ABSTRACTS

TORONTO, CANADA. Angiotensin-converting enzyme inhibitors (ACE inhibitors) and angiotensin II type 1 receptor blockers (ARBs) are both widely used to control high blood pressure. Among the more common ACE inhibitors are enalapril (Vasotec), lisinopril (Zestril), ramipril (Altace), and captopril (Capoten). The most popular ARBs are valsartan (Diovan), candesartan (Atacand), and irbesartan (Avapro). Both ACE inhibitors and ARBs inhibit the formation of aldosterone and are used interchangeably in the management of hypertension. There is also some evidence that both classes of drugs may be useful in preventing atrial fibrillation.

Cardiologists at two Toronto hospitals now point out that, while ACE inhibitors and ARBs may be equally effective in treating hypertension, their adverse effects are by no means equal. A clinical trial comparing the calcium-channel blocker amlodipine with valsartan found that patients in the valsartan group had a 13% higher incidence of stroke and a 19% higher incidence of heart attack. The CHARM trial showed that patients treated with candesartan had a 36% higher incidence of heart attack than did patients taking a placebo.

A study of diabetic patients with impaired kidney function found that irbesartan therapy was associated with a 36% increase in non-fatal myocardial infarction (heart attack) when compared to patients treated with amlodipine. In stark contrast to these findings are the findings regarding ACE inhibitors, which consistently produce a 20% reduction in the incidence of heart attack in patients with hypertension, atherosclerosis, diabetes, and renal insufficiency.

The Toronto cardiologists conclude that the potential adverse effects of ARBs are significantly greater than those of ACE inhibitors and that patients should be informed of this fact when discussing blood pressure lowering options with their physician.
Verma, S and Strauss, M. Angiotensin receptor blockers and myocardial infarction. British Medical Journal, Vol. 329, November 27, 2004, pp. 1248-49

CLEVELAND, OHIO. It is estimated that about 10% of afibbers undergoing pulmonary vein isolation (PVI) develop left atrial flutter (LAFL) or tachycardia as a result of the procedure. If the LAFL or tachycardia develops within the first week following the procedure it is usually transient and requires no treatment; however, it may develop as much as 2-3 months after the procedure and, in this case, treatment is required. Treatment may involve re-isolation of the pulmonary veins or the placement of long linear ablation lesions to interrupt the flutter circuit.

Electrophysiologists (EPs) at the Cleveland Clinic recently completed a study involving 730 afibbers who had undergone pulmonary vein antrum isolation guided by intracardiac echocardiography (ICE). Twenty-three patients (3.1%) developed LAFL after the procedure. All underwent a second procedure during which veins that had regained electrical conductivity were again isolated. During the procedure electroanatomical mapping (CARTO) was also carried out to determine the location of the flutter circuits and the presence of scar tissue in the left atrium.

After an average 496 days of follow-up 61% of the LAFL patients were free of all arrhythmias without the use of antiarrhythmic medication, 21% were able to maintain sinus rhythm with the use of previously unsuccessful antiarrhythmics, 2 patients (9%) required a third procedure during which linear lesions were made to interrupt the flutter circuit, and the remaining 2 patients (9%) developed recurrent persistent LAFL.

Imaging carried out during the initial PVI showed that 48% of the 23 LAFL patients had pre-existing scar tissue in their left atrium – possibly caused by fibrosis induced by long-term AF. The success rate for these patients was significantly poorer than for those without scar tissue. Only 36% were free of arrhythmia without antiarrhythmics, 27% had partial success (free of arrhythmia with the use of antiarrhythmics), and 36% experienced "complete failure". In comparison, 83% of the patients without scars remained free of arrhythmia without antiarrhythmics and the remaining 17% were free of arrhythmia with the use of antiarrhythmics.

The researchers conclude that most cases of post-PVI LAFL can be resolved by a second PVI, but that patients with pre-existing scar tissue may need additional linear lesions to resolve the problem. They also point out that in patients with coexisting AF and right atrial flutter, a standard PVI is often sufficient to resolve both arrhythmias, eliminating the need for the creation of ablation lines in the right atrium.

