A-Fib is age related. In particular, more people in their 80s are developing A-Fib.
Yet many A-Fib centers have a policy of not performing a catheter ablation on anyone 80 years old or older. But these are often the patients who need a PVI the most. Up to 25% of strokes occurring in octogenarians can be attributed to A-Fib.
It seems arbitrarily cruel to force someone to “live in A-Fib” just because they are older.
It seems arbitrarily cruel to force someone to “live in A-Fib” just because they are older. Isn’t this age discrimination? Why exclude octogenarians from a potentially curative treatment like catheter ablation (PVI)?
Study of Octogenarians Who Had a Catheter Ablation (PVI)
Dr. Pasquale Santangeli and his colleagues at the Texas Cardiac Arrhythmia Institute in Austin, TX examined data from 103 octogenarians who had an RF catheter ablation between 2008 and 2011. They compared this older group to younger patients who underwent the same procedure.
• There was no difference in the rate of success between the octogenarians and the younger group (69% vs. 71%).
• The rate of procedure-related complications was also not significantly different between the two groups, even when looking at different types of A-Fib such as paroxysmal and non-paroxysmal A-Fib.
• Octogenarians with paroxysmal A-Fib had more non-pulmonary vein trigger sites, and consequently required longer procedural time to effectively isolate such non-pulmonary vein areas. (Dr. Santangeli suggested a hypothesis that the underlying pathology of A-Fib in older patients might be different from younger patients.)
What Patients Need To Know
If you’re in your 80s, you’re not automatically doomed to a life in A-Fib and on A-Fib drugs. Dr. Santangeli’s work is very hopeful and encouraging. …Continue reading…
A-Fib Hospitalizations Up Sharply since 2000
US researchers found a 23% jump in overall hospitalizations due to A-Fib in the decade 2000 to 2010, and the costs of treating A-Fib rose 24%.
But the number of A-Fib patients dying in hospital decreased. There was a 29.2% drop in the mortality rate, which fell from 1.2% to 0.9%.
The study’s data was obtained from the ‘Nationwide Impatient Sample’ of 3.9 million medical records. The study author was Dr. Nileshkumar Patel at Staten Island University Hospital in New Your City.
Some of this increase in hospitalizations was due to the increase in US population (particularly older Americans). Older patients drove most of the total hospitalization increase.
Among people over the age of 80, the annual A-Fib hospitalization rate jumped from 9,361 to 11,045 million per year. Hospitals in the South had the highest percentage of A-Fib admissions (38%), while those in the West had the lowest (14%).
But part of the decade’s 23% increase is due to A-Fib co-morbidities (simultaneous presence of two chronic diseases or conditions). Patients with A-Fib often have other illnesses, too. The most common co-morbidities were hypertension, which was observed in 60%, diabetes (21.5%), and chronic pulmonary disease (20%).
This is not surprising news, but it is somewhat alarming. One of the reasons for the hospitalization increase is both doctors and patients are more aware of A-Fib and the health risks than they were in previous decades. (In 2009, the US Congress declared September as Atrial Fibrillation Awareness month.)
The good news is that fewer A-Fib patients are dying in hospitals probably due to better training and treatment options. But hospitalizations are expected to rise as the US population over age 80 increases from an estimated 11.4 million in 2008 to 19.5 million in 2030. It’s projected 1 out of 10 people over 80 will develop A-Fib. That’s nearly 2 million new patients with A-Fib!
The authors of this study point out that this “will lead to an enormous increased burden on the public health system and associated cost of care.” There will certainly be a lot more hospitalizations for A-Fib.
No Mention of Catheter Ablation: The authors discussed interventions for controlling costs such as the drug therapies of rate control vs. rhythm control. but did not mention catheter ablation (or Maze surgeries).
But the best and most cost-effective way to keep A-Fib patients out of the hospital is to make them A-Fib free, and also to take care of health conditions such as hypertension, obesity, diabetes, sleep apnea, smoking, and binge drinking. (Many EPs today recognize the importance of these health problems and how much they contribute to A-Fib. They require their patients to deal with these health problems before they can get a catheter ablation.)
From a public health perspective, shouldn’t we as citizens focus our efforts on strategies and treatments that offer the hope of a cure for A-Fib? That’s the best way to keep people out of hospitals.
Return to Index of Articles: Research and Innovations
Last updated: Sunday, February 15, 2015
Atrial Fibrillation patients often have loads of “Why?” and “How?” questions. Here are answers to the most frequently asked questions by patients and their families. (Click on the question to jump to the answer.)
5. “What is the difference between “Adrenergic” and “Vagal” Atrial Fibrillation? How can I tell if I have one or the other? Does it really matter? Does Pulmonary Vein Ablation (Isolation) work for Adrenergic and/or Vagal A-Fib?“
14. “I have paroxysmal A-Fib with “pauses” at the end of an event. Will they stop if my A-Fib is cured? My cardiologist recommends a pacemaker. I am willing, but want to learn more about these pauses first.”
16. “I am 69 years old, in permanent A-Fib for 15 years, but non-symptomatic. My left atrium is over 55mm and several cardioversions have failed. My EP won’t even try a catheter ablation. I exercise regularly and have met some self-imposed extreme goals. What more can I do? NEW!
Last updated: Friday, December 9, 2016
3. “Why do older people get Atrial Fibrillation more than younger people?”
