Atrial Fibrillation: Symptoms and Treatment

 

Course Number	LWN320                                                                                  2446
Objectives	At the end of this course, you will  describe 1. causes, 2. risks,  3. symptoms, 4. signs, 5. tests and 6. treatment of AFib.
Credit Hours and Fee	3.0 CE Credit Hours with a fee of $24.00
Instructor	Rudolf Klimes, PhD (Indiana University), MPH (Johns Hopkins University); Adjunct Professor, Folsom Lake College, Folsom, CA.

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Section 1-7 come in the main from the NIH, the CDC and ACC and present reliable up-to-date information. Sections 8 and 9 are more anecdotal reviews and need to be read critically and may or may not include some presently broadly accepted information.

Atrial fibrillations (AF) are electrical signals in the atria that are fired in a very fast and uncontrolled manner. Electrical signals arrive in the ventricles in a completely irregular fashion, so the heart beat is irregular.

Take this short introduction. http://www.nlm.nih.gov/medlineplus/tutorials/atrialfibrillation.html   http://www.heartpoint.com/afibgallery.html   A-Fib 101 [From the Atrial Fibrillation Page]

1. Causes, incidence, and risk factors   

2. Symptoms   

3. Signs and tests   

Listening to the heart with a stethoscope shows an irregular rhythm. The pulse may feel rapid, irregular, or both. Sometimes the pulse is too slow. The normal  heart rate is 60 to 100, but in atrial fibrillation the heart rate may be 100 to 175. Blood pressure may be normal or low.

An EKC shows atrial fibrillation. Continuous ambulatory cardiac monitoring -- Holter monitor (24 hour test) -- may be necessary because the condition is often sporadic (occurring at some times but not others).

Tests to determine the presence of underlying heart diseases may include:

4. Treatment  and Expectations (prognosis)    

The disorder is usually controllable with treatment. The natural tendency of atrial fibrillation, however, is to become a chronic condition.

Source: Medline Plus, Medical Encyclopedia. http://www.nlm.nih.gov/medlineplus/ency/article/000184.htm Update Date: 5/10/2002 by: Elena Sgarbossa, M.D., Department of Cardiology, Rush-Presbyterian St. Luke's Medical Ctr., Chicago, IL.

AFib Electrophysiology   EP Studies  ACC Management  AFib Controversies

5. AF Cases 

AF-related death rates for groups defined by age, sex, race/ethnicity, and state were determined by dividing the number of deaths by the population at risk (denominator) in each group. Rates of hospitalizations among Medicare enrollees aged >65 years with AF for each group were determined by dividing the number of hospitalizations by the population at risk (denominator) in the group. Age-adjusted death rates (per 100,000 population) and hospitalization rates (per 1,000 Medicare enrollees) were calculated by using the 2000 U.S. standard population (6).

In 1999, a total of 66,875 deaths with AF as a contributing cause occurred, resulting in an age-adjusted death rate of 24.7 per 100,000 population. Of these deaths, 56,138 (84.0%) were among persons aged >75 years. The greatest proportion of these AF-related deaths occurred among persons aged >85 years (47.4%), followed by those aged 75--84 years (36.6%), aged 65--74 years (12.3%), and aged <65 years (3.7%). Age-specific death rates increased for successive age groups. Age-adjusted death rates for AF were highest among whites (25.7) and blacks (16.4) and higher for men (34.7) than women (22.8). In 1999, for all decedents who had AF, the most common underlying causes of death were coronary heart disease (28.0%), AF (12.4%), and stroke (10.8%).

In 1999, a total of 1,765,304 hospitalizations (137.1 per 1,000 Medicare enrollees) were reported among persons with AF in the Medicare population . Rates increased among successive age groups. The rate of hospitalization among persons with AF was higher among whites (142.7) than among blacks (100.4). Although 55.7% of these hospitalizations were among women, men (162.9) had a higher rate of AF-related hospitalization than women (121.2). The most common diseases listed as the primary diagnosis for persons hospitalized with AF were congestive heart failure (11.8%), followed by AF (10.9%), coronary heart disease (9.9%), and stroke (4.9%). Source: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5207a2.htm

6. AF Research    

Recent data from the Cardiovascular Health Study suggest that age, male gender, clinical cardiovascular disease, and left atrial size are all important risk factors for AF.  Data from the Framingham Heart Study suggest that the risk of stroke attributable to AF increases significantly with age, rising from 1.5% for those aged 50-59 years to 23.5% for those aged 80-89 years.  The importance of AF persists into the oldest and most stroke-prone decades while the impact of other common risk factors, e.g., high blood pressure, lose their significance in the oldest old.  About 70% of persons with AF are between 65 and 85 years of age. Isolated AF occurs but is uncommon and most patients diagnosed with this arrhythmia have co-existing cardiovascular disease (e.g., ischemic heart disease, valvular disease, hypertension, heart failure or stroke).

