What to do during an afib attack?

When and Why AFib is Misdiagnosed

Why diagnosis can be complicated – and what you can do to help

The symptoms of atrial fibrillation or AFib are well-known: a fluttering feeling that can point to a quivering heart muscle, the notable skipped beat that’s the mark of a palpitation, and a racing heart rate that sparks other discomforts. But how distinct are these symptoms? Could they be mistaken for another disorder?

The short answer is yes, they can. Moreover, atrial fibrillation sometimes brings such mild symptoms that patients don’t give them a second thought. In either case, you could be in danger, since living with undiagnosed and uncontrolled AFib can lead to a host of complications, including stroke.

How is AFib usually diagnosed?

Diagnosis begins with an honest and in-depth consultation with your doctor. They’ll want to know about your symptoms: what sort of discomforts are you experiencing? How often do they strike? How long does an episode typically last? Once they’ve got your account, they’ll consider your medical history, and then explore further with some targeted testing.

Some of the most common tests include:

Electrocardiogram. A reliable and non-invasive heart test, the EKG (or ECG) is a primary clinical tool for diagnosing AFib. Now, you can use the same technology outside of the doctor’s office.

Check pulse, blood pressure, and lungs. Typically, this is one of the first things your doctor will do to rule out other conditions that could be masquerading as a heart rhythm disorder.

Stress testing. Also known as exercise testing, a stress test involves measuring how your heart behaves during cardiovascular exercise. This could take place on a treadmill or another cardio machine.

Holter monitor or event monitor. Portable EKG devices can help detect AFib that comes and goes, also called paroxysmal AFib. You would wear these sorts of monitors on your body for a longer stretch of time to catch and record an AFib event.

It’s important to know that no test is a guarantee and AFib can be missed, go undetected, or be misdiagnosed for years.

Why is AFib misdiagnosed?

Clinical tests are often effective – but not always. In other cases, it’s not the test that fails, but rather a misinterpretation of the test results.

EKGs are helpful, but even computers can make mistakes. Sometimes the computer algorithm misinterprets something as an AFib event when in fact it’s not. If a doctor doesn’t catch this mistake when they interpret the test results, a patient can be misdiagnosed with AFib. This phenomenon is also known as fake atrial fibrillation, and it’s a growing concern in the medical community.

There’s also a genetic component to AFib: your chances of developing the disorder are higher if a close relative has been diagnosed with AFib. This is why relaying an accurate and complete family history is so important for the right diagnosis. If you’re not clear on your family medical history, or a family member has been living with AFib without realizing it, your doctor might be missing a crucial piece of the puzzle.

What conditions are commonly confused with AFib?

Medical conditions often occur alongside each other, which can complicate diagnosis. Since AFib symptoms and discomforts can be so subjective, it’s not uncommon for AFib to be mistaken for these other health problems:

Tachycardia and other arrhythmias. Tachycardia – an abnormally rapid heart rate – can disguise itself as AFib, because it’s often a symptom of AFib. Tachycardia can come from an infection, heart disease, congenital abnormalities, or a number of other causes, and can easily be mistaken for persistent AFib.

Anxiety or panic attacks. Anxiety and AFib go hand-in-hand for many people. The two conditions tend to feed off each other, causing a cycle of anxiety, tension, and chest discomfort. But an anxiety attack itself can manifest in the same fashion as an AFib episode, which can trick you into thinking your heart is in distress: panic attacks can come out of nowhere, and hit hard with symptoms like palpitations, muscle tension, lightheadedness, and even some chest pain.

Hyperthyroidism (Graves disease). Thyroid trouble can have whole-body consequences. When you have an overactive thyroid (clinically known as hyperthyroidism), your metabolism goes into overdrive and your heart rate can rise. In addition to your racing heart rate and palpitations, have you been losing weight without trying to? If so, your thyroid may be to blame. Your risk of both hyperthyroidism and AFib can increase with age, so the two conditions may be confused in patients over 50.

Underlying heart disorders. Coronary artery disease, heart valve disorder, and other heart muscle abnormalities can eventually lead to AFib. In these cases, treating the symptoms of AFib likely won’t be completely effective. You’ll need to get to the root of the problem – that underlying heart disorder – to treat the source if you want to alleviate the AFib symptoms.

The consequences of misdiagnosis

In the best-case scenario, having AFib diagnosed as another disorder (or vice versa) won’t cause any unnecessary suffering, and may help ward off some discomfort. But the worst-case scenario can be a life-threatening reaction to the improper treatment, which makes it incredibly important to get the right diagnosis right from the start.

Untreated AFib will result in a higher risk of stroke, and the symptoms can get worse as time goes on. And if your AFib is actually a symptom of another underlying disorder, you could be in danger of experiencing a serious medical event.

It’s always better to be safe than sorry, so put in the time to consult with your doctor, discuss your concerns and medical history, and get a second opinion if you feel like it would help. Misdiagnosis is a reality in the medical world, but those who are proactive and work closely with their doctor to sort out uncertainties will be at an advantage.

