From the National Heart, Lung, and Blood Institute's Framingham
Heart Study, National Institutes of Health, Framingham, Mass (E.J.B., P.A.W.,
R.B.D., H.S., W.B.K., D.L.); Departments of Cardiology (E.J.B.), Preventive
Medicine (E.J.B., P.A.W., D.L.), and Neurology (P.A.W.), Boston University
School of Medicine, Boston, Mass; Department of Mathematics, Boston University
(R.B.D., H.S.), Boston, Mass; Division of Cardiology and Clinical
Epidemiology, Beth Israel Hospital, Boston, Mass (D.L.); and National Heart,
Lung, and Blood Institute, Bethesda, Md (D.L.).
Correspondence to Emelia J. Benjamin, MD, ScM, The Framingham Heart Study, 5 Thurber St, Framingham, MA 01702-6334. E-mail emelia{at}fram.nhlbi.nih.gov
Methods and Results—We examined the mortality of subjects 55 to
94 years of age who developed AF during 40 years of follow-up of the
original Framingham Heart Study cohort. Of the original 5209 subjects,
296 men and 325 women (mean ages, 74 and 76 years, respectively)
developed AF and met eligibility criteria. By pooled logistic
regression, after adjustment for age, hypertension, smoking, diabetes,
left ventricular hypertrophy, myocardial
infarction, congestive heart failure, valvular heart disease,
and stroke or transient ischemic attack, AF was associated with
an OR for death of 1.5 (95% CI, 1.2 to 1.8) in men and 1.9 (95% CI,
1.5 to 2.2) in women. The risk of mortality conferred by AF did not
significantly vary by age. However, there was a significant AF-sex
interaction: AF diminished the female advantage in survival. In
secondary multivariate analyses, in subjects
free of valvular heart disease and preexisting
cardiovascular disease, AF remained significantly
associated with excess mortality, with about a doubling of mortality in
both sexes.
Conclusions—In subjects from the original cohort of the
Framingham Heart Study, AF was associated with a 1.5- to 1.9-fold
mortality risk after adjustment for the preexisting
cardiovascular conditions with which AF was related.
The decreased survival seen with AF was present in men and women
and across a wide range of ages.
Although the morbidity of AF is well documented, it has not been
clearly established whether AF per se results in excess mortality. The
worsened survival seen with AF could reflect the increased mortality of
the cardiovascular conditions with which it is
associated. Using data from the Framingham Heart Study, we sought to
ascertain the mortality associated with AF after adjusting for
coexistent cardiac conditions and risk factors in a
population-based sample.
Definition of Clinical Covariables
Statistical Analyses
To examine the influence of age and sex on AF mortality, interaction
terms were introduced. To remove the impact of conditions with a high
case-fatality rate, in 1 analysis, subjects were excluded if
they died within 30 days of AF onset. Finally, to investigate whether
the poor prognosis with AF was limited to subjects with
valvular heart disease or preexisting
cardiovascular disease, a multivariate
analysis (adjusting for age, hypertension, smoking, diabetes,
and left ventricular hypertrophy) was limited
to subjects who were free of clinically apparent valvular heart
disease, myocardial infarction, congestive heart failure, or stroke or
transient ischemic attack.
For descriptive purposes, we used a matched-cohort analysis.
Approximately 2 subjects without AF were matched to each AF subject by
age, sex, and date of diagnosis of AF (index examination cycle). The
characteristics of the AF subjects and matched subjects without AF were
defined at the baseline index examination. To describe the mortality
after AF, a Kaplan-Meier analysis11 of
the matched-cohort subjects was used to estimate survival and produce
mortality curves. A log rank test was used to test the differences in
survival between AF and matched non-AF
participants.12 All analyses were sex
specific and were performed with the Statistical Analysis
System program13 on a Sun Sparc workstation.
The Kaplan-Meier mortality curves are displayed in the
Figure
To estimate the excess mortality attributable to AF, pooled logistic
regression analyses were undertaken (Table 3
Further tests failed to reveal a significant interaction between age
and AF with respect to mortality. The multivariate
coefficients for an age-AF interaction were 0.00811 (P=0.49)
in men and -0.00419 (P=0.69) in women, suggesting that the
risk of death with AF did not significantly vary over the 4 decades of
age studied. However, the risk of death in the setting of AF did vary
by sex. With men and women combined, in a full
multivariate model, there was a significant interaction
between sex and AF with regard to mortality. The presence of AF made
the sexes look similar for mortality: an OR of 1.2 (95% CI, 0.98 to
1.49) for men versus women with AF compared with an OR of 1.6 (95% CI,
1.4 to 1.7) for men versus women without AF.
