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One natural method for cardioversion by IV nutrient delivery is through the use of a moderately paced IV push of magnesium sulfate. The basic premise is to deliver 0.5 to 2.5 grams of magnesium sulfate (MgSO4) over 20 to 30 minutes. This treatment has largely fallen out of favor in conventional settings due to the higher success rates of treatments such as electrocardioversion and the conflicting evidence regarding its efficacy.15-18 The largest recent study, a trial of 199 patients in 2005, demonstrated that IV MgSO4 used in conjunction with other rate control therapies was significantly more likely to control rate and convert patients to NSR from AF-RVR.17 Despite outcomes, the studies generally agree on the safety of the intervention.
All of the normal contraindications to IV Mg apply: the absorption of digoxin, nitrofurantoin, and anti-malarials may be decreased by Mg; Mg may interfere with anticoagulants and quinolone or tetracycline antibiotics; Mg may interfere or have additive effects with beta blockers and calcium channel blockers. Most patients will experience a typical Mg "flush" during the treatment, and many will feel sedated or drowsy following the treatment and should have someone else drive them home.19
We often consider attempts to convert patients to a normal rhythm using homeopathy. Natrum muriaticum is the most indicated single or classical remedy for this purpose.20 We have seen the remedy convert patients from AF to NSR on three occasions, twice in the same patient. More frequently, we use a mixed, low-potency spagyric remedy indicated for tachycardia as a means of cardioversion. We have used it to success in several instances. The success rate is low, but the safety profile is high and the patient stands to lose very little for a trial of the therapy if the conversion circumstance is otherwise safe.
Finally, it is important to consider the potential association of irritation and inflammation in local tissues as a potential etiology of AF and a means by which to achieve its resolution. The most frequent association here is between AF and the sliding type of hiatal hernia. An excellent article was produced by Armaganijan et al. 2012 and published in Expert Reviews in Cardiovascular Therapy in October 2012 on this topic.21 Visceral manipulation and reduction of the sliding hiatal hernia can cause or help in the conversion of AF to NSR. We have experience with one patient in particular, in whom the association between paroxysms of AF and the position of his hiatal hernia superior to the lower esophageal sphincter appears to be completely unitary. In each instance that we have seen the patient during a paroxysm of AF, reduction/visceral manipulation of his hiatal hernia back to correct anatomical position alleviates his arrhythmia.
Antithrombotic therapy (AT) is a mainstay of treatment in virtually all instances of AF other than a single instance of a lone episode. AT is necessary to address the increased risk of thromboembolic events, especially stroke, which have a relative risk 10- to 20-fold higher or more in AF patients than in the average population.22 As AF patients age and comorbidities are compiled, they may reach an annual stroke risk over 15%.23
Whether antiplatelet therapy, by the use of aspirin (ASA) or anticoagulant therapy is more appropriate for a patient is determined by use of the CHADS2 score. The CHADS2 score helps predict the annual stroke risk by virtue of the patient's age and comorbidities. According to the CHADS2 score, we tally points for the patients risk based on: Congestive heart failure (past or present), Hypertension (controlled or uncontrolled), Age (≥ 75 years), Diabetes mellitus (controlled or uncontrolled), and Stroke or transient ischemic attack (TIA) history.24
The presence of each of the first four (CHAD) are worth 1 point each, whereas a history of stroke or TIA is worth two points (S2). According to the CHADS2 score system, 81 to 325 mg ASA/day is appropriate therapy for a score of 0 or 1 point and a score of greater than 2 points requires either warfarin therapy (to a target INR range of 2.0–3.0) or dabigatran, typically 150 mg/twice daily. A score of 2 points presents the managing physician and patient with a clinical decision between ASA therapy or anticoagulation with warfarin or dabigatran.
More recent modifications to the CHADS2 score have resulted in the development of the CHA2DS2-VASc score for AF. The CHA2DS2-VASc score (sometimes referred to simply as "ChadsVasc" score) helps us get a more precise assessment of the relative risk of vascular events, thus providing more clarity on the necessary level of AT intervention for a given patient. By contrast, the risk of the patient having a bleeding event while on AT is predicted utilizing the "HAS BLED" score.25,26
Many patients come to our practice seeking an alternative to pharmaceutical management of stroke risk. Many excellent natural therapies exist that may help to modify stroke risk and conventional AT. The greatest challenges with "natural blood thinning" (NBT) therapies are: (1) monitoring them and (2) educating patients that there is insufficient evidence of their efficacy to rely on them to prevent thromboembolic events without accompanying pharmaceutical stroke prophylaxis.
In order to monitor nontraditional blood thinning treatments (NBT), we use the Surgicutt Bleeding Time (BT) test. The bleeding time test has several different forms including: Ivy method, Duke method, template method, in vitro method, and the device methods including the Surgicutt and the Simplate (which is no longer available). The evidence surrounding BT for measuring primary hemostasis (ability to form a clot) is relatively robust.27-35 It is that indication which most concerns us as we are trying to create an iatrogenic disorder of primary hemostasis in order to lower stroke risk.
The test is widely criticized for the potential variability and (seemingly) subjective interpretation of its results. However, within individuals there is little biological variability, and most of the difference over time is due to observer variability.27 Despite criticism, it is still widely used in research as a measure of platelet function.
The strength of the BT is the same as its weakness: it is completely nonspecific. This is of great value to us when using NBTs because they achieve their effects by several different mechanisms. While several NBTs can interfere with or alter the INR, none are reliably measured by it. Moreover, the effects of conventional AT on the BT are exceptionally variable. With the BT we are measuring the furthest downstream effects on all aspects of hemostasis, the formation of a clot.