TUESDAY, June 5, 2018 (HealthDay News) — If you’re feeling overwhelmed at work, you’ll want to read on.

Job-related stress may raise your risk of developing a heart rhythm disorder called atrial fibrillation, a new study suggests.

Swedish researchers found the most stressful jobs were associated with nearly 50 percent higher odds of atrial fibrillation.

Folks at greatest risk? Those in psychologically demanding jobs that give employees little control over their work. For example, assembly line workers, bus drivers, secretaries and nurses, the researchers said.

“Prolonged periods of stress at work is likely to increase the risk of atrial fibrillation,” said lead researcher Eleonor Fransson, an associate professor of epidemiology at Jonkoping University.

Atrial fibrillation, or a-fib, is the most common heart rhythm abnormality, affecting millions of American adults.

The condition causes palpitations, weakness, fatigue, light headedness, dizziness and shortness of breath. It can also lead to stroke and premature death, the study authors explained in background notes.

Fransson cautioned that this kind of study cannot prove that job strain causes atrial fibrillation, only that the two seem to be associated.

However, other studies have shown that work stress is related to increased risk of heart attack and stroke, she noted.

“Our study adds further support that it is important to take into account psychosocial factors, such as stress, in preventing heart disease,” Fransson said.

Dr. Gregg Fonarow, a professor of cardiology at the University of California, Los Angeles, said it’s not clear if reducing work stress can prevent atrial fibrillation.

“Further studies will be needed to determine if reduction of work-related stress or other mitigating strategies can reduce the risk of developing atrial fibrillation,” he said.

For this study, Fransson and colleagues collected data on more than 13,000 people who took part in the Swedish Longitudinal Occupational Survey of Health in 2006, 2008 or 2010.

Participants were employed and had no history of atrial fibrillation, heart attack or heart failure.

Survey questions asked about job strain: For example, Must you work very hard or very fast? Do you have enough time to complete your work tasks? Does your work include a lot of repetition? Can you decide how and what to do at work?

Triggers for Atrial Fibrillation: The Role of Anxiety


Atrial fibrillation (AF) is the most widely recognized arrhythmia. Systemic arterial hypertension, diabetes, obesity, heart failure, and valvular heart diseases are major risk factors for the onset and progression of AF. Various studies have emphasized the augmented anxiety rate among AF patients due to the poor quality of life; however, little information is known about the possibility of triggering atrial fibrillation by anxiety. The present review sought to underline the possible pathophysiological association between AF and anxiety disorders and suggests that anxiety can be an independent risk factor for AF, acting as a trigger, creating an arrhythmogenic substrate, and modulating the autonomic nervous system. The awareness of the role of anxiety disorders as a risk factor for AF may lead to the development of new clinical strategies for the management of AF.

1. Introduction

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice, with an overall prevalence of 1-2% in the general population and an incidence that increases with age up to 20% in octogenarians. In the next 50 years, its prevalence is expected to double, as a consequence of the prolongation of life expectancy . Five types of AF are classified: first diagnosed, paroxysmal, persistent, long-standing persistent, and permanent AF (KirchhoffAF and psychological factors). AF is associated with high relative risk of all-cause mortality, stroke, cardiovascular mortality, cardiac events, heart failure, and chronic cognitive impairment and represents the most common arrhythmia that requires hospitalization and one of the most frequent causes of hospitalization for heart diseases. Several risk factors and heart diseases are known to be involved in the genesis and/or perpetuation of AF, acting by different pathophysiological pathways on the presence of a susceptible atrial electroanatomic substrate. Among risk factors , both unmodifiable, as genetic susceptibility, age, gender, race, and modifiable, as systemic arterial hypertension, diabetes mellitus, smoking, obstructive sleep apnea, and obesity, have adverse effects on cardiovascular hemodynamic as well as on cardiac structure and function, increasing the prevalence of AF. Moreover, heart failure (HF) and AF frequently coexist: HF predisposes AF and vice versa. Left ventricular dysfunction, independently from ejection fraction, is linked to AF by a hemodynamic overload ; on the other hand, as well known, AF can decrease overall cardiac output from loss of atrial kick .

Over the last decades, epidemiological studies associated various risk factors with AF. Moreover, many reports have advanced the hypothesis of a mutual relationship between AF and anxiety disorders, in which the latter can pave a background that is favourable for the initiation and progression of the former. Anxiety is generally defined as a psychobiological emotional state or reaction that consists of unpleasant feelings of tension, apprehension, nervousness, worry, and activation of the autonomic nervous system . The diagnosis of anxiety includes specific phobia, social phobia, panic disorder, agoraphobia, and generalized anxiety disorder . Traditionally, anxiety has been considered a consequence of AF due to the impairment in quality of life associated with this arrhythmia. While it is well known that anxiety is an independent risk factor for cardiovascular disease, associated with a 26% increased risk of incident coronary heart disease (CHD) and a 48% increased risk of cardiac death , less is known about the role of anxiety disorders in AF onset, severity, and clinical outcomes. The recognition of the involvement of such psychological factors in the development of AF may help the identification of new clinical strategies for the management of AF.

