When I think about the field of atrial fibrillation in 2013, several thoughts come to mind. There were technical advancements, some new drug therapies, and additions to our understanding of Atrial Fibrillation (and a few accomplishments for our A-Fib.com website).
Heart Imaging And Mapping Systems
Perhaps the most important technical innovations in 2013 for A-Fib patients were the introduction of two new heart imaging and mapping systems. A third system, the Bioelectronic Catheter, represents a whole new technology with tremendous potential for A-Fib patients.
The ECGI System
The ECGI system, combined with a CT scan, produces a complete 3-D image of your heart along with identifying all the A-Fib-producing spots. Think of it as an ECG with 256 special high resolution electrodes rather than 12. It greatly reduces your ablation time and your radiation exposure.
A day before your ablation, you simply don a special vest with 256 electrodes covering your upper torso, and lay down. The 3-D image created is a road map of your heart with all the focal and rotor areas (A-Fib-producing spots) identified. During your ablation your EP simply ablates the “guilty” areas. Read more of my article…
The FIRM System
The FIRM system uses a different approach to mapping the heart and the A-Fib producing spots. It uses a basket catheter inside the heart to map large areas in a single pass and reveal the location of foci and rotors. Read more of my article…
Why are these two technologies important? ECGI allows your imaging & mapping to be performed the day prior to your ablation, rather than during your ablation. This shortens the length of your ablation procedure. In addition it reduces your radiation exposure and produces remarkably accurate 3D images of your heart and identifies where A-Fib signals are coming from. The FIRM system, though performed during an ablation rather than before it, may be a significant improvement over the Lasso catheter mapping system now in current use. Both systems may mark a new level of imaging/mapping for A-Fib.
Stretchable Electronics Meets the Balloon Catheter
The merging of living systems with electronic systems is called “bioelectronics”. Key is a flexible, pliable circuit made from organic materials—the carbon-based building blocks of life. Bioelectronics have entered the EP lab with a prototype of a ‘bioelectronic catheter’, the marriage of a pliable integrated circuit with a catheter balloon.
In a mapping application, the deflated bioelectronic balloon catheter is slipped into the heart, then pumped up. The inflated integrated circuit conforms to the heart’s grooves and makes contact with hard-to-reach tissue. It can map a hundred electrical signals simultaneously, across a wider area and in far greater detail than had been previously possible. And it’s being developed to function in reverse. For ablation applications, instead of detecting current, it can apply precise electrical burns. This is a potentially breakthrough technology that may well change the way catheter mapping and ablation are performed. (Thanks to David Holzman for calling our attention to this ground-breaking research article.)
This is a remarkable time in the history of A-Fib treatment. Three very different technologies are poised to radically improve the way A-Fib is detected, mapped and ablated. We’ll look back at 2013 as a watershed year for A-Fib patients.
Three New Anticoagulants
In 2013 we saw three new anticoagulants, a welcome development for A-Fib patients. Note: the new anticoagulants are very expensive compared to the proven anticoagulant warfarin.
How do they compare to warfarin?
Warfarin seems to have a slightly higher chance of producing intracranial bleeding.
In general stay away from Pradaxa. There are horrible ER reports of patients bleeding to death from even minor cuts, because there is no antidote or reversal agent. Read more about my Pradaxa warning…
Eliquis, in general, tested better than Xarelto in the clinical trials, but it’s so new we don’t have a lot of real-world data on it yet. And, as with Pradaxa, neither have antidotes or reversal agents.
In addition, there was what some consider a major problem with the clinical trials comparing the new anticoagulants to warfarin. ‘Compliance’ rates by warfarin users were poor (many either weren’t taking their warfarin or weren’t in the proper INR range). Did this skew the results?
And finally, unlike warfarin where effectiveness can be measured with INR levels, we don’t have any way to measure how effectively the new blood thinners actually anticoagulate blood. Read more of my article “Warfarin vs. Pradaxa and the Other New Anticoagulants“.
Keep in mind: ‘New’ doesn’t necessarily mean ‘better’ or ‘more effective’ for You.
High Blood Pressure with Your A-Fib? Is Renal Denervation a solution?
As many as 30% of people with A-Fib also have high blood pressure which can’t be lowered by meds, exercise, diet, etc. There was hope that Renal Denervation would help.
With Renal Denervation, an ablation catheter is threaded into the left and right arteries leading to the kidneys, then RF energy is applied to the nerves in the vascular walls of the arteries, hopefully reducing ‘Sympathetic Tone’, lowering high blood pressure and reducing A-Fib. For many people Renal Denervation seemed the only realistic hope of lowering their high blood pressure. However, the Medtronic Simplicity-3 trial indicated that renal denervation doesn’t work. Read more of this article… For 2014 news on this topic, read more…
A Study of Obesity and A-Fib: A-Fib Potentially Reversible
Obesity is a well known cause or trigger of A-Fib, probably because it puts extra pressure and stress on the Pulmonary Vein openings where most A-Fib starts.
In 2013 A research study report focused on obese patients with A-Fib. Those who lost a significant amount of weight also had 2.5 times less A-Fib episodes and reduced their left atrial area and intra-ventricular septal thickness.
Good news! Losing weight can potentially reverse some of the remodeling effects of A-Fib. Related article: Obesity in Young Women Doubles Chances of Developing A-Fib.
Obstructive Sleep Apnea and A-Fib
Obstructive Sleep Apnea (OSA) is another well recognized cause or trigger of A-Fib. Anyone with A-Fib should be tested for sleep apnea.
Earlier studies have shown approximately two-thirds (62%) of patients with paroxysmal or persistent A-Fib suffer from sleep apnea. In 2013, research reports showed that the worse one’s sleep apnea is, the worse A-Fib can become. In addition, sleep apnea often predicts A-Fib recurrence after catheter ablation.
Before an ablation, Dr. Sidney Peykar of the Cardiac Arrhythmia Institute in Florida, requires all his A-Fib patients be tested for sleep apnea. If they have sleep apnea, they must use CPAP therapy after their ablation procedure.
A-Fib.com: Our New Website’s First Year
The original A-Fib.com web site was created using the phased out software MS FrontPage. Thanks to a “no strings attached” grant from Medtronic, A-Fib.com was reinvented with a more up-to-date but familiar look, and features more functionality (built on an infra-structure using Joomla and WordPress). We can now grow the site and add features and functions as needed.
It involved a tremendous amount of work. A special thanks to Sharion Cox for building the new site and for technical support. My wife, Patti Ryan, designed the look and all graphics. (I can’t thank Patti enough; I’m so lucky!)
Update the Directory of Doctors & Facilities
Back when I started A-Fib.com in 2002, there were less than a dozen sites performing ablations for A-Fib. Today our Directory of Doctors and Facilities lists well over 1,000 centers in the US, plus many sites worldwide.
Increasingly, doctors were writing me asking why they weren’t included, or why their info was incorrect since they had moved, etc. To update our records and our service to A-Fib patients, starting in July 2013, we prepared and mailed letters to over 1,000 doctors/facilities. We asked each to update/verify their listing (and include a contact person for our use).
