Yours in sinus rhythm – most of the time :~),
Hans

ROME, ITALY. Aspirin (acetylsalicylic acid) is widely used in the prevention of heart attacks and stroke. It works by preventing platelet aggregation in the blood, specifically that induced by collagen and adenosine diphosphate (ADP). Researchers at Rome's La Sapienza University now report that aspirin's antiplatelet effect decreases markedly with continued use. Their clinical trial involved 64 men and 86 women who were treated with aspirin (100 or 330 mg/day) and a matched control group of 80 patients who received 250 mg/day of ticlopidine (Ticlid), another antiplatelet agent. The researchers measured the degree of platelet aggregation induced by collagen and ADP at baseline and after 2, 6, 12 and 24 months. They also measured the delay (lag phase) between the addition of collagen and the beginning of aggregation. Their results were:

• Collagen-induced platelet aggregation declined from 88.2% to 37.9% after 2 months of treatment with aspirin. However, after 1 year it had risen to 58.5% and after 2 years to 61.9% indicating that most patients lost their sensitivity to aspirin with time. After 2 years 43% of all aspirin-treated patients had the same degree of collagen-induced platelet aggregation as they had prior to their treatment with aspirin.
• The collagen-induced lag phase was significantly prolonged after 2 months of treatment when compared to baseline (76.6 seconds versus 36.1 seconds). However, after 2 years the lag time had fallen to 42.5 seconds. After 2 years 42% of aspirin-treated patients had the same lag phase as before they began aspirin therapy.
• Aspirin inhibited ADP-induced platelet aggregation to a significantly lesser degree than that observed in regard to collagen-induced aggregation. The baseline value was 85.1% with a decline to 71.2% at 2 months and a subsequent return towards baseline after 2 years of treatment (24-month value was 71.2%).
• Ticlopidine did not affect collagen-induced aggregation or lag phase significantly, but did result in a substantial and sustained drop in ADP-induced aggregation from 86.1% at baseline to 37.2% after 2 years.

The aspirin results were not affected by dosage (100 mg or 330 mg/day). The finding that aspirin loses its platelet aggregation preventive effects with continued use, thus making patients insensitive to it over time, is a serious concern. Other research has shown that patients who are not sensitive to aspirin therapy have more than twice (24% versus 10%) the rate of cardiovascular events than do those who are sensitive to aspirin. The researchers urge further studies to determine if a combination of clopidogrel (Plavix) and aspirin may maintain antiplatelet aggregation benefits over time.
Pulcinelli, FM, et al. Inhibition of platelet aggregation by aspirin progressively decreases in long-term treated patients. Journal of the American College of Cardiology, Vol. 43, March 17, 2004, pp. 979-84

Editor's comment: The finding that aspirin loses its effectiveness with continued use is of particular concern to afibbers who rely on this for stroke prevention. For paroxysmal (intermittent) afibbers it may be better to just use aspirin when actually experiencing an episode or to switch to a stroke prevention program based on natural remedies.

DURHAM, NORTH CAROLINA. Some x-ray and CT scan procedures, notably angiography, use contrast media (x-ray dyes) to enhance the images. Most x-ray dyes contain substantial amounts of iodine and their use can result in further damage to the kidneys in patients already suffering from chronic renal insufficiency or diabetes. Researchers at the Duke University Medical Center now confirm that supplementing with n-acetylcysteine (NAC) prior to the x-ray procedure can help prevent contrast nephropathy (kidney damage from the use of contrast media). The researchers evaluated the results of 7 randomized, controlled trials involving 805 patients with chronic renal insufficiency who were scheduled to undergo angiography or angioplasty. Five of the trials compared placebo to 600 mg of NAC given orally twice daily for 4 doses prior to the procedure. One trial used 400 mg twice daily for 4 doses and one used 1200 mg once before the procedure and once after. The researchers found that patients who receive NAC prior to the procedure experienced a 56% lower risk of developing further renal insufficiency (rise in serum creatinine of at least 0.5 mg/dL) following the procedure.
Meine, TJ and Washam, JB. N-acetylcysteine to prevent contrast nephropathy. American Heart Journal, Vol. 147, March 2004, pp. 440-41

Editor's comment: Although the above findings apply to patients who already have dysfunctional kidneys, it would seem prudent for all patients about to be exposed to contrast media to supplement with NAC prior to the procedure.

