doctor check a woman's heart rate for signs of Arrhythmias



Last Section Update: 07/2023

Contributor(s): Shayna Sandhaus, PhD; Chancellor Faloon, Health & Wellness Author; Franco Melis

1 Overview

Summary and Quick Facts for Arrhythmias

  • Arrhythmias often occur in people with underlying heart disease; however, even healthy hearts can experience an abnormal rate or rhythm. Some arrhythmias are life-threatening, while others are not directly life-threatening, but can increase the likelihood of a stroke.
  • This protocol will explain the different types of arrhythmias, their causes and how they affect the heart. The important, though sometimes neglected, role of diet and lifestyle considerations in arrhythmia prevention and management will be discussed, and data on a number of scientifically studied natural compounds that may help maintain a healthy heart rhythm will be presented.
  • Conventional arrhythmia treatment strategies rely on pharmaceutical treatment with drugs that may have side effects, electrical synchronization procedures or surgical procedures that work in a certain percentage of patients. There are lifestyle considerations and several natural compounds including magnesium and coenzyme Q10 that have been shown to support a healthy heart and reduce occurrence of arrhythmia.

What are Arrhythmias?

Arrhythmias are irregularities in heart rate or rhythm. They are caused when the electrical signaling in the heart is disrupted. Arrhythmias often occur in people with underlying heart disease; however, even healthy hearts can experience an abnormal rate or rhythm. Some arrhythmias are life-threatening, while others are not directly life-threatening, but can increase the likelihood of a stroke.

“Arrhythmia” is a term that encompasses all kinds of irregularities; they can be classified by whether they slow or speed the heart rate, and which area of the heart is affected. There are many kinds of arrhythmias and they can each require different treatments.

Natural interventions such as magnesium and coenzyme Q10 may support heart health and reduce the risk of arrhythmias.

What are the Risk Factors for Arrhythmias?

  • Underlying heart conditions, including:
    • Coronary artery disease
    • Congestive heart failure
    • Cardiomyopathy
  • High blood pressure
  • Obesity
  • Smoking and alcohol abuse
  • Stress
  • Diabetes
  • Thyroid dysfunction
  • Using stimulants (eg, coffee, certain medications, and drugs like methamphetamine)
  • Participating in performance sports (ie, athletes)

What are the Signs and Symptoms of Arrhythmias?

Note: Many people with arrhythmias do not experience any symptoms. For those who do, symptoms may include:

  • Racing or pounding heart
  • Chest pain
  • Shortness of breath
  • Dizziness, lightheadedness, or fainting
  • Anxiety
  • Reduced capacity for exercise

What are Conventional Medical Treatments for Arrhythmias?

Note: Treatment options will vary depending on the type of arrhythmia. A doctor experienced in managing arrhythmias can determine the best course of treatment.

  • Vagal maneuvers
  • Medications such as sodium-, potassium-, or calcium channel blockers
  • Defibrillation
  • Ablation therapy
  • Implantable devices such as pacemakers
  • Surgery (for serious cases that do not respond to other treatments)

What Dietary and Lifestyle Changes Can be Beneficial for Arrhythmias?

  • Follow a heart-healthy diet (eg, Mediterranean diet)
  • Exercise
  • Maintain a healthy body weight
  • Quit smoking
  • Reduce alcohol and caffeine intake
  • Reduce stress

What Natural Interventions Can be Beneficial for Arrhythmias?

  • Omega-3 fatty acids. Higher levels of omega-3 fatty acids are associated with lower risk of certain arrhythmias. They offer other cardioprotective benefits as well.
  • Magnesium. Magnesium is essential for proper heart function. Symptoms of different arrhythmias can be improved with oral magnesium administration.
  • Potassium. Alterations in serum potassium levels can contribute to the development of arrhythmias. Treatment with intravenous magnesium and potassium may restore normal heart rhythm.
  • Hawthorn. Hawthorn may play a supportive role in cardiovascular health due to several mechanisms, including modulating ion channels. A clinical trial demonstrated hawthorn’s ability to improve heart function and reduce related symptoms.
  • N-acetylcysteine. N-acetylcysteine is an antioxidant that may reduce the incidence of post-operative atrial fibrillation (a type of arrhythmia).
  • Coenzyme Q10 (CoQ10). CoQ10 has been shown to exert therapeutic effects in various cardiac conditions. In patients who had heart attacks, CoQ10 supplementation lowered the occurrence of arrhythmias and improved antioxidant levels.
  • Other natural interventions include vitamins C and E, rhodiola, and resveratrol.

2 Introduction

Arrhythmias are abnormalities in heart rate or rhythm. They arise from disruption of the electrical conduction system within cardiac tissue, which must be properly synchronized to maintain normal heart rhythm. Arrhythmias often occur in people who have some form of underlying heart disease, such as coronary artery disease, but a healthy heart is not immune to abnormal heart rate or rhythm (UoMMC 2012; MayoClinic 2011a; NHLBI 2011a,b).

There are two main categories of arrhythmias: tachycardia, in which the heart beats too fast, and bradycardia, in which the heart beats too slow. Fibrillation, in which the heart beats irregularly or “quivers”, is an important heart rhythm irregularity sometimes classified as a subcategory of tachycardia (UoMMC 2012; Jeong 2012; MayoClinic 2011a; NHLBI 2011a,b; Katz 1999).

Arrhythmias are further classified depending on which part of the heart they affect; the 2 upper chambers of the heart are called atria and the 2 lower chambers are called ventricles (NHLBI 2011b).

Some arrhythmias, such as ventricular fibrillation, can be immediately life threatening because they impact the pumping action of the heart substantially enough to disrupt blood supply to the body, potentially leading to sudden cardiac death, one of the most common causes of death in the United States (Estes 2011; Tung 2012; Chugh 2008; MayoClinic 2011a). Atrial fibrillation is a common type of arrhythmia that is usually not life-threatening in its own right, but can dramatically increase risk of having a stroke because a blood clot can form within the fibrillating atria and then lodge in blood vessel(s) that supply the brain (Narumiya 2003; Schmidt 2011; Prasad 2012). Still other arrhythmias, such as premature ventricular contractions, are fairly common and not usually considered significant health threats (UoMMC 2012; NHLBI 2011b).

Conventional arrhythmia treatment strategies rely on pharmaceutical treatment with drugs that often have potentially serious side effects, electrical synchronization procedures, or surgical procedures that work in a certain percentage of patients.

There are lifestyle considerations and several natural compounds including magnesium and coenzyme Q10 that have been shown to support for a healthy heart and reduce occurrence of arrhythmia (Singh 2007; Weant 2005; Nagai 1985; Baggio 1993; Guerrera 2009; Bachman 2003; Falco 2012; Pepe 2010; Wu 2012).

This protocol will explain the different types of arrhythmias, their causes, and how they affect the heart. Conventional treatment strategies, including medications and procedures, will be reviewed and some promising new antiarrhythmic drugs will be examined. The important, though sometimes neglected role of diet and lifestyle considerations in arrhythmia prevention and management will also be discussed, and data on a number of scientifically studied natural compounds that may help maintain a healthy heart rhythm will be presented.

3 How the Heart Works

The heart consists of four chambers: two upper chambers, called atria, which receive the blood, and two lower ones, called ventricles, which push the blood out from the organ. The atria and ventricles alternately contract and relax to pump blood through the heart and to the rest of the body.

A heartbeat originates as electrical impulses are generated and pass through a pre-determined pathway in the heart. These electrical impulses originate in the sinoatrial (SA) node, which is a small mass of specialized tissue located in the right atrium; it is also known as the heart’s pacemaker. This electrical impulse first causes the atria to contract and squeeze blood into the ventricles. It then passes through the atrioventricular (AV) node and triggers the ventricles to contract, which having just been filled with blood by the contracting atria, pump blood out to the rest of the body (Patterson 2002).

