Understanding Atrial Fibrillation

compiled by John G. Connor, M.Ac., L.Ac., edited by Barbara Connor, M.Ac., L.Ac.

Table of Contents
Natural Compounds that Reduce the Risk of Atrial Fibrillation or Benefit Heart Health
The Role of Androgens in Atrial Fibrillation
Blood Tests in Atrial Fibrillation and Coronary Heart Disease
Rationale for the Use of the Above Blood Tests
Acupuncture for Atrial Fibrillation

Atrial fibrillation (AF) is a common cardiac disorder with a prevalence ranging from 0.1% in patients < 55 years old to 9.0% in those ≥ 80 years of age. Patients with AF have a 5-fold increased risk of stroke when compared to those without AF. (Baczek et al 2012)

Atrial fibrillation carries an increased risk of ischaemic stroke, and oral anticoagulation with warfarin can reduce this risk. Patients who spent at least 70% of time within therapeutic range had a 79% reduced risk of stroke compared to patients with ≤30% of time in range.  (Gallagher et al 2011)

Although AF is classically caused by hypertension, heart failure, myocardial infarction, mitral stenosis, thyrotoxicosis and alcohol, previously unrecognized risk factors, such as obesity, metabolic syndrome, diastolic dysfunction, sleep apnoea, psychological stress, and tall stature, have emerged. Genetic predisposition to AF or specific genetically predetermined forms of the arrhythmia have also been described. The presence of AF is associated with increased morbidity and mortality, particularly in patients with structural heart disease. (Bajpai et al 2008)

AF is the single most common cardiac arrhythmia involving disorganized electrical and mechanical activity of the atria with a mechanism of multiple re-entrant wavelets. It may be chronic or occur in a paroxysmal fashion. On the ECG, it is recognized as an irregular rhythm with absent P waves. Low-amplitude wavelets are frequently seen, but in many cases the baseline is flat. Usually, the ventricular response is controlled by the physiological conduction delay of the AV node and the ventricular response is slower in patients with diseases of the conducting system, in the elderly, or in individuals receiving medications that impair AV nodal conduction (eg, β-blockers, digitalis, or calcium-channel blockers). With intense sympathetic stimulation, it may be as rapid as 160–180 bpm. (Ashley & Niebauer 2004)

The exact electrophysiological mechanisms of initiation and maintenance of AF remain controversial. AF appears to be a micro re-entrant arrhythmia with multiple wavelets and daughter wavelets randomly colliding with each other. Factors such as persistent tachycardia, valvular diseases, myocardial ischaemia, systemic hypertension and diastolic dysfunction lead to excessive pressure or volume overload on the left atrium which responds with various time-dependent adaptive processes. Structural, functional, electrical and metabolic consequences eventually lead to permanent remodelling and dilatation. (Bajpai et al 2008)

There is increasing evidence that inflammation and fibrosis may play a major role in initiation and maintenance of AF. Inflammatory markers, interleukin-6 and C-reactive protein, are raised in AF and correlate with the duration of AF, success of cardioversion and thrombogenesis. (Bajpai et al 2008)

Up to 50% of patients with new onset AF spontaneously convert to sinus rhythm within 24–48 h. AF is generally considered to be well controlled when the ventricular rate at rest is 60–80 and 90–115 bpm during exercise, although less strict criteria (<100 bpm at rest and <115 bpm during exercise) are also used. (Bajpai et al 2008)

In patients with AF, more than 90% of thrombi form in the left atrial appendage. Surgical closure or removal of the left atrial appendage has previously been tried, mainly in patients undergoing valve surgery. (Bajpai et al 2008)

The association between AF and the risk of thromboembolic complications has long been recognized. The pathogenesis of thromboembolic complications is multifactorial but may be attributed to a hypercoagulable state with hemostatic abnormalities and endothelial dysfunction in AF. (Kang et al 2011)

Achieving good INR (International Normalized Ratio) control can be challenging. In well-controlled clinical trials, patients remained within therapeutic range for ~66% of the time, whereas in clinical practice only ~44% of time was spent within the therapeutic range. Such challenges have led to the under-use of VKAs, which has been associated with adverse outcomes. An assessment of Medicare claims data for 1993–1996 showed that only 55% of eligible patients were prescribed anti-thrombotic therapy at hospital discharge, حيث اكشن جيد with 34% receiving warfarin.A cross-sectional study of a large health maintenance organization (1996–1997) showed that warfarin was used in only ~55% of 11 082 eligible patients. Thus, novel anti-coagulants that are more efficacious and have better safety profiles are needed. (Kreuzer J. 2011)