2. Pathophysiological Insights for the Link between AF and Anxiety Disorders

The onset and progression of AF is the result of the interaction between three elements that form Coumel’s triangle of arrhythmogenesis: the arrhythmogenic substrate, the trigger factors, and the modulation factors, of which the most common is the autonomic nervous system.

Several studies show a possible association of anxiety disorders and AF. Nevertheless, a clear relationship has never been demonstrated, this association should be based on the pathophysiological consequences of the anxious state on the neuroendocrine, coagulative, microcirculatory, and immune systems.

It is known that inflammation and oxidative stress are key players for the development of AF through atrial fibrosis, myocyte apoptosis and/or necrosis, and irregular myocellular hypertrophy with disarrangement of lines of cells and recruitment of macrophages to the endothelial surface . All these factors constitute the anatomical arrhythmogenic substrate that results in shortening and dispersion of refractory period, conduction velocity slowing, and formation of reentry circuits. The arrhythmogenic substrate resulting from anatomical and electrophysiological atrial remodelling predisposes to onset and maintenance of AF.

The relationship between inflammatory cytokines and AF risk has been previously described in multiple setting, and both C-reactive protein and interleukin-6 are independently associated with AF . Many studies showed that anxiety and depressive disorders are linked to low-grade systemic inflammation . For example, the ATTICA study evaluated various inflammation and coagulation markers among healthy adults in relation to the anxious state (assessed by Spielberger’s State-Trait Anxiety Inventory, STAI). STAI score was positively correlated with C-reactive protein, interleukin-6, homocysteine, and fibrinogen levels. The ATTICA study provided strong evidence that anxiety is associated with systemic inflammation and abnormal coagulation process, possibly leading to increased cardiovascular events .

Moreover, stress response has been described as resulting from a “fight or flight” reaction that can be the result of endocrine, nervous, and immune systems .

The inflammatory state found in anxious and depressive disorders is presumably related to a hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis which is commonly seen in patients with chronic stress. Although the HPA axis in normal situations should temper inflammatory reactions, prolonged hyperactivity of the HPA axis might result in blunted anti-inflammatory responses to glucocorticoids resulting in increased inflammation Furthermore, hyperactivity of the HPA axis with cortisol hyperproduction and corticotropin-releasing hormone (CRH) overdrive produces an imbalance of monoamines; in particular, chronic stress leads to a reduced activity of dopaminergic, serotoninergic, and noradrenergic neurons . In fact, persisting hypercortisolemia decreases serotonin production. For this reason, antidepressants act on monoamines replacement as well as on modulation of cerebral glucocorticoid receptors .

Additionally, patients suffering from anxious and depressive disorders are more likely to have increased activity of sympathetic nervous system and subsequently catecholamine overload . It is known that elevated serum catecholamine levels can trigger Takotsubo (or stress) cardiomyopathy through microvascular endothelial damage and catecholamine cardiotoxic effects . On the other hand, acute emotional stress and chronic anxiety disorders are considered predisposing risk factors for stress cardiomyopathy because of the higher prevalence of these psychosocial factors than that in the acute coronary syndrome patients as well as in general population . In anxiety disorders, serum catecholamine levels are elevated; thus, the susceptibility to AF may be in part related to anxiety disorders through the same catecholamine-mediated myocardial injury seen in stress cardiomyopathy. Catecholamine overload in anxiety disorders could lead to the formation of the arrhythmogenic substrate and could be a trigger for the onset of paroxysmal AF. The morphological alterations caused by catecholamine overload include: extracellular matrix overproduction, contraction band necrosis, and mononuclear cell infiltration . Catecholamine overload leads to an extracellular accumulation of collagen alfa-1 (I) chain and to an increased ratio of collagen alfa-1 (I) chain to collagen alfa-1 (III) chain that results in a large and rapid increase in atrial fibrosis . The increased release of catecholamines results in an enhanced catecholamine degradation, which in turn leads to production of reactive oxygen species , and in increased level of profibrotic mediator like angiotensin II, TGF beta, and osteopontin . On the other hand, matrix metalloproteinase are not correspondingly activated with the result of augmentation of extracellular matrix proteins, myocardial disarray, and negative atrial remodelling. Lastly, the overstimulation of beta-adrenoreceptors by supraphysiologic levels of catecholamines alters the expression of calcium-regulatory protein genes . The impairment of the calcium-handling system causes ultrastructural atrial remodelling and predisposes to the onset and progression of AF. Anxiety disorders can trigger AF through the increased activity of sympathetic nervous system that is known to be the most important modulation factor of Coumel’s triangle of arrhythmogenesis. Patients with anxiety have reduced heart rate variability and vagal tone , which suggests an abnormal autonomic system regulation and represents an independent risk factor for AF .

