Survey Results � Part VI
Effect of Drugs (Antiarrhythmics)
My explanation of this finding, not substantiated by any other evidence that I am aware of, is that some antiarrhythmic drugs are slightly proarrhythmic at normal heart rates, thus more episodes, but do become antiarrhythmic at rapid heart rates, thus shorter episodes. The facts that antiarrhythmics can convert atrial fibrillation to atrial flutter, increase the frequency and duration of paroxysmal AF, and convert paroxysmal AF to chronic AF are well-documented.
There were no differences between drug users and non-drug users as far as average age, gender distribution or total years of LAF. The finding that overall, afibbers who take antiarrhythmics are no better off than afibbers who do not is indeed surprising and obviously needs further scrutiny. First of all it should be kept firmly in mind that none of the drugs prescribed for LAF have been specifically developed to deal with this condition and, as a matter of fact, several of them are not even approved for the treatment of atrial fibrillation as such. So essentially whenever a LAF patient is prescribed an antiarrhythmic it is a trial and error procedure � there is no guarantee of success. This is compounded by the fact that many afibbers are clearly receiving the wrong drugs for their particular condition. This is particularly pronounced among vagal afibbers.
Drugs in Vagal LAF
It was, unfortunately, not possible to establish the statistical significance of the above-mentioned differences because the individual sub-groups were too small and quite heterogeneous. Nevertheless, it seems clear that flecainide and disopyramide may be of benefit for vagal afibbers while other antiarrhythmics are not. Flecainide or disopyramide for that matter are not for the faint of heart though. They are highly dangerous drugs that should only be used by people with an absolutely sound heart. Side effects can be serious and potentially fatal.
Drugs in Adrenergic LAF
Drugs in Mixed LAF
The results and conclusions for the mixed group are somewhat confounded by the fact that the average age of the non-drug group was 48 years as compared to 58 years for the drug group. Looking closer at the regression analysis results it would appear that the age difference could account for about 25 extra hours of fibrillation in the older drug group. So even taking age into account it is still clear that drug users spent about 4 times longer in fibrillation and had almost 3 times as many episodes as did non-drug users.
Drugs and Chronic LAF
It is not immediately obvious why some chronic afibbers are on antiarrhythmics as there is no evidence that this will help them convert to sinus rhythm unless they are being prepared for cardioversion � none of the respondents were. Certainly being on digoxin can only make things worse and amiodarone has some very serious long-term side effects.
In conclusion the data collected in the LAF survey does not support the assumption that treatment with antiarrhythmics is beneficial to people with lone atrial fibrillation. There are clearly cases where afibbers have been helped by these drugs, e.g. flecainide for vagal afibbers, but in general terms they do not seem to be helpful and, in many cases, are clearly detrimental. It would appear to be up to each individual, in cooperation with his or her physician, to find the right drug or to forego antiarrhythmics altogether. Remember that LAF is not life-threatening, but antiarrhythmics can be. The best and safest approach for many afibbers may well be to just take verapamil during an episode to keep the heart rate under control.
The Inflammation Connection
Inflammation is the body�s immediate response to an injury, infection or other type of stress. It is usually time limited and ceases when healing is completed. However, in some cases, the inflammatory response continues unchecked and this can lead to the development of inflammatory diseases such as asthma, rheumatoid arthritis, and irritable bowel syndrome. An elevated erythrocyte (red blood cell) sedimentation rate (ESR) and high blood levels of interleukin-6 (IL-6) and C-reactive protein (CRP) are prominent features of inflammation.
There is mounting evidence that a systemic inflammation of the blood vessel lining is heavily involved in the initiation and progression of atherosclerosis. Austrian researchers have found that chronic dental infections, urinary tract infections, and chronic respiratory infections all substantially increase the risk of atherosclerosis. Italian researchers have found elevated blood levels of IL-6 and CRP in patients with unstable angina and have associated such higher levels with an increased risk of heart attacks. Very recently researchers at the Harvard Medical School found that high CRP levels are a potent risk factor for peripheral arterial disease (intermittent claudication).
Just recently diabetes, depression and most common cancers were also added to the list of inflammatory diseases[4,5,6]. It is probably not an overstatement to conclude that over 90% of all that ails us is caused by an underlying inflammation.
So why are we so inflamed? There are several possible explanations:
Whatever the reason, there is no doubt that inflammation and the many diseases resulting from it are rampant today.
Inflammation and LAF
The inflammation was found to be active in 3 of the 8 patients. These patients were treated with the anti- inflammatory medication prednisone. They had no further LAF episodes over a 2-year follow-up. The remaining patients were treated with propafenone, sotalol, flecainide or amiodarone and had numerous LAF episodes over the next 2 years.
