ABSTRACTS

ROME, ITALY. Atrial fibrillation is a common complication of coronary artery bypass graft surgery. Treatment with beta-blockers, sotalol or amiodarone can reduce the risk of AF development somewhat, but these drugs have several undesirable side effects.

Italian researchers now report that fish oil supplementation is highly effective in preventing post-operative atrial fibrillation. Their randomized clinical trial involved 160 patients (136 men and 24 women) scheduled for elective bypass surgery. The average age of the patients was 66 years and one of them had a previous history of AF. Half the patients were randomized to receive 2 grams/day of ethyl esters of EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) for at least 5 days prior to their operation and for the remainder of their hospital stay. The other half just received usual post-operative care.

All patients underwent continuous rhythm monitoring for the first 4 to 5 days after surgery. During this monitoring period, 27 patients in the control group (33%) experienced afib episodes lasting an average of 24 hours. In contrast, only 12 patients in the fish oil group (15%) experienced episodes and they lasted an average of only 15 hours. Non-fatal post-operative complications occurred in 7 patients in the control group and in 5 patients in the fish oil group; 2 patients died after the operation in the control group versus 1 patient in the fish oil group.

The researchers speculate that the beneficial effects of fish oil are associated with its documented ability to reduce inflammation as well as with its direct effect on cardiac myocytes (muscle cells), specifically in regard to resting membrane potential and an increase in phase 4 refractory period. They conclude that fish oil supplementation can safely be administered to all patients undergoing bypass surgery and that it is at least as effective as medication with beta-blockers, sotalol or amiodarone.
Calo, L, et al. N-3 fatty acids for the prevention of atrial fibrillation after coronary artery bypass surgery. Journal of the American College of Cardiology, Vol. 45, May 17, 2005, pp. 1723-28

Editor's comment: The findings of the Italian researchers support those of several afibbers who have found fish oils beneficial in dealing with their afib. I suspect fish oils would be most effective if inflammation is the underlying cause of the afib and prior to extensive remodelling. Fish oils have also been found effective in the prevention of ischemic stroke and, for this reason alone, should be part of every afibber's supplementation program.

MUNICH, GERMANY. After the discovery in 1998, by Professor Michel Haissaguerre, that atrial fibrillation originates mainly in the pulmonary veins ablation techniques have focused on electrically isolating these veins from the left atrium. Two different techniques are now widely used for the purpose – the segmental pulmonary vein isolation method (Haissaguerre method) and the circumferential anatomical pulmonary vein isolation method (Pappone method).

In the Haissaguerre approach electrophysiological mapping (using a multipolar Lasso catheter) is used to locate the pathways taken by aberrant impulses from the pulmonary veins and these pathways are then eliminated by ablation around the veins approximately 5 to 10 mm from the ostium of the veins.

In the Pappone approach anatomical mapping (CARTO) is used to establish the exact location of the pulmonary veins. Two rings of lesions are then created in the left atrium – one completely encircling the left pulmonary veins and another completely encircling the right pulmonary veins; the two rings are usually joined by a linear lesion. The Pappone method is somewhat quicker and easier to perform since it does not require the complex interpretation of pulmonary vein electrogram end points. Early results from Dr. Pappone and colleagues were highly encouraging with success rates of 85% for paroxysmal and 68% for permanent afibbers.

Dr. Hakan Oral and colleagues at the University of Michigan compared the Haissaguerre and Pappone methods directly in a series of 80 patients and found that 88% of patients in the Pappone group were free of afib during a 6- to 12-month follow-up as compared to 67% in the Haissaguerre group. It is important to bear in mind that only symptomatic episodes were considered in these two trials. It is now known that many afib episodes occurring after pulmonary vein isolation (PVI) are completely asymptomatic.

Researchers at the German Heart Center have just completed a comparison of the efficacy and safety of the two methods. Their study included 100 afib patients with highly symptomatic episodes (an average [median] of 10 episodes a month) despite the use of an average (median) of two antiarrhythmic drugs. The majority (89%) of patients had paroxysmal episodes with the remainder having persistent episodes. About 40% of the patients had lone AF. The study participants were randomly assigned to undergo either segmental PVI (Haissaguerre method) or circumferential PVI (Pappone method) and were then followed for 6 months. Twelve patients (24%) in the circumferential PVI group had a follow-up ablation within the first 6 months, as did 8 patients (16%) in the segmental group.

