Re: scary article

[Guest guest]

In a message dated 12/12/2004 9:22:30 PM Eastern Standard Time,

james@... writes:

no need to shoot the messenger george information is always useful -

it's the only way we can make the right decisions. I'm not sure there's

anything revelational in the article - it's a summary of the last 5 or 6

years research.

It is a statistician's playground though, the optimist might summarise

it as " improvements in so many heart disorders are now so good that

people will survive long enough to be given the opportunity to develop

AF "

Sounds like a pretty good epidemic given the alternative of popping your

clogs before you develop AF. We are living longer, we are surviving many

heart problems that used to be fatal, AF is on the increase. AF is now

appearing on the 'we should get around to fixing this' list - sounds

great to me

--

D

Thank you - As I said I had hesitated in posting this article (which I

had previously found posted by another affiber in the laf Phorum) because it is

written in a very serious manner with alot of statistics and info that I

believe we should all be educated about- I was suprised as a long time affiber

how

much the article disturbed me even though I already knew most of this info

from my own exposure to the research- Affibers will in most cases find nothing

new in this article but the tone of it is scary and that disturbed me enough to

look at and review my own treatment-I agree with your thoughts-the more info

we have on affib the better we as affibers can be part of better decision

making of our medical treatment with our Doctors who often do not know what is

best for us in treating affib-ie-many give out ameodorone like it was candy to

treat affib-The other excellent point you make is that as affib becomes more

prevalent in an aging population it will get the increased research/medical

attention that it has not yet gotten in relation to other disorders-Jerry

[Guest guest]

Boy ... You are just full of positive inspiration .. aren't you.

Many old and not so old people live a perfectly normal and healthy life with

AFIB ..... it will not kill you .. it is a nuisance to be sure ... but

with the right type of care and maintenence (aspirin, blood thinners etc

........ my betting is that these people will longer lives than the great

many without AFIB ..........

scary article

This is kind of scary- Jerry

Beyond the Numbers: Epidemiology and Treatment of Atrial Fibrillation

M. Lloyd-, MD, ScM, FACC

Medscape Cardiology 8(2), 2004. © 2004 Medscape

Posted 11/29/2004

Introduction

The incidence and prevalence of atrial fibrillation (AF) are on the verge of

reaching epidemic proportions. AF is already the most commonly occurring

dysrhythmia, currently affecting an estimated 2.2 million Americans.[1] The

lifetime risk for AF for men and women over age 40 is approximately 25%,

indicating

that 1 in 4 older individuals will experience AF before he or she dies.[2]

In

the coming decades, we may be victims of the substantial successes in other

arenas in medicine with regard to AF. Because AF is overwhelmingly a disease

of

older people, increases in longevity, improved survival after myocardial

infarction and congestive heart failure, and increasing prevalence of

cardiac

surgery are certain to lead to an increased prevalence of AF. Current

estimates

suggest that the prevalence of AF will reach 4 million by 2030 and climb to

5.6

million by 2050.[3-5]

These numbers are sobering in light of the substantial mortality and

morbidity associated with AF. In 2001, AF was the primary and/or

contributing cause of

more than 70,000 deaths. The age-adjusted death rate (per 100,000) has

climbed substantially from 27.6 in 1980 to 69.8 in 1998.[1] The Framingham

Heart

Study has shown that the presence of AF is independently associated with a

50% to

90% increase in the risk of death.[5]

In addition to the higher rates of mortality associated with AF, the

morbidity attributed to AF warrants particular attention. AF is associated

with a

5-fold increase in the risk of ischemic stroke, which is the leading cause

of

disability in the United States. Approximately 15% to 20% of all strokes, or

about

75,000 strokes per year in the United States,[6] are attributable to AF.

Furthermore, AF is an independent predictor of stroke recurrence and stroke

severity, with increased risk for ischemic stroke and embolism among

patients with a

history of previous stroke or transient ischemic attack (TIA; RR = 2.5).[7]

Finally, patients who experience symptomatic AF, even in the absence of a

complication, have impaired quality of life and lower functional status.