In an accompanying editorial Italian EPs question the routine use of linear lesions (usually between the mitral valve and the left inferior pulmonary vein) to reduce the risk of post-procedure LAFL. They point out that creating these lesions lengthens procedure and fluoroscopy time and may be less effective than a second PVI in resolving potential LAFL problems.
Cummings, JE, et al. Left atrial flutter following pulmonary vein antrum isolation with radiofrequency energy: linear lesions or repeat isolation. Journal of Cardiovascular Electrophysiology, Vol. 16, March 2005, pp. 293-97
Raviele, A, et al. Iatrogenic postatrial fibrillation ablation left atrial tachycardia/flutter: how to prevent and treat it? Journal of Cardiovascular Electrophysiology, Vol. 16, March 2005, pp. 298-301

MILAN, ITALY. A group of 10 prominent electrophysiologists (EPs) has just completed a worldwide survey of ablation procedures for afib to determine success rates and complications. The survey included 181 centers that had performed catheter ablations between 1995 and 2002. The number of procedures done at the centers varied from fewer than 30 to more than 300 and the success rates reflected this. Overall success rate (no afib, no medication) in 90 centers having treated 8745 patients was 52% after a 1-year follow-up with 27.3% of patients requiring a touch-up procedure to achieve this result. Another 23.9% were able to control their afib with antiarrhythmic drugs after the ablation although these drugs had been ineffective prior to the ablation. For centers having performed less than 30 procedures the average success rate (no afib, no medication) was 29.8% as compared to 63.8% among centers having done 300 or more. Adequate control with antiarrhythmic drugs was achieved among 30.1% of the patients treated at the smaller institutions versus 15.8% in the larger ones.

The type of procedure used was found to have evolved rapidly between 1995 and 2002. Between 1995 and 1997 simple compartmentalization was the predominant technique, searching for and ablating triggering foci was the favorite technique between 1998 and 1999, and pulmonary vein ablation or isolation became the standard in the year 2000. The total number of patients undergoing catheter ablation for atrial fibrillation rose from 15 in 1995 to 5050 in 2002. All centers reported treating paroxysmal AF, 53% also treated persistent AF, but only 20% treated permanent AF. Most centers (64%) would not treat patients with prior heart surgery, impaired left ventricular ejection fraction (between 30 and 35%) or a grossly enlarged left atrium (46%).

The most commonly used mapping techniques involved the use of the Lasso catheter (77%) and the CARTO system (43%). The most frequently used energy sources used in ablation were radiofrequency (84%), cryoablation (4%), ultrasound ablation (2%), and laser ablation (2%). Most centers (83%) required their patients to be on oral anticoagulation for between 1 and 6 months post-procedure, while 17% prescribed aspirin.

Major complications occurred in 524 patients (6%). The most common complications were chronic pulmonary vein stenosis experienced by 1.31% of patients, tamponade (piercing of the heart wall) experienced by 1.22%, and stroke or transient ischemic attack (TIA) experienced by 0.94%.

Success rates were found to vary with time. During the first 6 months post-ablation a cumulative total of 34% of ablatees became afib-free. This percentage rose to 66% after 12 months, but then declined again to 43% for those who had gone more than 2 years since their ablation. This decline in cumulative success rates is likely due to the less effective protocols used in the early years of AF ablation, but could also reflect on adverse evolution of the atrial substrate with time.
Cappato, R, et al. Worldwide survey on the methods, efficacy, and safety of catheter ablation for human atrial fibrillation. Circulation, Vol. 111, March 8, 2005, pp. 1100-05

Editor's comment: In my own survey of 112 afibbers who had undergone radiofrequency ablation (www.afibbers.org/sample.htm) I found that the 9 top-rated centers (in my estimation) had an average success rate of 68% in the first attempt and 76% with a touch-up. In comparison, the "B-class" centers had success rates of 21% and 29% (with touch-up) respectively. These results are quite similar to the ones reported in Circulation and, once again, emphasize the importance of lots of experience as the prime determinant in the outcome of an ablation.

STANFORD, CALIFORNIA. Several studies have concluded that an enlarged left atrium (as determined by conventional Doppler echocardiography) is associated with an increased risk of developing atrial fibrillation (AF). Most of these studies, however, included older patients, patients who were in afib during the examination, and patients who had experienced afib for a long time. It is also known that afib itself tends to lead to atrial enlargement.