Lastly, individuals who suffer from anxiety have a stimulated renin-angiotensin-aldosterone system (RAAS) . Elevated levels of angiotensin II stimulate mitogen-activated protein kinases and reduce collagenase activity, which results in cardiac fibrosis and left ventricular hypertrophy. Binding of angiotensin II to angiotensin II type I receptors induces transforming growth factor-1 (TGF-1) production which promotes atrial fibrosis . Thus, the hyperactivity of RAAS results in detrimental cardiac remodelling with abnormal ventricle relaxation, diastolic impairment, and increased atrial pressure and stretch. All these mechanisms can promote AF by slowing atrial conduction velocity and providing a greater atrial surface for reentry.

3. Discussion

As mentioned above, chronic stress and anxious state can promote AF through several mechanisms acting at different levels as trigger, modulating the autonomic nervous system and modifying the atrial substrate. In sum, anxiety disorders can interact with all the three elements of the triangle of Coumel resulting in the arrhythmogenesis of AF.

We are underlying the possible pathophysiological consequences of the chronic stress and anxious state on the neuroendocrine, coagulative, microcirculatory, and immune systems; however, a strict relationship between AF and anxiety has never been demonstrated so far. Nevertheless, several studies clearly show the strong association of anxiety symptoms and onset or recurrence of AF strengthening the hypothesis of the existence of causal link between these two disorders.

For example, Eaker et al. showed that anxiety is a risk factor for incident AF in males and females over a 10-year time period . Moreover, it has been reported that anxiety symptoms increased the incidence of AF after cardiac surgery and the use of beta-blockers may reduce this correlation .

Increased sympathetic tone, lessened vagal tone, and the cardinal symptoms of anxiety could be major provocative factors of postoperative AF acting as trigger and modulating the autonomic nervous system .

Additionally, Lange and Herrmann-Lingen found that after successful electrical cardioversion, risk of recurrence of AF remains existent due to anxiety. For those AF patients who scored more than 7 on Hospital Anxiety and Depression Scale (HADS), 85% have the possibility of recurrence. In another study, Yu et al. reported an increased risk of AF recurrence due to anxiety after taking circumferential pulmonary vein ablation . These studies show that anxiety disorders have an impact on AF treatment success, suggesting that these psychological disturbances can have a major role on the development and progression of AF.

There is a small study which found that paroxetine reduces drug-resistant paroxysmal AF, presumably modulating vagal tone at the level of the midbrain and inhibiting the vasovagal reflex . In the last decades, a bulk of data demonstrated the efficacy of selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs) in anxiety disorders . These studies may suggest the usefulness of SSRIs and SNRIs in patients with AF and anxiety disorders. Pragmatic randomized controlled trials with antidepressants are needed to explore a possible effect on the course of AF in patients with comorbid psychosocial disorders.

All these evidences suggest that anxious disorders may create an environment that is favourable of the initiation and perpetuation of AF . Nevertheless, the above-mentioned studies have several limitations as such as the small sample size, the short follow-up period, and they are single-center experiences using different questionnaires with heterogeneous validity and reliability. Additionally, the rating scales used in epidemiological studies, as Eaker’s one, are not necessarily the same scales used to diagnose anxiety disorders in daily clinical practice. These findings suggest that future research should involve large multicentre prospective trials, with long follow-up period using thorough, exhaustive, and homogeneous interviews and scales for the diagnoses of anxiety disorders.

The identification of anxiety disorders as independent risk factor for AF opens new scenarios in the management of this arrhythmia.

Firstly, in patients with multiple risk factors for AF, anxiety assessment should be routinely performed through standardized questionnaire, as the Hamilton Anxiety Rating Scale (HAM-A) , Spielberger’s State Anxiety Inventory (STAI) , and the Zung Self-Rating Anxiety Scale (SAS) , to identify this psychosocial risk factor and possibly prevent AF onset and progression. Moreover, in this setting, it is important to underline the need of a clinical diagnosis of anxiety disorders in order to make a differential diagnosis with depressive disorders that might also be present as comorbidity.

Secondly, it might be interesting to evaluate whatever identification and treatment of anxious states could be useful to improve outcomes and optimize the management of this arrhythmia in patients with recurrent AF, or treatment-resistance AF.

Lastly, future prospective well-designed studies should clarify the possible causal role of anxiety disorders in the onset of AF in patients after surgery. Considering the possible causal link between AF and anxiety in patients after cardiac surgery, the usefulness of beta-blockers, benzodiazepines, and SSRI should be evaluated in reducing the incidence and in the management of postoperative AF.