Exercise

intolerance, palpitations, fatigue, increased urination, congestive heart

failure, angina, hypotension, and presyncope are all conditions that greatly

reduce

the quality of life for patients suffering from AF.

The burden of healthcare costs associated with caring for patients with AF

is

also reaching astronomical proportions. Between 1985 and 1999, the number of

AF-related hospitalizations increased 190%. In 2001, AF was responsible for

416,000 hospital discharges, with $6041 paid to Medicare beneficiaries for

each

hospitalization.[1] In addition to the direct costs associated with AF

hospitalizations, one must also recognize the post-discharge costs,

including

medications, physician visits, procedures (including echocardiograms and

cardioversions), transportation, and loss of work experienced by patients

after diagnosis

of AF.

Why do these numbers matter? As with the statistics for coronary heart

disease and cancers, these numbers matter because they serve to put the

epidemic of

AF into perspective. For example, a 70-year-old woman has a lifetime risk

for

breast cancer of 1 in 14,[8] compared with a lifetime risk for AF of 1 in

4.[2] Given the potentially devastating consequences of AF, it is important

to

remember that beyond the financial repercussions, these statistics represent

our

patients, family members, and friends. This article was written with the

intent that an understanding of the presentation of AF and its clinical

consequences will help physicians identify patients at risk for AF and

prescribe

appropriate and effective therapy for their patients with AF.

What Is AF?

AF is a dysrhythmia that originates in the upper chambers, or atria, of the

heart. In normal sinus rhythm, the sinoatrial (SA) node, located at the

junction of the superior vena cava and the right atrium, initiates an

electrical

impulse that travels through the atria and causes the right and left atria

to

contract and pump blood into the ventricles. The electrical impulse is then

transmitted from the atria to the ventricles through the atrioventricular

(AV) node,

allowing for ventricular activation. In the presence of structural changes

and/or abnormal triggering impulses, the electrical activity of the atria

can

become uncoordinated and chaotic, suppressing the SA node and resulting in

AF.

Triggers for AF include premature beats, acute atrial stretch, and changes

in

sympathetic and parasympathetic tone and balance. In persistent AF, there

are

typically multiple reentrant wavelets that create a pattern of continuous

chaotic electrical activity. The atrial electrical activity usually exceeds

200 to

400 beats per minute, which can trigger uncoordinated atrial activation with

consequent deterioration of atrial mechanical function.[7] On the

electrocardiogram, AF is characterized by the absence of discrete sinus P

waves. Instead,

atrial activity is seen as rapid oscillations or fibrillatory waves that

vary

in size, shape, and timing.[9] The AV node cannot typically conduct all of

these impulses, but some of them are transmitted to the ventricles in an

erratic

pattern, creating an irregular heartbeat and potentially affecting the

heart's

ability to pump blood. One consequence is that 20% to 50% of patients

suffering from AF may develop heart failure. Furthermore, the loss of

coordinated

atrial contraction also results in stagnation of blood within the atria,

particularly in the left atrial appendage, which increases the probability

of

intracardiac thrombus formation and systemic thromboembolism.

Nomenclature of AF

In many patients, AF tends to be a progressive phenomenon. Types of AF are

characterized by the duration of dysrhythmia and the ability to convert from

AF

into normal sinus rhythm and include:

New-onset AF

Acute AF

Paroxysmal AF

Persistent AF

Permanent AF

A high percentage of new-onset AF episodes will spontaneously terminate

within 24 hours without treatment, particularly in younger individuals.

Acute AF

tends to refer to an episode that is diagnosed within 48 hours of its onset,

if

onset time can be determined reliably by symptoms or monitoring. Paroxysmal

AF

typically refers to intermittent, recurrent, self-terminating episodes of

AF.

In persistent AF, the rhythm does not self-terminate, but can often be

effectively cardioverted to sinus rhythm. Permanent AF is long-standing and

resistant to cardioversion; it may terminate for brief intervals, but tends

to persist

for the remainder of the patient's life. Refractoriness to cardioversion has

been found to be primarily dependent upon the duration of AF and the extent

of

structural changes and enlargement of the atria.