Researchers at Stanford University have now investigated left atrium size in 15 young lone afibbers (mean age of 39 years, range of 22-50 years) with no history of diabetes, hypertension, hyperthyroidism, previous heart attack or structural heart disease. All had a left atrial diameter less than 40 mm when measured in the conventional anteroposterior dimension. The 15 study participants and 15 age-matched controls all had two- dimensional and Doppler echocardiographic studies done while in sinus rhythm. There was no difference in left atrial size when considering only the anteroposterior dimension (average of 35 mm in both groups). However, when measurements were carried out in the inferosuperior dimension (vertical dimension between tricuspid/mitral valve openings and the top of the atrium – excluding pulmonary veins) a significant difference was found between lone afibbers and controls (average of 52.9 versus 46.7 mm). Significant differences were also found in the mediolateral dimension (width) of the left atrium (45.2 versus 39.7 mm) and area (19 versus 15.2 square centimeters). No significant differences were seen in right atrial dimensions, but the volume of the left atrium in afibbers was significantly greater than in controls (average 79.7 mL versus 68.2 mL).

The researchers conclude that left atrium volume is significantly greater in young lone afibbers than in age- matched controls and suggest that this, along with pulmonary vein foci, may be important in the initiation and maintenance of lone paroxysmal AF.
Phang, RS, et al. Echocardiographic evidence of left atrial abnormality in young patients with lone paroxysmal atrial fibrillation. American Journal of Cardiology, Vol. 94, August 15, 2004, pp. 511-13

CHIETI, ITALY. Warfarin therapy is recommended for AF patients at high risk of ischemic stroke. Despite this, its actual use is limited for a variety of reasons, including the difficulty in maintaining INR within prescribed limits (usually 2.0 to 3.0), the substantial risk of internal bleeding and hemorrhagic stroke, contraindication, interactions with herbs and other drugs, and the inconvenience of periodic blood testing. Thus, the search for viable alternatives to warfarin therapy is actively pursued.

Researchers at the Universities of Pisa and Chieti recently evaluated the combination of aspirin and clopidogrel (Plavix) versus warfarin in preventing thromboembolic complications in persistent and permanent afibbers. Their clinical trial included 30 afibbers between the ages of 45 and 75 years (11 women), 12 of whom had non-high- risk permanent afib and 18 of whom had persistent afib and were awaiting electrical cardioversion.

The study participants underwent transesophageal echocardiography (TEE) at the beginning of the trial to check for thrombi and dense spontaneous echo-contrast (SEC), a forerunner of thrombi. None of the participants had any indication of thrombi or SEC. The participants were then randomly assigned to receive warfarin (INR 2.0- 3.0) or aspirin/clopidogrel. Warfarin was given once daily before dinner; aspirin (100 mg) was given after lunch, and clopidogrel (75 mg) after dinner. For the first week of the trial aspirin was given alone followed by 3 weeks of the combination.

After 3 weeks on the assigned regimen all participants had another TEE, blood tests for INR and thromboxane B2 (an indicator of platelet activity), and determination of bleeding time. None of the participants had any evidence of SEC or left atrial thrombi. Patients on warfarin, as expected, showed no change in thromboxane B2 level or bleeding time. Patients on aspirin/clopidogrel, as expected, showed no change in INR, but an average 98% decrease in thromboxane B2 and an average 319% increase in bleeding time (from 4 to 16 minutes). Aspirin, on its own, increased bleeding time by 71% with clopidogrel adding an additional 144% increase.

Fourteen of the 18 persistent afibbers underwent successful electrocardioversion (7 in each group) and no SEC or left atrial thrombi occurred in either group during a 3-month follow-up. The researchers conclude that a combination of aspirin and clopidogrel is as effective as warfarin in preventing thromboembolic complications over the short term in low-risk permanent and persistent afibbers. A larger trial (ACTIVE) is now underway with the purpose of evaluating a combination of aspirin, clopidogrel and irbesartan (Avapro) in the prevention of vascular events in AF. NOTE: This study was partially funded by Bristol-Myers Squibb, Italy, a manufacturer of clopidogrel.
Lorenzoni, R, et al. Short-term prevention of thromboembolic complications in patients with atrial fibrillation with aspirin plus clopidogrel. American Heart Journal, Vol. 148, July 2004, pp. 11-18

GRONINGEN, THE NETHERLANDS. Dutch researchers involved in trials to determine the relative merits of rate control versus rhythm control in AF have studied the results in a subgroup of lone afibbers. They define lone atrial fibrillation as AF not associated with hypertension or any underlying heart disease. Their study group included 522 patients with AF of which 89 had the lone variety (persistent). The lone afibbers were more likely to be men, tended to be younger (average of 65 years versus 69 years), and had fewer complaints of fatigue and breathing difficulties. During a mean follow-up of 2.3 years three lone afibbers (3%) died from internal bleeding or hemorrhagic stroke. They were all on warfarin at the time of their death with an INR in excess of 3.5. Two patients suffered non-fatal bleeding (also on anticoagulants) and 2 experienced an ischemic stroke or TIA. The two lone afibbers having a stroke or TIA were not taking anticoagulants at the time even though they had one or more additional risk factors for stroke. Among non-lone afibbers, 6 (1%) died from bleeding, while another 16 (4%) suffered serious bleeding. Thirty-three (8%) had a stroke or TIA even though 70% of them were on anticoagulation at the time of their stroke.