During the 6-month follow-up 82% of patients in the segmental (Haissaguerre) group were free of afib symptoms as compared to 54% in the circumferential (Pappone) group. Six months after the initial ablation all participants underwent 7-day Holter monitoring. Sixty-six per cent of patients in the segmental group were found to be in constant sinus rhythm during the 7 days as compared to only 42% in the circumferential group. Atypical atrial flutter was observed in 9 patients after circumferential PVI, but in only 1 in the segmental group. There were no incidences of pericardial tamponade (piercing of the heart wall) in either group, but pericardial effusion (leakage) was noted in 44% of circumferential ablatees versus 10% of segmental ablatees. Transient ischemic attacks (TIAs) occurred in 2 patients after circumferential ablation and in 1 patient after segmental ablation. Asymptomatic pulmonary vein stenosis was observed in 6% of circumferential ablatees and in 12% of segmental ablatees.

The German researchers conclude that circumferential PVI is not superior to segmental PVI. Dr. David Callans of the University of Pennsylvania School of Medicine, in an accompanying editorial, concurs with the observation, "… it is strange and unprecedented to expect that less electrophysiological investigation will triumph over more."
Karch, MR, et al. Freedom from atrial tachyarrhythmias after catheter ablation of atrial fibrillation: a randomized comparison between 2 current ablation strategies. Circulation, Vol. 111, June 7, 2005, 2875-80
Callans, DJ. Comparing different strategies for catheter ablation of atrial fibrillation, Circulation, Vol. 111, June 7, 2005, 2866-68

Editor's comment: The German study confirms my own feelings about the relative efficacy of the two procedures. The circumferential PVI (Pappone method) relies more on technology (CARTO anatomical mapping system) than on skill, so it is probably easier to learn and perform than is the segmental PVI procedure. However, in skilled hands, the segmental PVI (Haissaguerre method) produces superior results. It is of interest that Dr. Andrea Natale at the Cleveland Clinic uses a modified segmental PVI approach and has found the circumferential approach to be inferior.

NEWCASTLE, UNITED KINGDOM. Maintaining an INR (International Normalized Ratio) in the therapeutic range (usually 2.0-3.0) when on warfarin (Coumadin) therapy can be problematical. Some studies have concluded that patients on warfarin are out of range at least a third of the time. Too low an INR increases the risk of an ischemic stroke, while too high a reading increases the risk of a hemorrhagic stroke or a major internal bleeding event. Warfarin works by reducing the amount of vitamin K available for the synthesis of clotting factors II, VII, IX and X. Patients on warfarin are therefore often counseled to avoid dark green leafy vegetables (the major dietary source of vitamin K) and to strictly avoid vitamin K-containing supplements.

British researchers now report that minimizing vitamin K intake while on warfarin might be precisely the wrong thing to do. Their study involved 26 patients (stable) whose INR had remained within the therapeutic range for at least 6 months without a change in warfarin dosage. The daily vitamin K intake of these patients was compared to that of 26 patients (unstable) whose INR had been varying considerably (standard deviation of INR values greater than 0.5) over a 6-month period and thus requiring continuous adjustment of warfarin dosage. All participants carefully weighed their food intake for two 7-day periods and completed detailed food diaries. Analysis of the data showed that the unstable patients had a significantly lower average daily intake of vitamin K (K1) than did stable patients (29 versus 76 micrograms/day). As a matter of fact, the daily vitamin K intake of the unstable patients was significantly lower than the daily intake of 60-80 micrograms estimated for the general UK population.

The researchers conclude that INR levels can be stabilized by increasing daily vitamin K intake. They point out that even a daily increase in vitamin K intake of 100 micrograms has comparatively little effect on INR (reduction of about 0.2). While it would be theoretically possible to improve the consistency of daily vitamin K intake through a strictly controlled diet, it is unlikely that this would be a viable solution. The researchers conclude their report with the statement, "Daily supplementation with vitamin K could be an alternative method in stabilizing anticoagulation control, lessening the impact of variable dietary vitamin K intake. We are currently evaluating this possibility."

