ABSTRACTS

MESTRE, ITALY. Pulmonary vein isolation (PVI) is now the standard when it comes to radiofrequency ablation for atrial fibrillation. There are two major methods for performing a PVI; the electrophysiologically guided segmental ablation (Haissaguerre method), and the circumferential anatomical ablation (Pappone method). Some electrophysiologists use a combination of the two methods. The Haissaguerre method specifically locates the pathways conducting aberrant impulses from the pulmonary veins and isolates those, while the Pappone method completely encircles the veins with lesions aided by anatomical mapping. The Haissaguerre approach has the advantage of requiring less application of radiofrequency energy, but usually does result in longer fluoroscopy exposure.

Italian researchers using the circumferential anatomical ablation approach have just completed a study aimed at determining if early recurrence of AF after a PVI predicts the long-term success of the procedure. Their study involved 143 consecutive patients who had undergone a PVI using the Pappone method. All patients were followed for an average of 19 months after the PVI at which time 102 (71%) were in sinus rhythm. The majority (62%) was still on antiarrhythmic drugs that had not been effective prior to their ablation. Twenty-two per cent of the 143 patients relapsed into AF during the first 48 hours following their PVI, another 20% had a relapse after the first 48 hours, but before a month had gone by, and another 3% experienced a relapse during the second and third months. Patients who did not relapse during the first 3 months had a 95% probability of long-term success as compared to only 43% among afibbers who did relapse. Only 10% of those ablatees who relapsed during the first month and continued to have episodes during the second and third month eventually achieved long-term success. However, 45.5% of patients who just relapsed during the first month achieved long-term success. The researchers conclude that the presence of structural heart disease and incomplete isolation of the pulmonary veins are the main predictors of the early relapse into AF.
Bertaglia, E, et al. Predictive value of early atrial tachyarrhythmias recurrence after circumferential anatomical pulmonary vein ablation. PACE, Vol. 28, May 2005, pp. 366-71

Editor's comment: This study shows that afibbers who have no relapse of afib during the first 3 months following their ablation have a 95% probability of having achieved a long-term cure. However, afibbers who have a relapse during the first month have a less than 50% chance of remaining afib-free in the long term, while those who have relapses in both the first, second and third months have only a 10% probability of a long-term cure.

TORONTO, CANADA. The anticoagulant warfarin (Coumadin) is routinely prescribed for elderly patients who have a prosthetic heart valve, have suffered a prior stroke or TIA (transient ischemic attack), or have been diagnosed with atrial fibrillation, diabetes, coronary artery disease, hypertension or heart failure. Although several studies have shown warfarin to be effective in preventing ischemic stroke in high-risk patients, it is also clear that anticoagulation increases the risk of internal bleeding and hemorrhagic stroke.

Researchers at the University of Toronto have just completed an investigation aimed at determining if patients (aged 66 years and older) are at increased risk of stroke if they discontinue warfarin therapy after suffering major trauma. Their study involved 8450 warfarin-taking individuals who had sustained major traumas (82% due to falls) in the period 1992 to 2001. During the 6 months following the trauma, 78% of the study participants resumed anticoagulation with warfarin, while the remaining 22% did not. During an average 3.3 years of follow- up a total of 592 patients (2.2% a year) sustained an ischemic stroke and 399 (1.5% a year) experienced a heart attack (myocardial infarction). There was no difference in the incidence of ischemic stroke and heart attacks between the patients on warfarin and those who had discontinued anticoagulation therapy.

The long-term risk of major hemorrhage (hemorrhagic stroke and internal bleeding requiring blood transfusion) was significantly higher among patients on warfarin (1.9% a year) than among those who had discontinued the drug (1.3% a year). The incidence of deep vein thrombosis was, however, almost twice as high among patients not on warfarin, but was fairly low overall (0.4% a year). There was no difference in the incidence of pulmonary embolism in the two groups. The researchers conclude that discontinuing warfarin in patients prone to falls will not increase their risk of stroke and heart attack, but will materially reduce the risk of major hemorrhage at the expense of a fairly small increase in the risk of deep vein thrombosis.
Hackam, DG, et al. Prognostic implications of warfarin cessation after major trauma. Circulation, Vol. 111, May 3, 2005, pp. 2250-56

Editor's comment: This study certainly casts considerable doubt on the wisdom of routinely anticoagulating elderly patients at risk for ischemic stroke, particularly if they are prone to falls. The slight increase in deep vein thrombosis could easily be counteracted by giving nattokinase to patients not on warfarin. At least one clinical trial has found nattokinase to provide very effective protection against deep vein thrombosis.