None of the lone afibbers suffered severe adverse effects from their antiarrhythmic drugs, while 3% of the non- lone afibbers did so. None of the lone afibbers died from heart disease or heart failure, while 5% of the non-lone afibbers did. Overall, death or serious adverse effects were significantly more common among lone afibbers using rate control than among those using rhythm control, but due to the small sample size the researchers could not conclude whether rate control is an acceptable alternative for patients with persistent lone AF. They do conclude though that lone AF is a far more benign disorder than is AF with underlying heart disease.
Rienstra, M, et al. Clinical characteristics of persistent lone atrial fibrillation in the RACE Study. American Journal of Cardiology, Vol. 94, December 15, 2004, pp. 1486-90

Editor's comment: Although the sample size was small, it is clear that the most serious complication facing lone afibbers is death or serious bleeding from inadequately controlled anticoagulation (warfarin) therapy. The study provided no evidence that lone afibbers with no additional risk factors for stroke would benefit from warfarin therapy – actually quite the opposite.

FRAMINGHAM, MASSACHUSETTS. Both obesity and atrial fibrillation are reaching epidemic proportions in the US. Nearly 65% of the population is overweight (BMI greater than 25) and 31% are obese (BMI greater than or equal to 30). About 2.5 million Americans have AF – a number expected to double over the next 4 decades.

Researchers involved with the Framingham Heart Study now suggest a strong link between obesity and the risk of developing AF. Their study involved 2384 men (mean age of 56 years) and 2898 women (mean age of 58 years). Seventeen per cent of the men and 16% of the women were obese at the beginning of the study.

During a mean follow-up period of 13.7 years, 10% (292 men and 234 women) developed atrial fibrillation. Compared to normal weight individuals (BMI less than 25) obese study participants had an average 50% greater risk of developing AF. This increased risk remained after adjusting for gender, age, and the presence of hypertension. Every one-unit increment in BMI (over 25) was associated with a 4% increase in risk. Detailed examination of study results revealed that the increased AF risk associated with obesity was almost entirely attributable to the fact that overweight and obese individuals tend to have larger than normal left atrial diameters (3.8 cm for normal weight men, 4.1 cm for overweight men, and 4.4 cm for obese men). The corresponding numbers for women were 3.5, 3.8 and 4.0 respectively. Obese persons also have a higher incidence of sleep apnea, a condition that has also been linked to an increased risk of AF. The authors note that weight reduction has been linked to a decrease in left atrial diameter and suggest that efforts to contain the obesity epidemic may also reduce the incidence of AF.
Wang, TJ, et al. Obesity and the risk of new-onset atrial fibrillation. Journal of the American Medical Association, Vol. 292, November 24, 2004, pp. 2471-77
Coromilas, J. Obesity and atrial fibrillation: is one epidemic feeding the other? Journal of the American Medical Association, Vol. 292, November 24, 2004, pp. 2519-20

Editor's comment: Our initial LAF survey did not find any indication that lone afibbers tended to be more overweight or obese than the general population.

GOTHENBURG, SWEDEN. Atenolol (Tenormin) is a popular beta-blocker used widely in the treatment of high blood pressure (hypertension). It is also used to lower heart rate in atrial fibrillation patients.

Swedish researchers recently released a report comparing atenolol to placebo and other antihypertensive drugs. The 4 studies comparing atenolol to placebo or no treatment found that atenolol was quite effective in lowering blood pressure, but had no effect in preventing heart attack, cardiovascular death, or death from any cause. One of the 4 studies did, however, conclude that atenolol reduced the risk of stroke. The 5 studies (involving 17,671 patients followed up for a mean of 4.6 years) comparing atenolol to other antihypertensives (hydrochlorothiazide, captopril, losartan and lacidipine) found that all drugs lowered blood pressure to a similar degree, but that atenolol-treated patients had a 13% higher overall mortality, and a 30% higher risk of stroke than did patients treated with the other drugs. Other studies have shown that other beta-blocking agents such as metoprolol, propranolol, and timolol significantly increase survival time after a heart attack, while atenolol has no such effect.