The response to our bulk mailing was great. The data input started in October and continued for several months (as time allowed). Recently, we cut over to the ‘new’ Directory menu and pages.
What’s Ahead for A-Fib.com in 2014
2014 Boston AFib Symposium Reports: Check out my new reports from the 2014 Boston A-Fib Symposium (BAFS) held January 9-11, 2014 in Orlando FL.
The first two reports are posted. Look for more reports soon. I usually end up with 12-15 reports in total.
Our a-Fib.com Directory of Doctors & Facilities: Work on updating our listings is still underway. We need to contact those who did not respond to our request for verification or updating of their listing. (Shall we write again or maybe make phone calls?)
Amazon Best Sellers list: Our book sales continue to grow. Did you know that our book ‘Beat Your A-Fib’ has been on Amazon’s Best Sellers list continually in two categories (Disorders & Diseases Reference and Heart Disease) since its debut in March 2012? Visit Amazon.com and read over 40 customer reviews.
Help A-Fib.com Become Self-sustaining: We plan to step up our efforts to make A-Fib.com a self-sustaining site. (Since 2002, Steve and Patti Ryan have personally funded A-Fib.com with an occassional reader’s donation.)
In our efforts toward sustainabiliy, several years ago we added a PayPal ‘Donate’ button (you don’t need a PayPal account to donate) and invited donations toward our onlline maintenance costs.
Our newest effort is our ‘A-Fib can be Cured! shop with T-shirts and more at Spreadshirt.com. With each shirt purchase $2 goes to support A-Fib.com. (We will roll out new designs every quarter or so).
Posted February 2014
Help A-Fib.com become self-sustaining! Help keep A-Fib.com independent and ad-free.
Will 2014 be the year you help support A-Fib.com?
Last updated: Wednesday, February 11, 2015
2015 International AF Symposium
by Steve S. Ryan, PhD
This overview should give you a sense of the topics floating through the three days in Orlando and the over sixty presentations by fifty A-Fib experts and researchers. (Most recent brief reports listed first)
(Please be advised that the Symposium organizers go to great lengths not to identify or unfairly publicize one device over another. When writing these reports I often have to do a good deal of research to correctly identify and describe particular devices that are demonstrated, as a service to readers. But this in no way implies or suggests that one device is superior to another.)
Dr. Gerhard Hindricks of the University of Leipzig in Germany gave a dynamic presentation of a catheter ablation of a 46-year-old female with paroxysmal A-Fib using the Rhythmia 3-dimensional multipolar mapping system by Boston Scientific. Along with his colleagues Drs. Andreas Bollmann and Jedrzej Kosiuk, they used the Rhythmia special basket catheter to generate a 3-D map of electrogram voltages and activation times. To me it seemed amazingly fast. The eight-splined bidirectional catheter produced 1,000 data points per minute. In what seemed like only a few passes, they produced a 3-D color reconstruction of the patient’s left atrium.
The actual ablation was routine. They terminated the A-Fib into sinus rhythm without having to use Electrocardioversion. But they found that the PV isolation was incomplete. Using the same Rhythmia 3-D mapping catheter, they were easily and quickly able to locate the gap in the Left Superior PV and ablate it.
Dr. Vivek Reddy from Mount Sinai School of Medicine in New York City gave a very well referenced and persuasive presentation on the Watchman device which closes off the Left Atrial Appendage to prevent clots and strokes. The theory behind the Watchman device is that most A-Fib clots originate in the Left Atrial Appendage (LAA). The Watchman closes off the LAA where 90-95% of A-Fib strokes come from. It’s a very low risk procedure that takes as little as 20 minutes to install. Afterward, you would usually not need to be on blood thinners. (For more, see my article, The Watchman Device: The Alternative to Blood Thinners).
Dr. Reddy certainly persuaded me that the FDA should approve the Watchman device. Dr. Reddy, earlier in Washington, had made the same persuasive arguments before the FDA.
Dr. Andrew Farb from the FDA took the bull by the horns and gave his perspective on the various LAA Closure (Occlusion) Devices. But as one would expect, he didn’t indicate how the FDA would rule on the Watchman device, since deliberations were still ongoing.
After his presentation, I asked him several pointed questions about this, but he was, of course, careful not to comment about current FDA deliberations. My guess? If body language, momentum, mood of the presentations, and more importantly recent research indicate anything, the Watchman device probably will not be approved by the FDA.
There was a palpable sense of sadness at the end of these presentations. The attendees realized that the game may be over for the Watchman device. I hope I am wrong, since the Watchman device would be an important tool to help A-Fib patients. Once the FDA rules and the current clinical trials of the Watchman device end, you will probably have to go to Canada or overseas to get a Watchman device installed.
(Happily I was wrong on this prediction. Update: The U.S. Food and Drug Administration (FDA) approved Boston Scientific’s WATCHMAN™ LAA closure technology for use in the U.S. on March 13, 2015. It has been available internationally since 2009. The FDA approval of the WATCHMAN device is based on the clinical program which consists of numerous studies, with more than 2,400 patients and nearly 6,000 patient-years of follow-up. The Watchman device will be available first at U.S. centers where it has been used in clinical studies.)
Watchman May Win FDA Approval
In my earlier brief reports on the Orlando AF Symposium, based on the recent research and the FDA presentation, I said the Watchman device probably won’t be approved in the US. I’m happy to say that I am most likely wrong.
At the LAA Symposium 2015 in Marina del Rey, CA, it was suggested that the Watchman device may be approved by the middle of this year. One presenter described how the FDA chairman talked with several people who were going to Canada to have the Watchman device installed. He seemed embarrassed that the Watchman was available everywhere in the world but not in the US and said that it has to be approved.
Other doctors I talked with at the LAA Symposium were of the same opinion. Presenters described how clinical trials for other LAA closure devices were on hold so that they could get approved in comparison to the Watchman (Non-Inferiority Trials). Dr. Dhanunjaya Lakkireddy of the University of Kansas Medical Center said that we are at a “tipping point” for the (A-Fib) industry.
As everyone, including the FDA, is well aware, A-Fib innovations usually start in Europe where they are more easily approved. Then only later do they move to the US for FDA approval, since the FDA generally requires more data than European regulators.
Drs. Jun Dong and Andrew Farb from the FDA described the FDA’s ‘Easy Feasibility Study’ (EFS) program where medical device innovations could be evaluated in the US without having to go to Europe first. He encouraged researchers and attendees to take advantage of the new EFS program. This is major news and may make the development of A-Fib innovations much easier to accomplish in the US.
For further information, contact: Andrew Farb, Email: Andrew.email@example.com. 301-796-6317
Dr. Luigi Di Biase from the Albert Einstein College of Medicine in the Bronx, NY and Dr. Daniel Singer from Massachusetts General Hospital in Boston each described potentially great developments in reversal agents for apixaban (Eliquis) and rivaroxaban (Xarelto).