Through recent correspondence with Dr. Frustaci I learned that 2 more patients had later shown signs of active inflammation and had been successfully treated with prednisone. Dr. Frustaci concurred that a relapse of atrial inflammation could result in new episodes of LAF and that it is quite possible that all the 12 LAF patients actually had signs of inflammation, but that the biopsy missed them in four of the cases. Dr. Frustaci also agreed that a high concentration of mercury or antimony in the heart tissue could produce electrical instability perhaps leading to LAF. Dr. Frustaci has earlier reported that some patients with congestive heart failure have levels of mercury and antimony in their heart tissue that are 22,000 and 12,000 times higher respectively than those found in healthy people. Canadian researchers at the University of Calgary have pointed out that dental amalgams (silver fillings) would be the most likely source of the mercury.
More recently Dr. Frustaci and colleagues reported a link between ventricular arrhythmias (tachyarrhythmias) and the presence of inflammation in the left ventricle. The inflammation in turn was linked to the presence of hepatitis C virus, enterovirus or influenza virus in the inflamed tissue.
Just last month a team of American and Greek researchers reported that many patients with congestive heart failure also have an active inflammation of the heart lining which, in some cases, can be treated successfully with prednisone. They observed that about one third of the patients with active inflammation had elevated erythrocyte sedimentation rates[14,15]. It is intriguing to speculate about a possible link between Dr. Frustaci�s findings of grossly elevated levels of mercury and antimony in the heart tissue of patients with congestive heart failure and this new finding.
The Source of LAF
The connection between the autonomic nervous system and inflammation is indeed an intriguing one and may well hold the key to the origin of LAF. Please note that the following is pure speculation on my part and not supported by any clinical evidence that I am aware of.
It would seem that LAF requires the presence of both an inflammation of the heart lining (myocarditis) and an imbalance in the autonomic nervous system. Is it possible that this combination of inflammation and autonomic nervous system dysfunction could trigger the damage to nerve endings (vagal or adrenergic) in the myocardium? Is it also possible that the body would compensate for this damage by increasing the output of norepinephrine (the adrenergic transmitter) and acetylcholine (the parasympathetic (vagal) transmitter) at adjacent nerve endings? If this were indeed the case it would explain the creation of highly sensitive foci on the surface of the heart. These foci in turn would initiate an LAF episode whenever the dominant (unbalanced) branch (adrenergic or vagal) of the autonomic nervous system became overloaded through physical or mental stress, etc. The highly sensitive foci would be discernible during an electrophysiology study and would be the ones destroyed during ablation therapy. Again I want to emphasize that this hypothesis is pure speculation on my part; however, it does seem to make sense and could be a plausible explanation for the initiation and continuation of LAF episodes.
Elimination of LAF
So how can the inflammation be eliminated? Clearly a two-pronged approach is required:
Bacterial, viral and fungal infections are potent triggers of inflammation. Both myocarditis (inflammation in the heart associated with LAF) and atherosclerosis have been linked to an infection with the Chlamydia pneumonaie bacterium[27-29]. Some researchers have reported the presence of Helicobacter pylori bacteria in atherosclerotic lesions, but the evidence of a causative link is not as convincing as for C. pneumonaie. There is also some evidence that a systemic Candida albicans infection can promote inflammation of the heart tissue (myocarditis) in severely immuno-compromised AIDS patients. Just recently American researchers reported that mice infected with the coxsackievirus (associated with the common cold, meningitis and encephalitis) or the cytomegalovirus (associated with mononucleosis, hepatitis and colitis) developed myocarditis within 2 weeks of becoming infected. Adding this evidence to Dr. Frustaci�s findings[9,13] it is clear that there is an association between bacterial, viral and fungal infections and the development of myocarditis and, furthermore, that there is an association between myocarditis and heart arrhythmias (both atrial and ventricular). So if you have LAF it would seem prudent to undergo testing for possible infections and follow-up with medical treatment to eradicate them as necessary.
Diet can also be a potent source of inflammation. In some people wheat, dairy products and certain foods of the nightshade family (potatoes, peppers, eggplant, tomatoes) can cause a chronic inflammation. I have found Dr. Peter D�Adamo�s book �Eat Right for Your Type� particularly helpful in sorting out what to avoid and what to emphasize in the diet.
Elimination of Persistent Inflammation
It is evident from Dr. Frustaci�s work that the inflammation (myocarditis) associated with LAF can be eliminated by treatment with prednisone. Unfortunately, rather high dosages are required, at least initially. Prednisone has the potential for serious adverse reactions and is use is generally not recommended for extended periods of time. Dr. Frustaci used 1 mg per kg bodyweight per day for 4 weeks tapered to 0.33 mg for 4 months. So while prednisone may do the job, at least if the inflammation is active, the overall benefit/risk ratio is not encouraging although probably no worse than that of long-term amiodarone (Cordarone) treatment.
An unfavourable benefit/risk ratio also applies to the use of aspirin and other NSAIDs to combat inflammation. They do not get at the root cause of the inflammation and can cause serious bleeding complications.