AF frequently progresses from transient and self-terminating (paroxysmal) to

episodes of longer duration requiring cardioversion (persistent), and then,

subsequently, to permanent AF. The progression from more benign patterns to

permanent patterns may be determined by anatomic structural changes such as

fibrosis, necrosis, fatty deposits, and inflammation.

Who Is the AF Patient?

Patients with AF may present with palpitations, including a sensation of

missed or extra heartbeats or an inappropriate rapid heartbeat. Others may

complain of a lack of energy or tiredness, dizziness, chest discomfort

(pain,

pressure, or other discomfort in the chest), and/or shortness of breath

(difficulty

breathing during activities of daily living). Hypertension is believed to be

the most prevalent risk factor associated with AF.[10,11] Other known risk

factors include valvular and other structural heart diseases, congestive

heart

failure, previous myocardial infarction, diabetes, obesity, excessive

alcohol

consumption (acute and chronic), and thyroid disease (particularly

hyperthyroidism).[12-14] Cardiac surgery, pericarditis, electrolyte

imbalances, and certain

pharmacologic and recreational drugs can precipitate AF as well. Demographic

variables, such as age, sex, and race/ethnicity, also appear to affect the

presentation and outcome of AF.

Age

A number of studies have shown that AF is more common in adults over the age

of 65 years than in their younger counterparts.[14] The prevalence of AF

increases from less than 1% among persons younger than 60 years to about 10%

among

persons aged 80 years and older. Data from the Anticoagulation and Risk

Factors in Atrial Fibrillation (ATRIA)[4] study support the relationship

between AF

and age. ATRIA found that the prevalence rates of AF were 0.1% in persons

younger than 55 years, 3.8% in those aged 60 and older, and 9.0% in adults

80

years and older.

Using data from the Framingham Heart Study, and colleagues reported

that for both younger and older age groups, the mortality of men and women

with AF was substantially greater than for non-AF subjects (P < .0001).[5]

They

also found that in subjects aged 55-74 years, 61.5% of men with AF vs 30.0%

of

men without AF died at 10-year follow-up; in women, 57.6% with AF died vs

20.9% of women without AF.[5] Additionally, individuals with AF, especially

after

age 65 years, had significantly shorter mean survival than those without AF.

Gender

In addition to age, several studies have examined the relationship between

gender and AF. The majority of studies published to date suggest that the

prevalence of AF is higher in men than in women. In the ATRIA study, for

example, AF

was more commonly reported in men (1.1% vs. 0.8%, P < .001).[4] Similarly,

20-year follow-up in the Renfrew-Paisley cohort demonstrated that the

prevalence

of AF was 8 per 1000 males and 5 per 1000 females.[15] In the Framingham

Heart Study, 2.2% of men had AF and women had a slightly lower prevalence of

1.7%.

Other Framingham Heart Study reports have also documented the increased risk

of AF among men. and colleagues reported that after adjusting for

age

and other risk factors, the risk of developing AF was 1.5 times higher in

men

than in women, and for each decade of advancing age, the odds ratio of AF

was

2.1 for men and 2.2 for women.[12] Absolute lifetime risk for the

development

of AF is slightly higher in men than in women, but the overall risks are

relatively comparable between men and women regardless of age.[2]

Despite a higher incidence of and risk for developing AF in men, it appears

that the risk of mortality associated with AF may be greater in women.

and colleagues identified AF as an independent predictor of mortality. After

adjusting for other risk factors, they found that AF was associated with a

1.5-fold risk of mortality in men and a 1.9-fold risk in women.[5] The

long-term

follow-up of the Renfrew-Paisley study[15] also demonstrated that AF was an

independent predictor of all-cause mortality, cardiovascular events, and

stroke

and that the risk was consistently higher in women than in men. According to

investigators, the relative risk of all-cause mortality related to AF was

2.2

in women vs 1.5 in men.

Race

Although risk factors for AF clearly differ between race/ethnic groups,

there

is no clear picture of the differences in racial patterns of AF. In the

ATRIA

study,[4] the incidence of AF was found to vary among race/ethnic groups.