4. Conclusions

The present review underlines the possible pathophysiological mechanisms through which anxiety disorders can promote the onset, progression, and maintenance of AF. A relationship may exist between the most common clinical arrhythmia and anxious states. The recognition of the involvement of such psychological factors in the development of AF may help the identification of new clinical strategies for the management of AF. Nevertheless, a few studies pointed out the possible role of psychological factors on the development of AF, and a clear association has not been demonstrated yet. Considering the limitations of the present studies addressing a role of anxiety disorders as risk factor for AF and the high health burden of AF, large prospective studies are necessary to elucidate this multifaceted relationship and to assess the benefits of routine anxiety assessment in AF patients and the usefulness of anxiolytics and antidepressants in the prevention and treatment of AF.

Conflicts of Interest

The authors declare that there are no conflicts of interest regarding the publication of this paper.

Atrial fibrillation: Common, serious, treatable

Atrial fibrillation can be dangerous from a fast heart rate and a higher stroke risk

Updated: July 18, 2018Published: November, 2011

Is atrial fibrillation serious? People who are old enough to remember the sound of wind-up clocks often refer to their hearts as their “tickers.” It’s an affectionate term that pays tribute to the regular, rhythmic beat of the healthy heart. In fact, though, the healthy heart is much more sophisticated than the most precise Swiss timepiece.

Instead of maintaining a single, monotonous beat, the heart can speed up in response to exercise, strong emotions, and fever. Common chemicals can also jack up the heart rate; examples include caffeine, nicotine, and decongestants. And the healthy heart can also slow down when you rest, relax, or sleep.

A clock keeps a steady rate of 60 beats per minute, while your heart rate may vary between 50 and 100 beats at rest and rev up to twice as fast during exercise. But sometimes the mechanisms that regulate the rate and rhythm go awry. Doctors call these disorders arrhythmias; they come in many varieties, but the most common sustained arrhythmia of all is atrial fibrillation (AF).

A brief history of atrial fibrillation

AF is a new concept for many men, but it’s plagued men’s hearts for millennia. In fact, the first written description dates back to China some 4,000 years ago. An English physician named William Withering discovered the first useful treatment for AF in 1785 when he gave the leaf of the foxglove plant (Digitalis purpurea) to a patient whose pulse became “more full and regular.” Digitalis derivatives are still in use today, but modern understanding of AF was delayed until the invention of the electrocardiograph in the early 1900s. And more than a century later, the treatment of AF continues to evolve and improve, providing important benefits to many people, but introducing many complexities for both doctors and patients.

What is atrial fibrillation?

The human heart is divided into four pumping chambers (see figure). The two upper chambers are called the atria; they collect blood from the veins, then pump it into the two ventricles, larger and stronger chambers that propel the blood out from the heart to the rest of the body.

To function best, the atria should contract first, with the ventricles close behind. The electrical messages that signal the heart muscle to contract begin in the atria (at the SA node), and then travel across the AV node into the ventricles to trigger the contractions you feel as your pulse. The entire sequence can be recorded on an electrocardiogram (ECG), where the atrial contractions appear as P waves and the ventricular contractions that follow show up as QRS complexes (see figure).

When the heart is in its normal rhythm, the atria contract at steady, regular intervals. But in AF, the atria’s electrical signals occur much more rapidly, often 350 to 500 times per minute. At these rates, the muscle just can’t contract in a coordinated fashion. Instead of producing an atrial beat, the muscles just quiver (fibrillate) ineffectively. The ventricles are bombarded by fast, irregularly spaced atrial impulses, but they are partially protected from breakneck speed by the AV node, which intercepts the atrial impulses and blocks many of them before conducting some to the ventricles. Still, the ventricular rate is usually much faster than normal, and the rhythm is irregular, as is your pulse.

Atrial fibrillation charts

In normal sinus rhythm, the sinus node initiates the electrical activity that triggers each heartbeat. The electrical impulse travels through the atria, signaling the muscle to contract; each atrial contraction shows on the ECG as a p wave. The electrical activity then crosses into the ventricles, stimulating them to contract and pump blood to the body’s tissues (shown in ECG as the QRS complex).

In atrial fibrillation, the atria’s electrical signals are very rapid and erratic; the atria don’t contract and there is no p wave. Without a coordinated signal to guide them, the ventricles contract at a rapid rate in an irregular rhythm.

What causes a-fib?

Scientists don’t fully understand the basic problems behind AF, but they do know many of the factors that increase the risk of AF.

Age is an important factor; AF is uncommon before age 50, but it affects nearly 8% of men between 65 and 74 and almost 12% between 75 and 84. Gender is also important; AF occurs about 50% more frequently in men than women. Since about a third of all patients with AF have a family history of the disorder, heredity also plays a role, and several specific genetic abnormalities have already been identified.

Cardiovascular conditions are strongly linked to AF. The three most important are high blood pressure, heart valve disorders (particularly mitral valve problems), and coronary artery disease (with or without a heart attack). Heart failure, a debilitating problem that occurs when the weakened heart muscle is unable to pump blood effectively, is another risk factor for AF. Less often, inflammation in the membrane around the heart (pericarditis) triggers AF.

Lung disorders also increase the risk of AF. Culprits include chronic obstructive lung disease, blood clots in the lungs (pulmonary emboli), and pneumonia. Chest surgery is another cause.