Dr. Di Biase described studies where leaving people on uninterrupted rivaroxaban and apixaban before, during and after an ablation dramatically reduced the amount of silent thromboembolic lesions and were as safe as warfarin with regards to stroke and TIAs. (This didn’t work with dabigatran [Pradaxa].) But if patients develop bleeding or effusion during the ablation, they are in trouble because there is no direct reversal agent as there is for warfarin. He has used Factor IV as an indirect reversal agent. Dr. Singer also described how Factor IV was used as a reversal agent for apixaban.
But there are new reversal agents for apixaban and rivaroxaban which promise to completely reverse the effects of these two drugs in less than four minutes. The FDA is speeding up studies on these reversal agents. But one never knows when or if the FDA will approve them.
Dr. John Day of the Intermountain Heart Institute in Murray, UT (and recently elected president of the Heart Rhythm Society) may be the first A-Fib leader to publicly question whether women should be given one point on the stroke risk CHA2DS2-VASc scale just because of their gender. Many doctors have said this in a circumspect way. Dr. Eric Prystowsky in a presentation at last year’s AHS meeting thought that most doctors would agree with Dr. Day, “as long as there wasn’t a camera focused on them.” He gave the example of a 45-year-old woman in good health and a 45-year-old man with hypertension who according to current guidelines should both be given one point on the stroke risk CHA2DS2-VASc score.
As readers of A-Fib.com, you know that’s been my opinion ever since the original European guidelines came out. Women in their child-bearing years are much less at risk of stroke because of the blood-thinning effect of losing blood each month. And even after menopause women have less risk of stroke. But eventually they do have more strokes. But not because of an innate inferiority, but because women live longer than men. Stroke is age related. An observational Danish registry study documents this.
For more, see The Denmark Study: Women in A-Fib Not at Greater Risk of Stroke Contrary to CHA2DS2-VASc Guidelines!) (Be advised that the original European guidelines were written by doctors with major conflicts of interest.) These guidelines may be a not so very subtle form of gender bias.
Living in A-Fib is more dangerous than having an ablation, according to Dr. Josef Kautzner from Prague, the Czech Republic. Studies have documented that the adverse effects of living in A-Fib, having to take A-Fib drugs and anticoagulants for life are both pragmatically and statistically worse than having an ablation. Dr. Kautzner discussed how A-Fib can cause or is associated with silent brain lesions and dementia. Any time you go into a hospital is a risk. And no one would say that a catheter ablation is a walk in the park. But an ablation is a low risk procedure, though not risk free. The risk is similar to having your tubes tied. The possible adverse effects of an ablation procedure (like bleeding at the groin) are generally temporary, unlike the lasting, permanent damage you can do to your heart, body and brain by living in A-Fib for years.
The most hotly discussed topic at this year’s symposium was rotors. The opinions expressed about rotors were at times very heated, more than I had ever seen at an AF Symposium. Dr. Shih-Ann Chen of Taipei, Taiwan disagreed with Dr. Sanjiv Narayan of Stanford, CA about the basic concepts of rotors and how they should be defined. Dr. Ravi Mandapati of UCLA and Loma Linda University disagreed with Dr. Narayan which was all the more striking in that he had worked with Dr. Narayan when he was at UCLA. Dr. Pierre Jais of Bordeaux, France said that the FIRM mapping system misses 40% of the atrium area.
Drs. Haissaguerre and Jais from Bordeaux and Dr. Sebastien Knecht of Brussels, Belgium gave presentations on how they were using the CardioInsight body surface mapping vest to perform ablations of “drivers” at many different centers, while Dr. Karl-Heinz Kuck from Hamburg, Germany using a different body surface mapping system said that he couldn’t ablate rotors. Dr. Narayan says the FIRM system finds a maximum of 2-3 rotors in the atria, while other systems find as many as seven. The FIRM system says rotors are usually relatively stable and can last as long as 30 seconds while others say they rotate in one fixed spot for only one or two rotations, that they tend to migrate within a certain area.
The presenters obviously didn’t share a consensus of basic concepts of what rotors are, how they work, their importance in A-Fib, how they should be correctly identified, used, and ablated. (It seems to me the Bordeaux group has the best understanding and pragmatic use of rotors. They refer to “rotors” and focal sources as “drivers.”) But the CardioInsight system Bordeaux uses isn’t currently available or isn’t being tested in the US.
Obesity was one of the most often discussed topics. There is a growing consensus among EPs that it isn’t enough to just give obese patients a catheter ablation while not dealing with their obesity. If the obesity isn’t dealt with, their A-Fib is very likely to re-occur. A-Fib will develop in other spots that haven’t been ablated. The condition (obesity) that triggered or caused the A-Fib will trigger or cause it again, if it isn’t taken care of.
Dr. Prashanthan Sanders of Adelaide, Australia described the great results he is getting in his clinic which includes a weight loss program and counseling. He convinces his overweight patients to buy into the program, lose weight, and keep it off. The program works so well that just by losing weight patients become A-Fib free. This program is a holistic approach to health and also is developed to work for diabetes, sleep apnea, hypertension, binge drinking and smoking.
Dr. Sanders foresees a world where some patients become A-Fib free simply by changing their life style, where they don’t have to have a catheter ablation to become A-Fib free.
Many other doctors commented that A-Fib treatment at many centers today includes or should include much more than A-Fib ablation and drugs. A-Fib centers should have nutritionists, exercise therapists, sleep apnea specialists, etc. as part of their A-Fib program.
Dr. John Day of the Intermountain Heart Institute in the Challenging Cases Discussion described his experience with the dreaded Atrial Esophageal Fistula. Though very rare, this is one of the few possible complications of a catheter ablation that can kill you. An ablation, if not done with caution, can irritate and damage the esophagus which often lies right next to the heart. Over 2-3 weeks stomach acid can eat through this damaged area to produce a hole or fistula from the esophagus into the heart.
As soon as Dr. Day saw this patient, he knew it was a fistula and immediately called surgeons and a GI doctor. All the surgeons were doing operations and didn’t want to do the surgery in the EP lab. Dr. Day described how he and his colleagues ran down the hospital hallway to the operating room while giving the patient a transfusion and at the same time pumping out the blood escaping from his heart.
The GI doctor got there first and put in a stent in the esophagus to plug the hole. There was lots of discussion as to whether this was the best approach, but it worked. The patient survived but had to spend a month in the hospital.
This cautionary and very dramatic tale certainly got the attention of all the attendees. No matter how rare a fistula is, every EP and A-Fib center must have an established protocol in place to deal with it. I remember Dr. Hugh Calkins in a previous Symposium advising, “There are only two kinds of EPs—those who have not had an Atrial Esophageal Fistula and those who have!” (Dr. Calkins’ patient with fistula also survived.)
Dr. Peter Kowey of Lankenau Hospital in Winnewood, PA described a case that illustrates the kind of dilemma both doctors and patients often have to face. A 92-year-old woman with paroxysmal A-Fib who had been treated for many years with warfarin had some bruising and nuisance bleeding, but never anything major.