The cholesterol-lowering drug pravastatin (Pravachol) is effective in reducing the level of the inflammation marker C-reactive protein (CRP). This could benefit patients with atherosclerosis or rheumatoid arthritis, but as far as I know no work has been done to investigate the use of pravastatin in lone atrial fibrillation. Unfortunately, pravastatin has many potentially serious side effects including liver dysfunction, myopathy, rhabdomylosis, and possibly cancer. Pravastatin has also been found to lower coenzyme Q10 levels possibly leading to impaired cardiac function and congestive heart failure.
Human growth hormone replacement is another possible route for combating inflammation. Researchers at the Harvard Medical School recently reported that levels of IL-6 (interleukin-6) and CRP were both significantly reduced by the administration of recombinant human growth hormone in men with adult-onset growth hormone deficiency. The reduction in CRP level (30%) was similar to that obtained with pravastatin. IL-6 levels decreased by almost 40% as compared to the placebo group. The researchers conclude that, �long-term growth hormone replacement in men reduces levels of inflammatory cardiovascular risk markers� (IL-6 and CRP).
It is interesting that one member of our group of afibbers has found growth hormone (HGH) therapy to be useful. Chuck, a vagal afibber, started using an oral sublingual HGH spray in early May (Sol RX available at www.atlantis.to/Products/gh-atlantis- home.htm). He used to have daily episodes lasting 4 to 5 hours. Since using HGH both his episode frequency and duration have decreased by about 50%.
Balancing the Immune System
Extensive research carried out at the University of Stellenbosch in South Africa has shown that a proprietary mixture of plant sterols and sterolins (Moducare) is very effective in increasing TH1 cell production (the �good� T cells) and decreasing TH2 cell production (the �bad� T cells). Moducare also normalizes the ratio between DHEA and cortisol. Moducare has strong anti-inflammatory effects and sharply reduces IL-6 production. It has been found useful in the treatment of chronic viral infections, tuberculosis, and HIV infection. Also it has been found to reduce the inflammatory response associated with excessive physical exertion. The recommended dosage of Moducare is two capsules one hour before the main meals for the first month and then one capsule one hour before breakfast, lunch and dinner.
I now firmly believe that the key to permanently overcoming LAF is to eliminate the dormant or active underlying inflammation of the heart lining. I have personally made some significant changes to my diet, lifestyle, and supplements in order to achieve this and will keep you informed of my progress. You can find the detailed �Larsen Protocol� for eliminating inflammation and LAF after the references. If you try it please let me know the results.
The Larsen Protocol
My approach to eliminating LAF is two-pronged - using dietary modifications and lifestyle changes to avoid �feeding� and constantly aggravating the inflammation, and using natural supplements to dampen and heal the inflammation. The �Larsen Protocol� does not replace whatever other measures you are now taking to control your LAF (e.g. Dr. Lam�s protocol) - it is solely designed to eliminate inflammation.
I should point out that I have experienced the adrenergic type of LAF for the past 11 years. I am not on any drugs and have had 8 episodes over the last six months with an average duration of 54 hours. Since beginning the protocol I have had zero episodes, my number of ectopic beats has dropped from 4-5/minute to 0-1/minute, and my autonomic nervous system is now in far better balance than it was prior to starting on the protocol. I have now gone 40 days without an episode � this is a bit of a record!!
This protocol has certainly made a great difference to me. Whether it will do the same for vagal, mixed and perhaps chronic afibbers remains to be seen.
If you decide to try the protocol please make sure you discuss it with your physician first. Although the components of the protocol are generally well tolerated and I am not aware of any side effects from the supplements there may be factors in your medical history or in any medicines you are taking that should be taken into account before you start. It may also be advisable to ease into the protocol over a one to two week period rather than start taking all the supplements all at once. I began by just taking Moducare, vitamin C, pancreatic enzyme and curcumin/bromelain for the first week.
I am not aware of any potential interactions between the recommended supplements and warfarin, but if you are on warfarin you may wish to check your INR a bit more frequently when you first start the protocol.
I would urge you to obtain one or both of Dr. D�Adamo�s books �Eat Right for Your Type� and �Live Right for Your Type� and then follow the diet appropriate for your blood type. Eating the wrong foods sets up an internal war that aggravates inflammation. You can purchase the books in your local book or health food store or you can order them by mail (Amazon.com) through the LAF Forum (www.yourhealthbase.com/lafforum.html).
DAILY SUPPLEMENT PROTOCOL
Upon arising (1 hour before breakfast):
I noticed a significant improvement in my heart stability and indeed in my general health and well-being within two weeks of beginning the protocol. I am very hopeful that four to six weeks on the protocol will eliminate my LAF episodes altogether � although individual results may depend on systemic mercury status.
The AFIB REPORT is published monthly by Hans R. Larsen MSc ChE
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