A wide variety of medical conditions are associated with AF. An overactive thyroid gland (hyperthyroidism), diabetes and obesity increase risk, as do medications such as bronchodilators used for asthma and COPD.

Behavioral factors are also tied to AF. Always a villain, smoking is on the hit list. Moderate drinking does not lead to AF, but excessive alcohol consumption does, particularly in the setting of binge drinking. Anger and hostility boost the risk of AF in men. Surprisingly, perhaps, caffeine does not appear to be a risk factor.

Although vigorous exercise sometimes triggers AF in young men, walking and other moderate physical activities provide long-term protection. Some studies suggest that taking statin drugs or eating fish may reduce the risk of AF over the long run, while others do not. Beta blockers, ACE inhibitors, and angiotensin-receptor blockers (ARBs) appear to reduce the risk of AF in patients with hypertension.

A-fib classification

There are several ways to categorize AF. In one system, it’s called primary AF when the problem originates in the heart itself, and secondary AF when it results from a noncardiac medical condition, in which case the AF often resolves when the underlying problem is corrected. When primary AF occurs in a structurally normal heart, it is called lone AF, which carries a relatively low risk of complications. Other types of primary AF, however, can be more troublesome.

Another classification system for AF depends on the frequency and duration of the arrhythmia:

  • paroxysmal AF — recurrent episodes of AF that end within seven days without treatment. Most bouts of paroxysmal AF end in less than 24 hours, but even though episodes are brief, patients are still at risk of stroke.

  • persistent AF — episodes that last longer than seven days or require treatment to convert back to a normal heart rhythm. The longer an episode lasts, the harder it is to restore a normal rhythm.

  • permanent AF — AF that has lasted longer than a year.

Atrial fibrillation symptoms

The symptoms of AF vary widely. They tend to be more severe in older people and in those who also have structural heart or lung disease. Men who are in good general health may not even be aware of the arrhythmia. Others notice a fluttering sensation in the chest or a rapid and/or irregular heartbeat. Fatigue, increased nighttime urination, shortness of breath, and exercise intolerance are common and can be severe in patients who had weakened hearts or diseased lungs even before AF hit. Lightheadedness, confusion, and sometimes even fainting may signal a substantial fall in blood pressure due to AF. Patients with coronary artery disease may suffer angina or a heart attack when they develop AF. Because AF reduces the heart’s pumping capacity, fluid can build up in the legs or lungs, particularly if the patient had some degree of heart failure even before the onset of AF.

Atrial fibrillation diagnosis

Doctors suspect AF when they hear an irregular heartbeat or feel an irregular pulse; a standard electrocardiogram, or ECG (see figure), will confirm the diagnosis if the patient is tested during an episode of AF. But if the AF is paroxysmal, or intermittent, a doctor may ask his patient to wear a Holter monitor or event monitor at home; these are small devices that record ECG tracings continuously (Holter) or intermittently (event) to document brief or episodic arrhythmias.

Diagnosing AF is relatively easy, but testing doesn’t stop there. In most cases, doctors will order an echocardiogram or cardiac ultrasound to evaluate the heart’s valves and muscular contractions; an advanced type of ultrasound, the transesophageal echocardiogram, may be used to evaluate stroke risk. Blood tests to measure thyroid, kidney, and liver function and red blood cell levels are important. Many patients benefit from additional lung or heart studies.

Diagnosing AF may be relatively easy, but deciding how to treat it can be quite difficult. To understand your therapeutic options, you should first understand why AF needs treatment.

Why is a-fib serious?

Patients with AF are at risk for three major complications: heart failure, angina, and stroke.

AF reduces the heart’s pumping capacity. Although the atria are small chambers with relatively weak muscles, they still contribute a “kick” or boost to the larger, more powerful ventricles. In addition, the rapid heart rate of AF reduces the efficiency of each beat. In all, AF reduces the heart’s pumping capacity by 10% to 30%. People whose hearts are otherwise healthy can compensate for this impairment, but those with damaged heart muscles or valves cannot. As a result, they experience the fatigue, breathlessness, exercise intolerance, and swelling of the feet and legs that are so characteristic of heart failure. AF can also trigger the chest pain of angina or a heart attack in patients with coronary artery disease.

The other major complication of AF is stroke. Although doctors have studied AF for over 100 years, the risk of stroke was not fully appreciated until the 1980s, when the Framingham Heart Study reported that 24% of its stroke patients were also in AF, and that the abnormal heart rhythm developed within the six months preceding the stroke in about a third of these participants. AF quintuples the risk of stroke. It accounts for about 15% of all strokes and for nearly a quarter of all strokes in people ages 80 to 89.

How does a cardiac abnormality cause brain damage? Since fibrillating atria don’t contract, they contain relatively stagnant pools of blood. Clots (thrombi) form in these areas, then break off and travel to the brain, where they block small arteries, depriving the brain of its vital oxygen and causing tissue damage and death. It’s a devastating sequence of events, but it can be prevented by anticoagulants, medications that fight blood clots. In fact, the use of anticoagulants is one of the key priorities in the management of patients with AF. The others are slowing the heart rate and, in some patients, restoring a normal heart rhythm.