Dr. Kowey thought that ethically he should tell her about the different new anticoagulants which may be superior to warfarin, then see if she wanted to change. She went with apixaban (Eliquis), then six months later had a stroke even though she was taking apixaban properly and conscientiously. Happily, she made an almost full recovery. She returned to warfarin which had worked for her in the past and which she was comfortable using.
One of the reasons Dr. Kowey discussed the new anticoagulants with his 92-year-old patient was because warfarin is considered more apt to cause bleeding in older patients. The newer anticoagulants in clinical trials caused less bleeding. But we don’t have much data from the clinical trials on people over 90 years old.
Can we say that apixaban didn’t work or was ineffective? No. Anticoagulants reduce but do not totally eliminate the risk of an A-Fib stroke. Just because she had a stroke doesn’t mean apixaban didn’t work.
Dr. Jeremy Ruskin pointed out that there has never been and probably never will be a head-to-head comparison of the three new anticoagulants. But in my opinion apixaban (Eliquis) appears to have tested better and is safer than the others
For more, see my 2013 BAFS articles, The New Anticoagulants (NOACs) and Warfarin vs. Pradaxa and the Other New Anticoagulants.
In the satellite case live presentations, Drs. Rodney Horton and Amin Al-Ahmad from the Texas Cardiac Arrhythmia Institute in Austin, TX surprised us by doing an ablation without wearing the standard lead aprons to prevent fluoroscopy exposure. Even more surprising was one of the lab assistants who was pregnant. She could work on the ablation because no fluoroscopy was used. The doctors did the whole ablation using ICE (Intracardiac Echo) and 3D mapping. They showed for example how ICE can be used to thread the catheter up into the heart and into the left atrium. Dr. Horton said that not having to wear those heavy lead aprons would probably add 5-10 years to his ablation career.
(They didn’t wear surgical masks during the ablation which was surprising to me. I will write them for an explanation.)
The live satellite case from Beijing, China was technically flawless and probably a first of its kind. But it wasn’t much of a learning experience for the attendees. The Chinese EPs only used one catheter and had to frequently pull out the mapping catheter and replace it with the ablation catheter, etc. When the expert panel asked them questions, the Chinese EPs either didn’t understand or simply didn’t answer them. They seemed very uncomfortable. It seemed like a throwback to ablation techniques of 20 years ago.
Drs. Claudio Tondo, Gaetano Fassini, Massimo Moltrasio, and Antonio Dello Russo from Milan, Italy showed how they do a catheter ablation for A-Fib and install the Watchman device in the same procedure, when it’s needed. They do the ablation procedure first. Then when the patient is in sinus rhythm, they install the Watchman device. (This can’t be done in the US, because the Watchman device hasn’t received FDA approval. In later discussions including representatives of the FDA, there was an all too real possibility that the Watchman will never receive FDA approval.)
Drs. Kevin Heist and Moussa Mansour from Massachusetts General in Boston showed in a live case how they used a Contact Force Sensing catheter combined with Jet Ventilation. (There are two Contact Force Sensing catheters approved by the FDA—the ThermoCool Smart Touch device by Biosense Webster (approved Feb. 24, 2014) and the TactiCath Quartz Contact Force Ablation Catheter by St. Jude Medical (approved Oct. 27, 2014). This live case used the TactiCath catheter but didn’t imply or suggest it is superior to the ThermoCool catheter. For a description of each, see my 2014 AF Symposium report The New Era of Catheter Ablation Technology: Force Sensing Catheters.
This combination of Force Sensing Catheter with Jet Ventilation for RF ablation probably represents the most advanced RF ablation strategy available today. Jet Ventilation doesn’t stop the heart from beating as in bypass surgery. But to this observer it seemed to put the heart in a type of slow motion with a lot less movement than when the heart is beating in normal sinus rhythm. You could really see a difference when they turned the Jet Ventilation off and on. Slowing down the heart like this helps the ablation doctor make lesions in hard-to-access areas and makes it easier to hold the catheter steady and apply the right contact pressure.
Drs. Michel Haissaguerre and Pierre Jais from Bordeaux/LYRIC gave presentations on the ECGI system. The day before their ablation, the patient lies down on his/her back and a technician places a vest-like device with 256 electrodes over his/her chest and stomach. These electrodes combine with rapid CT (Computed Tomography) scans to produce a very detailed 3D color map of the heart. (For a detailed description and discussion of the ECGI system, see 2013 BAFS: Non-Invasive Electrocardiographic Imaging [ECG]) The system automatically detects rotors and foci and computes them into a “Cumulative Map” or movie. These driver regions are ranked, based on statistical prevalence.
Then, Dr. Sebastien Knecht from CHU Brugmann, Brussels, Belgium, described the AFACART trial design and preliminary results using the CardioInsight ECGI system. Many centers in Europe including four in Germany are now using the CardioInsight. Requiring very little training, technicians and EPs using the CardioInsight system are getting similar great results like the Bordeaux group. Though these studies just started, it looks like the CardioInsight ECGI mapping and ablation system is poised to revolutionize the way EPs map and perform ablations.
Dr. Jose Jalife of the University of Michigan in Ann Arbor, MI, continued his exciting research on fibrosis and A-Fib. In previous Symposiums Dr. Jalife demonstrated how A-Fib produces fibrosis. When he paced sheep into A-Fib, their hearts became fibrotic within a very short time. The markers of fibrosis (collagen and scarring) increased progressively as the sheep went from paroxysmal to persistent A-Fib. (See A-Fib Produces Fibrosis—Experimental and Real-World Data.)
Fibrosis is tissue that has fiber-like characteristics which develop in place of the normal smooth walls of the heart. Fibrotic tissue is scarred, immobile, basically dead tissue with reduced or no blood flow and no transport function. It results in a loss of atrial muscle mass. Over time it makes the heart stiff, less flexible and weak, overworks the heart, reduces pumping efficiency and leads to other heart problems. Fibrosis, up to now, was considered permanent and irreversible. But Dr. Jalife gave his sheep a Gal-3 inhibitor GM-CT-01 that actually prevented and reduced fibrosis! (For his previous presentations, see 2014 BAFS: The Holy Grail: Preventing A-Fib by a GAL-3 Inhibitor.)
In his continuing studies of sheep, Dr. Jalife found that fibrosis predicts recurrence, and that fibrosis can not be reversed if it is well established, even with GAL-3 Inhibitors.
Last updated: Wednesday, January 18, 2017
by Steve S. Ryan, PhD, September 2014
Even though North America is a land of immigrants, the prevalence of A-Fib is much greater in the US than in our ancestral countries. There is ten-times more A-Fib in North America than, for example, in Asia. But once these Asians immigrate to the US, the incidence of A-Fib closely approximates that of other Americans.
Whatever protective effect Asians enjoyed in their native countries is lost when they immigrate. And the A-Fib epidemic is occurring not just in the US but also in most developed countries around the world.