Among patients 50 years or older, AF was more common in white than in black

patients (2.2% vs 1.5%, respectively; P < .001). Investigators found that

there was

no difference between races among patients 50-59 years of age, however, in

older age groups (60-69, 70-79, and >/= 80 years), AF was consistently more

common in whites vs blacks.

These findings were supported by results of the Epidemiology, Practice,

Outcomes, and Costs of Heart Failure (EPOCH)[16] study, which found that in

a

contemporary heart failure cohort, blacks had a 50% lower prevalence of AF

than

whites. The authors reported that these findings did not significantly

change

after adjusting for other variables by multivariate analyses.

The incidence of death related to AF is also higher in white vs black

patients. The AHA reports that the age-adjusted death rate (per 100,000)

associated

with AF in 2001 was 25.7 for white patients vs 16.4 for black patients.[1]

However, we should keep in mind some of the significant limitations

associated with some of these studies demonstrating a greater prevalence of

AF in

whites than in blacks. Specifically, the majority of epidemiology studies

conducted

to date have predominately studied whites.[17] In EPOCH,[16] for example,

conclusions regarding race were drawn from comparisons made between 223

blacks

and 1150 whites, and in ATRIA,[4] of the 17,974 patients evaluated, only

3.6%

were black. Furthermore, AF may be underdiagnosed in cross-sectional studies

that rely on patient self-report, that obtain only 1 electrocardiogram, or

that

do not have access to all medical records.

Treatment Strategies

Once the diagnosis of AF is confirmed by 12-lead electrocardiogram,

decisions

regarding the appropriate treatment strategy for a given patient may depend

on a number of factors. First, it is helpful to determine the length of time

the patient has had AF, if possible. If restoration of sinus rhythm is

deemed to

be desirable, the success rate for restoration of sinus rhythm with

medications or direct current (DC) cardioversion will depend on the length

of time that

AF has been present. Underlying structural heart disease and degree of

atrial

enlargement will also affect success rates. Furthermore, the duration of AF,

if known, will determine the need for prolonged anticoagulation and/or

transesophageal echocardiography prior to cardioversion. Rapid intervention

may

decrease the likelihood of remodeling and scarring of the atrial tissue,

which in

turn may reduce the likelihood of progression of transient bouts of AF to

permanent AF.[18] More chronic treatment options can include the use of

rate- or

rhythm-control strategies, pacemaker therapy for AF suppression, and/or

radiofrequency or surgical ablation of AF circuits, some of which will be

briefly

discussed below.

Rate vs Rhythm Control

Control of the ventricular rate is an important component of the treatment

of

AF. Drugs such as calcium-channel blockers, beta-blockers, and digoxin are

often used to improve both resting and exercise ventricular rates, largely

through slowing of conduction through the AV node. Beta-blocking agents

decrease

the resting heart rate and diminish the heart-rate response to exercise.

Calcium-channel blockers are also effective rate-control agents. Digoxin is

used for

rate control because it enhances vagal tone and prolongs AV nodal

refractoriness, but it has only been shown to be effective for rate control

at rest and is

typically used as a second-line agent for rate control in AF.[19] Digoxin

may

be effective in more sedentary and stable patients, but it is often utilized

in combination with a beta-blocker or calcium-channel blocker in more active

patients. Indeed, many patients will require 2 medications for effective

rate

control. Certainly, individual considerations must be made when prescribing

any

of the aforementioned medications. When using multiple agents for rate

control, clinicians must be aware of the potential for development of

digoxin

toxicity (especially in the presence of renal dysfunction, or in cases of

exposure

to verapamil or amiodarone), or of excessive AV nodal blockade, which can

lead

to symptomatic bradycardia.

Data from recent studies have challenged the long-held belief that

restoration and maintenance of sinus rhythm is the optimal treatment

approach to reduce

risks for morbidity and mortality, particularly due to stroke. Such a

strategy, known as " rhythm control, " employs electrical cardioversion and

antiarrhythmic drugs for those with persistent AF. The Atrial Fibrillation

Follow-up

Investigation of Rhythm Management (AFFIRM)[20] and Rate Control versus

Electrical

Cardioversion (RACE)[21] studies demonstrated that a rhythm-control strategy

was not superior to a rate-control strategy using drug therapy to control

ventricular rate. In some patient subgroups in the 2 trials, such as women,

patients older than 65 years of age, or those with hypertension, congestive

heart

failure, or coronary heart disease, rhythm control was actually associated

with

trends toward increased mortality.