A “normal” range for resting heart rate is approximately 60-100 beats per minute, with evidence suggesting that a heart rate at rest over 80 beats per minute may be cause for possible concern for underlying heart disease. For example, a study published in The Journal of Epidemiology & Community Health followed 50 000 healthy men and women over 20 years and found that for each increase of 10 heart beats per minute, the risk of dying of a heart attack increased 18% among women and about 10% in men (Nauman 2010). Any irregularities in the heart rhythm can affect the efficiency at which the heart pumps blood to the body, and may thereby lead to damage in various tissues and organs (NHLBI 2011a,b).

The normal conduction of electric impulses and normal heart muscle contractions depend on the levels of various electrolytes in the body. Impulses are generated due to the movement of electrolytes through passages called ‘ion channels’ that are present in the heart cells. Sodium, potassium, calcium, and magnesium are the chief ions required for generating electric impulses under normal circumstances. Inadequate levels of these ions prevent the proper formation of impulses, and/or their normal conduction, resulting in the development of arrhythmias. Most anti-arrhythmic drugs act by modulating these ion channels (Sanguinetti 2003).

4 Development of Arrhythmias

Mechanisms by which arrhythmias can develop (Jaeger 2010):

Enhanced or suppressed automaticity. Automaticity is the ability of the heart muscle cells to generate an electrical impulse. All cells in the heart have this capacity, but only certain cells, such as those in SA node, are responsible for generating heartbeats. The SA node is the heart’s natural pacemaker and it determines when an impulse should be fired. Any impulses fired from elsewhere in the heart before or concurrently with SA node firing can lead to premature heartbeats or sustained abnormal heartbeats. This can cause sinus node dysfunction (SND), a term used to describe various types of heart rhythm disorders. Enhanced automaticity, on the other hand, can lead to tachycardia (>100 beats per minute) and several types of atrial and ventricular arrhythmia. Various factors, including electrolyte imbalances, medications, and age can alter automaticity in specific areas of the heart, thereby leading to arrhythmias.

Triggered activity. Triggered activity, the abnormal propagation of electrical activity in individual heart cells, can lead to sustained abnormal heart rhythms (Wit 2007). Arrhythmias due to triggered activity are rare; when they occur, they are often due to problems in the ion channels in the heart muscle cells. They can also occur as a side effect of certain anti-arrhythmic drugs such as digitalis.

Re-entry. Re-entry is a common mechanism for the initiation of tachyarrhythmia (a rapid irregular heartbeat) (Merriam-Webster 2012). This happens when the electrical impulse travels backwards from the ventricles to the atria, initiating another heartbeat while the first heartbeat is still descending into the ventricles.

5 Types of Arrhythmias

Arrhythmias can be classified as follows (NHLBI 2011a):

Premature (Extra) Beats

Premature extra beats are a very common and mostly harmless type of arrhythmia. Those that occur in the atria are called premature atrial contractions (PACs), while those occurring in the ventricles are called premature ventricular contractions (PVCs) (Hebbar 2002b; Cha 2012). Premature atrial contractions have been linked to excess consumption of caffeine and alcohol, the use of sympathomimetic medications (drugs that mimic the effects of sympathetic nervous system signaling molecules called catecholamines), and are sometimes present in people who have structural heart disease (Hebbar 2002b). Premature ventricular contractions are often seen in the presence of structural heart disease, but they can also appear in the absence of any identifiable heart conditions (Cha 2012).

Premature Ventricular Contractions

Premature ventricular contractions (PVCs) are a transient ventricular arrhythmia that can cause the feeling of a “skipped beat” in the chest; they are typically benign in people without structural heart disease. PVCs are fairly common and are estimated to affect 1-4% of the general population, but they are much more common in the elderly, with a prevalence of 69% in individuals older than 75 (Cha 2012; Adams 2012).

Common causes of PVCs include electrolyte imbalance (eg, low levels of magnesium or potassium), ingestion of stimulants (eg, coffee), alcohol, and/ or exercise (Hebbar 2002a; MayoClinic 2011b). While PVCs are typically asymptomatic, they can sometimes cause signs and symptoms such as palpitations, chest pain, and heart failure. However, in the absence of structural heart diseases, PVCs rarely develop into serious arrhythmias (Hebbar 2002a; Cha 2012; Adams 2012).

  • PVC-induced cardiomyopathy is a condition in which the heart becomes enlarged and unable to pump blood efficiently due to very frequent PVCs. This condition is a diagnosis of exclusion, (ie, any underlying heart disease causing frequent PVCs must first be ruled out). A treatment called catheter ablation is performed in patients with over 10, 000-20, 000 PVCs in a 24-hour period. This procedure involves using electrical impulses or extreme cold to destroy the abnormal heart tissue that is causing the PVCs; the intervention usually stops the PVCs (Lee 2012; MayoClinic 2011a; Adams 2012).

Supraventricular Arrhythmias

Supraventricular arrhythmias start in the atria or in the atrioventricular node. Types of supraventricular arrhythmia include atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia, and Wolff-Parkinson-White (WPW) syndrome (Hebbar 2002b; MayoClinic 2011a).

Atrial Fibrillation

Atrial fibrillation is a common type of serious arrhythmia (NHLBI 2011b). The incidence of atrial fibrillation increases with age, with 0.1% of individuals under 55 years and approximately 10% of those over 80 being affected (Schmidt 2011; Go 2001). Post-operative atrial fibrillation, a common form of atrial fibrillation, occurs in 25-40% of patients following cardiac surgery (Gu 2012).

Atrial fibrillation involves the fast and irregular contraction of the atria. In atrial fibrillation, the heart's electrical signals are not initiated in the SA node; instead, they start in another part of the atria or in the nearby pulmonary veins. As the electrical signals do not travel along the normal path, their spread throughout the atria occurs in a rapid and disorganized way. This causes the atria to fibrillate (quiver in an abnormal manner), and blood is not pumped into the ventricles the way it should be (NHLBI 2011b). Atrial fibrillation is usually not life threatening, but can be dangerous if it causes the ventricles to beat very fast (NHLBI 2011b).

Atrial fibrillation has two major potential complications—ischemic stroke and heart failure (NHLBI 2011b; Gutierrez 2011; Knecht 2010).

  • Ischemic stroke may develop due to the incomplete emptying of blood from the atria, which facilitates the formation of blood clots within the heart. These clots, if they travel to the brain, may cause an ischemic stroke. Anticoagulant medications (eg, warfarin [Coumadin®]) are typically used as a stroke-prevention strategy for patients with atrial fibrillation.
  • Heart failure may occur if the heart is unable to pump enough blood to the body. This occurs if the ventricles do not completely fill with blood.

Atrial Flutter

Atrial flutter, another common pathological supraventricular tachycardia, occurs much less frequently than atrial fibrillation. Atrial flutter differs from atrial fibrillation in that the electrical signals move through the atria with a fast, but regular rhythm. Symptoms and complications of atrial flutter are similar to those of atrial fibrillation (NHLBI 2011b; Link 2012).

Paroxysmal Supraventricular Tachycardia

Paroxysmal Supraventricular Tachycardia (PSVT), the most common supraventricular tachycardia, refers to a fast heart rate that occurs from ‘time to time’. Symptoms of PSVT may begin and end suddenly. In PSVT, electrical signals can be transmitted in the reverse direction from the ventricles to the atria, causing extra heartbeats. PSVT may occur as a result of toxicity due to the medication digitalis, or in association with conditions such as Wolff-Parkinson-White (WPW) syndrome.

  • Wolff-Parkinson-White (WPW) syndrome is a type of PSVT wherein the electrical signals travel along an extra pathway from the atria to the ventricles, thereby disrupting the timing of the signals and causing rapid beating of the ventricles. While WPW can be life-threatening, other types of PSVT are typically not life-threatening and can occur without symptoms (Hebbar 2002b; NIH 2012b; Link 2012).

Ventricular Arrhythmias

Ventricular arrhythmias are initiated in the ventricles and represent the most common cause of sudden cardiac death. They can be life-threatening and require emergency medical care. Normally, these arrhythmias occur in patients with structural heart problems, but they may sometimes occur in patients who lack evidence of cardiac disease (Roberts-Thomson 2011).