Johannes Oldenburg, a German medical researcher, concurs and suggests that a continuous low-dose intake of vitamin K may stabilize the INR and subsequently reduce risk of bleeding complications.
Sconce, E, et al. Patients with unstable control have a poorer dietary intake of vitamin K compared to patients with stable control of anticoagulation. Thrombosis and Haemostasis, Vol. 93, May 2005, pp. 872-75
Oldenburg, J. Vitamin K intake and stability of oral anticoagulant treatment. Thrombosis and Haemostasis, Vol. 93, May 2005, pp. 799-800

Editor's comment: This is indeed a revolutionary study. The idea of avoiding vitamin K when taking warfarin is firmly entrenched in the medical community. So firmly in fact that vitamin K supplements and multivitamins containing vitamin K are banned in Canada, so as to "protect" the small minority of the Canadian population who are on warfarin therapy. Seemingly no thought has been given to the thousands and thousands of Canadians who may develop osteoporosis due to a lack of vitamin K. Hopefully, this will all change now! The immediate practical implication of the study is for anyone who has trouble controlling their INR to supplement with 50-75 micrograms/day of vitamin K – with their doctor's approval, of course.

CLEVELAND, OHIO. Ablation (pulmonary vein isolation or PVI) is usually only considered appropriate for afibbers with highly symptomatic episodes who have failed to obtain relief through the use of antiarrhythmic drugs. A group of American, German and Italian researchers now suggests that perhaps PVI should be considered the first-line approach for treating patients with symptomatic AF. They base their conclusion on a study of 70 patients (mean age of 54 years, range of 18-75 years) who had experienced highly symptomatic episodes for at least 3 months. The average time the participants had been suffering from AF was 5 months and 95% of them had the paroxysmal variety. About 25% of them had structural heart disease or hypertension, and about 60% of them were on beta-blockers.

The patients were randomized into receiving standard treatment with antiarrhythmic drugs (mainly flecainide – 100-150 mg twice daily, or sotalol – 120-160 mg twice daily) or a PVI procedure using the segmental procedure with the added feature of intracardiac echocardiographic (ICE) monitoring to ensure proper mapping catheter position and to guide energy delivery so as to avoid microbubble formation. All patients were treated in one German and two Italian centers specializing in AF treatment. Follow-ups were scheduled for 1, 3, 6 and 12 months after entering the study and all patients were given 24-hour Holter recordings prior to discharge from hospital and at 3, 6 and 12 months after enrollment. Event recorders were also used during the first and third months.

During the initial 2 months of follow-up, 20 patients (54%) of those in the medication group had at least one afib episode as compared to 9 patients (27%) in the PVI group. During the next 10 months, 63% of the afibbers on antiarrhythmics had recurrent, symptomatic AF episodes as compared to 13% in the PVI group. Asymptomatic AF was documented in 16% of the medication group as compared to 2% in the PVI group. Overall, the average (mean) number of episodes per 24-hour period decreased from 13 to 1 in the PVI group and from 12 to 6 in the medication group. The average duration of episodes prior to treatment was about 8-9 minutes in both groups. This decreased to 15 seconds in the PVI group and 45 seconds in the medication group after treatment. There were no transient ischemic attacks (TIAs), strokes, deep vein thrombosis or pulmonary embolism in either group during the follow-up period, but one patient (3%) in the PVI group developed moderate pulmonary vein stenosis, while 3 patients (9%) in the medication group developed bradycardia. Hospitalization during follow-up occurred in 54% of patients in the medication group versus 9% in the PVI group.

The researchers conclude that PVI is a feasible first-line approach for the treatment of selected patients with symptomatic AF. They caution that larger scale studies with longer follow-up are required before PVI can be considered standard care as first-line therapy for atrial fibrillation. NOTE: This study was partially funded by an unrestricted grant from Siemens, the manufacturer of the ICE system.
Wazni, OM, et al. Radiofrequency ablation vs antiarrhythmic drugs as first-line treatment of symptomatic atrial fibrillation. Journal of the American Medical Association, Vol. 293, June 1, 2005, pp. 2634-40

Editor's comment: The main conclusion from this study is that PVI successfully prevents recurrence of afib during the first year following the procedure in 87% of patients undergoing a first procedure. This compares to the 37% of afibbers on antiarrhythmic therapy who remained afib-free during the first year. Clearly the EPs at the three participating centers were highly skilled as they were able to achieve a first pass success rate of 87%. My surveys and published reports put the average success rate closer to 50% in "the real world". Perhaps my biggest problem with the study is that the participants were not typical of the real afib population. Having experienced afib for only 5 months with one or more monthly episodes lasting 8 minutes each would, in my opinion, not qualify for either aggressive drug treatment or a PVI. Furthermore, it should be kept in mind that about 60% of participants were taking beta-blockers on a continuous basis. This may well have impacted negatively on the medication group, which is bound to have contained at least some vagal afibbers. Finally, it is indeed unfortunate that the study did not include a placebo group – it may have fared just as well as the medication group.