AARHUS, DENMARK. Although there is some evidence that very high intakes of caffeine can produce cardiac arrhythmias, it is not known whether normal consumption increases the risk of developing AF or flutter. The Danish Diet, Cancer, and Health Study is designed to investigate the association between diet and cancer, but the data generated in the study are also being used to determine possible links between diet and other disorders.

Researchers at Aarhus University Hospital recently released the results of their investigation of a possible link between the consumption of caffeine, mainly in the form of coffee, and the risk of developing atrial fibrillation or flutter. A total of 22,533 men and 25,416 women between the ages of 50 and 64 years were followed for an average 5.7 years. During this time 373 of the men (1.7%) and 182 of the women (0.7%) developed AF or flutter. The researchers found no correlation between caffeine intake and the risk of developing AF or flutter. Participants with the lowest intake of caffeine (average 248 mg/day or about 2-3 cups of coffee a day) were no more likely to develop AF or flutter than were participants who consumed an average of 997 mg/day corresponding to about 10 cups of coffee a day. The researchers do point out that coffee intake in Denmark is generally high and that it is possible that someone with no caffeine intake would have a lower risk of developing AF or flutter.
Frost, L and Vestergaard, P. Caffeine and risk of atrial fibrillation or flutter: the Danish Diet, Cancer, and Health Study. American Journal of Clinical Nutrition, Vol. 81, 2005, pp. 578-82
Katan, M and Schouten, E. Caffeine and arrhythmia. American Journal of Clinical Nutrition, Vol. 81, 2005, pp. 539-40 (editorial)

Editor's comment: Several of our surveys have shown caffeine to be a strong trigger for afib episodes. Almost a third of adrenergic afibbers listed caffeine as a trigger as did 22% of vagal, and 20% of mixed afibbers. So, while caffeine may not be responsible for the development of afib, it certainly can be involved in triggering subsequent episodes.

VANCOUVER, CANADA. A nagging concern among paroxysmal afibbers is whether or not their AF will eventually become permanent (chronic). Researchers participating in the Canadian Registry of Atrial Fibrillation survey now report that about 25% of patients originally diagnosed with paroxysmal (intermittent) AF progress to permanent within 5 years of initial diagnosis. Their study included 757 patients diagnosed with a first episode of AF. The average age of the patients was 64 years (range of 14-91 years) and 38.3% were female. Eight-six per cent of participants reported symptoms (palpitations, chest pain, breathlessness, dizziness, fatigue or nausea), while 14% were asymptomatic (their AF discovered through an ECG). The majority of participants had a comorbid condition including heart disease (45%), hypertension (37%), respiratory disease (15%), thyroid disorder (10%) or diabetes (9%). Antiarrhythmic drugs were used by 41% and 12% used beta-blockers.

During the first year of follow-up, 8.6% of patients progressed to permanent status and by year five 24.7% had done so. The risk of becoming permanent increased by 40% for every 10 years of aging, by a factor of 3 if aortic stenosis was present, by a factor of 2.7 in the case of an enlarged left atrium (left atrial dimension greater than 45 mm), by 70% with moderate to severe mitral regurgitation, and by a factor of 2.4 in the presence of cardiomyopathy. Hypertension was not associated with an increased risk of progressing to permanent AF. A more rapid heart rate during fibrillation was associated with a slightly lower risk of progression to permanent with an increase of 5 beats per minute corresponding to a 6% decrease in risk.
Kerr, CR, et al. Progression to chronic atrial fibrillation after the initial diagnosis of paroxysmal atrial fibrillation. American Heart Journal, Vol. 149, March 2005, pp. 489-96

Editor's comment: As is unfortunately common in studies of atrial fibrillation, no attempt was made to treat lone afibbers as a separate group in the evaluation of the data. Thus, it is not known whether the findings would apply to lone afibbers. However, since the most important variables associated with progression involve heart disease, I would guess that the progression among lone afibbers would be considerably slower. Nevertheless, a significant increase in left atrial diameter, degree of mitral regurgitation, or a drop of 30-50 bpm in heart rate during fibrillation may be a good time to consider an ablation or maze procedure.