Ventricular Tachycardia

Ventricular tachycardia is a fast (greater than 100 beats per minute) but regular beating of the ventricles that can last from a few seconds to much longer. While mild episodes may not be life threatening, continued ventricular tachycardia that lasts for more than a few seconds is dangerous and may evolve into ventricular fibrillation, which can be fatal (Hebbar 2002a; NHLBI 2011b). It is important to keep in mind that individuals with ventricular tachycardia may sometimes have minimal symptoms (Compton 2012; MayoClinic 2011a; Piccini 2012; Hebbar 2002a).

Ventricular Fibrillation

As its name suggests, ventricular fibrillation (v-fib) makes the ventricles quiver due to disorganized electrical signals. When this happens, the heart is unable to pump blood to the body and death may occur within minutes. V-fib is treated by using a machine known as a “defibrillator” to deliver an electrical shock to the heart and restore its normal rhythm (NHLBI 2011b).


Bradyarrhythmia, or slow heart rate, is defined in adults as a heart rate of less than 60 beats per minute. This may cause insufficient blood to reach the brain. Except for certain individuals, such as people who are very physically fit, in whom a slower heart rate can be normal, bradyarrhythmias may occur as a result of serious medical conditions (eg, heart attacks), medication(s) (eg, beta-blockers and calcium-channel blockers), hypothyroidism, and electrolyte imbalances in the blood (NHLBI 2011b).

6 Symptoms of Arrhythmias

Approximately one-third of people with arrhythmia do not exhibit any symptoms, preventing their timely diagnosis and treatment. For individuals who do have symptoms, these may include feelings of a racing or pounding heart, chest pain, shortness of breath, dizziness, lightheadedness, anxiety, fainting or near fainting, and reduced capacity to exercise, which can impair the quality of life (Schmidt 2011; NHLBI 2011b). In some cases, symptoms can be dangerous and life-threatening, and may even lead to sudden cardiac death (Sali 2007).

What are palpitations?

Palpitations are sensations or feelings of a racing or pounding heart that may be felt in the chest, neck, or throat (NHLBI 2011c). These may or may not be accompanied by an abnormal heart rhythm (NIH 2012c). Typically they are harmless, and in up to 16% of cases no underlying cause can be found (Abbott 2005; Raviele 2011). Palpitations can result from non-cardiac causes such as anxiety, drug use, low blood sugar, electrolyte imbalance, or fever. Caffeine, alcohol, tobacco, and certain drugs can also lead to palpitations, as can panic attacks. Avoiding these triggers typically resolves the condition (NIH 2012c; WebMD 2012).

When accompanied by dizziness or fainting, palpitations may indicate the existence of a more serious condition, such as tachyarrhythmia. However, most patients with arrhythmias do not report palpitations. Non-arrhythmia causes of palpitations include coronary heart disease and congestive heart failure.

An electrocardiogram can be used help determine the cause of palpitations. In cases where structural heart disease is absent, further monitoring of the heart beat using a Holter monitor (instrument that records the heart rate over a period of 24-48 hours) may be used to make a diagnosis (Abbott 2005).

7 Causes of and Risk Factors for Arrhythmias

Conditions or Events that Affect the Heart

Arrhythmias are frequently associated with conditions or events that affect the structure or function of the heart including (MayoClinic 2011a; NHLBI 2011a; Hebbar 2002a,b; Brown 2010):

  • Coronary artery disease
    • The narrowing of arteries in coronary artery disease can lead to arrhythmias (NHLBI 2011a; Haugaa 2011; MayoClinic 2011c; Ghuran 2011).
  • Congestive heart failure
    • Congestive heart failure (deterioration of the heart’s ability to pump blood) is associated with a high risk of sudden cardiac death from arrhythmia (Nessler 2007; Johns Hopkins 2012).
  • History of heart attack
    • Some form of heart rhythm abnormality is present in over 90% of individuals who have had a heart attack (Hebbar 2002a; Merck Manual 2008).
  • Infectious myocarditis
    • Infections that damage the heart (ie, infectious myocarditis) have been associated with some types of arrhythmia (Friedman 1994; Maury 2008).
  • Cardiomyopathy
    • A damaged or dysfunctional heart muscle (ie, cardiomyopathy) can cause arrhythmias (Nava 1992; Ji 2004).
  • Congenital heart defects
    • Being born with certain heart malformations may lead to disturbances in the heart rhythm (Rekawek 2007; MayoClinic 2011a; Haugaa 2011).

Indirect and Non-Cardiac Risk Factors for Arrhythmias

In addition to inherited and/or acquired structural/functional heart problems, several other risk factors have well-established relationships with arrhythmias. These risk factors (such as cigarette smoking) may beget arrhythmias either by contributing to chronic structural or functional heart abnormalities over time, or temporarily altering the biochemistry of the body in such a way as to trigger a transient arrhythmia (such as from excessive intake of stimulants like caffeine).

  • Imbalance of electrolytes
    • Imbalanced blood levels of electrolytes such as sodium or potassium alter the excitability of the heart muscle and the conduction of the electrical impulses, and may lead to arrhythmias (MayoClinic 2011a).
  • High blood pressure
    • High blood pressure is thought to increase the thickness and stiffness of the left ventricular walls over time, which changes the way in which electrical impulses travel through the heart (MayoClinic 2011a).
  • Obesity
    • Obesity may increase risk of developing arrhythmia and lead to cardiac problems in several ways: it can affect the heart indirectly, by increasing lipid levels, blood pressure, and glucose intolerance, or directly, by increasing the blood volume, which elevates cardiac output and causes thickening of the heart muscle in the left ventricle (Mathew 2008; MayoClinic 2011d).
  • Smoking
    • The mechanisms that explain the link between smoking and arrhythmia are complex. It is thought that nicotine promotes the formation of excess fibrous tissue in the heart and increases susceptibility to stress hormones. Other constituents of tobacco smoke, such as carbon monoxide, along with oxidative stress, appear to play additional roles. Moreover, smoking causes coronary artery disease and chronic obstructive pulmonary disease, which independently predispose to arrhythmia (D’Alessandro 2012).
  • Alcohol abuse
    • Chronic alcohol use may lead to disease/dysfunction of the cardiac muscle and cause the heart to beat less efficiently (Podrid 1987; Witchel 2003; Barnes 2010; MayoClinic 2011a).
  • Stress
    • Acute emotional and psychological stress may trigger potentially deadly arrhythmias (Taggart 2011; Hansson 2004; Ziegelstein 2007).
  • Diabetes
    • Uncontrolled diabetes increases the risk of developing coronary artery disease and hypertension. Also, episodes of low blood sugar may trigger arrhythmia (MayoClinic 2011a).
  • Thyroid dysfunction
    • Atrial fibrillation occurs in 10-15% of patients with hyperthyroidism, and low serum thyroid stimulating hormone (TSH) concentrations are an independent risk factor for atrial fibrillation (Fazio 2004; Jayaprasad 2005).
  • Stimulants
    • Stimulants such as caffeine and certain prescription medications may lead to various types of arrhythmias. Certain illegal drugs, such as methamphetamine and cocaine, may lead to arrhythmias or sudden death due to ventricular fibrillation (MayoClinic 2011a; Hebbar 2002a).
  • Oxidative stress
    • Oxidative stress has been implicated in the development of ventricular tachycardia and fibrillation, particularly in situations wherein the blood supply to the heart is temporarily interrupted and then restored (eg, following a heart attack) (Wolin 2005).
  • Performance sports
    • Athletes are at increased risk for developing atrial fibrillation, a relatively common arrhythmia in the athletic community; it is more frequently seen in middle-aged than young athletes. Autonomic nervous system alterations, systemic inflammation, and increased atrial size are some of the factors thought to be involved (Sorokin 2011; Turagam 2012; Maisel 2003).
  • Certain medications
    • Certain medications including digoxin (Lanoxin®), tricyclic antidepressants, and antipsychotics can sometimes cause arrhythmias (Hebbar 2002a). Other compounds that can induce arrhythmia are some antiemetics, antibacterial agents, anesthetics, and bronchodilators. Even certain anti-arrhythmia medications such as flecainide (Tambocor®), dofetilide (Tikosyn®), and sotalol (Betapace®) may induce or worsen other types of arrhythmia (Podrid 1987; Witchel 2003; Barnes 2010; MayoClinic 2011a).
  • Major surgery
    • The onset of arrhythmic disorders after major surgery is a common complication, particularly in the elderly. Both cardiac and non-cardiac surgeries carry this risk. Local and systemic inflammation, including from sepsis, is one potential cause. Nervous system and hormonal changes after surgical trauma and anesthesia are also suspected causes. Injury to the heart and surrounding tissues during cardiac surgery, effects of medications, and electrolyte disturbances may also play a role. Most postoperative arrhythmias occur in the first four days after surgery, but can last much longer. Atrial fibrillation is the most common type, and is predictive of further cardiovascular complications, though ventricular arrhythmias can also occur. Pre-existing structural heart disease predisposes to development of post-surgical arrhythmia (Peretto 2014; Walsh 2007; Koshy 2019; Sigmund 2017).

