. No part of the body is immune to this process.

If we select a specific part of the body, such as the heart, at a given point in this continuous process of deterioration, we can ask how much of the remaining heart function is determined by the heart's intrinsic condition, and how much is determined by various other body control systems which have the capacity to affect the heart.

There is abundant evidence that the heart's intrinsic condition is far more important, as it should be.

For instance, the heart is designed to function normally even when the other body control systems, which normally can affect heart function are dead.

For instance, there are no examples that the body's heart control systems, which normally can affect heart function to a degree, have been able, by themselves, to force the heart to stop functioning. And, if the heart's intrinsic condition results in the heart's functioning to stop, the body's heart control systems cannot restore heart function.

For instance, the various medical operations which are able to cure a-fib, do so by removing the ability of the more deteriorated heart tissue to interfere with more of less normal heart operation. The medical operations in no case affect the heart's control systems. But, after the medical operation the control systems are able to again control heart function normally. Therefore, the control systems are able to affect heart function, but not nearly to the degree that intrinsic heart condition does.

Those of you that focus on the body's heart control systems, which in marginal situations ARE able to noticably affect heart function, while not acknowledging that the intrinsic heart condition is far more important, are focusing on the wrong part of the problem.

Admittedly, focusing on intrinsic health of the heart leads to a degree of helplessness. Our power to restore deteriorated tissue is limited to changing fundamental living habits and hoping that we can thereby allow normal body repair mechanisms to somewhat improve the condition of the deteriorated tissue. For most people changing fundamental living habits is strongly resisted, especially in the absence of positive proof of the efficacy of the changes.

Pam,

The info re. VT that I viewed (somewhat neurotically) a couple of years ago and which I related to (from memory) in my above post was from a website relating to army aviators and waiver from duty further to discovery of VT. I just had another quick look and came up with this webpage which kinda backs up what I stated earlier.

[wwwsam.brooks.af.mil]

which states:

'Ventricular tachycardia (VT) is defined as three or more consecutive, ventricular ectopic beats at a heart rate greater than or equal to 100 bpm. Sustained VT is that which lasts greater than 30 seconds or any duration with associated hemodynamic impairment/symptoms.'

and:

'Sustained VT or any duration of VT associated with hemodynamic symptoms is permanently disqualifying. However, in the absence of underlying cardiac disease, limited episodes of short duration VT carry a benign prognosis.'

I'm only pointing this out to you so you don't think I was just spouting on without any reference! Though I'm hardly in a position to debate VT with your goodself considering your background and experience (-:

Wil,

Point taken. I guess it all boils down to whether the issue is fibrosis (heart damage/wear and tear) OR inbalances within the ANS..... or some of both.

MIke F.

Thanks Pam for the insights into VT and Wil for highlighting the need to pay more attention to intrinsic heart health.

Pam, you stated you've noticed that VT always deteriorates into VFib. I assume you meant a sustained VT will do that or or did you also mean that those who have unsustained VT incidents will eventually have VFib?

Wil: In discussing the processes affecting AFib, I sometimes just parrot the literature which I have studied and shut out new theories. When I went back and looked at the origonal topic/reference to this thread I was reminded of this. i.e., Quoting the reference: "For decades, one of modern medicine's dictums was that, like the brain, the heart, once damaged, could not heal. The heart could not grow new tissue or be repaired. But scientists have begun to try to do what was once unthinkable -- grow new heart muscle." Your comments seem to partially refute this new premise.

The damaged or fibrotic heart tissue does something to explain the start of AFib but doesn't satisfactorily explain why AFib stops. (the tissue doesn't heal!?) And remembering the goat experiments leading to "AFib begets AFib" remodelling theory, those hearts were healthy at least. (even tho goats!) And young healthy hearts do have AFib problems, and the category "lone AF" is part of medicine's admission of that. This phorum has a certain dedication to uncovering alternative paths to curing AFib and kudos to that!

Having said all that, my heart is a 67 year old mixed bag of LAF, Flutter(now ablated) and runs of monomorphic VT, so I'm more than aware of the aging process. But then great (and older) posters like Erling Waller come along and defeat these rising and falling ectopic disturbances. Thanks for all input; I'm still trying--- Anton

Anton:
I suppose that nonsustained VT wouldn't always lead to or deteriorate into VF, but how does one know, if one has nonsustained VT that it will not go on? Just as a person who has pauses. At what point does he need a pacemaker?
In my experience, people who have long runs of VT always get ICDs. What has been your experience with it? If you have runs of VT, how long do they last in seconds? Are you symptomatic with them? How long do they run in terms of beats, and at what kind of rate?


Pam, you stated you've noticed that VT always deteriorates into VFib. I assume you meant a sustained VT will do that or or did you also mean that those who have unsustained VT incidents will eventually have VFib?

Pam

Pam- I'm contemplating ICD now, vs. ablating VT and AF at CClinic. Looking for additional input from Dr. Natale vs another EP here in CT. Natale seems to favor ablation as my condition is good. My latest Holter showed VT during exercise while in AF, the longest run of which was 13 sec/220 BPM. (Yes, I knew it and slowed down) Being only a little over 2 months since a flutter ablation, it was'nt good news!

Still studying--- Anton

Anton,

I didn't know that VT could be ablated. But I'm sure glad to hear that it can - though I wonder - is it more difficult to ablate VT than AF given that the location of the focus is in the ventricles?? And, of course, my best wishes for whatever course of action you decide upon - do keep us informed as to what decision you take as regards sorting out your arrythmias. The website which I referred to in an earlier post to this thread should provide you with more than a little reassurance as regards non-sustained VT.

Mike F.

Anton:
It seems to me that VT ablations have been in practice longer that AF ablations, and with more success. I certainly agree that it's daunting in view of your recent flutter ablation. I can promise you that 13 seconds of VT IS a concern. I will look for more info on the success of VT ablations, and the history of the procedure. I would think that in a reasonably fit and active person like yourself that ablation would be preferable to ICD. I'll post you if I find anything.

Best Regards,
Pam

Yes, VT can be ablated and dependant on the type and the location, the success rate can be quite good. Some are 90% successful and are easier than PVI’s. Mine is monomorphic (from one focus) which is good, but from the left side, which is bad. I’ve got a lot of these “good and bad” characteristics that make my decision to go for ablation difficult.

For example, there is little reason to get an ablation for AFib and another for VT if a year down the road I develop another area of “irritability” or for other reasons need an ICD. When time I’ll further post my story which gets a bit complicated, at least to my simple way of thinking.

Still consulting and studying. –Anton