TAIPEI, TAIWAN. The discomfort associated with atrial fibrillation is not primarily due to the fibrillation of the atria, but rather to the fact that the fibrillation affects the AV (atrio-ventricular) node and causes the ventricular rate (pulse rate) to be fast and irregular. An obvious solution to this problem is to isolate the AV node (the ventricular beat controller) from the chaotic impulses originating in the atria from any extraneous impulses and feed it "its marching order" from an implanted pacemaker. This procedure has three major drawbacks:

• It does nothing to stop the fibrillation of the atria, which in itself can be quite uncomfortable, and necessitates continuing anticoagulation (warfarin) therapy.
• It makes the patient entirely dependent on the pacemaker. If it malfunctions or the batteries run out the patient dies.
• It does nothing to remedy the fatigue and reduced exercise capacity caused by the fibrillation of the atria.

AV node ablation is performed in much the same way as a RF ablation except that it is the area around the node that is ablated.

Taiwanese researchers have now compared the long-term efficacy of AV node ablation and pacemaker implantation with pulmonary vein isolation. Their study included 69 elderly patients with AF not controllable with medications. The patients were given the choice of a PVI or the AV node ablation. Thirty-two chose the AV ablation and 37 the PVI. All patients were followed for an average of 52 months after their procedure. At the end of the follow-up, all members of the AV node group experienced a regular pulse rate as compared to 81% in the PVI group. However, the prevalence of persistent AF was substantially higher in the AV node group than in the PVI group (69% versus 8%). The prevalence of heart failure was significantly higher in the AV node group (53% versus 24%) and a decline in left ventricular ejection fraction was also noted in the AV node group (from 51% to 44%), but not in the PVI group. The researchers conclude that AV node ablation and pacemaker implantation is superior to PVI in maintaining a steady ventricular rate, but carries with it an increased prevalence of persistent AF, atrial enlargement, heart failure, and decreased left ventricular ejection fraction.
Hsieh, MH, et al. Catheter ablation of atrial fibrillation versus atrioventricular junction ablation plus pacing therapy for elderly patients with medically refractory paroxysmal atrial fibrillation. Journal of Cardiovascular Electrophysiology, Vol. 16, May 2005, pp. 457-61

Editor's comment: The Taiwanese study confirms that AV node ablation with pacemaker implantation should be the very last resort for atrial fibrillation patients, particularly for those with the lone variety.

CENTO, ITALY. Dr. Paolo Alboni and colleagues at the Civic Hospital present an excellent overview of the treatment options for patients with atrial fibrillation. The following groups of afibbers, in their opinion, are better off with no treatment at all:

• Patients who have only experienced one episode.
• Patients with infrequent, short and well-tolerated episodes.
• Patients whose first afib episode occurred after surgery or during or after a heart attack.
• Patients whose episodes are due to binge drinking (they should be counseled to avoid excessive alcohol consumption).

Afibbers who have longer episodes less than once a month should preferably use the on-demand (pill-in-the- pocket) approach to convert to normal sinus rhythm and thus avoid a visit to the emergency room for conversion. The on-demand approach involves taking propafenone (Rythmol) or flecainide (Tambocor) as soon as possible after the onset of the episode. The recommend dose is 200 mg of flecainide or 450 mg of propafenone for persons weighing less than 70 kg (154 lbs) and 300 mg of flecainide or 600 mg of propafenone for people weighing 70 kg or more. The on-demand approach is effective in achieving conversion within 2 hours in 94% of episodes. However, it is not appropriate for all afibbers and should be tried in the hospital or the doctor's office for the first time. The researchers conclude that the use of the on-demand approach can reduce the number of emergency visits and hospitalizations by 90%.

Continuous treatment with antiarrhythmics should be reserved for those afibbers who have frequent, debilitating episodes. Amiodarone is the most effective drug for afibbers with underlying heart problems, but for lone afibbers beta-blockers (for those with the adrenergic variety) and disopyramide (Norpace) or flecainide (for those with vagal afib) are the drugs of choice.

Patients with frequent and/or badly tolerated episodes that markedly reduce their quality of life and are resistant to drug therapy should consider ablation or maze surgery, either on its own or in combination with antiarrhythmic drugs.
Alboni, P, et al. Antiarrhythmic drugs in patients with recurrent atrial fibrillation: where are we? Italian Heart Journal, Vol. 6, March 2005, pp. 169-74

MILANO, ITALY. Dr. Carlo Pappone and his colleagues at the San Raffaele University Hospital have published a fascinating review of the current and future status of radiofrequency ablation for AF. Some of the highlights of the article are:

• The San Raffaele Hospital treats afibbers who fulfill the following criteria:

  - At least one weekly episode of paroxysmal AF, or
  - At least one monthly episode of persistent AF, or
  - Permanent AF
  - At least one failed trial of antiarrhythmic drugs, or more than one antiarrhythmic drug needed to control symptoms.