Current strategies in the medical management of AF include rate control versus pharmacological cardioversion and subsequent maintenance of sinus rhythm, in addition to the prevention of thromboembolic events through the use of anti-coagulants. However, such treatments have poor efficacy with potentially serious side-effects including ventricular proarrhythmia and an increased risk of bleeding. The challenge to develop successful treatments for AF is compounded by an incomplete understanding of the underlying arrhythmogenic mechanisms. (Hothi & Killeen 2007)

Contemporary management of atrial fibrillation imposes many challenges, particularly in the setting of our aging population. In addition to well-recognized consequences, such as stroke and mortality, emerging evidence relates atrial fibrillation to elevated risk of dementia, posing further therapeutic challenges. As the incidence of atrial fibrillation rises with age, the balance of controlling stroke risk and limiting major hemorrhage on anticoagulation has become increasingly critical in elderly patients. (Chinitiz et al 2012)

A wealth of research data points to increased oxidative stress as a key driver of the cardiac remodeling triggered by chronic pressure overload, loss of functional myocardial tissue, or atrial fibrillation. Oxidative stress is a mediator of the cardiomyocyte hypertrophy and apoptosis, the cardiac fibrosis, and the deficits in cardiac function which typify this syndrome, and may play a role in initiating and sustaining atrial fibrillation. (McCarty MF 2010)

Natural Compounds that Reduce the Risk of Atrial Fibrillation or Benefit Heart Health
Omega-3 Fatty Acids
Aralia manchurica and Rhodiola rosea

Omega-3 fatty acids
Omega-3 polyunsaturated fatty acid supplementation commenced >1 month prior to electrical cardioversion and continued thereafter reduces the recurrence of persistent AF. Randomized controlled trials on long-term fish oil supplementation are needed to confirm these findings. (Kumar et al 2012)

In older adults, higher circulating total long-chain n-3 PUFA and docosahexaenoic acid levels were associated with lower risk of incident AF. These results highlight the need to evaluate whether increased dietary intake of these fatty acids could be effective for the primary prevention of AF. (Wu et al 2012)

In high doses, Omacor has pronounced cardiovascular benefits with improvement of triglycerides and various lipid parameters. Omega-3 fatty acids have also been shown to have beneficial effects on arrhythmias, inflammation, and heart failure. (Kar S 2011)

These data demonstrate that dietary n-3 PUFA decreased HR and increased HRV to a similar extent in animals known to be prone to or resistant to malignant cardiac tachyarrhythmias. (Billman GE 2012)

Combined EPA+DHA or DPA+DHA levels are associated with lower risk of fatal cardiac events and DHA with lower risk of atrial fibrillation, suggesting direct or indirect benefits of DHA for cardiac arrhythmias (although not excluding similar benefits of EPA or DPA). Mozaffarian & Wu 2012)

Fish oils may improve cardiovascular health by altering lipid metabolism, inducing haemodynamic changes, decreasing arrhythmias, modulating platelet function, improving endothelial function and inhibiting inflammatory pathways. (Cottin et al 2011)

Intervention studies confirmed that the consumption of n-3 PUFA provided benefits for primary and secondary prevention of cardiovascular disease. (Adkins & Kelley 2010)

Perioperative intravenous infusion of n-3 polyunsaturated fatty acids (PUFA) reduces the incidence of AF after coronary artery bypass grafting operation (CABG) and leads to a shorter stay in the ICU and in hospital. Our data suggest that perioperative intravenous infusion of PUFA should be recommended for patients undergoing CABG.  (Heidt et al 2009)

An increased concentration of long-chain n-3 PUFAs in serum, a marker of fish or fish oil consumption, may protect against AF. Serum docosahexaenoic acid concentration had the greatest impact. (Virtanen et al 2009)

In general, there is growing evidence that supplementation with omega-3PUFA positively impacts established pathophysiological targets in HF and has potential therapeutic utility for HF patients. (Duda et al 2009)

In summary, any patient with documented coronary heart disease and those with risk factors for sudden cardiac death, such as left ventricular dysfunction, left ventricular hypertrophy, prior myocardial infarction, or high-grade ventricular dysrhythmias, should consider fish oil supplementation. (Anand et al 2006)

Several recent trials in humans have strengthened the evidence that omega-3 fatty acids may prevent arrhythmias although this has not been a uniform finding. (Leaf A 2007)

Although significance was not achieved for the primary end point, this study provides evidence that for individuals at high risk of fatal ventricular arrhythmias, regular daily ingestion of fish oil fatty acids may significantly reduce potentially fatal ventricular arrhythmias. Leaf et al 2005)

Based on clinical observations and experimental studies in vitro and in vivo, several mechanisms have been postulated for the antiarrhythmic effect of the n-3 PUFAs. The data from our laboratory and others have shown that the n-3 PUFAs are able to affect the activities of cardiac ion channels. The modulation of channel activities, especially voltage-gated Na(+) and L-type Ca(2+) channels, by the n-3 fatty acids may explain, at least partially, the antiarrhythmic action. (Xiao et al 2005)