A-FIB HAS INCREASED 71% IN THE LAST 20 YEARS
Dr. John D. Day of Intermountain Healthcare in Utah has performed more than 3,000 A-Fib ablation procedures. But he asks, “Am I even making a dent in this disease? I cannot remember seeing so many new patients, even young patients, with atrial fibrillation when I began my cardiology fellowship nearly 20 years ago.”
A-Fib has increased 71% in the last 20 years. The general consensus is we are seeing more A-Fib due to our aging population (and also because we are looking more for A-Fib and have better tools to diagnose it).
But that doesn’t explain why A-Fib is increasing more than our aging population.
Though he poses it as a question, Dr. Day suggests strongly that obesity is causing the increase in A-Fib. “Could the lifestyle of modern civilization and our obesity epidemic explain the marked spike in new atrial fibrillation cases we are now seeing?”
WEIGHT LOSS CAN REVERSE A-FIB
In a study at the Mayo Clinic, bariatric surgery helped to prevent A-Fib in patients with morbid obesity. New onset A-Fib occurred in only 6.4% of patients with bariatric surgery, compared to 16.1% in the control group.
Dr. Day described a new program (DARE—Drive Atrial fibrillation into Remission Evaluation) started at Intermountain Healthcare in January, 2014, to encourage aggressive lifestyle modification.
Even though less than 5% of people successfully change their lifestyle to maintain long-term weight loss, 92% of his patients are still actively engaged in this lifestyle modification program.
They’ve lost an average of 16 pounds over the last few months and a 42% reduction in their A-Fib symptom burden. They “feel better than they have ever felt before.” Patients who had failed multiple ablations were now A-Fib free.
A-Fib can be prevented or reversed by lifestyle changes. Dr. Day encourages doctors to take a holistic approach, to not just treat A-Fib but to help patients become aware of and overcome the toxic lifestyles of our culture. “A large percentage of cases in the USA are unnecessary.”
Weight loss improves A-Fib ablation success & symptoms
Researchers in Australia found that obese patients who had a catheter ablation and then lost weight, had nearly a five-fold greater probability of staying A-Fib free.
Two groups of obese patients had catheter ablations for A-Fib. The first group agreed to participate in an aggressive risk factor management program. Each group was monitored for two years. The life-style change weight management group experienced more weight loss, better systolic blood pressure, better glycemic control and lipid profile.
Ablation success rate much better with weight control
The single procedure A-Fib free rate was greater for the weight management group (32.9% vs 9.7%), while the multiple procedure results were markedly better (87% vs 17.8%). [A 32.9% success rate is relatively low compared to other centers.] A-Fib frequency, duration, severity, and symptom severity were better in the aggressive risk factor management group.
A previous study had found that a weight management program for highly symptomatic A-Fib patients reduced symptom burden and severity and reduced antiarrhythmic drug use. The authors wrote that these benefits, “may be attributable to a decrease in left atrial area and ventricular wall thickness, thereby reducing the left atrial hypertension that is a common finding in obese patients.”
The authors concluded that current A-Fib management guidelines should be changed to include risk management when treating A-Fib.
Before this study, many doctors were already requiring that A-Fib patients with pre-existing conditions or risk factors get these taken care of before getting a catheter ablation. If they didn’t, they were much more likely to have a recurrence than other patients. These Australian researchers also developed risk factor management strategies not only for weight, but also for hypertension, diabetes, sleep apnea, cholesterol, alcohol use and smoking.
Catheter Ablation often isn’t enough if pre-existing health problem
The beauty of this Australian research is it confirms scientifically what we already knew, that just performing a catheter ablation on someone with a pre-existing health problem like obesity, isn’t enough. Doctors must take a holistic approach and treat not just the A-Fib, but also the pre-existing health condition that caused or triggered the A-Fib in the first place. Let’s take the example of an obese patient who has a catheter ablation and is A-Fib free. That person’s PVs are isolated. But the ongoing obesity (which produces left atrial hypertension) can potentially trigger other areas of the heart to produce A-Fib signals.
Many doctors today emphasize a holistic approach. For example, new patients with A-Fib are routinely tested for sleep apnea. The EP works with other doctors in his practice to develop a sleep apnea strategy for this patient. The patient isn’t given a catheter ablation till they address their sleep apnea problem.
For more about a taking a more holistic approach, see our FAQs: Natural Therapies & Holistic Treatments
Last updated: Sunday, February 15, 2015
by Steve S. Ryan, PhD, June 2014
Ed Grossman recently wrote and asked me about recurrence of A-Fib after a successful catheter ablation:
“I’ve read studies from the French Bordeaux group that talk about A-Fib recurring after a catheter ablation, that A-Fib tends to come back. Can A-Fib be cured permanently by a catheter ablation? After a successful catheter ablation, what are my chances of A-Fib recurring?”
The French Bordeaux group pioneered the original Pulmonary Vein Isolation procedure.
The studies you refer to were done in 2001-2002 with 100 patients. There’s been a great deal of improvement in the procedure since then, such as the use of irrigated tip catheters and the increased use of circumferential pulmonary vein isolation (PVI). (For example, when I had my procedure done in Bordeaux in 1998, they did what was then called a focal ablation in only one of my pulmonary vein openings. I’ve been A-Fib free “cured” for 16 years. Today though, they routinely isolate all four pulmonary veins.)
Don’t let the threat of recurrence put you off of having a catheter ablation. Recurrence is often influenced by several factors unrelated to the actual catheter ablation procedure, some of which you can control.
Certain Health Conditions Cause Recurrence of A-Fib
There are health conditions which tend to cause A-Fib to recur including hypertension, obesity, sleep apnea, diabetes, smoking and binge drinking. Controlling these conditions will reduce the risk of recurrence.
For example, let’s say patient “Joe” has A-Fib and sleep apnea, then has a successful A-Fib ablation and is A-Fib free. Because of his sleep apnea, Joe’s A-Fib is more likely to recur than someone without sleep apnea. So much so, that Electrophysiologists (EPs) today are insisting that A-Fib patients with sleep apnea be treated and use devices like a CPAP breathing machine before they can get a catheter ablation. In one study sleep apnea was an independent predictor for catheter ablation failure after a single procedure.
Also, those with long-standing persistent A-Fib, or those with vascular heart disease, or cardiomyopathy are more likely to have a recurrence.
Less recurrence for those with Lone A-Fib
Around 50% of A-Fib patients have no apparent pre-existing medical condition—called “lone A-Fib” because there’s no other contributing health condition. After a successful catheter ablation, those with lone a-fib are less likely to have a recurrence. But some lone A-Fib patients do have recurrences. (Some studies estimate a 7% chance of recurrence out to five years, though most recurrences occur in the first six to 12 months.)
So why the recurrence for lone a-fib patients? Heart tissue is very tough and tends to heal itself after an ablation. Or, there may be gaps in the ablation lines and the spots may require a touch-up ablation (usually with a much shorter procedure time and easier to perform than the first ablation).