• They do not treat patients over the age of 80 years or those with a life expectancy of less than one year. They also exclude patients with serious heart failure (NYHA functional class IV), those with a thyroid dysfunction, contraindications to anticoagulation, thrombi in the left atrium or a left atrial diameter at or above 65 mm. Patients with mitral and/or aortic metallic prosthetic valves are not excluded.

• A review of the outcome for 589 patients who were recently treated with circumferential pulmonary vein ablation yielded the following results: –

  - Total procedure time – 162 minutes
  - Mapping time (using CARTO or NavX) – 75 minutes
  - Fluoroscopy time – 29 minutes
  - Number of patients needing reablation – 30 (6%)
  - Extent of ablated area – 4.9 sq cm (28% of total left atrial area)
  - Procedural success rate – 98.5%
  - Freedom from afib after 29 months – 81% for paroxysmal and 76% for chronic afibbers
  - Procedure related mortality – 0%
  - Transient ischemic attack – 0.2%
  - Stroke – 0.03%
  - Tamponade – 0.1%
  - Atrio-esophageal fistula – 0.03%
  - Pulmonary vein stenosis – 0%
  - Left atrial tachycardia – 6%

• Overall mortality (from any cause) in this group of ablated afibbers was similar to that found among age- and gender-matched persons in the Italian population.

• It is clear that there is a steep learning curve in developing expertise in performing a successful circumferential pulmonary vein ablation and complications are significantly more common when the EP has done less than 150 procedures.

• There are many exciting new developments on the horizon. Among them: –

  - Integration of anatomical mapping (CARTO and NavX) with magnetic resonance imaging or CT scans.
  - Remote control of mapping and eventually ablation catheters, largely eliminating the need for extensive operator experience.
  - Denervation of vagal ganglia in the left atrium to further improve ablation outcome.

The above summary gives the gist of Dr. Pappone's article in the Italian Heart Journal, but for anyone seriously interested in a thorough review of the current and future status of pulmonary vein ablation this article is a must read. It can be found at www.italheartj.org
Pappone, C, et al. Atrial fibrillation ablation. Italian Heart Journal, Vol. 6, March 2005, pp. 190-99

TIP OF THE MONTH

Recently I have noticed several postings from afibbers who are having a rough time post ablation. I believe there are two important aspects that could be contributing to this.

1. Low potassium levels may occur after surgery. My own level after my recent ablation was 3.2 mmol/L; well below my normal level and also outside the normal range of 3.5 – 5.0 mmol/L. A low potassium level is likely to increase the number of PVCs (premature ventricular complexes) and PACs (premature atrial complexes). The PACs can set off afib episodes and the PVCs, if frequent enough, can result in very uncomfortable palpitations. The way to overcome this problem is to increase your potassium intake. This can be done through the diet (www.afibbers.org/conference/session32.pdf), through supplementation with potassium chloride or potassium gluconate, or through consumption of low sodium V8 juice or a potassium-rich drink such as the PAC-Tamer (www.afibbers.org/conference/session39.pdf). It is a good idea to have your serum potassium level measured just after the ablation. If it is below about 4.1 mmol/L (mEq/L) then an increase in potassium intake is definitely needed.

2. Ongoing inflammation – It is almost certain that the serious trauma experienced by the heart during the ablation will result in an inflammation of the heart tissue (myocardium). My own C-reactive protein (CRP) level went from 0.3 mg/L to 7.0 mg/L after my ablation indicating the presence of a serious inflammation. The Cleveland Clinic has recognized this problem and used to prescribe statin drugs to help prevent inflammation. I believe they are now using prednisone to prevent and, if necessary, treat the inflammation. I am not entirely sure of this, but in any case, a course of prednisone post ablation would probably be a good idea. For those of us who are not keen on pharmaceutical drugs, there are lots of alternative means of combating an inflammation. My own anti-inflammatory regimen (for one month after the ablation) consisted of:
   
   • Fish oil (3 x 2 grams daily)
   • Beta-sitosterol (3 x 113 mg daily)
   • Zyflamend (2 capsules with dinner)
   • This in addition to my normal supplementation with vitamins, minerals and antioxidants.

I am sure there are other just as effective natural protocols.