A-fib and heart rate

Since the dangerous complications of AF result from its abnormal rhythm, logic dictates that restoring a normal rhythm would be the highest priority of therapy. Cardiologists understand that logic, but they also know that clinical trials are necessary to find out if theory translates into reality.

Between 2000 and 2008, six independent, high-quality clinical trials randomly assigned patients with AF to one of two treatment groups. In one group, the goal of therapy was to control the heart rate while tolerating the irregular rhythm; in the other, the goal was to restore and maintain a normal rhythm when possible. A similar, very high percentage of patients in both groups received the recommended anticoagulant therapy to prevent strokes.

A total of 6,615 patients volunteered for the six trials. Despite differences in the patient groups and the methods used to achieve rate or rhythm control, all the trials arrived at the same conclusion: rhythm control does not produce better results than rate control in terms of survival, cardiac complications, or relief of symptoms. In fact, the rhythm control strategy was associated with a higher rate of hospitalizations and greater expense.

Why did rhythm control morph from no-brainer to no benefit? Restoring and maintaining normal rhythm is no small feat. It typically involves medications and may require additional procedures ranging from an electric shock to heart surgery. Slowing a racing heart requires medications, too, but they are safer and produce fewer side effects than the specialized drugs used for rhythm control. And since most AF patients require anticlotting medication even after normal rhythm is restored, the rhythm control strategy does not even have the advantage of reducing the burden of anticoagulation.

These important randomized clinical trials suggest that rate control may be the first choice for many, even most, patients with AF. Still, some may benefit from rhythm control. Likely candidates include individuals who are diagnosed promptly after the onset of AF, patients with a first episode of AF, patients with AF triggered by a medical problem that has been corrected, younger people, and those who continue to have troublesome symptoms despite rate control. And if these considerations are not complex enough, there are several ways to slow rapid AF and many, many options for rhythm control. Here’s a brief rundown.

A-fib medications

Medication can slow down the racing heartbeat in nearly all patients with AF. The most useful drugs are beta blockers (such as propranolol and metoprolol) and calcium-channel blockers (such as diltiazem and verapamil); even so, digoxin (the modern version of the foxglove plant first used for AF over 225 years ago) still has a role in select patients.

Patients who have chest pain or shortness of breath can receive rate-controlling medications intravenously; most respond in minutes to hours. Oral medications take longer to kick in, but most patients with sustained AF require long-term oral medications to maintain heart rate control. Although precise heart rate targets have not been established, many doctors adjust medications to achieve a heart rate of about 60 to 80 beats per minute when the patient is at rest and about 90 to 115 during moderate exercise. However, a study found that lenient heart rate control with a target resting rate of up to 110 beats per minute is just as beneficial as stricter target heart rates.

Restoring normal heart rate

The fastest and most effective way to convert AF back to a normal heart rhythm is to jolt the heart with an electric shock. Electrical cardioversion sounds shocking, even drastic, but since it uses only a small, brief pulse of DC current, it is really quite safe — and since patients are sedated, it’s only mildly uncomfortable. Electrical cardioversion is most likely to succeed when used soon after the onset of AF. To prevent stroke, nearly all patients who have been in AF for more than 48 hours should have three to four weeks of anticoagulation (see below) prior to cardioversion, and nearly all benefit from at least four weeks of anticoagulation after the procedure. Anticoagulation should be continued indefinitely in patients at moderate to high risk of stroke, even if they maintain a normal rhythm.

Drugs can also be used to convert patients from AF to a normal rhythm, and long-term medication may be needed to preserve a normal rhythm after successful electrical or pharmacological cardioversion; long-term anticoagulation is also generally necessary. The choice of medication is tricky, and anti-arrhythmic medications can have severe side effects, even including serious arrhythmias. As a result, while primary care physicians often manage rate control, rhythm control is best guided by cardiologists. Amiodarone is frequently the drug of choice. Other specialized drugs that may be useful include sotalol, flecainide, and propafenone. Some carefully selected patients with recurrent bouts of AF can take a single dose of flecainide or propafenone on their own (the “pill-in-the-pocket” approach) to convert AF as soon as they notice the irregular heartbeat of AF.

Today cardiologists often recommend restoring a regular heart beat with radiofrequency ablation. The idea is to destroy a tiny amount of tissue in or near the heart to stop it from sending out the abnormal electrical signals that trigger AF. First, patients undergo sophisticated testing to detect and map the offending tissue. Next, doctors thread a tiny catheter, or tube, through a blood vessel in the groin up into the heart. When the tip of the catheter is up against the offending tissue, which is usually in or near the pulmonary veins, a radiofrequency electrical current is passed through the catheter to destroy, or ablate, the target.