The joy of Years of living in ‘Normal Sinus Rhythm’
Let’s discuss a worst-case scenario. You have a catheter ablation that makes you A-Fib free. Then three years later you develop A-Fib again. But the bottom line is you’ve been “cured” for three years. (The dictionary defines “cure” as “restoration of health; recovery from disease”.)
Most people with symptomatic A-Fib are overjoyed to have a normal heart beat and a normal life for three years, to be freed from both A-Fib symptoms and from the anxiety, fear and depression that often accompany A-Fib.
(See the personal experience stories by patients who had recurrence and a successful second ablation: Jay Teresi, “In A-Fib at Age 25“ and Robert Dell’s A-Fib Experience: “Daddy is always tired”.)
Only people with A-Fib appreciate how wonderful it is to be in ‘Normal Sinus Rhythm’ (NSR). For most of us, catheter ablation provides “acceptable” long-term relief from A-Fib. And it’s comforting to know, you can go back for another ablation, if you need it.
Catheter Ablation is the Best Hope for a “Cure”
Today, catheter ablation is the best A-Fib treatment offering hope for a “cure”—for making you A-Fib free. Current medications, for the most part, don’t work or have bad side effects or lose their effectiveness over time. Electrocardioversions usually don’t last. Surgical approaches work, but are generally more invasive, traumatic, and risky, and not recommended as first-line therapy for A-Fib.
Yes, A-Fib can return after a catheter ablation; the benefit may not be permanent. But, as a point of reference, consider heart by-pass operations or heart stents—are they always permanent? (Often they aren’t.) Do patients need additional surgeries? (Often they do.) With the option to return for an additional or “touch-up” procedure, catheter ablation is still today’s best hope for a life free from the burden of Atrial Fibrillation.
Last updated: Monday, August 17, 2015
Obesity Strong Predictor of A-Fib Risk and Recurrence
Report by Steve S. Ryan, PhD
Dr. David Wilber of Loyola University Medical Center in Chicago, IL gave a presentation entitled “Obesity, Inflammation and Atrial Fibrillation.”
Dr. Wilber described the findings of several studies on obesity and A-Fib:
1. Obese Patients Are at Greater Risk of Developing A-Fib.
In the Framingham Heart Study of 5,282 patients followed for 13.7 years, obese patients had a 1.5 greater risk of developing A-Fib. (Wang et al. JAMA 2004; 2022:2474)
In studies involving 68,000 people, obese patients had a 49% increased risk of new onset A-Fib (Wanahita et al. AHJ 2008; 155:310-315)
Increase In BMI (Body Mass Index) Is associated with a risk of developing A-Fib
♦ 16% for a BMI increase of 5-15%
♦ 46% for a BMI increase of 16-35%
♦ 90% for a BMI increase of over 35%
2. Obesity Produces Left Atrium Volume Changes and Overload
In the MONICA study of 1212 patients followed for ten years, 36% had hypertension, 34% were obese. Only obesity predicted Left Atrium volume changes and produced volume overload. (Hypertension produced pressure overload.) (Stritzke et al. JACC 2009; 54:1982-9)
3. Predictably Progress to Permanent A-Fib
In the Olmstead County study of 3,248 patients with Paroxysmal A-Fib (1980-2000), BMI greater than 35 (obese) predicted progression to permanent A-Fib independent of age, gender and clinical variables.
Obesity Factors Influencing or Responsible for A-Fib
Dr. Wilber then examined what factors or elements of obesity were responsible for affecting A-Fib.
1. Epicardial fat had more local chemokines, cytokines, and cellular infiltrates (fibrosis) than subcutaneous fat. He described an experimental study where epicardial and subcutaneous fat were added to atrial rat tissue. (Epicardial fat had higher levels of activin A and other biomarkers of fibrosis.)
2. In the Framingham Offspring study, only pericardial fat volume was significantly associated with A-Fib risk. 13% increased risk of A-Fib per 10 ml volume of pericardial fat.
3. In sheep experiments, obesity was profibrotic (increase in interstitial and cytoplasmic TGF-B1, PDGF-BB, and CTGF levels). Increasing weight produced significant increase in A-Fib burden (more and longer A-Fib episodes)
4. Risk of recurrence increases with obesity (Guijian et al, PACE 2013; 36:748-756). Left Atrium fat volume was the only significant predictor of recurrence (Tsao et al 2011)
5. A 19% decrease in weight significantly decreases A-Fib burden.
Dr. Wilber’s Conclusions
• Obesity is a strong independent predictor of A-Fib risk
• Obesity produces cardiac structural remodeling, notably LA volume and diastolic dysfunction
• Local direct effects which promote Left Atrium fibrosis through inflammatory and profibrotic cytokines
• Epicardial fat volume may be a useful way to measure or be a marker for local direct effects like fibrosis. Epicardial fat is independently associated with A-Fib risk relative to BMI, Left Atrial Volume, and other risk factors
• Obesity significantly impacts A-Fib recurrence after ablation
• Weight lost reduces the risk of new onset A-Fib, and subsequent progression/recurrence after A-Fib onset
Obesity is a major problem particularly in the US, so we can expect to see an increased number of the obese developing A-Fib (along with a host of other problems like hypertension, diabetes, coronary disease and sleep apnea).
The most startling statistic Dr. Wilber cited was that a BMI increase of 35% in men from age 25 to 50 increased the risk of developing A-Fib by 90%. Practically speaking, almost everyone who becomes obese in their lifetime will develop A-Fib. That’s a really scary statistic with enormous public health consequences.
And paroxysmal A-Fib patients who are obese will predictably progress to persistent (chronic) A-Fib.
“Is it a waste of time to perform a catheter ablation on someone who is obese? Aren’t they more at risk of recurrence?” They certainly are more at risk of recurrence. But a successful catheter ablation will change their lives and improve their quality of life. However, EPs should insist that obese patients who have a successful ablation must lose weight. But that should be easier to do if the obese person is in normal sinus rhythm and isn’t plagued by A-Fib symptoms like being unable to exercise because of a racing heart.
As Dr. Wilber suggests, measurement of epicardial fat volume should become a routine part of a yearly physical. For example, if a patient has a certain amount of epicardial fat volume, they should be told they are at a greater risk of developing A-Fib (and other health problems).
The good news is that weight loss both reduces the risk of developing A-Fib and reduces A-Fib burden (how badly A-Fib affects us). And it lowers the risk of recurrence after a successful catheter ablation.
Return to Index of Articles: AF Symposium: Steve’s Summary Reports
Last updated: Tuesday, February 9, 2016
What are the Causes of A-Fib?
It’s estimated as many as 5.1 million people in the U.S. have A-Fib. By the year 2050, the number will be 12-16 million.1 Each year there are over 340,000 new cases in the US. A-Fib is the most common heart arrhythmia.2 In the U.S. people over 40 have a one in four lifetime risk of developing A-Fib.3
HOW DO YOU GET A-FIB?