Nonetheless, rhythm control remains an appropriate strategy for many

patients, particularly those with moderate to severe symptoms, such as

frequent or

intolerable palpitations or exercise intolerance, and in cases where a

strong

patient preference is stated. The most important consideration in

rhythm-control

strategies is the ongoing need for anticoagulation. AF will frequently recur

transiently and repetitively in patients despite antiarrhythmic medications,

and the presence of these medications may make it less likely that the

patient

will detect the AF. If anticoagulation is discontinued but AF recurs, the

patient will be at an unacceptably high risk for stroke. In recent studies,

patients who were not treated with anticoagulants had a 2.1-fold increased

risk for

recurrent stroke and a 2.4-fold risk for recurrent severe stroke.[1] In both

the AFFIRM[20] and RACE[21] studies, most strokes occurred in patients who

discontinued anticoagulation or had subtherapeutic (< 2.0) international

normalized

ratios (INRs).

Rhythm control employs the use of antiarrhythmic drug therapy, usually with

amiodarone or class IC antiarrhythmics, and can also include the use of

cardioversion and catheter-based or surgical ablation to restore sinus

rhythm.

Amiodarone has been shown to be superior to other drugs such as sotalol, but

no

antiarrhythmic has been uniformly effective in preventing the recurrence of

AF. In

patients with persistent AF who have been successfully cardioverted, only

about 50% will be free of a recurrence of AF at 1 year, even with the best

antiarrhythmic regimen. Drug choice is typically based on factors such as

the age of

the patient, the presence of structural heart disease, convenience of

dosing,

efficacy of the drug, and potential toxicity. Amiodarone, the most effective

available agent, is associated with potentially severe toxicities including

pulmonary and hepatic fibrosis, both of which are related to the cumulative

dose. Thyroid disorders, most commonly hypothyroidism, are also associated

with

amiodarone, and can occur early in the course of therapy, particularly among

the

elderly. The occurrence of hypothyroidism typically necessitates thyroid

hormone replacement therapy, whereas the occurrence of hyperthyroidism often

causes recurrence of AF and necessitates discontinuation of amiodarone and

more

complicated treatment for control of the thyroid. The greatest concern with

use

of antiarrhythmic drugs is their potential for proarrhythmic effects, which

can

lead to lethal heart rhythms and/or hemodynamic collapse.

Cardioversion. When managing new-onset AF, initial efforts are focused on

rate control to decrease the potential for myocardial ischemia or congestive

heart failure, and to promote the possibility of spontaneous conversion to

sinus

rhythm. Chemical conversion is typically most successful when the patient is

without important structural heart disease and if the duration of AF has

been

less than 48 hours. However, because of the risk of serious ventricular

arrhythmias, patients must be monitored closely in a hospital setting. DC

cardioversion involves the use of an electrical shock to depolarize all of

the atrial

myocardium simultaneously, with the aim of restoring organized electrical

activity. This allows the SA node to resume its role as the primary

pacemaker for the

heart. In patients with persistent AF, synchronized electrical cardioversion

under sedation is safe and effective, with success rates usually in the

range

of 65% to 90%.[22] The use of defibrillators that utilize biphasic shock

waveforms has increased the success of cardioversion and decreased the

energy

required when compared with monophasic shocks. In patients with

long-standing AF, AF

recurrence after cardioversion is common and primary antiarrhythmic drug

therapy can be used to help maintain sinus rhythm.