ANN ARBOR, MICHIGAN. Cardiologists at the University of Michigan report that the success rate of pulmonary vein isolation (PVI) varies depending on whether the patients has adrenergic, vagal or random (mixed) episodes prior to the ablation. Their study involved 188 paroxysmal (intermittent) afibbers with a mean age of 53 years – 72% had random episodes, 16% had predominantly adrenergic episodes, and 12% had mainly vagal episodes. Patients whose episodes occurred at least 90% of the time during sleep, while relaxing or after dinner were classified as vagal. Those whose episodes occurred at least 90% of the time during or shortly after strenuous exertion or other adrenergic activation were classified as adrenergic and those with no clear pattern to their episodes were classified as random.

All patients underwent segmental ostial radiofrequency ablation during which the left superior, left inferior, and right superior pulmonary veins were completely isolated from the left atrium. The right inferior vein was also successfully isolated in 41% of the patients. There were no significant differences in age, gender distribution, frequency of episodes, number of years AF had been present, left atrial size, presence of heart disease or low left ventricular ejection fraction among the three types of afibbers. The patients were followed for over a year (mean of 445 days) during which time only 50% of vagal afibbers remained free of AF episodes as compared to 83% of adrenergic afibbers and 69% with random episodes. The presence of vagal AF was the only statistically significant predictor of PVI success, although the number of years AF had been present also correlated with success rate with an increasing duration of AF associated with a lower success rate. The researchers conclude that, while the pulmonary veins are clearly the most likely sources of AF initiation in adrenergic and random episodes, there are equally clear additional triggers in the atrium itself when it comes to vagal AF. They suggest that ablation of vagal afibbers should take this into account.
Oral, H, et al. Pulmonary vein isolation for vagotonic, adrenergic, and random episodes of paroxysmal atrial fibrillation. Journal of Cardiovascular Electrophysiology, Vol. 15, April 2004, pp. 402-05

CLEVELAND, OHIO. The finding by Professor Haissaguerre and colleagues that most AF episodes are triggered by foci firing from the pulmonary veins has led to the widespread use of pulmonary vein isolation (PVI) in the treatment of atrial fibrillation. The PVI technique involves the creation of scar tissue (by radiofrequency or cryogenic ablation) around the circumference of the 4 pulmonary veins at the point where they enter the left atrium. Initially the scar tissue was placed inside the pulmonary vein itself. This, however, was found to markedly increase the risk of severe narrowing (stenosis) of the vein. Today most PVI procedures aim to place the scar tissue in the left atrium itself in a ring around the opening where the vein enters (ostial ablation). This has markedly reduced the risk of stenosis. Since the perfection of ostial PVI hundreds of patients have undergone the procedure and enough data is now available to determine the relative effectiveness of PVI in relation to the age of the patient and the type of AF experienced (paroxysmal, persistent or permanent).

Researchers at the Cleveland Clinic have looked at the outcome of ostial PVIs performed on 325 patients (259 men and 64 women aged between 18 and 79 years). All procedures were done using radiofrequency ablation with a 4-mm cooled-tip catheter and circular mapping. The majority (53.8%) of the patients had paroxysmal (intermittent) AF, 10.8% persistent AF, and 35.3% permanent AF. They were divided into 3 groups – 106 patients below the age of 50 years, 114 patients between the ages of 51 and 60 years, and 103 patients over the age of 60 years (mean age of 66.6 years). Highlights of their findings were:

• Patients over the age of 50 years had a higher prevalence of hypertension and/or structural heart disease (60%) than did patients 50 years of age or younger.
• There were no significant differences in duration of AF (6 years on average), left atrial size (43 mm on average) or left ventricular ejection fraction (53%) between the 3 groups.
• About 12% of all patients needed a touch-up ablation to achieve complete isolation. The overall recurrence rate of AF, after 1 year, was 17% with no significant difference between the 3 age groups. The recurrence rate among permanent afibbers was about 22% as compared to 13% for paroxysmal patients.
• The incidence of severe stenosis (narrowing in excess of 70%) was about 2%. There were 2 TIAs (transient ischemic attacks) among the 325 patients (one in the under 50 years of age group and one in the over 60 years of age group). No strokes occurred in the two under 60 years groups, but 3 non-fatal ischemic strokes occurred in the over 60 years group. All the stroke victims had hypertension and permanent AF and one had suffered a previous stroke.