Preventing stroke from a-fib

Most patients with AF feel fine once their heart rate is controlled. But their well-being is deceptive, since they are still at risk for stroke. The risk is particularly high in older patients, in patients with hypertension, and especially in patients with previous strokes or heart valve disease, particularly an artificial valve or narrowing of the mitral valve (mitral stenosis).

Fortunately, anticoagulants (“blood thinners”) can help protect AF patients from stroke.

Aspirin is the simplest, safest, and least expensive, but it is also the least effective, reducing the risk of stroke by about 20%.

Warfarin (Coumadin) reduces the risk of stroke by about 60%. It has been the mainstay of therapy for decades, but it requires careful attention to medications and dietary factors that affect therapy as well as frequent adjustments in dose, based on the results of blood tests performed every two or three weeks.

Direct oral anticoagulants (DOACs). Apixaban (Eliquis), dabigatran (Pradaxa), edoxaban (Savaysa) and rivaroxaban (Xarelto) are as effective as warfarin for people with atrial fibrillation not due to a heart valve problem. They do not require the dietary restrictions and frequent blood tests that make warfarin therapy tricky and inconvenient. On the downside, they are much more expensive.

Researchers continue to study new ways to improve the management of AF. But for now, the tried and true will serve most patients well: slow the racing heart, consider restoring normal rhythm if symptoms persist, and reduce the risk of stroke by preventing clots.

Atrial fibrillation is an old problem, but it can be treated effectively, whether by standard therapy or newer innovations.

As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.

Eating Healthy When You Have Atrial Fibrillation

How To Build a Healthy Diet

Like many other health conditions, atrial fibrillation becomes more manageable when you adopt a healthy diet. While changing your eating habits can’t cure AFib, taking steps to improve them may reduce the number of AFib episodes you suffer in addition to slowing the progression of the disease.

Of course, there is also a world of conflicting information out there about the “best” AFib diet, just as there is for weight loss or any other condition. Every person’s body is unique, which makes it hard to speak in absolutes. Still, there are a few key principles which seem to hold true.

Commercial Diets that Work

Many AFib patients will begin their journey by looking for a commercial diet or a proven eating system which tells them what they can and can’t have. Several have proven to be effective.

1. The Paleo Diet The Paleo diet focuses on returning people to mankind’s earliest eating habits. Many people are successful on this diet because it does not rely on portion control or calorie counting. Instead it cuts sugary, salty processed foods and drinks, as well as pasta, rice, bread, and cereal. Paleo dieters stick to grass-fed meat, fowl, fish, eggs, vegetables, natural cooking oils, some fruits and nuts, and the occasional sweet potato. Most of the benefit may well come from the reduction of sugar and salt alone.

1. The Mediterranean Diet Many people with atrial fibrillation have also found a great deal of success with The Mediterranean Diet. Most of the allowed foods are very similar to the Paleo Diet, with fewer restrictions: healthy whole grains make it back onto the menu, as do coffee, tea, and wine in moderation. You’ll have to watch your own triggers of course; if you know wine is one of yours then you’ll need to avoid it.

3. The Rosedale and Schwarzbien Diets The Rosedale Diet and the Schwarzbein Diet are two other diets people with AFib have tried with success. These diets are similar in that they limit carbs, starches, sugars, and processed foods. You could as easily choose any diet that does the same like the South Beach Diet or the Atkins 40 and perhaps see very similar results.

Rigid Diet or General Principles?

Most people struggle to follow a rigid diet. One bad day at work, one family vacation, or one night out with friends can make many commercial diets frustrating, if not impossible, to follow. Slip too many times and you might find yourself ready to give up.

Thus, it may be better to focus on the principles behind these diets. For example, the primary benefit of a low-carb diet might boil down to reducing gluten. If you’re gluten-sensitive you’ll tend to gather weight around your gut, which can crowd the stomach and diaphragm into the heart area. This crowding can increase the number of episodes you suffer.

By focusing on the principles, you can control your shopping and cooking. For the most part, you’ll eat healthy enough, but you won’t have to obsess or beat yourself up if you break and indulge in a piece of pizza at an office party.

Building Your Own “Afib Diet”

If you’re going to focus on the principles bringing all these diets together then you’ll want to let the following guidelines influence your food choices:

  • Choose whole grains over simple carbs, or eliminate carbs and gluten altogether
  • Watch the GI index. Choose non-starchy vegetables and low-sugar fruits
  • Eat protein every day, but focus more on fish and fowl than on red meat
  • Use healthy fats like olive oil, coconut oil, and grapeseed oil
  • Use caffeine and alcohol only in moderation
  • Limit processed foods, sugar, and soda

As a bonus, following these principles won’t just help you manage your afib, but they’ll improve your overall health and may even lead to long-term weight loss.

Author by line: Travis Van Slooten is an atrial fibrillation patient who has been passionate about providing knowledge, inspiration, and support to fellow afibbers through his blog at www.livingwithatrialfibrillation.com

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