MILAN, ITALY. Both myocarditis (inflammation of the heart lining) and atherosclerosis have been linked to a bacterial infection involving Chlamydia pneumonaie. There is also some evidence that the Helicobacter pylori bacterium may play a role in the formation of atherosclerotic lesions. Italian researchers now report that H. pylori may play a role in atrial fibrillation as well. The researchers had noted that many of their afib patients appeared to have gastric problems also. Based on this finding they instituted, as standard practice, that all newly admitted afib patients be tested for H. pylori. This, in turn, spawned a pilot study in which 59 consecutive patients with paroxysmal or persistent afib and no structural heart disease were tested for blood levels of C-reactive protein (CRP), a marker of inflammation and IgG antibodies to H. pylori. Their results were compared to those obtained by testing 45 healthy volunteers without heart disease, diabetes, or acute or chronic infections.

The researchers found that the average IgG level in the afib group was 97.2 IU/mL as compared to 5.3 IU/mL in the control group. A value higher than 20 IU/mL is usually considered indicative of a H. pylori infection (seropostive). The CRP levels among afibbers were also significantly higher with an average value for afibbers of 8 mg/L as compared to 1 mg/L in the control group. Within the group of afibbers persistent afibbers had higher IgG levels than paroxysmal afibbers (100 IU/mL versus 60.2 IU/mL) and higher CRP levels as well (9 mg/L versus 7 mg/L) indicating a more serious H. pylori infection.

The researchers speculate that the H. pylori bacterium may adversely affect the Na+/K+-ATPase pump responsible for maintaining homeostatic balance in individual heart cells. A disturbance of this balance may trigger afib by creating abnormal automaticity or triggered activity that causes a depolarization delay, which can result in very rapid premature atrial contractions (PACs) – a forerunner for a full-blown afib episode.
Montenero, AS, et al. Helicobacter pylori and atrial fibrillation: a possible pathogenic link. Heart Vol. 91, July 2005, pp. 960- 61

Editor's comment: The finding that a H. pylori infection could be associated with atrial fibrillation is indeed an exciting one and should be confirmed in larger trials. What is, unfortunately, less clear is what can be done about eradicating the bacterium if indeed it does reside in the heart lining. H.pylori can be eradicated successfully in the stomach through a 2- or 3-week course of an antibiotic, a proton pump inhibitor (omeprazole), and bismuth subsalicylate. The H. pylori bacterium "hides" in the folds of the stomach lining and it is believed that the bismuth subsalicylate is essential for "opening up" the access to the bacteria so that the antibiotic can do its work. Presumably, the mechanism for eradicating H. pylori in the heart lining would be quite different and it is not at all clear that the present drug regimen for H. pylori eradication would work for this.

CHELTENHAM, VICTORIA, AUSTRALIA. Warfarin therapy is recommended for afibbers over the age of 75 years in order to lessen the risk of an ischemic stroke. However, there is some concern that the reduced risk of ischemic stroke may be offset by an increased risk of hemorrhagic stroke and internal bleeding. Australian researchers recently addressed this concern in a study involving 933 patients (aged 76 years and older) admitted to hospital with atrial fibrillation during the period July 1, 2001 to June 30, 2002. All the patients had at least one other risk factor for stroke (previous stroke, diabetes, hypertension or heart failure) and all were quite frail (average age of 81 years). About 25% (228 patients) were prescribed warfarin upon discharge (INR between 2.0 and 3.0). The researchers followed these patients until October 1, 2003 at which time 158 (69%) were still alive and 70 (31%) had died. (Editor's note: It is indeed unfortunate that the remaining 705 patients not on warfarin were excluded from the study. Having followed them as well would have provided a baseline against which the efficacy of warfarin could have been compared.)