OSLO, NORWAY. Statin drugs such as atorvastatin (Lipitor), lovastatin (Mevacor), pravastatin (Pravachol), and simvastatin (Zocor) are primarily used to reduce cholesterol levels, but have also been found to reduce oxidative stress and inflammation. American researchers found that they help to prevent the development of atrial fibrillation (AF) in patients with coronary artery disease and Japanese researchers recently reported that statin drugs might also be helpful in preventing the recurrence of AF after cardioversion in patients with persistent lone atrial fibrillation. The Japanese study, however, was small (10 patients on statin drugs) and not controlled or randomized.

Now Norwegian researchers report the results of a randomized clinical trial aimed at determining the effects of pravastatin on AF recurrence in 114 patients who were scheduled to undergo electrical cardioversion for AF. The patients were randomized to receive a placebo or 40 mg of pravastatin once daily for 3 weeks prior and 6 weeks after the attempted cardioversion. During this time they also received warfarin to a standard INR of 2.0- 3.5. Twelve patients (6 in each group) converted spontaneously prior to cardioversion leaving 102 patients to be converted. The conversion was successful in 80 patients (78%). Six weeks after conversion 35% of patients in the pravastatin group had experienced a recurrence of AF as compared to 33% in the control group. Overall, 50% of the 114 patients were in AF 6 weeks after the attempted cardioversion either because the conversion was unsuccessful or because AF had recurred after a successful conversion. The researchers conclude that statin drugs are unlikely to have a clinically relevant effect on the rate of recurrence of AF after electrical conversion.
Tveit, A, et al. Analysis of pravastatin to prevent recurrence of atrial fibrillation after electrical cardioversion. American Journal of Cardiology, Vol. 93, March 15, 2004, pp. 780-82

Editor's comment: The Norwegian study was significantly larger and better controlled than the Japanese one. Thus it is likely that the Japanese findings were coincidental and that the effect of statin drugs in preventing AF recurrence is not significant.

PARIS, FRANCE. The risk of suffering an ischemic stroke during radiofrequency ablation of atrial fibrillation trigger points in the left atrium, notably around the pulmonary vein entrances, is estimated at from 0 to 8%. Blood clot (thrombus) formation could, presumably, take place through one of the following three mechanisms:

• dislodgement of preexisting thrombi by movement of catheters;
• formation of thrombi at ablation sites;
• formation of thrombi on the surface of catheters or the plastic sheaths enclosing them.

Researchers at the Lariboisière Hospital now report that increasing the flow of saline solution through the transseptal sheath during the procedure can markedly reduce stroke risk. Their study involved 86 patients who underwent a total of 153 ablation procedures involving the left atrium. For the first group of 32 patients a flow rate of 3 mL/hour (1 drop per minute) was used in irrigating the transseptal sheath. The flow rate used in the second group of 54 patients was 180 mL/hour or roughly 1 drop per second. No strokes were observed in the high-flow rate group while a total of 5 strokes (all non-fatal) occurred in the low-flow rate group. There were no other significant differences between the low- and high-flow groups that could explain the substantial difference in stroke incidence.

The researchers believe that a high saline flowing through the transseptal sheath prevents clot formation by preventing reflux of blood during catheter movement or by washing out any blood that does get into the sheath or perhaps, by diluting activated coagulation factors. The researchers recommend further studies to determine the optimum irrigation rate and to test the possible advantage of adding heparin to the saline solution.
Cauchemez, B, et al. High-flow perfusion of sheaths for prevention of thromboembolic complications during complex catheter ablation in the left atrium. Journal of Cardiovascular Electrophysiology, Vol. 15, March 2004, pp. 276-83

HERSHEY, PENNSYLVANIA. A team of American cardiologists reports the case of a 53-year-old man who experienced afib episodes whenever he swallowed a large mouthful of bulky food. The cardiologists believe there is a connection between the act of swallowing and the initiation of afib episodes. They speculate that the mechanism could involve direct mechanical stimulation of the left atrium by food passing through the esophagus, activation of the vagus nerve through the act of swallowing or activation of the cardiac sympathetic nerve. They believe activation of the adrenergic (sympathetic) nervous system is unlikely to explain the association between swallowing and afib in this particular patient since he did not respond to treatment with a beta-blocker (atenolol).

The cardiologists point out that earlier research has shown that AF can be reproduced at will by blowing up a balloon in the esophagus at the level of the left atrium. The medications procainamide (Procan), reserpine (Harmonyl), quinidine (Quinaglute), and verapamil have been found useful in dealing with swallowing-induced AF. The patient was prescribed verapamil and is currently symptom-free with regular doses of this calcium channel blocker.
Baman, NS, et al. Swallowing induced atrial fibrillation. PACE, Vol. 27, April 2004, pp. 555-56

Editor's comment: Several afibbers, myself included, have observed that having gas in the stomach can precipitate ectopic beats, which presumably could initiate afib if not immediately relieved by burping.