8 Diagnosis

Cardiac arrhythmias can be diagnosed in a physician’s office. By studying the characteristic wave pattern of a series of heartbeats, physicians can determine what kind of arrhythmia is present. The most common diagnostic tool is the electrocardiogram (ECG or EKG) (NHLBI 2011b).

Diagnosis may include one or more of the following:

History and physical examination. The presence of heart disease or a history of heart disease, thyroid problems, or high blood pressure in the patient or in family members is associated with increased risk; family history of sudden death, diabetes, or other illnesses also increases risk (NHLBI 2011b). Listening to the heart and measuring the rate and rhythm of the heartbeat, listening for heart murmurs, checking for swelling in the feet, and taking the pulse can all aid in the diagnosis of arrhythmias (NHLBI 2011a).

Electrocardiogram (ECG or EKG). The ECG is a test that detects and records the heart’s electrical activity (MayoClinic 2011a).

  • An ECG may be performed at a doctor’s office; however, in case the arrhythmia is intermittent, a portable ECG monitor (eg, Holter monitor) that is attached to the patient may be employed. The Holter monitor can record the heart’s electrical signals for a period of 24-48 hours, after which the doctor may be able to detect the arrhythmia and reach a diagnosis (Abbott 2005).
  • Another ECG monitoring method is an implantable loop recorder, a device that performs continuing ECG monitoring and can detect abnormal heart rhythms. The device is placed under the skin on the left chest area through minor surgery performed under local anesthesia. It can be used for as long as 12-24 months and allows prolonged continual monitoring (Cumbee 1990; Parry 2010; NHLBI 2011b; Edvardsson 2011).

Intracardiac electrophysiology study (EPS). EPS is a procedure used to test the heart’s electrical system. It is typically used in cases of serious arrhythmia to pinpoint the location and cause of the arrhythmia and to plan the therapeutic strategy. EPS involves directing a thin, flexible wire through a vein in the upper thigh/groin or arm to the heart to record the heart’s electrical signals (NHLBI 2011b).

Echocardiography. Echocardiography is a test that uses sound waves for the dynamic visualization of the heart and to observe the flow of blood. It can provide information about the size and shape of the heart and its chambers and valves, and it can identify heart areas that do not function normally (such as areas with poor blood flow, areas that are not contracting normally, or areas with previous injury) (NHLBI 2011b).

Stress test. Some arrhythmias are triggered or worsened by exercise, and certain heart problems are easier to diagnose when the heart is working hard. The stress test involves testing for arrhythmias while the patient is exercising on a treadmill or a stationary bicycle. In patients who have difficulty exercising, the test involves being injected with a drug, such as adenosine, to stimulate the heart to mimic exercise. Heart activity is monitored during the test (Faulds 1991; MayoClinic 2011a; NHLBI 2011b).

Coronary angiography. This procedure uses dye and X-rays to visualize the inside of the coronary arteries (NHLBI 2011b).

Tilt table test. This test is recommended in patients who have fainting spells. Heart rate and blood pressure are measured while the patient is lying flat on a table. Subsequently, the table is tilted, and the heart and nervous system are monitored during the change in the angle (MayoClinic 2011a).

Blood tests. Thyroid hormone and electrolyte levels may be measured as abnormal levels are associated with increased risk of arrhythmia (NHLBI 2011b).

Electromechanical wave imaging – a novel diagnostic technique

Electromechanical wave imaging (EWI) is a newer non-invasive technique based on ultrasound imaging that can map the electrical circuitry of the heart. Unlike previously available diagnostic techniques, EWI can detect minute changes/deformations in the heart and be performed with real-time feedback. Moreover, this technique is adaptable to already existing ultrasound imaging machines (Provost 2011b).

A study conducted on mice demonstrated the feasibility of EWI use as a non-invasive technique to visualize the electrical circuitry of the heart and enable the early detection of arrhythmias (Konofagou 2010; Provost 2011a). Additional exploratory experiments showed that EWI may be viable for mapping heart rhythms in canines and humans (Konofagou 2012; Provost 2011a).

EWI technology may enable doctors to precisely evaluate arrhythmias in real time, diagnose them, and design treatments appropriate for each patient (Provost 2011a).

9 Conventional Treatment Strategies

Several strategies are available for treating arrhythmias, and the approach varies depending on the type of arrhythmia. For bradycardia, or slow heart rate, a pacemaker can be implanted to help ensure the heart beats quickly enough. Tacchycardias (fast heart rate) and fibrillations (irregular heart rate) can be treated with medications to slow the heart rate. A procedure called cardioversion uses electrical current, either synchronized or unsynchronized (defibrillation) with the cardiac cycle, to treat abnormally fast heart rate (tachyarrhythmia) or uncoordinated & irregular electrical activity in the heart (fibrillation). Another treatment option involves ablation of portions of heart tissue from which improper electrical signals are originating. In addition, since atrial fibrillation increases ischemic stroke risk, anticoagulant medications such as warfarin (Coumadin®) or dabigatran (Pradaxa®) are used to prevent blood clot formation in people with this arrhythmia (Gallego 2012; Ho 2012; MayoClinic 2011a).

This section will outline several arrhythmia treatment considerations:

Vagal Maneuvers

It may be possible to stop an arrhythmia that begins above the ventricles by using vagal maneuvers that affect the vagus nerve, which is a part of the nervous system responsible for controlling the heartbeats. Some examples of these maneuvers, which often cause the heart rate to slow, include holding your breath and straining (Valsalva maneuver), dunking your face in icy water, and coughing; a physician may be able to recommend other maneuvers to slow down a fast heartbeat (NHLBI 2011b).


Arrhythmias can be treated with a variety of medications. The type of arrhythmia present and the unique characteristics of each patient determine which type of drug should be used and how. Because the clinical assessment of arrhythmias and the algorithm that physicians employ to determine the best pharmacologic treatment strategy is complex, this protocol will not discuss all of the specific roles of drugs in the various types of arrhythmias. Rather, we will outline the basic classification of drugs that may be utilized as part of pharmacologic arrhythmia management. Individuals with any type of arrhythmia should consult with a physician experienced in arrhythmia management to be properly evaluated and treated.

A classification method called the Vaughan-Williams system is widely used to categorize antiarrhythmic agents based on their effects on the electrophysiological system of the heart. This classification system characterizes antiarrhythmic drugs as follows (Weirich 2000; Ganjehei 2011; Homoud 2008):

Class I agents: Sodium-Channel Blockers. Class I antiarrhythmic agents are further subclassified as class IA, IB, or IC agents depending on how strongly they block sodium channels. Examples of class I agents include procainamide (Procanbid®), disopyramide (Norpace®), and flecainide (Tambocor®).

Class II agents: Beta-Adrenergic Blockers or “Beta-Blockers”. Some common beta-blockers are carvedilol (Coreg®), metoprolol (Lopressor®), and propranolol (Inderal®).