Perhaps the most important anti-inflammatory measure you can take is to avoid strenuous exercise for at least 4-6 weeks after the ablation. Strenuous and prolonged physical activity will markedly "fan the flames" of an inflammation and may also deplete you of important electrolytes, especially potassium and magnesium. Swedish sports medicine experts are adamant that exercise should be totally avoided whenever myocarditis (inflammation of the heart tissue) is suspected[1]. Very recently Greek researchers found that participants in a 36-hour long distance run experienced a 152-fold increase in CRP levels and an 8000-fold increase in the level of interleukin-6 (IL-6), another important marker of systemic inflammation. They conclude that the increases in the inflammation markers noted, "amount to a potent systemic inflammatory response"[2].

While not many afibbers will run a 36-hour marathon following their ablation, the Greek study, nevertheless, clearly supports the contention that prolonged, heavy exercise is very detrimental when it comes to preventing or combating an inflammation. I would suggest that no exercise at all would be the best approach for the first two weeks after the ablation followed by one or two daily walks for the next month or so. Jumping right into a strenuous physical activity program right after an ablation is, in my opinion, a very unwise thing to do.

In conclusion, I strongly believe that ensuring an adequate potassium intake, following a suitable anti- inflammatory protocol, and going very easy on the exercise for the first month, at least, can go a long way to preventing a miserable recovery period and may even help ensure the success of the ablation.

References

1. Friman, G and Wesslen, L. Special feature for the Olympics: effects of exercise on the immune system: infections and exercise in high-performance athletes. Immunol Cell Biol, Vol. 78, No. 5, October 2000, pp. 510-22
2. Margeli, A, et al. Dramatic elevations of interleukin-6 and acute phase reactants in athletes participating in the ultradistance foot race "Spartathlon": severe systemic inflammation and lipid and lipoprotein changes in protracted exercise. J Clin Endocrinol Metab, April 26, 2005 (Epub)

American College of Cardiology Conference

Diabetes and risk of AF
A very large study involving almost 850,000 American veterans has shown that patients with diabetes have a substantially increased risk of developing atrial fibrillation. The researchers found that the incidence of AF among diabetics was 14.9% as compared to 10.3% among a control group of veterans with hypertension but no diabetes. The incidence of atrial flutter was 4% and 2.5% respectively. Veterans with diabetes also had a 3 times higher risk of congestive heart failure and twice the risk of coronary artery disease.
Abstract 1050-267, p. 97A

Survival of lone afibbers
Mayo Clinic researchers have reviewed the clinical records of 4618 residents of Olmsted County, Minnesota who were diagnosed with a first episode of atrial fibrillation during the period 1980-2000. About 9% (413 subjects) were classified as having lone AF. While lone afibbers below the age of 70 years at diagnosis had a mortality rate similar to that of the general population, those over 70 years of age had a 25% higher mortality rate over the 8.3-year follow-up period. The incidence of transient ischemic attacks (TIAs) was 1.5% over the follow-up period. Stroke was experienced by 5 lone afibbers (1.2%), while 2.4% developed angina (ischemic heart disease), 6.5% congestive heart failure, and 3.9% died from cardiovascular disease. The researchers conclude that lone afibbers have a low incidence of cardiovascular events and a survival rate similar to that of the general population.
Abstract 1050-272, p. 98A

Cryoablation associated with lower stroke risk
Researchers at the University of Hong Kong report that the use of cryoablation rather than radiofrequency ablation significantly reduces the risk of thromboembolic complications during the procedure. They measured the platelet and coagulation activation before and during the procedure and found that both were elevated immediately after the transseptal puncture. However, the increase in platelet activation was considerably less during cryoablation indicating that this procedure may have an inherently lower risk of TIAs and stroke.
Abstract 847-3, p. 120A

More extensive ablation required for persistent and permanent AF
Catheter ablation, whether radiofrequency (RF) or cryo, is generally much less successful in persistent and permanent afibbers. Italian researchers now report that the creation of additional ablation lines (including disconnection of the superior vena cava) in the right atrium markedly improves the success rate of RF ablation in persistent and permanent afibbers. Their study involved 60 patients, 35 with persistent AF and 25 with permanent, who were randomized to receive the standard pulmonary vein ablation (including cavotricuspid isthmus ablation) or the standard plus additional ablation in the right atrium. After an average 12 months of follow-up, 87% of the patients who were ablated in both the left and right atria were afib-free as compared to 63% in the conventional left atrium ablation group.
Abstract 847-8, p. 121A