MAASTRICT, THE NETHERLANDS. Atrial flutter can effectively be cured by radiofrequency ablation of the cavotricuspid isthmus region of the right atrium. Now Dutch researchers report that cryoablation (ablation using a nitrogen-cooled probe cooled to about –80o C) is also effective in eliminating atrial flutter. Their clinical study involved 35 patients with a mean age of 53 years with common atrial flutter; 34 of the patients exhibited counterclockwise rotation. Eighty per cent of the patients also had a history of AF. In 31% of these patients the afib had developed during treatment of the flutter with antiarrhythmic drugs.

The ablation line was created by point-by-point application of the cryo-probe to the tissue for 3-5 minutes. A median of 14 "burns" was applied at 10 sites along the line. The mean fluoroscopy time was 40 minutes and the total procedure time was 220 minutes for the first 17 patients versus 100 minutes for the subsequent patients indicating a very steep learning curve. After a mean follow-up of 17.6 months, 89% of the cryoablated patients were still flutter-free. Three of the remaining patients underwent a repeat ablation and have been free of atrial flutter for 5, 6 and 11 months respectively. It is noteworthy that 46% of the patients who also experienced AF prior to the ablation experienced no further episodes after the ablation. It is also worth noting that the patients felt no pain during the procedure; radiofrequency ablation can be quite painful.
Manusama, R, et al. Catheter-based cryoablation permanently cures patients with common atrial flutter. Circulation, Vol. 109, April 6, 2004, pp. 1636-39

ALICANTE, SPAIN. Electrical cardioversion is used extensively in attempts to terminate persistent AF. It is, unfortunately, unsuccessful in at least a quarter of all cases. Spanish researchers recently investigated whether an infusion of flecainide prior to cardioversion would increase the immediate rate of success, would reduce the number and strength of shocks needed or would extend the time the patients remained free of afib after a successful cardioversion.

Their randomized, double-blind study included 54 persistent afibbers who had been in AF for 3-18 weeks (mean of 8 weeks). Half the group received flecainide (2 mg/kg as a 30-minute infusion) and half received a 5% glucose solution prior to the cardioversion attempt. No differences between the groups were observed in the number and strength of shocks delivered during the procedure. The percentage of patients who converted was not significantly different between the two groups (82% in the placebo group versus 73% in the flecainide group) nor was the percentage still in sinus rhythm 30 days after cardioversion significantly different (55% in the flecainide group and 52% in the placebo group). The researchers conclude that pretreatment with flecainide does not improve the efficacy of electrical cardioversion.
Climent, VE, et al. Effects of pretreatment with intravenous flecainide on efficacy of external cardioversion of persistent atrial fibrillation. PACE, Vol. 27, March 2004, pp. 368-72

BOSTON, MASSACHUSETTS. There is still considerable controversy as to whether type A behaviour, anger and hostility are risk factors for coronary heart disease (CHD) and there is no data regarding a possible association between these traits and AF. Researchers at the Boston University School of Public Health have now remedied this situation with the release of the results of a major new study. The study involved 1769 men and 1913 women who were enrolled in the Framingham Offspring Study. The age of the participants varied between 18 and 77 years with the average being 48.5 years.

Between 1984 and 1987 the participants underwent baseline tests for behaviour type (type A or B), anger expression (retain it, take it out on others, discuss it), anger symptoms (headache or feeling weak), typical experience with anger (Spielberger Trait-Anger Scale), and degree of hostility towards others. Participants who felt that others are inconsiderate, immoral, selfish and deserving to be punished scored high on the hostility scale. They noticed a strong correlation between smoking and hostility in both men and women.

During 10 years of follow-up, 7.5% of the men and 2.5% of the women developed CHD. There was no correlation between the likelihood of developing CHD and any of the personality measurements described above. During follow-up, 7.5% of the men and 3.2% of the women developed atrial fibrillation or flutter. Sixty-six per cent of the AF cases occurred before the age of 60 years and 87% of cases involved no underlying heart disease – in other words, the vast majority of cases were lone afibbers.

After controlling for age, diabetes, hypertension, valvular heart disease, and history of heart attack or failure, the researchers concluded that a high degree of hostility, symptoms of anger, and a high score on the Spielberger Trait-Anger Scale were all associated with an increased risk of AF in men, but not in women. A high level of hostility corresponded to a 30% increase in the risk of afib while a high score on the Spielberger Trait-Anger Scale corresponded to a 20% increase in overall mortality among men.