During the follow-up there was a total of 17 strokes affecting 16 people. Five of the strokes occurred among patients who were within the specified INR range of 2.0 to 3.0 at the time of the stroke, 6 occurred while patients had an INR below 2.0, and the remaining 6 occurred while the patients had stopped taking warfarin. The total follow-up period for the study was 530 person-years corresponding to an annual ischemic stroke rate of 2.6%. During this period 41 patients experienced 53 episodes of major bleeding. The annual event rate of major hemorrhage was 10% and that of fatal hemorrhage was 0.9%. Forty-five per cent of the 53 major bleeding events were classified as serious, 45% as life threatening, and 10% as fatal. Most of the hemorrhages (64%) occurred in patients who had been on warfarin for more than a year. Two gastrointestinal hemorrhages, 2 intracranial hemorrhages (hemorrhagic stroke), and 1 acute anemia caused the 5 fatal bleeding events. The researchers conclude by recommending that warfarin be used in preventing ischemic stroke in an older, frail population.
Johnson, CE, et al. People aged over 75 in atrial fibrillation on warfarin: the rate of major hemorrhage and stroke in more than 500 patient-years of follow-up. Journal of the American Geriatrics Society, Vol. 53, April 2005, pp. 655-59

CLEVELAND, OHIO. The current standard for the pulmonary vein isolation (PVI) procedure involves the use of radiofrequency (RF) energy (0.3 - 3.0 MHz) to create lesions around the pulmonary veins so as to isolate the left atrium from any aberrant impulses originating in the veins. Most RF delivery systems consist of a "pinpoint" catheter electrode and a second large-surface electrode (ground pad) placed underneath the patient's back. The main problem with this system is that the current density declines very rapidly with increasing distance from the catheter. This makes it difficult to produce deep enough lesions (burns) to ensure adequate isolation without at the same time risking carbonization, steam popping and coagulum formation – all risk factors for stroke. Several approaches are being evaluated to overcome this problem. Electrodes where the current flows between two closely opposed small electrodes contained within the catheter are used extensively in electro-surgery, but have not yet been evaluated in RF ablation. Cooled or irrigated catheters allow a deeper burn without surface carbonization and are becoming increasingly popular. Other methods of energy delivery for ablation are based on microwaves, lasers, ultrasound, and freezing (cryoablation).

Microwaves (0.3 – 300 GHz) induce oscillation of water molecules which, in turn, create enough heat to "cook" the tissue at the desired spots. There are still significant problems in creating an antenna catheter that will work inside the atrium, but microwave ablation has been used successfully in maze procedures.

Laser beams produce photon energy that can heat tissue and create a lesion. Laser technology for pulmonary vein isolation is still very much in the developmental stage. Some very exciting work is currently underway to develop a laser balloon that would produce a ring of laser energy which, in turn, would completely isolate a pulmonary vein in one application.

High intensity ultrasound (2 – 20 MHz) can be used to create lesions and has been extensively evaluated in prostate surgery. Ultrasound can be focused in much the same fashion as light beams making it possible to target a specific area for ablation. Work is underway to develop a balloon delivery system, but so far results have been disappointing. There is also some indication that current ultrasound delivery systems are associated with a higher incidence of phrenic nerve paralysis.

Cryoablation makes use of a hollow catheter whose tip is cooled to -75oC through the use of liquid nitrogen. The cryo-catheter produces ice formation inside and outside the cells, a mechanism of irreversible cellular injury. Cryoablation is slower than RF ablation (4-8 minutes per lesion versus 1 minute or less), but does avoid the complications (charring, steam popping, thrombus formation) associated with RF ablation. There is also some indication that it is less likely to produce pulmonary vein stenosis. There is some concern that the risk of afib recurrence is higher with cryoablation; however, new catheter developments are expected to overcome this problem and could well make cryoablation the preferred form of pulmonary vein ablation.
Cummings, JE, et al. Alternative energy sources for the ablation of arrhythmias. PACE, Vol. 28, May 2005, pp. 434- 43

TORONTO, CANADA. Warfarin (Coumadin) is prescribed for the prevention of ischemic stroke and deep venous thrombosis in patients with atrial fibrillation, prosthetic heart valves, venous thromboembolism, and coronary artery disease. The major potential adverse effects of warfarin are hemorrhagic stroke and internal bleeding. The blood level of warfarin must be controlled within very narrow limits in order to ensure that clots don't form while avoiding internal bleeding. It is becoming increasingly clear that controlling warfarin levels is not a simple matter and that many drugs and foods either potentiate warfarin's effect making bleeding more likely, or reduce warfarin's effect making thrombosis and stroke more likely.