Although there are several treatment options available to manage AF (i.e., secondary prevention) including therapies to maintain sinus rhythm following cardioversion to control ventricular rate, and therapies to prevent thromboembolism and stroke through anticoagulation, most treatments are associated with potentially harmful side effects.  Accordingly, the NHLBI is sponsoring the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM).  This ongoing trial in 5,300 elderly patients is comparing two strategies for long-term management of AF:  antiarrhythmic agents to maintain normal sinus rhythm and a different group of drugs and/or catheter ablation for heart rate control only.  Yet, despite the importance of AFFIRM, more attention needs to be directed to the importance of age-related changes (both structure and function) in the atria and the impact of these changes on the development of AF in older persons with co-existing cardiovascular disease.

Neither the specific molecular nor precise physiologic bases for AF are well defined.  It has been suggested that the left atrium enlarges, stiffens, and develops fatty infiltrations - especially within the atrial septal region.  These changes are accompanied by other age-related changes that have been observed in humans or animals.  These include:  increased interstitial collagen deposition (which may interfere with normal electrical conduction); changes in elastin content; increased cardiac amyloid deposition; shortening of atrial refractory period; depressed sinoatrial and atrioventricular nodal function; increased sinoatrial and atrioventricular conduction time; decreased number of atrial myocytes, including a decrease of up to 90% in the number of sinoatrial pacemaker cells by age 75 in humans; and atrial myocyte hypertrophy.

Age-related changes in atrial anatomy are likely to be involved in the genesis of AF.  Compared with ventricular anatomy, atrial anatomy is exceedingly complex in nature.  The atria are composed primarily of highly branched, distinct muscle bundles; i.e., pectinated trabeculae.  These trabeculae provide multiple conduction pathways that split the atrial excitation wavefront as it conducts throughout the upper chambers of the heart.  Within this anatomical arrangement, conduction slowing may lead to reentry of atrial excitation and induction of AF. Unexcitable fibrous tissue proliferation increases with age, and appearance of this tissue may represent an important way by which atrial conduction is altered during aging.  Understanding the interactions between fibrous tissue (unexcitable) and atrial muscle (excitable) will help define factors leading to AF in old age.  This information will foster development of treatment strategies targeting atrial fibroproliferative changes.  This research, along with a better elucidation of the electrical interactions occurring within the complex atrial anatomy, should provide the basis for the development of new treatments for the prevention of AF in the elderly. Source: http://grants1.nih.gov/grants/guide/pa-files/PA-99-035.html

The preferred and most frequently used initial therapy for the common heart rhythm disorder atrial fibrillation (AF) is a strategy to restore and maintain a normal heart rhythm. However, a study supported by the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health found that this "heart rhythm" strategy prevents no more deaths than the alternative, often secondary, approach to treatment which merely controls the rate at which the heart beats — and may have some disadvantages, including more hospitalizations and adverse drug effects.

Furthermore, the rhythm approach does not result in a lower risk of stroke, improved quality of life, or improved cognitive function — all of which had been presumed to be benefits over the "heart rate" strategy. These results, from the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial were published in the December 5 issue of The New England Journal of Medicine.

One classification of AF includes:

• Acute AF (onset within 48 hours).
• Paroxysmal AF (terminated spontaneously on at least one occasion).
• Persistent AF (duration greater than 48 hours and has not terminated spontaneously).
• Permanent AF (resistant to pharmacological or electrical cardioversion). http://www.ahcpr.gov/clinic/epcsums/atrialsum.htm

7. Vagal AF (VMAF)

The heart's rate control system consists of inputs from the two branches of the autonomic (involuntarily controlled) nervous system.  The cardiac nerve is the sympathetic branch of the autonomic nervous system; stimulation by this will speed the heart rate up (adrenergically- mediated).  The vagus nerve is the parasympathetic branch of the nervous system, and slows the heart rate.  These two controls respond to and balance the body's requirements such as speeding up blood flow during exercise or calming it again afterwards. 

Overstimulation of either branch can cause Atrial Fibrillation due to the resultant, and similar but not equal, nerve impulse transmitter chemicals' effects on changes in the heart's electrical status.  This may or may not occur in the presence of other predisposing factors - i.e. it is suggested that some autonomic activity can cause fibrillation even if there is nothing wrong with the heart. It is a fallacy that AF is always caused by excessive cardiac nerve activity; this is unfortunately a persistent misconception among some.

Given no external control an isolated heart would adopt its own rate, controlled by the sinus node, which would be higher than the usual resting heart rate of around 65-75 bpm (beats per minute).  Thus, in a normal heart, the vagus nerve is active. This is called the "vagal drive".  Thus in a "normal" heart (with no underlying heart disease) any AF is more likely to be vagal.

Classically, for those suffering from AF, [and where there is no established cause such as hyperthyroidism, post-operatively, and similar,] the condition of "lone" AF has been associated with a speeding up of the heart triggering it into an AF episode.  This is not always the case.  A significant proportion of people may have their AF brought on by factors causing a slowing down of the heart. 

The importance of this distinction is that certain drug treatments are at the minimum unhelpful, and at worst harmful, to the condition.  Further, correct active management of the condition at the paroxysmal stage must be adopted to prevent it possibly progressing to permanent AF.