The researchers note that the relatively small number of women developing AF made finding strong correlations unlikely, but they did notice a trend for women who took their anger out on others to have an increased risk of afib. They conclude that anger and hostility recognition and management may help prevent AF in young and middle-aged people.
Eaker, ED, et al. Anger and hostility predict the development of atrial fibrillation in men in the Framingham Offspring Study. Circulation, Vol. 109, March 16, 2004, pp. 1267-71

Editor's comment: At the end of the 10-year follow-up, 7.5% of the men involved in the study had AF (mostly lone). This is clearly a very high prevalence and obviously poses a huge burden on the heath care system. The finding that the development of AF is associated with psychological factors, especially anger and hostility is clearly of major importance. Anger and hostility is certainly on the rise (road rage, for example) and this can only further fuel the afib epidemic.

American College of Cardiology Conference

Cancer risk and ablation
A group of American and German researchers have determined the radiation exposure associated with pulmonary vein isolation (PVI) for atrial fibrillation (15 patients) and with ablation for atrial flutter (5 patients). They used a biplane pulsed fluoroscopy system with a pulse rate of 7.5/sec. The mean fluoroscopy time was 68 minutes in the PVI procedure and about 15 minutes in the atrial flutter procedure. The researchers estimate that this would correspond to an excess risk of dying from radiation-induced cancer of 2 per 1000 male patients and 1.5 per 1000 female patients in the case of PVI. In contrast, the excess fatal cancer risk for the flutter ablation would be only 0.3 per 1000 patients.
Abstract #1090-221, p. 124A

PVI and persistent afib
Pulmonary vein isolation (PVI) is quite effective in eliminating afib episodes in patients with paroxysmal (intermittent) atrial fibrillation (AF). Electrophysiologists at the University of Michigan now report that the procedure is much less effective for persistent afibbers. Persistent AF is defined as AF lasting more that 7 days, but convertible to sinus rhythm through cardioversion. The researchers performed PVI on 167 patients with paroxysmal AF and 20 patients with persistent AF. After 2 years of follow-up 70% of the paroxysmal afibbers were still in sinus rhythm as compared to only 25% among the persistent afibbers. The researchers conclude that alternative ablation techniques need to be developed for persistent afibbers.
Abstract #828-1, p. 132A

Cure rate after second ablation
Cleveland Clinic researchers have evaluated the cure rate among paroxysmal (intermittent), persistent and permanent afibbers after a first and second pulmonary vein isolation (PVI) procedure. They studied the afib recurrence rate after 6 months in 185 paroxysmal afibbers and 171 non-paroxysmal afibbers (33 persistent and 138 permanent). The recurrence rate after the first PVI procedure was 15% among paroxysmal afibbers and 25% among the non-paroxysmal ones. After a follow-up ablation the recurrence rates were 5.4% and 7.1% respectively. The researchers conclude that non-paroxysmal afibbers are more likely to require a second procedure to completely eliminate afib. They noted that 31% of the paroxysmal afibbers suffered from hypertension as compared to 64% among the non-paroxysmal ones.
Abstract #828-3, p. 133A

Four- versus three-vein isolation
Isolation (ablation) of three of the four pulmonary veins (left superior, left inferior, and right superior) is often, but not always, successful in eliminating paroxysmal atrial fibrillation. Researchers at the University of Michigan have just completed a study to see if also isolating the right inferior vein would improve outcome. They followed 176 PVI patients for one year after their procedure. A total of 106 patients underwent ostial 3-vein isolation while the remaining 70 had all 4 veins isolated. At the end of the follow-up period 58% of the 3-vein patients were free of afib (using no antiarrhythmic drugs) as compared to 73% among the patients who had all 4 veins isolated. The researchers conclude that whenever feasible, the right inferior pulmonary vein should also be isolated during the first ablation procedure.
Abstract #828-4, p. 133A

Silent afib is common
Most afibbers know when they are in afib and have one or more of the common symptoms of violent palpitations, breathlessness, dizziness, and frequent urination. Some afibbers, however, have no symptoms at all and their condition is only discovered through a routine electrocardiogram. Researchers at the Mayo Clinic have now determined that silent afib (AF with no symptoms) may be present in as many as 24% of all patients referred for a routine electrocardiogram. The likelihood of diagnosing silent afib increases significantly with age, male gender, and a slower heart rate during afib episodes.
Abstract #1166-210, p. 144A