A team of Canadian medical doctors and pharmacists recently reviewed the medical literature from 1993 to March 2004 in order to compile a verified list of important interactions between warfarin and foods, supplements, and other drugs. The most probable and best-verified interactions are presented in the tables below.

There are no credible studies supporting an interaction between warfarin and the following drugs and foods – alcohol, antacids, atenolol, clopidogrel, fluoxetine (Prozac), metoprolol, naproxen, psyllium, ranitidine, vitamin E, atorvastatin (Lipitor), coenzyme Q10, ginkgo biloba, ibuprofen, and influenza vaccine.

The researchers point out that there are now so many potential interactions between warfarin and other drugs that it would be impossible for a physician or pharmacist to remember them all. They recommend that doctors prescribing other drugs to patients on warfarin keep in mind that many drugs in the following groups can increase or inhibit the effect of warfarin:

• Antibiotics and antifungal agents
• Cardiovascular drugs (including propafenone, amiodarone, and cholesterol-reducing drugs)
• Painkillers
• Anti-inflammatories
• Central nervous system drugs (citalopram, sertraline)
• Gastrointestinal drugs (cimetidine, omeprazole)
• Anabolic steroids

Holbrook, AM, et al. Systematic overview of warfarin and its drug and food interactions. Archives of Internal Medicine, Vol. 165, May 23, 2005, pp. 1095-1106

Editor's comment: It is of particular interest that this latest study found no credible evidence that supplementing with vitamin E, ginkgo biloba, or coenzyme Q10 has any effect on the efficacy or safety of warfarin therapy. The study did, however, note that concomitant use of fish oils is likely to potentiate warfarin.

As some of you already know, I have been a lone afibber since December 1989 and in the intervening 15 years have tried pretty well everything (trigger avoidance, dietary changes, supplementation and antiarrhythmics) to vanquish the beast – all to no avail. My situation was complicated by the fact that it was discovered a couple of years ago that I had hyperaldosteronism, which makes it very difficult to maintain a normal potassium level. My episodes increased in frequency and duration until I began using the on-demand approach (450 mg of propafenone (Rythmol) at the onset of an episode). Using this approach I was able to keep episode duration to about 3 hours. However, the fatigue and depression accompanying my frequent episodes were wearing me down, so during the summer of 2004 I decided to have a pulmonary vein isolation (PVI) procedure here in Victoria, BC with Dr. Richard Leather. It was eventually scheduled for December 22. Just as well, during the first 3 weeks of December I had 10 episodes.

The procedure went well and the next two weeks were pure bliss with no afib at all. Unfortunately, the bliss did not last. On January 6 I experienced a pretty debilitating episode with accompanying enormous disappointment and depression. From then on things got steadily worse. In January I had 7 afib episodes and a 50-hour episode of bradycardia (very slow heart beat) that was later attributed to the propafenone. I found the bradycardia more frightening than the afib, so I reluctantly gave up the on-demand approach. This meant that my episodes now lasted considerably longer. I had 9 episodes lasting a total of 98 hours in February and 12 episodes in March totaling 129 hours. Things were definitely going from bad to worse. A touch-up was scheduled with Dr. Leather, but the earliest I would be able to have it would be the end of June and even that was not guaranteed – waiting times are very long in Canada.

Now a bit of a miracle happened. A good friend of mine is scheduled for an ablation in Bordeaux on July 11th. On Friday, April 1 (no fooling :~)) he received an e-mail from Mlle. Deixonne (Professor Haissaguerre's secretary) informing him that there had been a cancellation for April 11 and enquiring if he would be able to come. He had to decline since he had not been on warfarin for the requisite two months prior to the procedure. Fortunately, he immediately thought of me (I had been on warfarin ever since my December 22 PVI) and over the weekend contacted me with the news. Judi and I did not need a great deal of discussion before deciding that this was one opportunity we could not miss – no matter what the cost. So on Sunday I e-mailed Laurence (Mlle. Deixonne) and said that I would like to come for the procedure. Monday morning I received an e-mail with confirmation that I was "on" for April 11 along with detailed information about the whole procedure including cost, preparation, and even a list of recommended hotels close to the hospital – a very impressive start to my relationship with Hopital Cardiologique du Haut-Leveque.