Internal cardioversion with percutaneous electric catheters can also be used

in patients in whom external cardioversion has failed. Delivery of

synchronized low-energy shocks between the right atrium and coronary sinus

or left

pulmonary artery can restore sinus rhythm in an additional 80% to 90% of

patients

under sedation.[23]

Ablation. Ablation is another means of rhythm control and is often reserved

for patients who remain symptomatic despite optimal medical care. Elegant

electrical mapping studies of AF in animal models and humans have indicated

the

important role played by electrically active tissue at the juncture of the

left

atrium and pulmonary veins. Ablation techniques attempt to isolate these

foci

that initiate and perpetuate AF. Catheter-based radiofrequency ablation has

become an increasingly viable treatment option for patients with paroxysmal

or

persistent AF. In essence, radiofrequency pulses are applied

circumferentially

around the ostia of the pulmonary veins in order to disrupt the electrical

connections between the left atrium and pulmonary veins. Success rates vary

but

typically range from 60% to 90%, depending on patient selection.

Radiofrequency

ablation in and near the pulmonary veins can, in rare cases, lead to

pulmonary

vein stenosis and the possibility of pulmonary hypertension. A variety of

surgical techniques have also now been described for electrical isolation of

the

pulmonary veins. These techniques are being used increasingly for patients

with AF who are undergoing cardiac surgery for other reasons, and have in

some

cases been the primary indication for surgery in severely symptomatic

patients.

Another surgical procedure, known as the Maze procedure, involves making

multiple linear incisions in the atrial tissue. In theory, this should

isolate

regions of the atria and create regions of tissue that are too small to

sustain

AF.[24] Postoperative complications include fluid retention (occurring in 5%

of

all patients) and frequent atrial arrhythmias in the early postoperative

period. The Maze III procedure is the most current technique used today for

treatment of permanent AF and has had 95% success in the treatment of AF in

patients

with structural heart disease.[25]

Finally, for those with chronic AF and uncontrollable tachycardia, ablating

the AV node is another option. Ablation of the AV node will require

permanent

pacing to restore appropriate ventricular rates and responsiveness. Results

from The Left Ventricular-Based Cardiac Stimulation Post AV Nodal Ablation

Evaluation Study (PAVE)[26] study demonstrated that the use of a

biventricular

pacemaker instead of a dual-chamber pacemaker yielded better functional

outcomes.

Anticoagulation

Regardless of which treatment strategy is employed, we must all be aware of

the critical role of anticoagulation in the treatment of AF. As discussed

above, AF increases the risk of stroke 5-fold and accounts for 15% to 20% of

all

strokes.[1] Numerous studies have documented the benefits of anticoagulation

in

AF patients, regardless of the underlying etiology. Although anticoagulation

therapy has been shown to reduce the risk of stroke, its use is limited by

low

prescription rates, poor patient compliance, and potential bleeding

complications. For most patients in AF, adjusted-dose warfarin is indicated,

unless they

are at low risk for stroke or have a specific contraindication to the use of

warfarin (eg, thrombocytopenia, recent trauma or surgery, or

alcoholism).[27]

For low-risk patients, adult-strength aspirin (325 mg daily) may be

appropriate.

Patients on active warfarin therapy require frequent monitoring to ensure

INR

levels are optimized. The optimal INR for an AF patient is between 2.0 and

3.0. Studies indicate that levels below 2.0 are not adequate to protect

against

thromboembolic complications, whereas levels above 3.0 can increase the

chance

of bleeding. As noted earlier, in both the AFFIRM[20] and the RACE[21]

studies, the majority (70% in the AFFIRM cohort) of all strokes occurred in

patients

who had stopped receiving anticoagulation or who had subtherapeutic INRs (<

2.0).

Despite convincing evidence for the effectiveness of warfarin prophylaxis,

concern has been expressed that the efficacy of warfarin in clinical trials

may

not translate to clinical practice. This therapy requires that patients

undertake frequent laboratory testing and its use is associated with an

increased

risk of bleeding. These factors tend to adversely affect patient compliance.

Nonetheless, until newer agents become available, warfarin is the drug of

choice

for most patients with AF, and patients must understand the potentially

devastating complications of noncompliance.

Conclusion

The aging of the population, improved survival after myocardial infarction

and congestive heart failure, and the increase in the number of cardiac

procedures will all contribute to the inevitable increase in the burden of

AF. With

roughly 2.2 million people currently suffering from AF, it is imperative

that we

focus on earlier detection, better individualized patient management, and,

most importantly, reduction of the morbidity and mortality of patients

suffering

from AF with evidence-based therapies, as well as good clinical judgment.