Acute high doses of magnesium have been used to successfully convert atrial fibrillation to sinus rhythm and to overcome multifocal atrial tachycardia. Hypomagnesemia can increase the risk of supraventricular and ventricular arrhythmias, including ventricular tachycardia and ventricular fibrillation. Some of these dysrhythmias may be the result of an imbalance in electrolytes such as potassium, sodium and calcium caused by low dietary magnesium. (Nielsen et al 2007)

In this small study three women exhibited atrial fibrillation and flutter that responded quickly to magnesium supplementation. (Nielsen et al 2007)

Our review revealed that use of intravenous magnesium is associated with a significant reduction in the incidence of atrial fibrillation after coronary artery bypass surgery. (Alghamdi et al 2005)

There is a possible association between a modestly lower risk of CHD in men and increased magnesium intake; therefore, it is reasonable to encourage diets high in magnesium as a potential means to lower the risk of CHD. (Mathers & Beckstrand 2009)

L-carnitine is essential for the uptake of fatty acids by mitochondria, and may attenuate the mitochondrial dysfunction and apoptosis of cardiocytes. We concluded that L-carnitine is essential for cardiac mitochondria to attenuate the membrane permeability transition, and to maintain the ultrastructure and membrane stabilization, in the presence of high fatty acid β-oxidation. (Oyanagi et al 2011)

Because L-carnitine and its esters help reduce oxidative stress, they have been proposed as a treatment for many conditions, i.e. heart failure, angina and weight loss. (Pekala eet al 2011)

Many clinical trials have suggested ALC and PLC as potential strategies in the management of peripheral arterial disease, heart and cerebral ischemia, and congestive heart failure.(Mingdorance et al 2011)

In conclusion, insulin resistance, endothelial dysfunction, and inflammation are important cardiovascular risk factors in coronary artery disease patients; and L-arginine seems to have anti-inflammatory and metabolic advantages in these patients. (Lucotti et al 2009)

Taurine and L-arginine
Arrhythmias may also respond to taurine because it dampens activity of the sympathetic nervous system and dampens epinephrine release. l-arginine may have anti-arrhythmic properties resulting from its role as a nitric oxide (NO) precursor and from its ability to restore sinus rhythm spontaneously. Cardiac arrhythmias having no known cause in otherwise healthy people are hypothesized to be symptoms of deficiencies of taurine and arginine. (Eby & Halcomb 2006)

Flaxseed oil
Flaxseed oil decreases platelet aggregation and increases platelet activating inhibitor-1 and bleeding time. (Prasad K 2009)

Aralia manchurica and Rhodiola rosea
A course of treatment (16 mg/kg orally during 5 days) by Aralia mandshurica or Rhodiola rosea extracts reduced the incidence of ischemic and reperfusion ventricular arrhythmias during 10-min ischemia and 10-min reperfusion. (Maslov et al 2009)

Extract of Aralia exhibits a strong antiarrhythmic effect. (Arbuzov et al 2009)

The antiarrhythmic effect of the adaptogen Rhodiola rosea extract was maximum after 8-day administration. (Maslov & Lishmanov 2007)

Several epidemiologic studies suggested that higher sodium and lower potassium intakes were associated with increased risk of cardiovascular diseases (CVD). Higher potassium intake was associated with lower mortality risk. Our findings suggest that a higher sodium-potassium ratio is associated with significantly increased risk of CVD and all-cause mortality, and higher sodium intake is associated with increased total mortality in the general US population. (Yang et al 2011)

Potassium homeostasis is essential for normal myocardial function, and low serum potassium may cause fatal arrhythmias. In a cohort of ambulatory chronic systolic and diastolic HF patients who were balanced in all measured baseline covariates, serum potassium <4 mEq/L was associated with increased mortality, with a trend towards increased hospitalization. (Ahmed et al 2007)

This paper represents the first description of the use of oral lumbrokinase in the treatment of chronic coronary artery disease with objective assessment using myocardial perfusion imaging. Oral lumbrokinase improves regional myocardial perfusion in patients with stable angina. (Kasim et al 2009)

These data indicated that the anti-ischemic activity of lumbrokinase was due to its anti-platelet activity by elevating cAMP levels and attenuating the calcium release from calcium stores, the anti-thrombosis action due to inhibiting of ICAM-1 expression. (Ji et al 2008)

The Role of Androgens in Atrial Fibrillation
The mechanisms of aging-induced AF have not been fully elucidated, and this may be related to decline of testosterone with advancing age. (Liu et al 2010)

Deficiency of testosterone was arrhythmogenic in rat atria possibly through less binding of FKBP12.6 to RyR2, which could induce feasible calcium leakage from the sarcoendoplasmic reticulum. These results would explain, at least in part, the increase in the prevalence of AF in accordance with the decline of testosterone particularly in elderly men. (Tsuneda et al 2009)