The researchers conclude that their meta-analysis casts doubt on the suitability of atenolol as a first-line antihypertensive drug and as a reference drug in the evaluation of other antihypertensive drugs. NOTE: Most of the authors of this study had received grants from pharmaceutical companies including AstraZeneca, the manufacturer of Tenormin.
Carlberg, B, et al. Atenolol in hypertension: is it a wise choice? The Lancet, Vol. 364, November 6, 2004, pp. 1684- 89

Editor's comment: This study basically concludes that, while atenolol does not increase overall or cardiovascular mortality compared to placebo or no treatment, there are other antihypertensive drugs that do indeed reduce mortality compared to atenolol.

Hans kindly asked me to contribute my story this month. First I'd like to say that I'm a bit new at this afib business and I'm not sure my success is long-lived enough to qualify as an example (and it is still a work in progress), however, I'm happy to contribute so that others can possibly learn from my experience. I can say that I'm sure I would not have the success I've had without the work of Hans, PC, Jackie, PeggyM, Fran and the many others who've come before me and generously shared their expertise and experience. For this I'm very grateful.

I'm a 49-year-old male vagal afibber. Like many on this site, I've been a life-long exerciser. I played American Football in college and then continued running until about 10 years ago, when I took up 4 miles of daily walking at a pace of about 11-12 minutes/mile. I found this kept me in sufficiently good condition to compete annually in a 13 1/3 mile race up Pikes Peak (a 14,000 ft peak, the race gains 7,850 ft in elevation). I could finish within 20 minutes of the 4 hr 20 min median time. I've also had a mostly vegan diet for 15 years and my blood chemistry has been excellent since then. In my early 20's, I was diagnosed with "white-coat hypertension." So, I've routinely taken my own blood pressure with a stethoscope and cuff since.

This last summer, I was again training for the Pikes Peak race. I was climbing 14,000 ft peaks on the weekends here in my home state of Colorado. One Thursday morning, in early July, I woke up and decided to take my blood pressure. It was fine, however, my pulse "sounded" weird. I took my pulse rate. It was about 80. This was unusual for me as my resting pulse is normally in the low 50's (and I had done no activity). I put on an old heart rate monitor and started walking around. Going up the stairs, my pulse soared to 150. Normally it would be 80 or 90 doing this. I really wondered what was happening to me. Was I having a heart attack? So I drove myself to the ER. They put me on a monitor, but my pulse converted to NSR before they could get a printout. The doctor did a variety of tests, chest x-rays, asked me if I drank (no), etc. The doctor sent me home with a Holter and said he thought it might be atrial flutter. The one significant item out of these tests was a low serum potassium (K) value of 3.2 mmol/l (normal range is 3.5-5.2 mmol/l). They did give me a potassium pill at the ER.

The following Tuesday, I went to my GP. He said my Holter was normal, one nonspecific run of 10 seconds and an average of 24 PVC's and 2 PAC's per hour. He wasn't too concerned, started me on a baby aspirin/day and told me to schedule a treadmill test, and a 30-day event monitor test.

The event monitor/treadmill tests were scheduled for a month hence. In the meantime, nobody was too concerned about my condition. I also learned that for me, it wasn't an ER event. This was important as I've been self-employed for 18 years and carry only very high deductible medical insurance. My ER bill was $2,500 and it would be very costly to keep paying for those visits. About two weeks after the 1st event, I had another one. It came on at 3 AM. This time, I put on my HR monitor and decided to watch it. I went ahead and went to the office and around noon I decided to see what would happen if I did a little exercise (I knew very little about my condition and did not even know that it was afib at this point). I found I could walk at a 15 min/mile pace and my HR would go to 140. When I slowed down, my HR would drop, so I wasn't too concerned. At one point, I had to sprint across a street to avoid traffic. My HR monitor shot up to 233 (I'm still not sure if this was real, as readings like this can also happen if one of the leads looses contact). I was a little concerned, however, after a couple of minutes, I had converted to NSR. I called my GP and told him what I had done. He said that I had acted properly.