Class III agents: Potassium-Channel Blockers. Drugs in this class include sotalol (Betapace®), dofetilide (Tikosyn®), and ibutilide (Corvert®).

Class IV agents: Calcium Channel Blockers. A few common drugs that fall into this category include amlodipine (Norvasc®), diltiazem (Cardizem®), verapamil (Calan®).

Other agents: There are several antiarrhythmic drugs whose mechanisms are complex and/or not fully understood; they are usually grouped into this category. One frequently used drug that falls into this category is digoxin (Campbell 2001).

It should be noted that the Vaughan-Williams System has some considerable limitations because some drugs – such as amiodarone (which is typically considered a class III agent) for example – exhibit actions characteristic of more than one Vaughan-Williams class (Schmidt 2011). Therefore, physicians cannot rely solely on classification of antiarrhythmic agents in this manner when determining the best drug strategy for each patient.

Newer alternatives to amiodarone – budiodarone and dronedarone

Amiodarone (Cordarone®) is one of the most frequently used antiarrhythmic agents because it effectively treats potentially deadly ventricular arrhythmias; it is also used in the management of atrial fibrillation (Siddoway 2003; Singh 2005). However, it can cause some serious side effects, including the development of fibrous tissue in the lungs and thyroid dysfunction (Maseeh uz 2012; Van Herendael 2010). Therefore, a drug capable of delivering similar efficacy with less side effects would be a promising antiarrhythmic agent (Morey 2001).

One reason that amiodarone can cause significant side effects is that it remains in the body for a long time (ie, it has a very long half-life) and can build up in tissues (Morey 2001; Mason 2009).

Budiodarone and dronedarone (Multaq®) are similar to amiodarone in both chemical structure and mechanism of action. However, they are metabolized more quickly than amiodarone, potentially resulting in less tissue accumulation and side effects (Mason 2009). Dronedarone was approved by the Food and Drug Administration (FDA) in 2009 for atrial fibrillation and atrial flutter; budiodarone is still undergoing trials as of the time of this writing (FDA 2009; Ezekowitz 2012).

Clinical trials and data analyses have shown that both of these new drugs have efficacy and side effect profiles comparable or superior (at least in some aspects) to amiodarone.


In a comprehensive analysis of data from 4 trials involving nearly 6000 subjects with atrial fibrillation, treatment with dronedarone significantly reduced stroke risk compared to placebo treatment (Dagres 2011). In another analysis, this time grouping data from 39 atrial fibrillation treatment trials, dronedarone was again shown to reduce stroke risk and produce fewer arrhythmic events than amiodarone, and amiodarone was shown to be associated with a higher mortality rate than dronedarone. However, dronedarone was not as efficacious at preventing recurrence of atrial fibrillation as amiodarone (Freemantle 2011).

Dronedarone is associated with increased risk of cardiovascular death, stroke, and heart failure in patients with permanent atrial fibrillation (ie, those who cannot be converted to normal heart rhythm). Therefore, the FDA does not advise that doctors prescribe dronedarone to this population (FDA 2011).


In a 12 week study, patients with atrial fibrillation and a previously implanted pacemaker who stopped taking antiarrhythmic agents for a period sufficient to “wash out” the drug from their systems were treated with budiodarone for 12 weeks. In the group receiving the highest dose of the drug (600 mg twice daily), atrial tachycardia / atrial fibrillation was reduced by 74% (Ezekowitz 2012).

Although more studies are needed before dronedarone and/or budiodarone can be asserted as unequivocally superior or inferior to amiodarone, data so far suggest that these agents may become an important treatment consideration for select arrhythmia patients.

Electrical Cardioversion

In some cases of arrhythmia, cardioversion (ie, the process of delivering an external electrical jolt through the chest to the heart) may be utilized to reset the heart to its normal rhythm. The machine used to deliver the electrical current is called a defibrillator (Hebbar 2002a; Shea 2008; Sucu 2009).

Ablation Therapy

Another technique often employed to treat arrhythmias is catheter ablation. This procedure involves the insertion of a thin wire catheter into a blood vessel in the groin, arm, or neck, which is then guided to the heart. Radiofrequency energy is then delivered through the wire to generate heat and destroy (ablate) small sections of tissue in the heart responsible for triggering the arrhythmia (Davoudi 2012). Other ablation techniques include application of extreme cold (ie, “cryoablation”) or high frequency ultrasound through the catheter to destroy the arrhythmogenic tissue (Narayan 2012; Joseph 2012).

Implantable Devices

Treatment for heart arrhythmias may also involve the use of an implantable device. Several types of such devices are currently available.


A pacemaker is an implantable, battery-operated device that is used in cases of slow or irregular heart rate. Implanting a pacemaker involves surgically placing the device under the skin, near the collarbone. An insulated wire connects the device to the right side of the heart, where it is permanently anchored. In cases of slow or abnormal heart rhythms, the device emits an electrical signal that stimulates the heart to beat at a normal rate. The device typically remains in a “switched off” mode when the heartbeat is normal (NHLBI 2011a; ExitCare 2012).

Implantable Cardioverter-Defibrillator

In ventricular fibrillation, which is a potentially life-threatening disorder, an implantable cardioverter-defibrillator (ICD) may be placed near the left collarbone, similarly to a pacemaker. The ICD does not turn off and monitors heart beats continuously. It acts as a pacemaker in cases of bradycardia and sends high-energy electrical impulses to reset the heart in cases of ventricular fibrillation or tachycardia (Estes 2011; Vlay 2009; NHLBI 2011a).

Surgical Treatments

In some cases, surgery may be the recommended treatment for heart arrhythmias.

Maze Procedure

This procedure involves making surgical incisions in the atria, which heal into carefully placed scars that force cardiac electrical impulses to travel along a preset pathway and cause the heart to beat efficiently. The resulting scars form boundaries and create a ‘maze’ for electrical impulse to travel along. Rather than using a scalpel, scars can be created by using a ‘cryoprobe’ to apply extreme cold or a radiofrequency device that applies heat. Since this procedure requires open-heart surgery, it is typically reserved for patients who do not respond to other types of treatment (Nakamura 2012; MayoClinic 2011a).

Coronary Bypass Surgery

Coronary bypass surgery or coronary artery bypass graft (CABG) is performed in cases of severe coronary artery disease with frequent ventricular tachycardia. This procedure may help improve the blood supply to the heart and reduce the frequency of ventricular tachycardia (MayoClinic 2011a).

Stroke Prevention in Atrial Fibrillation

A major potential complication of atrial fibrillation is ischemic stroke that occurs as a result of blood stagnating and clotting in the fibrillating atria (Manning 2022). The blood clot can then travel to the brain and lodge in a blood vessel, causing an ischemic stroke (Kamel 2016; Kamel 2017). Therefore, anticoagulant medications, which reduce the likelihood of blood clots forming, are an important stroke-prevention strategy in patients with atrial fibrillation (Manning 2022). (Concomitant treatment with anticoagulants and antiplatelets is not recommended for most patients as dual therapy significantly increases the risk of major bleeding) (American Academy of Family Physicians 2017).

Without anticoagulants the rate of ischemic stroke in patients with atrial fibrillation ranges from 1‒20% per year. In an analysis of five primary prevention trials, adjusting the dose of warfarin (an anticoagulant) reduced the annual stroke rate from 4.5% in control patients to 1.4% in patients assigned to adjusted-dose warfarin (Alshehri 2019).

Atrial fibrillation patients are stratified according to their stroke risk (generally measured via CHADS2 or CHA2DS2-VASc score), and for those with an increased stroke risk oral anticoagulants are strongly recommended (American Academy of Family Physicians 2017; American College of Cardiology 2019; Manning 2022). Most cardiovascular medicine authorities, including the American College of Cardiology, recommend direct oral anticoagulants (DOACs) over vitamin K antagonists like warfarin or antiplatelets such as aspirin. While warfarin has been shown to reduce the risk of stroke and all-cause mortality, it has a very narrow dosage range within which it is effective as an anticoagulant. Below this range the compound is ineffective, and above these levels it is extremely toxic; therefore, patients on warfarin must be closely monitored (American Academy of Family Physicians 2017).

