new affib study

Public release date: 11-Nov-2003
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Contact: Sherry Baker
emoryheartnews@aol.com
404-377-1398
Emory University Health Sciences Center

Emory scientists link atrial fibrillation with decrease in nitrous oxide
ORLANDO - Emory research presented at the Abstract Oral Sessions of the American Heart Association's Scientific Sessions today entitled "Atrial Fibrillation Causes Increased Oxidative Stress and Decreased Nitric Oxide Bioavailability in the Left Atrial Appendage" offers a possible explanation for one of the most serious, and sometimes deadly, complications associated with the heart rhythm disorder known as atrial fibrillation (AF) -- stroke.
AF, which is characterized by a rapid and irregular beat originating from the upper chambers of the heart, is the most common sustained heart rhythm disorder. According to the Centers for Disease Control (CDC), an estimated 2.2 million adults in the United States have been diagnosed with this arrhythmia. A-fib increases the risk for heart disease and stroke, both leading causes of death in the United States. AF associated stroke is known to be due almost exclusively to blood clot ( hrombus) formation in the left atrial appendage (LAA), a small, thumb-shaped pouch in the heart's left upper chamber.

"Previous studies have indicated that more than 90 percent of non-rheumatic AF-related strokes are the result of blood clots that form in the LAA and then travel to blood vessels leading to the brain, causing stroke, " says Emory Heart Center and Atlanta Veterans Administration Medical Center cardiologist Samuel C. Dudley, MD, who headed the Emory research team. "The mechanisms underlying AF perpetuation and localized formation of LAA thrombus continue to be poorly understood. However, we recently found that AF is associated with decreased endocardial nitric oxide (NO) in the LAA . We believe that may play a role in blood clot formation."

The Emory researchers, working with pig hearts, examined atrial tissue (from the upper chambers of the heart) from animals that had experienced induced AF and compared them with the hearts of control animals. They found that superoxide (O2) levels were twice as high in the LAA of animals with AF compared with controls and this increase in O2 was associated with a significant decrease in NO.

"Nitrous oxide is known to have has antithrombotic properties that can protect against blood clots, so we believe these changes may explain the predisposition to LAA thrombus in people with AF," says Dr. Dudley. "These findings may provide new avenues for the study of therapeutic interventions in humans with AF."


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The Emory Heart Center is comprised of all cardiology services and research at Emory University Hospital (EUH), Emory Crawford Long Hospital (ECLH) Carlyle Fraser Heart Center, the Andreas Gruentzig Cardiovascular Center of Emory University and the Emory Clinic. Ranked in the top ten of U.S. News & World Report's annual survey of the nation's best Heart Centers, the Emory Heart Center has a rich history of excellence in all areas of cardiology - including education, research and patient care. It is also internationally recognized as one of the birthplaces of modern interventional cardiology.

Media Contacts: Sherry Baker, 404/377-1398, emoryheartnews@aol.com
Kathi Baker, 404/727-9371, kobaker@emory.edu

Jerry,

Perhaps the antithrombotic properties of Vitamin E, Mg and several other supplements owe this to their ability to quench the superoxide anion and other free radicals. NO may be just another way to measure this.

PC

Jerry,

Thank you for sharing this article. You may find this article very important, too, especially in how the antioxidant amino, Glutathione, relates to nitric oxide, with the latter being formed from the amino acid, Arginine. This link says that the lungs have 140x's more Gluthathione than anywhere else in the body, and that makes sense, being that the lungs are exposed to toxic elements every time we take a breath. What I find important about this, is the fact that after the blood leaves the lungs, it enters the left atrial of our heart, and if the toxicities weren't handled in the lungs, due to lack of Glutathione, then does this leave the pulmonary vein and left atrial vulnerable to these toxicities? In light of the fact that the aminos, cysteine (a breakdown product from methionine), glutamate, and glycine, form Glutathione, could taking N-acetyl-cysteine help with toxicities of free glutamate, by combining with the excess of the latter? By having more available Glutathione in our bodies, this may help with nitric oxide delivery, as well as, having the benefits of reversing fibrosis, if that is an issue. Glutathione also is the strongest antioxidant within the cell, keeping the cell free of injury. I don't know about anyone else, but I am convinced that this should be at the top of our priority list of supplementation. It must be known, however, that it is equally important to take N-acetyl-cysteine with Vit. C, as they work synergistically together.

[members.tripod.com]
See pg. 6 and 7, but read the whole article, as it is very interesting.

Richard

Jerry,

Very interesting article. Actually this subject was discussed in some detail in the opening postings of Conference Room sessions 10 and 15.

Hans