I suffered terribly from chronic (permanent) afib from April 1986 (I was 41 years old) to July 2003. For most of that period I was medicated with some combination of digoxin, a beta-blocker, verapamil, Coumadin, and an anti-arrhythmic (Sotalol, Norpace, Amiodarone, Flecainide, etc.). Each change of drug tended to work for a while at a low dosage, then I'd be fibbing almost all the time again, the dosage got upped, and eventually I'd go to the next, stronger drug. I remember blacking out many times under a new drug, getting dizzy and looking for a comfortable piece of the floor to roll down onto. Even after we settled on the same, ineffective dose of Flecainide, I fainted many times just standing up, especially in the morning after I'd been lying down for hours.

Between the medicines and the condition itself, many parts of my life got badly messed up: sleep, digestion (chronic constipation), cognition, sexual function (impotence is listed as one possible side-effect of many of those drugs), general physical condition (I couldn't exercise at all, really--and in the '80's I had run 7 full marathons, played full-court basketball at a high level, etc.), and family life, especially in the role of father of two young children.

I made many trips to the emergency room, my heart racing so fast that no recognizable "beat" could be felt. I was cardioverted about a dozen times, but the last few times the arrhythmia came back before I made it to my car. My cardiologist then advised me not to be cardioverted again.

Before that, a good few times that I went to the emergency room, my heart settled down nicely before cardioversion was attempted. I now see that I had developed terrible anxiety from the afib, though I had been told it's nothing like a fatal condition; it just felt like I would die, or collapse in public, and I developed panic-attack syndrome. My panic culminated in some awful episodes in my car (where I had to pull over on the freeway, pull off the road, etc.) and at work. Eventually my brother-in-law, who is a doctor, prescribed me some Ativan (lorazepam), and that helped a lot. I went to some classes at Kaiser about panic attack, and they helped as well, and I got off the Ativan. But I never was confident about walking anywhere, speaking in public, or just doing anything "exciting" that would raise my heart rate and get the arrhythmia more chaotic--anything that would get my juices flowing, and as a result, I became very careful, detached. It's impossible to be bon vivant and full of good cheer and positive chi when you're in afib or dreading that you soon will be back in afib.

No cardiologist ever made the connection between emotion and heart function for me. More generally, my cardiologists tended not to be interested in what put me into afib and what got me out of it, even while those were the most important things in my life. With all due respect, the cardiologists became well-meaning pill- pushers.

I had my first catheter ablation operation in 1999. I looked forward to it as a possible cure for my condition: just take it out, burn away the "hot spots" in the atrium that were sending the extra signals. Well, it didn't work. One thing I saw was that the surgeons could only go on what they were seeing that day, that moment. Afib is a chaotic heart rhythm, and while they did stimulate my heart and burn away a number of apparent "hot spots," quite evidently there were more, as I was back in afib two days after the operation. I had my second catheter ablation in 2001: same story.

By the time I had my third ablation, Dr. Lauer was confident that the procedure had come a long way. Instead of looking for specific "hot spots", they would essentially wall off the whole area of the pulmonary vein from which extra signals develop. The extra signals would still be there, but they wouldn't make it out into the area where they could mess up the heartbeat. To make a long story short, I had one brief (but scary) episode of afib about a month after the procedure, converted spontaneously back to sinus rhythm, and have been in sinus rhythm ever since, about nine months now.

The differences in quality of life are huge. I exercise pretty vigorously; I am potent again; I think better; I have more endurance; I am far more relaxed, happier, and easier to live with; more productive at work; braver, out more, keeping up with my kids; eating more and gaining weight--not really a good thing, but I had been semi- starving myself, as food put me right into afib. I am off digoxin fully, and have cut back on my other drugs. I hope to be off all but a little beta-blocker by next month.

I hope my experience with being (for now) cured of atrial fibrillation soon becomes the norm. I'd advise all afib sufferers to go for some such cure for the condition, not be satisfied with "rate control" and some partial relief from anti-arrhythmic drugs. I had come, I think, to live with chronic afib pretty well: I didn't get upset, despondent, or anxious any more when I went into it, and when in it, I slogged on the best I could, just kind of breathed deeply, lived in the moment and tried not to get too run down. But the cure has made all that seem like part of another life already, one I'd rather forget. Hooray for Dr. Michael Lauer and the Kaiser system for covering the three operations.

I hope you all come to feel as good as you did before afib struck.