The week starting Monday, April 4th turned out to be rather hectic. The hospital requires you to have a TEE (transesophageal echocardiogram) prior to the procedure in order to ensure that there are no clots in the left atrium or left atrial appendage. They could do this procedure in Bordeaux, but if they did find a clot they would not proceed so the trip would have been in vain. Monday morning I called Dr. Leather's office to see if he could arrange for a TEE (normal waiting time for this procedure would probably be about 2 months) and also to obtain copies of my medical records so I could fax them to Bordeaux. Dr. Leather was most cooperative and pulled the necessary strings to let me have the TEE done on Wednesday morning. I faxed my medical records to Laurence later on the Monday. Tuesday was spent arranging flight and hotel reservations. The TEE turned out to be OK so Wednesday afternoon we picked up our tickets for a KLM flight from Vancouver to Amsterdam followed by an Air France flight to Paris.

We left Victoria Friday, April 8th and caught the early morning flight from Vancouver on the Saturday. Sunday, April 10th we arrived at the Charles de Gaulle airport in Paris and walked to the train station located right in the airport. Here we obtained tickets for the TGV to Bordeaux leaving at 1:44 pm and arriving at Gare St. Jean in Bordeaux at 6 pm. Going by TGV is a bit like low-level flying with speeds of almost 200 miles/hr (300 km/hr). From Bordeaux we took a rather expensive cab ride to the hotel Chantafred in Pessac, a suburb of Bordeaux where the hospital is located. At this point, we were somewhat tired to say the least! Just prior to arriving in Bordeaux I had gone into afib – an episode that was to last 40 hours.

As scheduled, we checked into the hospital at 2 pm and handed over the bank draft for 11,731 Euros ($14,400 US) which covered the cost of the 5-day hospital stay, the procedure done by Pr. Haissaguerre and Dr. Jais (chief EP) and all tests, catheters etc. as well as room and board for Judi. NOTE: Full payment is normally required one month prior to admission. We were shown to a very pleasant, spotlessly clean room with two beds, and a large wardrobe, which also housed a very solid looking safe for storing our valuables. Shortly after settling in two nurses arrived to take blood samples, blood pressure and ECG. Then Pr. Haissaguerre arrived for a chat. He is a very personable physician, extremely intelligent and with a complete grasp of the intricacies of afib. To say that I was impressed would be an understatement. He said that my procedure was scheduled for Tuesday afternoon and that Dr. Jais would be doing the actual ablation. Later another doctor arrived and asked a lot of questions. Then a nurse's aide came in with a special surgical scrub solution that I was supposed to use when having a shower before bed and in the morning. At 6 pm I was taken for an x-ray and at 7 pm we had a nice supper served in the room. Later on a nurse came in and gave me a heparin injection as my INR had proven to be a bit low (I had stopped warfarin 48 hours earlier as instructed). I also received a potassium supplement as the initial blood test had shown that I was low on that as well. Just before bed I was hooked up to a wireless Holter monitor, which transmitted my vital signs to the nurses' station. At 2 am I was woken up for another heparin injection.

Tuesday morning was taken up with more blood samples, ECGs, blood pressure measurements, heparin injections, groin and chest area shaving and in general, procedure preparations. At 9:15 am I finally reverted to sinus rhythm after 40 hours of afib. Around noon Dr. Jais arrived for a chat. Again I was mightily impressed. One of the questions he asked me was whether I had ever had episodes lasting over 24 hours. I said that I certainly had and he then remarked that, in their experience, this probably meant that there were one or more ectopic sources outside the pulmonary vein area – so after having isolated the pulmonary veins he would go looking for other sources on the atrium wall and ablate them as well. As I understand it, the procedure is done while the atrium is fibrillating; thus when the fibrillation stops, it is likely that the ablation is complete. Nevertheless, several attempts are made to induce fibrillation before the catheters are withdrawn.

