Re: More on Chronic Lone AF and the Maze Operation

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Posted by steve giddings on August 05, 2001 at 19:09:11:

In Reply to: More on Chronic Lone AF and the Maze Operation posted by Osman M. Nassar on August 04, 2001 at 06:21:18:

A few comments on origin of lone af, lack of understanding, and so on.
1) It is pretty darn hard to "overwork" or "strain" a normal heart.
2) Enlargement of the heart in endurance athletes is a normal, physiologic response to increased work load, just like hypertrophy of any other muscle in response to increased use. There is no information to suggest that chronic endurance training is harmful, despite what the superslow guy says. In fact, there is plenty of evidence to suggest that it is heart protective. Is there a point beyond which endurance training is counterproductive? Perhaps, but no one has been able to prove it, and it has been looked at carefully.
3) There is a definite correlation between the capacity to develop a fib and heart size. Small animals do not ever go into af. You cannot even induce it experimentally. Larger animals can, and it is a realatively common problem in horses, and has been documented in less studied animal species, like elephants. The reason is simple, af continues when a circular electrical pathway develops, for whatever reason. If the atrium is small enough, there isn't enough atrium for circles to form. Normal heart cells respond to electrical activity by changing the permability of their cell membrane to different ions, sodium, potassiumm, calcium and chloride, predomiannlty, in a very controlled fashion. As the permeability to each ion changes, the potential difference across the membrane of the cell changes and as this passes from cell to cell, it creates an electrical signal. For a period of time after permeablity changes, the cell is incapable of responding to further signal. As the permeabilities change back to the basal state, the responsiveness changes. This wave of change can become circular for a number of reasaons and when it does, af may develop. Atrial premature contractions, spontaneous depolarizations at sites other than the sa node, may set these off. These sites are the target of focal ablation efforts. Unfortunately,there are usually so many, and each one is so hard to find, that focal ablations don't have the success that was hoped for them. Back to heart size, the bigger the heart, even if it is pretty much normal,the more likely it is to go into Af, given the right circumstances. Once af occcurs, the pathway appears to be imprinted in some way, so that the likelihood of af occurring again is increased. Big people, endurance athletes, and especially big endurance athletes, tend to have big hearts. Successful endurance athletes, in addition to developing big hearts in response to training, probably had bigger than average hearts to begin with, which made them better than other people at endurance sports when they were starting out. People tend to persist in activities in which they enjoy success and drop activities in which they don't.
4) With regards to not understanding why folks can't figure what causes af and an effective medical treatment. It ain't like nobody with a brain is workin' on it. It is the biggest non-circulatory cardiac problem around, and it remains just about the only significant (PACs by themselves don't put folks at increased risk for anything) atrial arrhythmia that there isn't successful treatment for.

There is likely a genetic component. There is a familial form of af that has been mapped to a specific gene locus. What percent of af is the result of problems with specific genes remains top be determined. The problem is extraordinarily complex. Faulty ion channels may be (one of) the culprit(s). Since the first chloride channel was mapped and cloned in the search for a cure for cystic fibrosis, at least 29 separate ion channel genes have been identified. The products of these genes may be present or absent in any given tissue, their production is likely regulated and the regulating signals may be faulty point, rather than the gene itself. It may require interactions between subtle defects in several different channels in order to cause af, or other conduction system problems.
So you can't fix af by putting a penny in a blown out fuse.

We have come a long way since the first time a person was put on bypass for open heart surgery in 1964. It took James Cox and many colleagues a long time to even prove the circular theory for the origin of af which formed the basis of the maze operation, and longer to work out the specifics of the surgical intervention. It may be like hitting a fly with a sludge hammer, but we've come along way since we learned to use tools. Admittedly we have a ways to go.


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