The typical picture of Vagal AF is :

• Prevalence: 80% male
• Typical age - young (45 +/- 10 years) at onset
• Generally fit individual
• No underlying heart disease
• Classical times for episodes: at night, during rest, after large meals
• Other notable triggers: gastric discomfort or problems, cold drinks, straining, postural triggers (e.g. bending over), tendency to faint as patient stands up, tendency to slow heart rate (athletes)

The indicated drug treatments for vagally-mediated AF are Flecainide or Disopyramide, possibly for difficult cases, Amiodarone (though this has serious side-effects). Beta blockers and Digoxin are contra-indicated for vagal AF, and can actually make it worse.

It is crucial to actively manage the AF to prevent episodes.  This is because AF can, when it persists, display a characteristic whereby "AF begets AF" - that is, as the AF occurs, the heart muscle's properties become altered in such a way as to engender further and more persistent AF.

Active AF management should include not only drug treatment (if appropriate), and of course the correct drug(s), but also correction of any underlying issues such as chronic gastric problems. This is because the vagal stimulation caused by such problems can actually modify the heart muscle and make it likely to fibrillate, even if originally healthy.

It is vital to obtain medical care from a Cardiologist or Electrophysiologist who understands the distinction and is up-to-date with the characteristics and treatments for vagal AF.

A similar report is found at http://www.acc.org/clinical/guidelines/atrial%5Ffib/vi%5Fassociated.htm

 8. A Patient's View

It may take from 2 to 15 years for episodic attacks to develop into daily attacks.  The commonest feature is that of weekly episodes, lasting from a few minutes to several hours.  The essential feature is the occurrence of the attacks at night, often ending in the morning.  Rest, digestive periods (particularly after dinner), and alcohol absorption also are favoring factors.  Exercise or emotional stress does not trigger the arrythmia.  On the contrary, on feeling the sensation of an incoming arrythmia (repeated atrial extrasystoles), many patients observed that they could prevent it by exercising.  But the relaxation period that follows an effort or an emotional stress frequently coincides with the onset of AF."

For patients with VMAF, vagal stimulation can bring on or terminate episodes of AF. This includes activities such as:

bending down, sitting down, or lying down
drinking cold water or eating cold food (e.g., popsicles, frozen yogurt)
jumping into a cold swimming pool
gas buildup in the stomach
eating a heavy meal
coughing hard
alcohol ingestion
straining with a bowel movement.

These activities are especially likely to bring on AF in late afternoon until early morning, when vagal tone is predominant.  So can vagal maneuvers (carotid sinus massage, particularly when lying down, Valsalva maneuver (sitting, bending forward, and trying to blow out), plunging face into a basin of ice water while holding breath for half a minute).

In my experience, vagal maneuvers have worked sometimes to terminate my AF, but usually not on the first try.  Light exercise can also terminate AF, particularly when it has lasted into the morning or early afternoon.  Several posts to the atrial fibrillation message board have also reported that sleeping on the left side can trigger AF during the night (this has also been my experience), and I have found that I can avoid AF by sleeping on the right side or on the back.  It can also help to elevate the head and upper part of the body when sleeping, either by using several pillows or a bed that can be adjusted to do
this.

My own experience is that flecanaide (also known as tambocor) works for me.  It may also be significant that the first time I went into the ER for AF, I was given digoxin, and stayed in AF for nearly 48 hours until I was cardioverted.  It seems quite possible that the digoxin actually made the AF worse in my case.

My electrophysiologist has started me on a regime he calls "pulse therapy" under which I take flecainide (at a somewhat higher dosage than would usually be taken) only at the onset of an attack.  This way I am not on the drug all the time.  Source: A patients view: http://www.afibbers.org/victor2.html

 9. Dealing with AF

Individuals with many AF symptoms will usually call 911, those with very few symptoms will see their doctor or cardiologist.

"Over time, the pattern of AF may be defined in terms of the number of episodes, duration, frequency, mode of onset and possible triggers, and response to therapy..". Source: http://www.acc.org/clinical/guidelines/atrial%5Ffib/iii%5Fclassification.htm

Here is one way of keeping track of information on AF that may show useful patterns:

For recurring paroxysmal AF with minimal or no symptoms, anticoagulation and rate control drugs may be given as needed, but no drugs for AF prevention. These may be reserved for disabling symptoms. http://www.acc.org/clinical/guidelines/atrial%5Ffib/figure10.htm 

Check food interactions: http://media.seniorconnection.org/pdfs/FD-handout1.pdf  http://64.58.76.136/search/cache?p=anticoagulants+dietary&url=e3rLNkJpuYoC:www.aecom.yu.edu/family/presentations/vitk.ppt  

Some individuals are reducing the occurrence of their AF episodes by following the TopWell Lifestyle Program at www.learnwell.org/topwell.htm in addition to their prescribed medications. This may work for some but not for others.  There are many home interventions that individuals have tried on their own but as far as the author knows, none have proved successful for the larger AF population.

This is a health education page and no part of it should be considered medical advise.

10.  AF Library 

Management of AF: http://www.ahcpr.gov/clinic/epcsums/atrialsum.

AF Resources: http://www.a-fib.com

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