We know that those over 60 years old are in the higher risk group for developing A-Fib. This may be related to what is called “Interstitial Fibrosis” which is often part of the aging process.
The Pulmonary Vein openings (where most A-Fib signals originate) sometimes become fibrous as we age. The Pulmonary Vein openings are similar in structure and have similar smooth muscle tissue as the Sinus and AV Nodes which generate your normal heart beat signal. The Pulmonary Vein openings are electrically active in the heart like the Sinus and AV Nodes but usually beat in sync with them. When the Pulmonary Vein openings become fibrous, they tend to beat out of sync with the Sinus and AV Nodes which results in A-Fib.
Please be advised that the above statement is an observation, an attempt to explain, rather than a medical fact. Further research is necessary to confirm this observation.
2014 Boston AF Symposium
A-Fib Producing Spots Outside the Pulmonary Veins
Report by Dr. Steve S. Ryan, PhD
Dr. Vivek Reddy of Mount Sinai Hospital in New York gave a presentation entitled “What is the true rate of Non-PV triggers?”
Why do ablations fail?
Dr. Reddy posed the question, ‘Why do ablations fail?’ The most common reason is a gap in an ablation lesion. Dr. Reddy showed slides of a typical wide area antrum isolation ablation with remarkably precise point-by-point burns. But there was a slight gap which let A-Fib signals escape from the pulmonary veins into the rest of the heart. But Non-PV triggers can also cause ablation failure.
Dr. Reddy asked the BAFS attendees:
“What is the rate of non-PV triggers after an extra-ostial PV isolation procedure?”
The choices ranged from 5% to over 25%.
The actual rate of non-PV triggers is approximately 23%.
Carina important origin of A-Fib triggers
Dr. Reddy showed how the ‘carina’ (the area in the heart between the left and right pulmonary vein openings) is often a source of A-Fib triggers and of recurrence after an ablation. According to the study cited, “the carina region (has an) apparently unique electrical behavior.” To effectively isolate PVs, it is frequently necessary to target within the circumferentially ablated veins in the carina region, even though there is a risk of stenosis.
Where are the non-PV triggers usually from?
In an older study of 248 Paroxysmal A-Fib patients, 28% had non-PV triggers. (These earlier studies often used segmental or ostial isolation and weren’t as durable as later procedures.) The most common locations were:
▪ LA Posterior Free Wall: 38% ▪ Superior Vena Cava: 37% ▪ Crista Terminalis: 13.7% ▪ Ligament of Marshall: 8.2%
(In this study, the Carina area and newer areas of interest such as the Left Atrial Appendage were not mentioned)
Left Atrial Appendage (LAA)
In a study of nearly 4,000 A-Fib patients that looked at redo procedures for paroxysmal, persistent and long-term persistent A-Fib, 27% had LAA firing (the LAA is the source of arrhythmia), much more in the long-term persistent (58%) compared to paroxysmal (18%). Most wound up having a LAA isolation procedure. (Many centers, as part of their protocol, now routinely first look at the LAA after isolating the PVs. See Bordeaux Five-Step Ablation Protocol for Chronic A-Fib.)
Paroxysmal patients over 80 years old had many more non-PV triggers than other patients.
Recurrence Associated with Predominately Non-PV Triggers
In a study of 197 paroxysmal A-Fib patients from 2009 to 2012 using irrigated tip RF catheters and extraostial PV isolation, there were non-PV triggers in 23.7% of patients. In patients who had recurrence, 70.8% had non-PV triggers.
In patients who had recurrence, 70.8% had non-PV triggers.
Dr. Reddy’s research is important for EPs who will now look more closely at areas like the Carina and the Left Atrial Appendage to find and ablate/isolate non-PV triggers.
What does Dr. Reddy’s research mean for patients? Since 23% of A-Fib ablation triggers are found in other areas of the heart than the pulmonary veins, a simple Pulmonary Vein Isolation (PVI) or Maze surgery may not be enough to cure your A-Fib.
One of the most important findings of Dr. Reddy’s research is that recurrence (a failed ablation) is most often associated with non-PV triggers (70.8%). When searching for the right Electrophysiologist (EP) to do your ablation, they have to have experience in tracking down these non-PV triggers. When interviewing EPs, maybe one of the questions needs to be “How often do you find non-PV triggers? How do you track them down and ablate them?”
You should probably avoid any EP who only isolates the PVs. [I’ve read Operating Room reports from EPs who only do a PVI, never look for non-PV triggers, and don’t terminate the A-Fib by ablation. Instead they shock the patients back into sinus rhythm, then load them up with powerful but toxic antiarrhythmic meds like amiodarone. This usually doesn’t work.)
If you are considering (Wolf) Mini-Maze surgery, be aware that most Mini-Maze surgeries only isolate the PVs. Your chances of having non-PV triggers which a Mini-Maze surgery will not ablate/isolate are approximately 23%. That translates to at least a 23% chance of failure.
If you have non-PV triggers or A-Fib/Flutter coming from the right atrium, most Maze surgeries won’t make you A-Fib free. Surgeons currently do not access the right atrium during most Maze surgeries. To take care of these other A-Fib spots, you will have to schedule a catheter ablation.
Return to Index of Articles: AF Symposium: Steve’s Summary Reports
Last updated: Friday, August 28, 2015
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.↵