I had two additional episodes before my treadmill test. They both came on about 3 AM and I converted them with exercise. When I took my treadmill test, it showed no underlying disease, and it did not put me into afib. I went quite a bit longer than my expected time. During the test, I told the cardiologist that my events came on at around 3 AM and I had been able to convert them to NSR with exercise. I asked, "How common is this?" He told me that I was the first patient he'd seen who could do this. Wow, I thought, I'm unique. I went home wearing an event monitor. Sure enough, I had another event. I even took a reading while in afib and exercising, then converted it and took another reading. These readings showed that I did have atrial fibrillation. Of course the HR that was reported was the one while I was exercising, not resting. My GP suggested a consultation with the cardiologist, but I hadn't scheduled one yet.

I went ahead and did my Pikes Peak race, with no problems. In the meantime, I'd done some Internet searching and found a couple of papers that reference vagal afib. The early morning initiation of afib and return to NSR with activity described in those papers fit my situation. I now knew I wasn't a solitary case. I also knew I wasn't going back to the cardio who had done my treadmill test! Three days after the race, I had another event. The only thing that was different is that I didn't convert on this one.

I asked around and got referrals to a cardiologist and an electrophysiologist. It turns out they were partners. I didn't know any different, so I went to see the cardio. By the time I had an appointment, I'd found www.afibbers.org and read Hans' book. Feeling well armed, I went to my first meeting and talked to the cardio about my 3 AM events and (up until now) conversion with exercise. I said I thought I was vagal. He said, "I don't believe in that." I was a bit shocked. I offered to bring in some papers to discuss with him. He said, "don't bother, I won't read them." He also said, "I'm sure I could find some papers in your field that you wouldn't agree with." Then he told me that digoxin was his favorite drug. I was really worried then. He ordered an echocardiogram and scheduled another appointment. He started me on Coumadin. My echo came back fine, but after 6 weeks in persistent afib my ejection fraction had dropped some. I could tell this in daily activities, as I got winded more easily. I was such a pain that he referred me to his partner the EP. I told the EP my story (3 AM and exercise conversion). He said, "you're obviously vagal, and there are a whole category of drugs that are contraindicated for you. We will not prescribe them." "Wonderful, finally somebody who has a clue!" I thought to myself. This guy sent me home with a Holter, so he could see what my average HR was, out of rhythm.

During the weeks this was happening, I read more and also had a few tests ordered by my GP and my integrative MD. These included an EXATEST for cellular levels of Mg (and other minerals), a Comprehensive Digestive Stool Analysis (CDSA) test, and a C-Reactive Protein (CRP) test. The EXATEST showed that I had low-normal magnesium levels, the CDSA, a very small amount of Candida and everything else looked good; and the CRP was very low. So, there was nothing obvious to treat. I did add some magnesium to my supplement plan.

The results of my Holter were that my average rate was ~80 when out of rhythm. The EP suggested that the best course of action was not to convert me, because of the risks of treating me with rhythm drugs if I converted and the fact that I was doing OK out of rhythm. We had already talked about this, so I had done my research. I'd read Hans' book and looked at all the reports of those who had managed to stay in rhythm with supplements. I also learned about flecainide on demand. So, I proposed my plan "B." It was 1) to convert me, 2) I would try to stay in rhythm with supplements and trigger avoidance, and 3) I would take flecainide on demand if 1 and 2 didn't work. He accepted my plan. He gave me a prescription for flecainide and at first thought he'd give me a 300 mg dose to see if I converted. Then he came back and said that the studies showed that this was only effective if given right after going out of rhythm. I'd been out of rhythm for 2 ½ months at this time. He told me to schedule a cardioversion in a couple of weeks. I got the prescription and went home. I looked at the pills and thought, "Well, I've already been cleared to take these, what do I have to lose?" I took a 300 mg dose and converted in about 18 hours. Needless to say, I was ecstatic after being out of rhythm for so long. I faxed a note to the EP who asked me to come in for an EKG to make sure I was doing OK on the flecainide. This turned out fine.

I went on my supplement program big time, determined to stay in rhythm (the conversion took me by surprise). This has worked well for 5 months. I did have one event at exactly 4 weeks. I determined that eating a bunch of junk, late was a trigger. I then thought back to my other events in the summer and could also remember similar triggers. At this point I decided to not eat after 7 PM. I wasn't sure if the trigger was GERD, hypoglycemia or a vagal response to eating, but early eating will help all of these.