Warfarin therapy is monitored by the PT/INR test, but this makes it the exception rather than the rule among conventional ATs, which typically undergo no monitoring at all and have few reliable or cost-effective monitoring test options. Moreover, other than ASA, antiplatelet therapy is not used in the conventional management of AF. Yet, platelet aggregation and dysfunction, as well as blood viscosity, are as important in thrombus formation as are the factors of the clotting cascade antagonized by warfarin and dabigatran.
We believe that monitoring and optimization of the BT test in AF is an important element of integrative AF management. It is also important to monitor scrupulously for changes in the INR, for drug/herb/nutrient/metabolism interactions and for signs or symptoms of increased bleeding when combing conventional AT with NBTs.
We utilize several different therapies to optimize platelet function and bleeding time. We typically begin with optimization of polyunsaturated fatty acid (PUFA) intake. PUFAs exert several important effects on platelet function, blood thinning, AF, and cardiovascular function. They are well-tolerated, essential nutrients, which are inexpensive and easy to incorporate into the daily regimen for most patients.
The essential omega-3 (n-3) PUFAs, EPA and DHA, appear to increase the BT in a dose-dependent manner, but results of studies are mixed on its AT effects and are far from conclusive.36-39 In addition, PUFAs have important effects on cardiovascular conditions that are often concomitant to AF such as high blood pressure and poor lipid profiles.40-49
PUFAs can exert an antiarrhythmic effect in AF. This point is hotly contested throughout the medical literature, and the studies which analyze these effects vary substantially in the type of AF that is scrutinized, the sample sizes, the doses used, and the ratio of n-3 PUFAs used.50-55 However, in the studies of patients with permanent AF taking 6 grams or more of n-3 PUFAs daily, antiarrhythmic properties have been reliably demonstrated.50,51
We typically begin by recommending that patients get 4 to 8 tablespoons per day of ground flax seeds and 2 to 4 tablespoons per day of ground chia seeds. Additional PUFA support comes by way of vegetarian or fish-oil supplementation based on the other indications present in a particular case and the BT.
Our second-line intervention to optimize BT is a nattokinase supplement that has been analyzed after manufacture for its fibrinolytic activity. The product that we use has 2000 FU (fibrinolytic units) per capsule, and we initiate therapy at 1 cap once or twice daily; we may escalate to as much as 4 caps twice daily, but we never exceed this amount based on safety and cost.
The nattokinase research is also controversial, but studies have shown fibrinolytic activity as well as an upregulation in the endogenous activity of tissue plasminogen activator (tPA) by the vascular endothelial cells, decreased red blood cell aggregation, and low-shear blood viscosity.56-59 One compelling prospective study of 186 patients taking a proprietary combination of nattokinase and Pycnogenol before air travel demonstrated that no thrombotic events occurred in the treatment group while the control group demonstrated five instances of deep vein thrombus and two of superficial venous thrombus.57 Nattokinase has also shown side benefits on concomitant cardiovascular conditions such as high blood pressure.60
We use a sustained-release grape-seed extract as our third-line intervention to optimize BT. Several small studies show that grape-seed extract may have very potent antiplatelet activity.61-68 This evidence, too, is conflicting; however, we have seen its use routine raise BT in our practice. In one particular patient, her BT remains suboptimal at 7 minutes on PUFA and nattokinase therapy; the addition of sustained-release grape-seed extract reliably elevates her bleeding time over 12 minutes and its removal returns the BT to 7 minutes. Like those above, grape-seed extract has cardiovascular side benefits, including effects on blood pressure.69 It is rich in polyphenols, especially anthocyanidins, and has demonstrated compelling effects on many systems outside of the cardiovascular system.
Finally, we do not hesitate to use 81 to 325 mg of ASA therapy to achieve optimal platelet function and BT when necessary and appropriate. To be sure, there are many patients who come to us because they cannot use ASA due salicylate sensitivity, medication interactions, or gastrointestinal bleeding events; and in these, as well as others, ASA may not be appropriate. In the instance of a stubborn bleeding time or suboptimal platelet function in the absence of contraindications, however, it can be just the extra push that is needed. Moreover, the research surrounding its ability to prevent a first instance of heart attack in men or a first instance of stroke in women is virtually absolute.
Atrial fibrillation is a complex management scenario. Depending on AF type and duration, as well as on patient comorbidities and preferences, there are many opportunities for the improvement of patient health via the integration of CAM therapies with conventional management. In this and in previous articles in this journal, we have discussed CAM protocols to improve patient arrhythmias and endothelial function. Certain CAM therapies can be effective in conversion of arrhythmias back to normal rhythm, when appropriate. Finally, the optimization and monitoring of platelet function and bleeding time in AF patients may be one of the most important contributions that CAM can make to conventional management of this common arrhythmia.
Dr. Jeremy Mikolai
Heart & Lung Wellness Program
Center for Natural Medicine Inc. (CNM)
1330 SE Cesar E Chavez Blvd.
Portland, Oregon 97214
503-232-1100
HLResident@cnmwellness.com
CNMWellness.com
This author has no financial conflicts of interest to declare.
 Jeremy Mikolai, ND, is professor of cardiology in the naturopathic medicine program in the School of Health Sciences at Universidad del Turabo in Gurabo, Puerto Rico, and cofounder of the Naturopathic Institute of Cardiovascular and Pulmonary Medicine (NICVM). He is the attending physician in cardiovascular and pulmonary medicine at the National College of Natural Medicine (NCNM) and co-attending physician in the Heart & Lung Wellness program at the Center for Natural Medicine (CNM), both in Portland, OR. Dr. Mikolai is in his third year as the Heart & Lung Resident and is the Chief Resident for 2012–2013 at NCNM. He is also an adjunct faculty member in the Masters of Science in Integrative Medicine Research (MSiMR) program at the Helfgott Research Institute at NCNM. He is actively working to create the first ND fellowship in cardiology.
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