If you’ve had other heart problems, this could lead to diseased heart tissue which generates the extra A-Fib pulses. Hypertension (high blood pressure), Mitral Valve disease, Congestive Heart Failure, coronary artery disease, and obesity6 seem to be related to A-Fib, possibly because they stretch and put pressure on the pulmonary veins where most A-Fib originates. Coronary artery disease reduces blood flow and oxygen (stagnant hypoxia) which can trigger A-Fib.
A lot of A-Fib seems to come from uncontrolled high blood pressure. Many EPs recommend that all hypertension patients get a home BP monitor and aggressively work at controlling their blood pressure.
About 25% to 35% of stroke survivors experience atrial fibrillation;7 Up to 40% of patients8 get A-Fib after open heart surgery. “Pericarditis”—inflammation of the pericardium, a sack-like membrane surrounding the heart—can lead to A-Fib.
Heavy drinking may trigger A-Fib, what hospitals call “holiday heart”—the majority of A-Fib admissions occur over weekends or holidays when more alcohol is consumed. No association was found between moderate alcohol use and A-Fib.9 (Heavy drinking reduces the ability of cells to take up and utilize oxygen [histotoxic hypoxia] which in some people may produce or trigger A-Fib. [Thanks to Warren Stuart for this insight.]) See the personal A-Fib story by Kris: “Binge Drinking Leads to Chronic A-Fib, Amiodarone Damages Eyesight” pp. 144-150 in my book, Beat Your A-Fib.
See the personal A-Fib story by Kris: “Binge Drinking Leads to Chronic A-Fib, Amiodarone Damages Eyesight” pp. 144-150 in my book, Beat Your A-Fib.
But if you already have A-Fib, even moderate use may trigger an A-Fib attack, “…people with atrial fibrillation had almost a four and a half greater chance of having an episode if they were consuming alcohol than if they were not.”10 (Thanks to David Holzman for calling our attention to this article.)
Otherwise healthy middle-aged women who consumed more than 2 drinks daily were 60% more likely to develop AF.11
Steve Walters writes “that red wine brings on A-Fib attacks for him, but not beer, white wine, or cordials. Has anyone else had similar experiences with red wine?” E-mail: bicwiley(at)gmail.com.
Neville writes that “taking a heavy dose of Magnesium/Potassium tablets and bananas for breakfast kept him out of A-Fib during a golfing weekend with significant drinking.” He uses the same strategy to get out of an A-Fib attack. firstname.lastname@example.org
Severe Body & Mind Stress
Severe infections, severe pain, traumatic injury, and illegal drug use can be a trigger. Low or high blood and tissue concentrations of minerals such as potassium, magnesium and calcium can trigger A-Fib. Thyroid problems (hyperthyroidism), lung disease, reactive hypoglycemia, viral infections and diabetes.
To learn the impact of anxiety and emotional stress on A-Fib, see Jay Teresi’s personal story “Anxiety the Greatest Challenge”
Extreme fatigue, anxiety and emotional stress can trigger A-Fib.
Smoking can trigger A-Fib. Smoking reduces the ability of the blood to carry oxygen (anemic hypoxia). Smoking cigarettes raises the risk of developing A-Fib even if one stops smoking, possibly because past smoking leaves behind permanent fibrotic damage to the atrium which makes later A-Fib more likely.12
As we put on pounds, our risk of developing A-Fib increases. In recent studies overweight adults were 39% more likely, and obese adults 87% more likely, to develop A-Fib than their normal-weight counterparts.13
Health problems linked to obesity, like high blood pressure and diabetes, can contribute to A-Fib. And obesity may put extra pressure on the pulmonary veins and induce A-Fib. Left atrial hypertension is a common finding in obese patients.
14 Do you have a parent or other immediate family member with A-Fib? Research says you have a 40% increased risk of developing A-Fib yourself. And the younger that family member was when they got A-Fib, the more likely you are to develop A-Fib.
According to Dr. Dan Roden of Vanderbilt University, genetic research may become important to A-Fib patients. He postulates that “Lone A-Fib” (A-Fib without a known cause) may actually be caused by genetics.
We’ve had reports that A-Fib can be triggered by antihistamines, bronchial inhalants, local anesthetics, medications such as sumatriptan, a headache drug,15 tobacco use, MSG, cold beverages and eating ice cream, high altitude, and even sleeping on one’s left side or stomach. One person writes that hair regrowth products seem to trigger his A-Fib.
I used to include caffeine (coffee, tea, sodas, etc.) in this list, but some research suggests that coffee and caffeine in moderate to heavy doses (2-3 cups to 10 cups/day) may not trigger or induce A-Fib.16 Coffee (caffeine) may indeed be antiarrhythmic and may reduce propensity and inducibility of A-Fib both in normal hearts and in those with focal forms of A-Fib.17
Possible Food-Related Triggers
Chocolate in large amounts may trigger attacks. Chocolate contains a little caffeine, but also contains the structurally related theobromine, a milder cardiac stimulant.
Another reader writes that the natural sweetener and sugar substitute Stevia seems to trigger her A-Fib.
GERD (heartburn) and other stomach problems (like H. pylori) may be related to or trigger A-Fib. If so, antacids and proton pump inhibitors like Nexium may help your A-Fib. A report from England suggests that the veterinary antibiotic “Lasalocid” found in eggs and poultry meat may cause or trigger A-Fib.18
Recent research indicates sleep apnea (where your breathing stops while you are sleeping) may contribute to A-Fib, probably by causing stress on the Pulmonary Vein openings and/or by depriving the lungs and body of adequate oxygen supply (Hypoxemic Hypoxia).
Over 25 million Americans currently have sleep apnea, but 80% of these people don’t know they have it
In one study of patients with A-Fib, 43% had sleep apnea. (An additional 31% had “central sleep apnea/Cheyne-Stokes respiration” which is a different type of sleep apnea.)19
If you have A-Fib, it’s wise to have yourself checked for sleep apnea. You can do a “quick” check of how much oxygen is in your blood with a Pulse Oximeter, such as the Contec Pulse Oximeter for about $20 from Amazon.com and in drug stores. A reading below 90% would indicate you need to have a sleep lab study.
You may want to check out the web site, MySleepApnea, http://www.myapnea.org, an online community for people with sleep apnea to s hare health info and personal experiences. (The Shaquille O’Neal video is terrific!)
Gail writes that “both her sleep apnea and her A-Fib were cured by a CPAP [Continuous Positive Airway Pressure] breathing machine.” (E-mail her: gail(at)bonairwine.com.)
Mechanically Induced A-Fib
Be careful if you work around equipment that vibrates. Certain frequencies and/or vibrations may possibly trigger or induce A-Fib. (If anyone has any info on how or why high frequencies and/or vibrations may possibly affect A-Fib, please let me know.)
Jerry writes that “high powered magnets, such as the N50, may trigger A-Fib due to the electromagnetic fields they generate.” (If you have any info on this, please email me.)