I also wanted a finer gauge of how I was doing than "either I'm in afib", or "I'm not". To this end, I purchased a Polar S810 HR monitor, and the FreezeFramer HR monitor. They both accomplish the same thing, namely a beat to beat recording of your heart rate. The Polar records, and then the data is downloaded to your computer. The FreezeFramer has a finger cuff (now an ear cuff, too), which you wear while hooked up to your computer. You can watch the display in real time. Both devices suffer from artifacts and noise if you move around too much. I've taken to monitoring myself while meditating, as I am most still then. In recent testing with an EKG device[1], I've determined that I can differentiate PAC's from PVC ectopic beats. The PAC's have an anomalously fast beat or fast immediately followed by an anomalously slow beat. The PVC's have an anomalously slow beat[2]. Both the Polar and the FreezeFramer have the same PAC/PVC response. In testing the Polar with my EKG, I found that several anomalies that I thought were ½ period artifacts turned out to be real PVC's per the EKG. If you use a FreezeFramer, you need to make sure that the Enable Artifact Detection box is unchecked (this defeats the purpose), as well as uncheck the Enable HRT Filter box. In counting ectopics in a 20-minute period (the length of most meditations), I can see if I'm doing well with my program. My initial July Holter showed 24 PVC's and 2 PAC's per hour. Generally, I'm way below that now. My readings have ranged from 0 to 20 per hour, but most range in the 3 to 10 range. There is data to show that ectopics increase to 5 or 6 per minute right before the initiation of afib. I actually feel very few of my ectopics; in fact, I feel them only rarely and then only when I'm sitting quietly with a monitor on and my attention on my throat. The monitors pick up several orders of magnitude more ectopics than I feel.

I also wanted to address the possibility that my trigger was a hypoglycemia event. In addition, I had added about 10 pounds during my 2½-month afib event, and my blood pressure had crept up to 130/85. I wanted to address these issues also. I purchased a Bayer Ascencia home blood glucose monitor. It was the most accurate I could find. Many home models are very inaccurate (according to their own specs – OK for a diabetic, but not for my purposes). What I found was that hypoglycemia wasn't my problem, but hyperglycemia was. Hans' first book had also referenced that vagal afibbers might have a "flat" blood glucose response. This was not my case. I found that high glycemic index (GI) carbs could spike my blood sugar. Also the addition of fat, even "good" fat would keep my blood glucose high on a fasting test and so would a high GI meal. In a literature search, I found that this is because circulating lipids impair insulin's ability to work[4-7]. For me, I could get a 112 mg/d (6.2 mmol/l) reading on a fasting test by eating solely two helpings of ice cream for dinner, however, this would drop to the mid 80's (~4.7 mmol/l) the next day on a fasting test following a day of eating my no added fat, whole food vegan diet. I also found that drinking 1 liter of a whole fruit drink, that I make by grinding up whole apples, oranges and other fruits hardly moves my blood sugar at all.

After two weeks of paying attention to keeping my blood sugar even, I'd dropped the 10 pounds I'd added, and my fasting glucose and my blood pressure normalized. One detriment to this approach is the lack of essential fatty acids (EFA's) in the diet. There has been discussion of the fact that people don't convert fat from flax seeds to EFA's; however, there are some interesting abstracts on one of Hans' other sites. One reports the non- conversion of the flax-type fatty acid (percent of dietary fat not stated). However the other shows that people do convert, if their dietary fat intake is limited to 20% of calories (see the first two abstracts listed at www.oilofpisces.com/weightcontrol.html).

Now some people may think "this guy goes nuts buying stuff to measure himself." You would probably be correct. However, you must remember that I have very high deductible insurance and if I can save one ER visit, I've paid out my monitoring investment many times.

Here is my supplement program:

Morning supplements, normally around 7 AM, with breakfast
2 mg Copper
1000 mg Taurine
800 mg NOW brand Trace minerals
200 mcg Selenium
B-50 B-complex
500 mg Vitamin C
400 IU Vitamin E
1000 mg Acetyl L-Carnitine
500 mg L-Tyrosine
500 mg L-Lysine

Mg & K
400 mg Magnesium Glycinate
400 mg Magnesium Maleate (will switch to only Glycinate when done with this bottle)
1.5 grams Now Brand KCl powder

Evening, normally around 6 PM, with dinner
Repeat the Mg & K

I also take CANDEX per directions to rid myself of any Candida, as per Jackie's suggestion.