At 12:30 pm I was given a sedative and had a painkiller patch put on my groin area to reduce the risk of pain when the catheters were inserted. I was then wheeled down to the operating room and prepared for the procedure. After administering a local anesthetic Dr. Jais inserted the catheters and started the procedure – at about 2 pm I believe. I was given more sedative (intravenously) and really did not feel a lot until I woke up about 2 hours later. Occasionally it hurt a bit, but not intolerably so. At 3:30 pm Pr. Haissaguerre told Judi that the procedure was over and all had gone well. I don't remember too much of what went on during the rest of the day, but I know I had more tests and heparin injections. I was also hooked up to the wireless Holter monitor again and would be continually monitored for the next three days.

Wednesday started out with more tests. While I had the ECG Pr. Haissaguerre came in and immediately noticed that I had a lot of PVCs (I was feeling them as well). He took one look at the ECG as it rolled off the machine and said: "You must be very low in potassium". A blood test immediately confirmed that my level was low at 3.2 mmol/L and within ½ hour I was hooked up to an intravenous feed of potassium chloride and within another ½ hour the PVCs were gone – a clear demonstration of the importance of potassium in preventing PVCs. Otherwise the day was pretty routine with more tests and heparin injections as well as a nice lunch and dinner. I pretty well spent the whole day resting while Judi went for a long walk around the hospital grounds.

Thursday morning Dr. Jais came in for a long chat. He explained in detail how the procedure had gone. They had found no signs of stenosis after the first ablation in Victoria, but had discovered that three of the four veins isolated during that procedure had become conductive again. So he had re-isolated them and had then attempted to put me into afib again. I did go into afib so he went hunting for the offending cluster of rogue cells and found it on the atrial wall. After ablating it he was no longer able to induce afib. On the way out from the left atrium he had done a standard flutter ablation in the right atrium. Apparently, from 10 to 20% of afib ablations result in the development of atrial flutter, so in order to prevent that, they routinely do the flutter ablation on their patients from overseas. His overall conclusion was that everything had gone well and he would not expect me to have anymore afib episodes. However, just to make sure he would send me for a bicycle stress test to make certain that did not put me into afib. I passed this test with flying colors. I was certainly apprehensive before I went into it, since the last time I had a stress test, I went straight into afib after finishing. Later on I had a standard echocardiogram, which proved normal.

Friday morning I had more blood tests and an ECG and we were shown how to self-inject heparin. This had to be done every 8 hours over the weekend. I also had to continue with an oral potassium supplement and spironolactone in order to keep my potassium level up. After lunch we packed our things and went back to the Chantafred where we were to spend the next two nights since the special ward we were on closes for the weekend. In retrospect, we would have been better off staying in Bordeaux because there is not much to do in Pessac, especially on a Sunday. We did take the train from Pessac to Bordeaux on the Saturday and explored the city a little. It is a wonderful city with lots to see and do. While there we arranged to stay at a delightful small hotel (the Hotel Acanthe) in the old part of town from Monday until our return to Canada via Paris on Thursday April 21.

Monday morning (April 18) we returned to the hospital for final tests and consultation. If I had experienced any signs of afib, or shown any abnormalities in the tests, Dr. Jais would have gone back in and fixed the problem on Monday afternoon and I would then have had to stay a couple more days in the hospital before being discharged. As it turned out, everything was fine, so after lunch I was finally discharged with prescriptions for Coumadin (to be taken for one to three months), the beta-blocker bisoprolol (to be taken for one month) and time-release potassium chloride (to be taken as needed to keep potassium level above 4.0 mmol/L). After saying our goodbyes we headed for Hotel Acanthe where we spent a most delightful 3 days exploring Bordeaux and nearby St. Emilion – but that, as Hans Christian Andersen would have said, is another story!

Postscript:
After returning home I continued supplementing with potassium in order to ensure my potassium level remained above 4.0 mmol/L. I have found that taking about 800 mg/day of elemental potassium (in the form of potassium gluconate) spread throughout the day keeps the level at about 4.4 mmol/L – not taking any potassium supplements drops it to 4.0 mmol/L. In any case, PVCs are a thing of the past and I have now gone 12 weeks without the slightest hint of an afib episode. Life is great – and I am eternally grateful to Dr. Jais and Prof. Haissaguerre for giving it back to me!

The Bordeaux clinic can be contacted at [email protected]