Direct oral anticoagulant drugs include dabigatran, apixaban (Eliquis), rivaroxaban (Xarelto), and edoxaban (Savaysa), all of which inhibit components of the blood coagulation cascade. Dabigatran inhibits a coagulation factor called thrombin, while the other three are direct inhibitors of factor Xa, a component of the coagulation cascade (American Academy of Family Physicians 2017). In multiple meta-analyses of randomized controlled trials, DOACs have been shown to be superior or noninferior to warfarin, with a generally superior safety profile and in a broad range of patient populations, for reducing stroke risk (Connolly 2009; Granger 2011; Patel 2011; Giugliano 2013; Wang 2021).

Advantages of DOACs versus warfarin include (Leung 2021; Wolters Kluwer 2022; Mekaj 2015; López-López 2017):

  • Rapid onset of action; rapid clearance from body
  • Predictable pharmacological properties
  • Wide safe and effective dosage range
  • Lower potential for drug and food interactions
  • No requirement for anticoagulant blood test monitoring
  • Efficacy and safety advantages (or at least noninferior)
  • No need for dietary restriction to maintain low vitamin K levels, which may confer a risk of bone fracture, particularly in patients with preexisting osteoporosis

Disadvantages of DOACs versus warfarin include:

  • Rapid clearance necessitates more frequent dosing of some DOACs; warfarin is available in a once-daily dosage
  • Warfarin is typically less expensive than DOACs, although apixaban has been thought to be equally cost-effective (taking into account adverse effects and efficacy)
  • Must be used especially carefully in patients with chronic kidney or severe liver disease
  • Dose titration generally not available, and has not been validated

Unfortunately, randomized trials directly comparing the efficacy and safety of different DOACs have not been conducted and are considered unlikely in the near future (Link 2021). Therefore, clinician preference, economic considerations, and use of indirect comparison by means of network meta-analysis and real-world observational or retrospective studies must determine the choice of DOAC (López-López 2017; Ganse 2020; Okushi 2021). However, a large retrospective cohort study found that treatment with rivaroxaban was associated with a significantly higher risk of major ischemic or hemorrhagic events compared with apixaban (Ray 2021). Similarly, a cohort study published in late 2022 showed that apixaban was associated with lower relative risks of ischemic stroke or blood clots than rivaroxaban among people with atrial fibrillation and valvular heart disease (Dawwas 2022). Although there is not unanimity in the field, multiple analyses have also ranked apixaban ahead of or equal to other DOACs for safety and effectiveness (Link 2021; López-López 2017; Ganse 2020; Okushi 2021). Still, the choice of which DOAC agent to use in preventive anticoagulant therapy in patients with atrial fibrillation must ultimately be made on a case-by-case basis. Rigorous randomized direct comparison trials are necessary to fully establish the correct indications for drugs in this class (López-López 2017; Tritschler 2019).

10 Alternative Therapies & Dietary and Lifestyle Considerations


Acupuncture refers to a procedure involving stimulation of a variety of points on the body using needles that are inserted manually (NCCAM 2012). A study that enrolled 80 patients with persistent atrial fibrillation was conducted to evaluate whether acupuncture treatment had any effects on recurrence rates and whether it was able to prevent arrhythmias. After patients had their normal heart rhythms restored via cardioversion, they were treated with amiodarone (Cordarone®), acupuncture, sham-acupuncture (a procedure wherein acupuncture needles are inserted into the “wrong” points), or given no treatment. The results revealed that recurrence rates were lower in the acupuncture group (35%) than the sham (69%) or control (54%) groups (Lomuscio 2011). The recurrence rates in patients treated with amiodarone were 27%. Analysis of data from 8 separate studies showed that 87-100% of participants converted to normal heart rhythm after acupuncture treatment (VanWormer 2008).

Mediterranean Diet

The Mediterranean diet has been shown to provide cardioprotective effects. A study conducted in 2011 sought to study the relationship between this type of diet, vitamin intake, and the incidence of arrhythmias. The study recruited 800 subjects, 400 of which had detected their first episode of atrial fibrillation. Low adherence to this diet was associated with the development of atrial fibrillation, and high adherence with spontaneous conversion back to normal electrical impulses in the heart. While further studies in a larger population are required to corroborate these findings, high adherence to a Mediterranean diet may potentially prevent atrial fibrillation episodes (Mattioli 2011).

Lifestyle Changes

Other lifestyle measures that may reduce risk of arrhythmia include (Pepe 2010; Park 2009; Mattioli 2011):

  • Adequate exercise (Shea 2008)
  • Maintaining a healthy body weight (Fuster 2011; Tedrow 2010)
  • Quitting smoking (Chamberlain 2011; Shea 2008)
  • Cutting back on caffeine (Fuster 2011; Mattioli 2008, 2011; Shea 2008)
  • Cutting back on alcohol (Shea 2008; Fuster 2011; Kodama 2011)
  • Reducing stress (Magri 2012; Shea 2008)
  • Avoiding stimulant medications (eg, pseudoepinephrine) (Shea 2008)

11 Nutrients

Omega-3/Fish Oil

The omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are important health-promoting lipids found in certain fish and seafood as well as some marine plant sources (Lavie 2009; Kromhout 2011). In addition to their well-known anti-inflammatory effects, EPA and DHA may also have anti-arrhythmic properties, and have been found in multiple studies to benefit heart disease patients by improving lipid levels, lowering blood pressure, and reducing the risk of sudden death (Colussi 2018; Siscovick 2017). Omega-3 fatty acids may help regulate heart rhythm by normalizing sodium and calcium channel function in heart muscle cell membranes, thereby stabilizing electrical activity in the heart (Glück 2016).

In a randomized crossover trial (in which subjects participated in both treatment and placebo groups in separate phases in random order) that included 87 patients with implanted cardioverter defibrillators, supplementing with 3.6 grams EPA plus DHA per day for six months reduced the number of ventricular arrhythmia episodes. The average number of episodes was 1.7 during the EPA plus DHA phase versus 5.6 during the placebo phase (Weisman 2017). Another trial in 115 heart attack patients found 1.8 grams EPA daily for one month, beginning one day after the heart attack, reduced the likelihood of ventricular arrhythmia: the incidence of ventricular arrhythmia was 7.0% in the EPA group and 20.6% in the control group (Doi 2014). A controlled trial in 80 patients with known heart disease already using anti-arrhythmic drugs found adding 1 gram of omega-3 fatty acids daily for six months further reduced the number of ventricular arrhythmia events (Gavva 2012).

Omega-3 Fatty Acids and Atrial Fibrillation

The effects of omega-3 fatty acid supplementation on atrial fibrillation risk appears to be more complex (Curfman 2021). A report from an ongoing observational study that included data from 6,546 participants who had no cardiovascular disease at the beginning of the study found those with higher baseline levels of DHA, but not EPA or EPA plus DHA, were less likely to develop atrial fibrillation over a median of 14 years of monitoring (Kapoor 2021). In a meta-analysis that included nearly 55,000 participants published in 2023, higher blood or adipose tissue omega-3 fatty acid levels were not associated with an increased risk of atrial fibrillation. In fact, higher levels of docosapentaenoic acid (DPA), DHA, and EPA plus DHA were associated with reductions in risk for atrial fibrillation (Qian 2023). On the other hand, some clinical evidence suggests taking EPA or EPA plus DHA supplements may increase atrial fibrillation risk. A meta-analysis of five randomized placebo-controlled trials with a combined total of more than 50,000 participants, all of whom had established or high risk of cardiovascular disease, found omega-3 fatty acid supplementation was associated with a 29% increased incidence of atrial fibrillation, despite reducing the risk of cardiac events in some trials (Lombardi 2021). It is important to note that the trials in the meta-analysis were designed to identify a relationship between omega-3 fatty acid supplementation and major cardiovascular events (eg, heart attack, stroke, heart failure, and cardiovascular death), and atrial fibrillation incidence was reported as a secondary or tertiary outcome.