Chronic AF affects DNA
South Korean researchers have analyzed the gene expression in atrial tissue taken from patients with permanent atrial fibrillation of more than 6 months duration and compared it to tissue from patients without AF. They found consistent, significant differences in 66 genes with 31 being down-regulated and 35 being up- regulated more than 2-fold. The overall result of the changes in gene expression was an increase in apoptosis (self-destruction [suicide] of individual cells to avoid a threat to the survival of the organism as a whole) in the cardiac myocytes (heart muscle cells) of patients with permanent AF. The researchers speculate that drugs, which help prevent the unfavourable changes in gene expression, may be helpful in the treatment of permanent afib.
Abstract 1163-256, p. 122A

I am a 66-year-old male, retired US Air Force Heavy Jet Tanker/Transport pilot, with a long history of afib, and currently living in Cincinnati, Ohio. My afib doesn't make me unique; there are over 2 million afib sufferers today, in the US alone. Though many don't suffer any discomforting symptoms and have a relatively low frequency of episodes, there are a substantial number of us that are "symptomatic" and very aware of our afib. This is my story.

After several years of acid reflux (a possible warning sign), I had my first afib episode 14 years ago (June, 1991) under conditions of extreme psychological work stress as a mid-level executive, program manager in the aerospace industry. An Emergency Room visit was able to convert me back to sinus rhythm with intravenous (IV) drugs over a period of about 8 hours. This episode was followed a few weeks later by what appeared to be a flu-like viral infection resembling the worst case of flu one could imagine (aching joints, fever, cough, night sweats, continuous headache, back aches, etc.). This illness lasted unabated for 9 weeks. My family doctor tried numerous medications and treatments without success and ultimately diagnosed the problem as possible viral pericarditis (heart lining inflammation).

I went for another year without any heart medications until I had my second isolated episode. This was triggered by an improper drug prescription (Hytrin), which was prescribed by an urologist to treat BPH (prostate enlargement), at an initial dosage level contrary to the manufacturer's warning/recommendation. The first application of this drug (designed for hypertension) caused me to pass out and I awoke in afib. Again I was converted at the ER with IV medications, this time taking over 15 hours.

I remained arrhythmia free, without medication, after that for 5 years (until 1997) when the arrhythmia episodes began again in very short duration (less than an hour) and in frequencies many days apart; they converted spontaneously and were of a mostly vagal nature. Gradually the episodes got longer and the interval between them became shorter. I was aware from the www.afibbers.org website that atrial fibrillation was not a heart condition, but was a neurological problem in the electrical system that controlled the heart pulses, so I opted to make initial contact with an electrophysiologist (EP). He took my history, made no tests (except an EKG which showed a normal sinus rhythm, at that point in time), and prescribed several drugs, including antiarrhythmics, beta-blockers, and digoxin. These had no positive effect, as the episodes got progressively worse. By March of 1999, my afib had worsened to the point that it had become permanent (chronic). Meanwhile, I had changed to a different EP who merely changed the variety and dosage of medications as he unsuccessfully tried to treat the symptoms without determining any possible cause(s). Neither EP suggested or attempted to use electro-cardioversion.

By this time, the ongoing afib had caused my first episode of congestive heart failure (CHF) symptoms (shortness of breath, cough, and swelling ankles), with my EP seemingly remaining uninterested and unconcerned. My family doctor diagnosed a fluid build up in my lungs with an X-ray and started me on a temporary regimen of Lasix (a diuretic) to purge the fluid build- up. After this experience, at the suggestion of my family practitioner, I changed cardiologists again, and the new doctor was quite upset that no one had attempted to electro-cardiovert my afib early on. He scheduled me for the procedure after stopping all medications in May '99. This attempt proved unsuccessful.

I remained in continuous afib, and was referred to another EP, 120 miles away in Indianapolis, Indiana, who assured me that he could successfully cardiovert me. The second attempt was scheduled for July 1999. This new EP hospitalized me for 3 days while he loaded my system up on Tambocor (flecainide), digoxin and beta-blockers. The attempted electro- cardioversion was again unsuccessful and I had to remain in hospital for two additional days while they attempted to bring my heart rate and blood pressure under control. I left the hospital on medications substantially elevated from those used prior to the attempt, but still in continuous afib. Up to this point I had been prescribed virtually every one of the popular anti- arrhythmic and/or heart drugs currently in use and all without any apparent affect other than a variety of undesirable side affects. These included Quinaglute, Toprol-XL, digoxin, sotalol (BetaPace), flecainide (Tambocor), propafenone (Rythmol), Cardizem-CD, Lopressor, and Altace, all in individual and in multiple combinations and various dosage levels incurring a variety of combinations of the side-affects known for each.