Physical and Gender Characteristics
Men get A-Fib more than women. But women may have more symptoms.
Men get A-Fib more than women. But women may have more symptoms.
Men get A-Fib more than women. But women fail more antiarrhythmic drugs therapies than men and may have more symptoms. For more see my article: The Facts About Women with A-Fib: Mother Nature and Gender Bias.
A-Fib is associated with aging of the heart. As patients get older, the prevalence of A-Fib increases, roughly doubling with each decade. 2-3% of people in their 60s, 5-6% of people in their 70s, and 8-10% of people in their 80s have A-Fib.21,22,23Approximately 70% of people with A-Fib are between 65 and 85 years of age.24 This suggests that A-Fib may be related to degenerative, age-related changes in the heart. Inflammation may contribute to the structural remodeling associated with A-Fib.25
No Known Cause
But in many A-Fib cases (around 50% of Paroxysmal A-Fib26), there is no currently discernible cause or trigger (called “Lone” or “Idiopathic A-Fib”).27 (Some research suggests that inflammation may initiate Lone A-Fib.)28
Last updated: Sunday, April 10, 2016
- Miyasaka, Yoko, et al, Secular Trends in Incidence of Atrial Fibrillation in Olmsted County, Minnesota, 1980 to 2000, and Implications on the Projections for Future Prevalence Circulation, 2006;114:119-125. Last accessed Feb 15, 2013. URL: http://www.circ.ahajournals.org/cgi/content/full/114/2/119↵
- Nelson, Bryn. “Places In The Heart,” NYU Physician. Spring, 2009, p. 8.↵
- Van Wagoner, David “Atrial selective strategies for treating atrial fibrillation.” Drug Discovery Today: Therapeutic Strategies Vol 2, No. 3, 2005. “We have detected increased levels of the systemic inflammatory marker C-reactive protein (CRP) in patients with A-Fib.”↵
- S. S. Chugh, et al. Worldwide Epidemiology of Atrial Fibrillation: A Global Burden of Disease 2010 Study. Circulation, 2013; DOI: 10.1161/CIRCULATIONAHA.113.005119↵
- Camm, “Stroke in atrial fibrillation: Update on pathology, new antithrombotic therapies, and evolution of procedures and devices.” Annals of Medicine, 39:5, 371-391, 2007↵
- The Link Between Infections and Inflammation in Heart Disease. Life Extension Vitamins. Last accessed November 5, 2012 http://www.lifeextensionvitamins.com/cadico6otco.html↵
- Bottom Line Personal, October 15, 2014, p. 11. Kallmunzer, Bernd et al. Peripheral pulse measurement after ischemic stroke. Nuerology, Published Online May 6, 2014 http://www.neurology.org/content/83/7/598.abstract?sid=f532228b-5314-46d3-bdca-a7db9bc7fa7d↵
- Frost L., et al. “Atrial fibrillation and flutter after coronary artery bypass surgery: epidemiology, risk factors and preventive trials. International Journal of Cardiology. 1992;36:253-262.↵
- Calkins, H. and Berger, R. “Atrial Fibrillation The Latest Management Strategies.” The Johns Hopkins Medicine Library, p. 10.↵
- Alcohol May Trigger Serious Palpitations in Heart Patients. American Journal of Cardiology (August 1, 2012) http://www.newswise.com/articles/alcohol-may-trigger-serious-palpitations-in-heart-patients↵
- Conen D, Tedrow UB, Cook NR, Moorthy MV, Buring JE, Albert CM (December 2008). “Alcohol consumption and risk of incident atrial fibrillation in women”. JAMA 300 (21): 2489 96.
doi:10.1001/jama.2008.755. PMID 19050192. PMC 2630715. http://jama.ama-assn.org/cgi/content/full/300/21/2489.↵
- Heeringa J, et al. Cigarette smoking and risk of atrial fibrillation: the Rotterdam Study. Am Heart J. 2008 Dec;156(6):1163-9. doi: 10.1016/j.ahj.2008.08.003. Last accessed Jan 6, 2013 URL: http://www.ncbi.nlm.nih.gov/pubmed/19033014↵
- Vivek Y. Reddy, M.D., Joins The Mount Sinai Medical Center as Director of Electrophysiology Laboratories.Â May 6, 2009 . http://www.prweb.com/printer/2396634.htm↵
- Brugada R. “Identification of a genetic locus for familial atrial fibrillation,” New England Journal of Medicine 1997;336:p. 905-911. Ellinor et al., 2005, 2008. Sinner et al., 2011.↵
- The Link Between Infections and Inflammation in Heart Disease. Life Extension Vitamins. Last accessed November 5, 2012 http://www.lifeextensionvitamins.com/cadico6otco.html↵
- Katan, M, Schouten, E. Caffeine and arrhythmia1,2,3. Am J Clin Nutr March 2005 vol. 81 no. 3 539-540. Last accessed November 5, 2012 http://www.ajcn.org/cgi/content/full/81/3/539↵
- Rashid, Abdul et al. “The effects of caffeine on the inducibility of Atrial fibrillation.” J Electrocardiol. 2006 October, 39(4): 421-425. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2257921/↵
- Barclay, L. Caffeine Not Associated With Increased Risk of Atrial Fibrillation. Mar 10, 2005. Medscape News Today. Last accessed November 5, 2012. http://www.medscape.com/viewarticle/501279?src=search↵
- Bitter, T. et al. Sleep-disordered Breathing in Patients With Atrial Fibrillation and Normal Systolic Left Ventricular Function. Dtsch Arztebl Int 2009; 106(10): 164-70 http://www.aerzteblatt.de/pdf/di/106/10/m164.pdf. DOI: 10.3238/arztebl.2009.0164↵
- “The tallest patients in a recent study were 32% more likely to have A-Fib than the shortest ones. Doctors estimate that for every six-inch increase in height, the risk for A-Fib increases by 50%.” Bottom Line Health, July, 2006, p. 14.↵
- Go, “Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) study. Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention.” JAMA, 2001:285:2370-2375.↵
- Philip A. et al. Atrial Fibrillation: A Major Contributor to Stroke in the Elderly, : The Framingham Study. Arch Intern Med 1987;147:1561-1564.↵
- Feinberg, “Prevalence, age distribution, and gender of patients with atrial fibrillation: analysis and implications.” Arch Intern Med 1995;155:469-473.↵
- Laish-Farkash, A. et al. Atrial Fibrillation in the Elderly—To Ablate or Not to Ablate, J Cardiovasc Electrophysiol. 2013;24(7):739-741. http://www.medscape.com/viewarticle/807303.↵
- Van Wagoner, David “Atrial selective strategies for treating atrial fibrillation.” Drug Discovery Today: Therapeutic Strategies Vol 2, No. 3, 2005. “We have detected increased levels of the systemic inflammatory marker C-reactive protein (CRP) in patients with A-Fib.“↵
- Allessie, Maurits A. et al. “Pathophysiology and Prevention of Atrial Fibrillation.” Circulation. 2001;103:769.↵