One trial included in the analysis included 8,179 participants with established or high risk of cardiovascular disease and compared 4 grams of a specialized icosapent ethyl formulation of EPA (with no DHA) daily with a mineral oil placebo. During a median of 4.9 years of monitoring, incidence of cardiovascular events was significantly lower in those receiving EPA, but the risk of atrial fibrillation was noted to be higher (5.3% vs. 3.9%) (Bhatt 2019). Another trial in the analysis that included 13,078 participants found 4 grams daily of a specialized carboxylic acid formulation of EPA plus DHA had no effect on cardiovascular events compared with a corn oil placebo, but was linked to an increased rate of reports of new atrial fibrillation (2.2% vs. 1.3%) (Nicholls 2020). In a third trial, 12,513 participants were given 1 gram of omega-3 fatty acids daily in their naturally occurring ethyl ester form or an olive oil placebo and followed for a median of five years. The ratio of EPA:DHA in the supplement ranged from 0.9:1 to 1.5:1. No significant difference was found in the occurrence of atrial fibrillation between groups; in women, hospitalization or death due to cardiovascular events was reduced (Roncaglioni 2013). The two other trials in the analysis found non-statistically significant increases in atrial fibrillation with combinations of EPA plus DHA, at doses of 1.8 grams and 840 mg per day, and no significant effects on risks of cardiovascular events (Nicholls 2020; Kalstad 2021; Bowman 2018).

In contrast, a randomized controlled trial including 25,119 participants aged 50 years and older without cardiovascular disease found 840 mg omega-3 fatty acids (460 mg EPA plus 380 mg DHA) daily in their ethyl ester form did not impact the incidence of atrial fibrillation compared with a corn oil placebo during a median of 5.3 years of follow-up (Albert 2021). Furthermore, a meta-analysis of 14 randomized controlled trials with a total of 3,570 participants found supplementing with EPA plus DHA reduced the risk of post-operative atrial fibrillation after cardiac surgery compared with usual care, but not compared with other oils, and only when the dose of DHA was higher than the dose of EPA (Wang 2018).

Further research is needed to explore the possible protective role of DHA, and establish optimal doses, forms, and ratios of omega-3 fatty acids to prevent or treat atrial fibrillation and identify characteristics of patients most likely to benefit from omega-3 fatty acid supplementation. Until more is known, Life Extension recommends older patients with a history or high risk of atrial fibrillation use only marine omega-3 fatty acid formulations that include DHA and use moderate amounts (less than 4 grams daily).

Magnesium and Potassium

As both magnesium and potassium are intricately involved in the heart’s electrical stability, maintaining normal functional blood levels and ratios of each of these ions is important. Low concentrations of magnesium and potassium in the body are associated with increased risk of developing ventricular arrhythmias (Sultan 2012).


Magnesium deficiency may result in congestive heart failure, hypertension, and angina (Guerrera 2009). The American Heart Association recommends administering magnesium sulfate intravenously (up to 2 grams in 2 minutes) to treat some types of ventricular tacharrhythmia. Oral magnesium oxide (15 mg/kg) added to a regimen of beta-blockers helped to improve some markers of imminent ventricular tachyarrhythmia, even in cases where the beta-blockers failed to make a difference on their own (Bachman 2003). Additionally, oral magnesium (3 grams daily for 30 days) improved symptoms of premature ventricular and supraventricular complexes in 93.3% of patients taking magnesium as compared with only 16.7% of patients administered placebo (Falco 2012).


Potassium is important for the maintenance of cardiac electrical stability, and alterations (deficiency or excess) in serum potassium levels, such as can be induced by diuretic drugs, can contribute to the development of cardiac arrhythmias (Zaza 2009; Abdel-Qadir 2010; Berkova 2012). Assessing potassium levels via blood testing and increasing potassium intake via supplementation if levels are found to be low is an arrhythmia treatment consideration. In a study that enrolled 170 patients with symptomatic persistent atrial fibrillation, pre-treatment with intravenous potassium/magnesium improved the success rate of achieving conversion to a normal heart rhythm (Sultan 2012).


Hawthorn is a fruit-bearing shrub whose constituents have been used since the 1800s to support cardiovascular health (Edwards 2012). Modern scientific inquiry has shown that hawthorn is rich in several antioxidant compounds such as flavonoids and anthocyanins, and that it may play a supportive role in several cardiovascular diseases (Rigelsky 2002; Chang 2005; Edwards 2012). It is thought that hawthorn supports heart and vascular health via modulation of ion (eg, potassium and calcium) channels, blood flow, inflammation, and oxygen utilization, as well as by scavenging damaging free radical molecules, which cause oxidative stress (Rigelsky 2002; Tadic 2008).

In an animal model, infusions of hawthorn extracts reduced the number of arrhythmias compared to a control infusion following experimental deprivation and subsequent reinstitution of blood supply to the heart (“ischemia/ reperfusion”), a paradigm that mimics some of the effects of a heart attack (Garjani 2000). In another similarly designed animal model, long-term supplementation with a standardized hawthorn extract was associated with 6-fold fewer incidence of potentially deadly ventricular fibrillation following deprivation and subsequent reinstitution of blood flow to the heart (al Makdessi 1999). A 24-week long human clinical trial involving over 1000 patients with heart failure found that hawthorn supplementation improved heart function and reduced symptoms such as fatigue and palpitations. Supplementation also increased the amount of time subjects’ heart rhythms remained normal (Tauchert 1999).

Vitamin D and Atrial Fibrillation

The role of vitamin D in the health and function of the cardiovascular system is complex, and scientists’ understanding of the potential of vitamin D supplementation to support cardiovascular health is evolving (Carbone 2023; Cosentino 2021). With regard to heart rhythm abnormalities, and atrial fibrillation more specifically, preclinical research indicates there may be a link to vitamin D. For instance, activation of the vitamin D receptor on animal ventricular heart cells improves the action of their potassium channels, which may reduce the risk of atrial fibrillation by modulating the excitability of the heart (Tamayo 2018).

In humans, there is some evidence suggesting that avoidance of vitamin D deficiency as well as vitamin D supplementation may be associated with a normal heart rhythm. Several observational studies have shown that vitamin D deficiency (defined as < 20 ng/mL) is associated with an increased risk of developing atrial fibrillation (Liu 2019). However, the evidence from controlled interventional trials involving vitamin D supplementation is mixed.

In 2022, a randomized-controlled trial evaluated the risk of cardiovascular disease and cancer in 2,495 Finnish men and women (average age 68 years). The participants supplemented daily with 1,600 IUs (40 mcg) or 3,200 IUs (80 mcg) vitamin D or placebo for five years (Virtanen 2022). Although those who supplemented with 3,200 IUs (80 mcg) daily had slightly less major cardiovascular events compared with the other groups, the trial failed to show any significant differences between both vitamin D groups and placebo. In 2023, a secondary analysis of the trial data was conducted to retrospectively evaluate the risk of atrial fibrillation among the participants (Virtanen 2023). Compared with placebo, those who received 1,600 IUs (40 mcg) and 3,200 IUs (80 mcg) vitamin D experienced a 27% and 32% risk reduction, respectively. However, because atrial fibrillation was not a prespecified endpoint in the initial randomized-controlled trial, the results should be interpreted with caution. Moreover, other confounding factors were not accounted for. More research is needed to understand vitamin D’s role in atrial fibrillation.

In contrast, in 2021, a randomized-controlled trial that evaluated the effects of supplementation with 2,000 IUs (50 mcg) vitamin D daily on atrial fibrillation risk over a 5.3-year period did not show significant benefits compared with placebo (Albert 2021).

Vitamin D and Post-Operative Atrial Fibrillation

Coronary artery bypass grafting is a procedure used to treat coronary artery disease wherein veins or arteries obtained from other parts of the body are used to bypass narrowed heart arteries. About 11–40% of people who undergo this procedure develop atrial fibrillation (Filardo 2009).