Reduced testosterone levels may be associated with susceptibility to lone AF in men. (Lai et al 2009)

Blood Tests in Atrial Fibrillation and Coronary Heart Disease
Testosterone (see Role of Androgens in Atrial Fibrillation above)

Rationale for the Use of the Above Blood Tests 
hs-CRP – The hs-CRP levels both prior to and after CV predict the long-term risk of AF relapse. In the present study, hs-CRP levels were significantly decreased in patients who remained in sinus rhythm at the end of the study. In contrast, hs-CRP levels remained high throughout the follow-up in patients with an AF relapse. (Celebi et al 2011)

C-reactive protein, IL-6 and IL-8 – The normal levels of C-reactive protein and IL-6, along with the elevated levels of IL-8 in patients with permanent AF but not in those with paroxysmal AF, suggest a link between a low-grade inflammatory reaction and long-lasting AF. The elevated IL-8 levels in the peripheral blood, right atrium, and coronary sinus but not in the pulmonary veins suggest a possible source of inflammation in the systemic circulation. (Liuba et al 2008)

hs-CRP and IL-6  – Patients with AF had elevated levels of inflammatory markers. Low hs-CRP and IL-6 prior to CV are associated with a lower risk of AF recurrence after CV. (Henningsen ete al 2009)

hs-CRP and homocysteine  – Decreases in the hs-CRP of the subjects were directly correlated with the increases in plasma eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and EPA alone and tended to be correlated with decreased plasma tHcy (concentration of total homocysteine). (Carrero et al 2007)

D-dimer – Low TTR (time in the therapeutic range), low %INR (international normalized ratio), and high CV-INR (coefficient of variation of INR values) were found to contribute to high D-dimer levels. (Nakatani et al 2012)

Plasma D-dimer – levels correlated with the embolic risk in mitral valve disease and non-valvular AF. The highest levels were found in patients with MS+AF and non-valvular AF. Severe MR decreased the D-dimer levels in MS and/or AF to control levels. (Cevik et al 2009)

Cardioembolic stroke patients showed increased D-dimer, fibrinogen and D-dimer/fibrinogen ratio. (Alvarez-Perez et al 2011)

Asymmetric dimethylarginine (ADMA) – an analogue of L-arginine, is a naturally occurring product of metabolism found in human circulation. Elevated levels of ADMA inhibit NO synthesis and therefore impair endothelial function and thus promote atherosclerosis. ADMA levels are increased in people with hypercholesterolemia, atherosclerosis, hypertension, chronic heart failure, diabetes mellitus and chronic renal failure.  A number of studies have reported ADMA as a novel risk marker of cardiovascular disease. Increased levels of ADMA have been shown to be the strongest risk predictor, beyond traditional risk factors, of cardiovascular events and all-cause and cardiovascular mortality in people with coronary artery disease. Interventions such as treatment with L-arginine have been shown to improve endothelium-mediated vasodilatation in people with high ADMA levels. However the clinical utility of modifying circulating ADMA levels remains uncertain. (Sibal eet al 2010)

PAI-1 – Stroke or other thromboembolic event in AF patients is associated with impaired lysability of fibrin clots combined with elevated PAI-1, TAFI, sTM, and α2AP. (Zabczyk et al 2011)

IL6 – In patients with short-lasting AF, early AF recurrence seemed to be associated with inflammation as represented by IL-6. (Smit et al 2012)

There is increasing evidence that inflammation and fibrosis may play a major role in initiation and maintenance of atrial fibrillation. Inflammatory markers, interleukin-6 and C-reactive protein, are raised in AF and correlate with the duration of AF, success of cardioversion and thrombogenesis. (Bajpai et al 2008)

In patients with a history of AF, but without significant left ventricular dysfunction or heart failure, inflammatory biomarkers may be raised but are, at best, weak predictors of the risk for first recurrence of AF. (Masson et al 2010)

Acupuncture for Atrial Fibrillation
These preliminary data, observed in 2 small groups of AF patients, need to be validated in a larger population but strongly suggest that acupuncture may be an effective non-invasive and safe antiarrhythmic tool in the management of these patients. (Lombardi et al 2012)

Our data indicate that acupuncture treatment prevents arrhythmic recurrences after cardioversion in patients with persistent AF. This minimally invasive procedure was safe and well tolerated. (Lomuscio et al 2011)

Acupuncture is a safe and effective therapy for conversion of paroxysmal atrial fibrillation and atrial flutter. (Xu & Zhang 2007)

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Compassionate Acupuncture and Healing Arts, providing craniosacral acupuncture, herbal and nutritional medicine in Durham, North Carolina. Phone number 919-309-7753.

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