After being in continuous afib for over 15 months, and suffering a worsening quality of life including occasional CHF symptoms, in desperation I made contact via email and finally went to the Cleveland Clinic some 250 miles away. They recommended immediate attempt at cardioversion, again by hospitalization and loading up my system with appropriate drugs prior to the cardioversion. After three days of high-level loading again with Tambocor (to a level nearly 50% higher than the previous cardio-version attempt) and other drugs, I spontaneously converted just mere hours before the electro- shock was to take place – having been in continuous afib for exactly 17 months (since Aug. 2000). When I was discharged, I was on a very elevated Tambocor dosage along with BetaPace, digoxin and beta-blockers, but was suffering from headaches and BP in the 160/100 range. The Tambocor at the high levels (525 mg/day) completely scrambled my brain, affecting hand-eye coordination, balance and cognitive functions.

After five days the afib returned, slowly at first and then once again increasing. At this point I self-discontinued the digoxin and the afib stopped within 27 hours of my last dose. When I told the Cleveland Clinic EP that I had quit the digoxin, he just agreed that, "this was probably a good idea and was an old drug and essentially not indicated for afib". (I wondered why was I paying a doctor for care and advice?). Eventually I reduced my daily level of Tambocor from 525 mg/day to 300 mg/day. This largely alleviated the severe side affects, that I had been experiencing, to a tolerable level. However, the afib once again started up on an intermittent basis.

In Feb 2002, I began to suffer from angina induced by walking my dog outside in the frigid sub-zero wind chill. After 5 increasing attacks over four weeks, I went to the ER. An angiogram was performed and I was scheduled for an immediate dual bypass graft. My afib abated somewhat after the bypass surgery, but again began to increase. I remained on the Tambocor at 300 mg/day. By mid summer 2002 I was again in near-continuous afib.

By Nov 2002, I was suffering from over 30 health issues that were all traceable directly to published Tambocor side affects. At this point I had been on this drug since 1999 and it was no longer controlling the afib. Upon presentation of this list to my family doctor he agreed to phase me off of the Tambocor and substitute amiodarone, a highly toxic and dangerous anti- arrhythmic drug; a "medication of last resort".

I related the shortness of breath to the Tambocor toxicity and tried to offset this as a temporary initiative by taking hyperbaric treatments, making hyperbaric chamber "dives" to 2 atmospheres for an hour every other day. This helped somewhat, but had no lasting benefit. On Dec 26, 2002, I went to the ER to obtain a supplemental oxygen prescription. They diagnosed CHF and admitted me for IV treatments to purge the retained fluids and reduce heart rate and blood pressure. While still heavily under the effects of Tambocor toxicity, which I had just fully eliminated in the previous 24 hours, and while still full of fluids, the "holiday assigned" resident junior cardiologist ordered an echocardiogram. With the retained fluid, high heart rate and residual effects of the Tambocor, my ejection fraction was reported as 15% (norm is 50 to 60%) and the resident wanted me to take an immediate angiogram with a preliminary diagnosis of stenosis of my bypass graphs, or possibly the need for additional bypass grafts. I refused on the basis that according to my family doctor, if this had been my typical ejection fraction, I would have needed a pacemaker long before now. Also I had taken a cardiolite stress test (treadmill plus nuclear trace dye) a mere two months previously, which had shown normal circulation in the heart. I insisted on obtaining a second opinion before undergoing what I believed to be an unwarranted angiogram. Changing cardiologists, once more, I was again diagnosed with elevated heart rate and B/P, and he focused on bringing these numbers into the normal range by medication. Once this was achieved, a follow-up echocardiogram was taken in April 2002 which showed a "remarkable" recovery of ejection fraction to 40% (confirming my earlier suspicion that the first echo was not representative due to the circumstances). Though the rate control technique reduced my symptoms, I was still plagued with significant quality of life issues (depression, fatigue, malaise, anxiety, insomnia, lost libido, a feeling of being much older, etc.) and increasing episodes of congestive heart failure.

In the meantime, the University of Cincinnati, and Dr. Randall Wolf were making breakthrough technology on a capability to perform the "maze procedure" using micro-surgery and an endo-scopic device, rather than as an open-chest procedure. Called the "mini-maze", this procedure is performed by making a 3 to 4 inch incision on the side between the ribs, high in the rib cage, with a smaller incision several ribs below for the endo-scope, which is used to observe the surgical field.