A randomized-controlled trial evaluated the effects of high-dose bolus vitamin D supplementation on the occurrence of post-operative atrial fibrillation after coronary artery bypass grafting. The study was conducted on 116 patients who had vitamin D deficiency (defined as < 21 ng/mL) or insufficiency (defined as 21-29 ng/mL) prior to surgery. Participants were divided equally into two groups to receive either vitamin D or serve as a control. Forty-eight hours before surgery, participants in the vitamin D group received supplemental vitamin D according to their baseline vitamin D status: 300,000 IU (7,500 mcg) if vitamin D deficient or 150,000 IUs (3,750 mcg) if vitamin D insufficient. Five days after surgery, the number of cases of atrial fibrillation was seven in the vitamin D group and 16 in the control group, a statistically significant difference. These results suggest that high-dose vitamin D before coronary artery bypass grafting may reduce the risk of post-operative atrial fibrillation among patients with vitamin D deficiency or insufficiency at baseline (Kara 2020). More randomized controlled trials, including those with larger sample sizes, are needed to clarify the role of pre-operative vitamin D supplementation in reducing the risk of atrial fibrillation after coronary artery bypass grafting.


Oxidative stress and inflammation have been implicated in the development of atrial fibrillation, and this is particularly true in the case of post-operative atrial fibrillation (Ozaydin 2008). Various studies have attempted to determine the usefulness of antioxidants in the treatment of atrial fibrillation (Rasoli 2011).


The beneficial effects of N-acetyl-cysteine (NAC) treatment are attributed to its antioxidant and anti-inflammatory properties (Ozaydin 2008). Since oxidative stress has been implicated as a factor in post-operative atrial fibrillation, various trials have tried to assess the effectiveness of N-acetyl-cysteine (NAC) in preventing the condition. An analysis of data from 8 separate trials that included a combined population of over 500 patients concluded that NAC supplementation may effectively reduce the incidence of post-operative atrial fibrillation (Gu 2012). In a trial conducted to study the effects of NAC treatment on post-operative atrial fibrillation, intravenous infusion of NAC was compared to a group receiving saline infusion. Post-operative atrial fibrillation was found in only three patients from the NAC-treated group, as compared with 12 patients from the saline group (Ozaydin 2008).

Vitamins C and E

Vitamins C and E may also exert a protective effect against post-operative atrial fibrillation by virtue of their antioxidant properties. An analysis of data from 5 clinical trials that examined a total of 567 patients demonstrated that vitamin therapy caused a significant reduction in the incidence of post-operative atrial fibrillation and all-cause arrhythmia. This effect was independent of the type of surgery. There is also evidence of a synergistic effect between antioxidant vitamins and beta-blockers (Harling 2011). A separate study that enrolled 100 patients undergoing bypass surgery showed that a combination of oral vitamin C (2 grams on the night prior to surgery and 2 grams daily for 5 days thereafter) and a beta-blocker was more effective in preventing post-operative atrial fibrillation than the beta-blocker treatment alone. The incidence of post-operative atrial fibrillation was only 4% in the vitamin C group as compared with 26% in the control group (Rodrigo 2010). Vitamin C treatment showed similar benefits in another study where a group of 44 patients receiving standard treatment following conversion to normal heart rhythm received either vitamin C or no additional treatment. Atrial fibrillation recurred in only 4.5% of the patients in the vitamin C group, as compared with 36.3% of the patients who did not receive any treatment (Korantzopoulos 2005). Similarly, pre-operative treatment with vitamin E for 28 days followed by vitamin C on days 27-29 reduced the incidence of arrhythmias in a group of 37 patients undergoing bypass surgery (Rasoli 2011).


Resveratrol is a polyphenol found in grapes and Japanese knotweed (Polygonum cuspidatum) with antioxidant and anti-inflammatory properties. An animal model revealed that resveratrol can attenuate inflammatory responses and oxidative stress after myocardial infarction, which can lead to decreased inducibility of ventricular arrhythmias (Xin 2010). A pre-clinical study revealed that resveratrol treatment significantly suppressed myocardial infarction-induced ventricular arrhythmias and improved long-term survival. Resveratrol acts by a variety of mechanisms, and exerts its effects in a concentration-dependent manner, by inhibiting the calcium current, which reduces the intracellular calcium overload, or opening certain potassium channels (Hung 2004; Chen 2008).

Coenzyme Q10

Coenzyme Q10 (CoQ10) is a powerful antioxidant and an important component of cellular energy production. A number of studies have revealed a therapeutic role for CoQ10 in conditions of impaired cardiac function, such as heart failure (Singh 2007; Weant 2005). Animal data has shown that CoQ10 can exert powerful antiarrhythmic action following deprivation and subsequent reinstitution of blood flow to the heart (Nagai 1985). Several clinical trials have revealed that CoQ10 possess antiarrhythmic action in situations of impaired cardiac function or metabolic disease such as type 2 diabetes. In a trial involving 27 diabetic individuals, CoQ10 supplementation was found to be beneficial in reducing premature ventricular contractions (Fujioka 1983). A trial involving 2500 heart failure patients found that 3 months of supplementation with 50 – 150 mg of CoQ10 daily was associated with an improvement in arrhythmia signs and symptoms in 62% of subjects (Baggio 1993). Another trial evaluated the effects of CoQ10 supplementation (150 mg daily) for 7 days preceding scheduled coronary artery bypass grafting (CABG) procedures in 40 subjects who were divided to receive CoQ10 or act as a control group. Following CABG, CoQ10 supplementation was associated with lower markers of oxidative stress and significantly lower incidence of potentially deadly ventricular fibrillation (Chello 1994). In a controlled clinical trial among 144 subjects who had a heart attack, 28 days of supplementation with 120 mg of CoQ10 daily was associated with a 2.6-fold reduction in occurrence of arrhythmias. Moreover, subjects receiving CoQ10 also exhibited less evidence of oxidative stress, and levels of other antioxidants such as vitamins A, C, and E increased to a greater degree following heart attack in the group who received CoQ10 than those who received placebo (Singh 1998).


Rhodiola reduced the incidence of ventricular arrhythmias and increased the ventricular fibrillation threshold in an animal model of heart attack (Maslov 2009). Preclinical research suggests the anti-arrhythmic effect of rhodiola may be due to activation of opioid receptors (Maimeskulova 2000). Experimental pre-clinical research has demonstrated pretreatment with rhodiola improved several measures of heart cell health following induced ischemic injury (Wu 2009).


  • Jul: Added section on vitamin D to Nutrients


  • Jan: Updated section on stroke prevention and atrial fibrillation in Conventional Treatment Strategies


  • July: Updated section on omega-3 fatty acids and atrial fibrillation in Nutrients
  • May: Updated section on omega-3 fatty acids in Nutrients
  • May: Added section on omega-3 fatty acids and atrial fibrillation to Nutrients


  • Dec: Comprehensive update & review

Disclaimer and Safety Information

This information (and any accompanying material) is not intended to replace the attention or advice of a physician or other qualified health care professional. Anyone who wishes to embark on any dietary, drug, exercise, or other lifestyle change intended to prevent or treat a specific disease or condition should first consult with and seek clearance from a physician or other qualified health care professional. Pregnant women in particular should seek the advice of a physician before using any protocol listed on this website. The protocols described on this website are for adults only, unless otherwise specified. Product labels may contain important safety information and the most recent product information provided by the product manufacturers should be carefully reviewed prior to use to verify the dose, administration, and contraindications. National, state, and local laws may vary regarding the use and application of many of the therapies discussed. The reader assumes the risk of any injuries. The authors and publishers, their affiliates and assigns are not liable for any injury and/or damage to persons arising from this protocol and expressly disclaim responsibility for any adverse effects resulting from the use of the information contained herein.

The protocols raise many issues that are subject to change as new data emerge. None of our suggested protocol regimens can guarantee health benefits. Life Extension has not performed independent verification of the data contained in the referenced materials, and expressly disclaims responsibility for any error in the literature.

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