My best estimate is that the Mg, K, Taurine and Acetyl L-Carnitine are the most active with respect to afib. Also the B6 helps the absorption of magnesium. If you decide to go this route, start slowly and increase your dosages. Also, make sure your kidneys are OK, so have your BUN and creatinine levels checked. PeggyM says that when your stores of Mg are full, your bowel tolerance for Mg will decrease. At this point, just reduce your dosage till you don't have a problem maintaining your Mg levels.

I don't know that I've optimized this. At some point, I plan to repeat the EXATEST and see how I'm doing bringing the Mg levels up in my cells, or as PeggyM suggests, I can wait till I have a bowel tolerance problem and cut back my dosage then. All of these supplements have not helped my digestion, however, the addition of Betaine HCl and dietary enzymes seems to help this. I may add a pre-bedtime dose of K, as my morning ectopic samples are much lower if I do. However, I think that the chlorine in the KCl negatively affects my blood pressure. I may substitute the potassium gluconate and see if this will still lower my ectopics while not affecting my blood pressure.

My digestive system doesn't really like all those fillers and capsules. However, if I can back off at all, my ectopic rate is right back up again. At some point, I'd like to see if I can accomplish the addition of these nutrients mostly within the confines of my vegan diet. However, since what I'm doing has kept me in NSR for 4 months, I'm loath to change it too much. One reason I chose the supplement route to begin with is that a dietary approach takes a lot more analysis and organization (perhaps not for the paleo or blood-type diet folks, but it does with my vegan plan and, otherwise, I do very well as a vegan with a lot more energy than my peers). Also, I'm very active, leading a youth group of 14- to 20-year-olds camping on a regular basis. It is much easier just to pack a few supplements.

As an aside, several months ago a friend also had his first two afib episodes. I suggested that he up his intake of Mg and K. He did this and now makes his own version of the PAC-Tamer. He has had no more afib episodes since he started the Mg and K.

Thanks to all for suffering through this long-winded story and I hope some of you find it useful.

References

1. http://www.afibbers.com/forum/read.php?f=6&i=6277&t= 6277
2. http://www.afibbers.com/forum/read.php?f=6&i=6278&t= 6278
3. http://www.afibbers.com/forum/read.php?f=6 &i=4134&t=4111#reply_4134
4. http://www.diva- portal.org/diva/getDocument?urn_nbn_se_umu_diva-26-1__fulltext.pdf
5. Sweeny, J.S. 1927 Dietary factors that influence the dextrose tolerance test. Arch. Int. Med. 40:818-30
6. Felber, J. P., and Vannotti, A. 1964 Effects of fat infusion on glucose tolerance and insulin plasma levels. Med Exp. 10:1536
7. Anderson, J. W., et al. 1973, Effect of high glucose and high sucrose diets on glucose tolerance of normal men. Amer. J. Clin. Nutr. 26:600-607

I sent my story to Hans before going on a snow cave outing with my youth group. I snow shoed into our camp for 3 ½ hours carrying a 70-pound (32 kg) pack, breaking trail much of the time in >3 feet (1 meter) of snow. I then worked for another 4 ½ hours constructing a snow cave. Although I wasn't wearing a heart rate monitor, I can tell you that I was working at maximum exertion for those 8 hours. Also, the elevation was 10,500 ft (3,200 meters).

I crawled into my sleeping bag around 8 PM. At about midnight, I went into afib. I brought my flecainide along, so I decided to take a 300 mg dose (my conversion prescription). The instructions given on this board are to take it crushed in warm water as soon as possible after the start of the afib. Well, my water bottle had ice in it, as the cave temperature was below freezing (better than the –5 deg. F (-21 deg. C) outside). So, I chewed the three tablets and washed them down with ice water. Happily, I converted in less than 30 minutes. This was much better than my first two conversions on flecainide, 18 and 22 hours, and even exercise conversions I'd had. These ranged from 7 to 10 hours.

So, I've broken my four-month spell of not having to use my flecainide on demand as backup. However, I'm not unhappy – the plan I presented to my EP is still working. On this trip, I certainly stressed my system and probably messed up my electrolytes as well as being dehydrated from the exertion and altitude. The flecainide worked much more quickly than before. I would attribute this to all of the supplements I've taken. As I mentioned, this is a "work-in-progress", and I obviously need to fine tune my program if I want to continue exerting myself like this (some would observe that this would not be a bright move).

In addition, my blood glucose observation program has yielded an 18-pound weight loss in 8 weeks (usually with much more modest exercise than this latest outing). All in all, I'm very pleased with my progress. NSR to all readers!