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rhythm control in patients with recurrent persistent atrial fibrillation. N

Engl J Med. 2002;347:1834-1840.

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knowledge and recommendations for management. Working Group on Arrhythmias

of the

European Society of Cardiology. Eur Heart J. 1998;19:1294-1320.

Schmitt C, Alt E, Plewan A, et al. Low energy intracardiac cardioversion

after failed interventional external cardioversion of atrial fibrillation. J

Am

Coll Cardiol. 1996;28:994-999.

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fibrillation. Cardiol Clin. 1997;15:739-748.

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lone

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first prospective, randomized study evaluating BV pacing after ablate and

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therapy. Program and abstracts from the American College of Cardiology

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2003;139:1009-1017.

M. Lloyd-, MD, ScM, FACC, Assistant Professor, Preventive

Medicine and Medicine, Feinberg School of Medicine, Northwestern University,

Chicago,

Illinois; Staff Physician, Cardiology, Northwestern Memorial Hospital,

Northwestern Memorial Faculty Foundation.

Disclosure: M. Lloyd-, MD, ScM, has disclosed that he has served

as an advisor or consultant for Merck and Novartis.

[Guest guest]

> Boy ... You are just full of positive inspiration .. aren't you.

> Many old and not so old people live a perfectly normal and healthy life with

> AFIB ..... it will not kill you .. it is a nuisance to be sure ... but

> with the right type of care and maintenence (aspirin, blood thinners etc

> ....... my betting is that these people will longer lives than the great

> many without AFIB ..........

no need to shoot the messenger george information is always useful -

it's the only way we can make the right decisions. I'm not sure there's

anything revelational in the article - it's a summary of the last 5 or 6

years research.

It is a statistician's playground though, the optimist might summarise

it as " improvements in so many heart disorders are now so good that

people will survive long enough to be given the opportunity to develop

AF "

Sounds like a pretty good epidemic given the alternative of popping your

clogs before you develop AF. We are living longer, we are surviving many

heart problems that used to be fatal, AF is on the increase. AF is now

appearing on the 'we should get around to fixing this' list - sounds

great to me

--

D

[Guest guest]

<<These numbers are sobering in light of the substantial mortality

and morbidity associated with AF. In 2001, AF was the primary and/or

contributing cause of more than 70,000 deaths. The age-adjusted

death rate (per 100,000) has climbed substantially from 27.6 in 1980

to 69.8 in 1998>>

<<The Framingham Heart Study has shown that the presence of AF is

independently associated with a 50% to 90% increase in the risk of

death>>

<<In addition to the higher rates of mortality associated with AF,

the morbidity attributed to AF warrants particular attention. AF is

associated with a 5-fold increase in the risk of ischemic stroke>>

<<Finally, patients who experience symptomatic AF, even in the

absence of a complication, have impaired quality of life and lower

functional status>>

And a lot of doctors, including EP's, still call afib just a nuisance.

P <MI>

[Guest guest]

> This is kind of scary- Jerry

>

> Beyond the Numbers: Epidemiology and Treatment of Atrial

Fibrillation

>

>

> M. Lloyd-, MD, ScM, FACC

> Medscape Cardiology 8(2), 2004. © 2004 Medscape

> Posted 11/29/2004

>

>

>]

This article is not really surprising. In mid 1993, Pappone

published an article on the differences in health outcomes between

people treated with medications and those who elected ablations in a

particular study group. The study of about 1,200 people in Italy,

though somewhat flawed in its methodology due to self selection of

treatment by the patients, indicated that in the study group those

who were treated with medication had worse morbidity and mortality

statistics than those who elected ablation, and that within the

group studied, the ablation group's morbidity and mortality

statistics tended to mirror the general population. Dr. Natale told

me at the time not to read too much into such a small study, but

this new article is somewhat consistent with the Pappone study.

I had an ablation by Dr. Natale which has been successful for 13

months, so my bias may be showing here. Nevertheless, there is much

to think about in choosing a treatment.