Through my current cardiologist, I received a referral to see Dr. Wolf for an evaluation to see if I might be a candidate for this newly developed procedure. Initially he was reluctant to consider me as a candidate due to the prior bypass surgery (which could cause potential difficulties due to related scar tissue), and the length of history I had with afib (recognizing that this was still a new and developing technique). However, I was able to prevail on him to take on my case with some added latitude that would permit him to abort the procedure, with my advance agreement, if it proved questionable.

The procedure was performed and the results were better than anticipated. During accomplishment of the mini-maze procedure, Dr. Wolf discovered that an adhesion had taken place during my Feb. 2002 dual bypass surgery, which had fused the top of my right lung to my heart. This adhesion had caused unexplained substantial muscle pain and spasms on a near 24/7 basis for nearly three years following the bypass surgery and had triggered and aggravated my arrhythmia. He was able to separate and cauterize this adhesion. He also removed the left atrium appendage (cause of 90+% of heart related blood clots that trigger strokes). He found that one of the bypass grafts had formed an adhesion to the appendage and he had to separate that adhesion very carefully before the appendage could be removed. He also conducted NPT (neurological path testing) on the nerve bundles in the heart and found several nerves that were hyperactive (a probable source of the afib extra pulses). He surgically desensitized or neutralized these.

I awoke from the surgery in wonderful sinus rhythm and have remained continuously in sinus rhythm, ever since. The recuperation period lasted about ten weeks with gradual reduction of the soreness and restrictions from the surgery. Recovery to a nearly pain-free state took approximately 5 months (unique in my case due to the added scope of surgery to clear scar tissue from the prior surgery).

A follow-up exam was done two weeks after the surgery, and again at six weeks. Dr. Wolf kept me on my pre-surgery medications so that any changes that occurred were attributable only to the surgery. At the six-week follow-up, Dr. Wolf terminated my amiodarone antiarrhythmic medication with no negative affects. At nine weeks after the surgery, a follow-up echocardiogram was performed to see what the impact was on my ejection fraction and mitral regurgitation. The results were very positive showing a noticeable reduction in the size of the left atrium, a substantial reduction in the mitral regurgitation to "trace" levels, and an improvement in the ejection fraction (up from the pre-surgery reading of 40% to near normal range of 46%). At twelve weeks (dictated by being off amiodarone for six weeks), I was monitored on a 24/7 basis by a portable CardioNet device for a period of two weeks to assess if there are any remaining episodes of arrhythmia. This verified a stable sinus rhythm with absolutely zero abnormal beats. At this point my Coumadin medication was next eliminated. Subsequently, my energy levels and routine have returned to normal levels. The symptoms of CHF have disappeared. And I am no longer on the Lasix medication.

I must add a personal observation. At the outset of my atrial fibrillation in 1997, I was acutely aware anytime my heart went into or came out of afib. It even would wake me up from a sound sleep; it was so conspicuous. During one pre-bypass period of 17 months, I was in continuous afib. After the bypass, I was again in persistent and near-continuous afib for more than a year, but I had either become acclimatized to it, or there was less of a transition since I didn't perceive the afib initiation as much. For the past 10 to 14 months, I had once again been in continuous afib. My post mini-maze surgery with its total return to sinus rhythm gave rise to a surprising and delightful psychological effect. The long-term continuous afib had subconsciously created a sense of anxiety, depression, and malaise — things weren't right in my physical condition, and there was little motivation to pursue new long-term goals, adventures, or even any desire to travel far from home. After the surgery, I awoke in strong sinus rhythm and euphoria that "all was well with the world" and I now have motivation, energy, and a bright outlook on life (even though I just turned 66 two days before the surgery). My health continues to improve as the various bodily organs resume to full oxygen circulation that was deprived by the chronic afib. I now walk two plus miles every day when the weather is not wet, and can do so without becoming winded or strained. I have begun a course of physical exercise to limber and strengthen muscles left weak from the fatigue caused by the afib.

Dr. Wolf is now traveling all over the US and a half dozen international sites (including Canada) teaching his new mini-maze procedure. In the US, Medicare and most major medical insurance policies have certified this procedure for coverage. I highly recommend this advanced surgical procedure to anyone afflicted by major, uncontrolled afib problems. Not only will it successfully improve your quality of life, it may also save you from congestive heart failure.

Dr. Randall Wolf can be contacted, as follows:
Univ. of Cincinnati
Director, Center for Surgical Innovation
231 Albert B. Sabin Way
PO Box 670558
Cincinnati, OH 45267-0558

(513) 558-0914

email: [email protected]