Secondary analyses explored the impact of AF in subsets of
subjects with AF (Table 3
Cause of Death
We performed secondary analyses to see whether the increased
mortality risk was limited to subsets of subjects with AF. One
possibility is that AF merely served as a marker for terminal illness.
After elimination of 30-day mortality, AF remained associated with a
50% greater mortality in women. However, in men who survived 30 days
after AF was diagnosed, AF was no longer significantly associated with
increased mortality, suggesting that in men the worsened survival with
AF was heavily influenced by early mortality. Another potential
explanation is that the increased mortality of AF was confined to
subjects with structural heart disease or more severe clinically
evident cardiovascular events. When our
analysis was limited to subjects free of baseline myocardial
infarction, congestive heart failure, valvular heart disease,
and stroke or transient ischemic attack, AF was still
associated with about a doubling in mortality.
Comparison With Previous Literature
Evidence of mortality risk in broader series of AF subjects comes from
several sources. Gajewski and Singer24 in 1981
examined insurance applicants and found that after 3.3 years of
follow-up, applicants with chronic AF or paroxysmal AF in the setting
of mitral stenosis or coronary artery disease had
increased mortality. In a 1982 hospital-based study,
Godtfredsen25 found that subjects with
AF had a worse mortality compared with the general population. A number
of cohort studies have also examined the issue, with samples ranging
from male air force recruits26 to male civil
servants27 to population-based
samples.28 29 30 31 32 Given the diverse study designs,
it is not surprising that the reported 1-year mortality has varied
widely, from 2.6% in the Gajewski and Singer24
series describing insurance applicants with asymptomatic
chronic AF to 16% in patients >70 years of age with AF detected on
hospitalization.33 While 1 study found that the
1.9-fold mortality risk was not statistically
significant,30 most studies have found that
AF conferred excess risk of death,24 26 27 28 29 31 32
with a risk of all-cause mortality ranging from an adjusted relative
risk of 1.326 to an unadjusted relative risk of
2.6.27
However, the studies of broader samples of AF subjects have been
limited by a number of factors, including a small number of AF
cases29 30 31 32 and the inclusion of prevalent AF
cases.24 25 27 28 29 30 32 34 Prior studies have also
had the disadvantages of being
retrospective,24 25 34 case
series,25 34 or case-control in
design.28 30 Most of the prior studies have not
shed light on possible sex differences in the mortality of AF because
they have been all male cohorts26 27 or lacked
sex-specific analyses.24 25 28 30 32 34
With regard to clarifying the independent impact of AF on mortality,
the fundamental limitation of most prior studies was their lack of
time-dependent or multivariate
analyses.24 25 27 28 30 31 32 34
Study Strengths and Limitations
The study sample was largely white; our results may not be
generalizable to other racial groups. Similarly, the results may not be
relevant to subjects outside the age range studied (55 to 94 years of
age), particularly younger subjects without any evidence of structural
heart disease. In addition, we combined AF and atrial flutter, as well
as chronic and paroxysmal AF; hence, we do not comment on differences
in the prognosis of these AF subsets. Although the primary
analysis controlled for covariates such as myocardial
infarction, we were unable to control for infarct severity, which has
been associated with risk for both AF and death. Most of the follow-up
occurred before the availability of
echocardiography and the widespread use of
anticoagulants and antiarrhythmics for AF. The lack of routine
echocardiography undoubtedly contributed to some
misclassification of valvular heart disease. Moreover, we have
insufficient data to comment on whether the mortality of AF is altered
by anticoagulants35 or
antiarrhythmics,36 as suggested by others.
However, studies suggest that only about one third of eligible AF
patients in the United States receive
warfarin.37 38 Therefore, we believe that our
mortality data may have relevance to most subjects with AF, given
current treatment practices.
Clinical Implications
Received January 23, 1998;
revision received April 21, 1998;
accepted May 3, 1998.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Impact of Atrial Fibrillation on the Risk of Death
The Framingham Heart Study
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—Atrial fibrillation (AF)
causes substantial morbidity. It is uncertain whether AF is associated
with excess mortality independent of associated cardiac conditions and
risk factors.
Key Words: fibrillation, atrial • mortality • prognosis • stroke • cerebrovascular disorders • risk factors • aging
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Atrial fibrillation
(AF) is the most common chronic arrhythmia associated with an
adverse prognosis. It is estimated that 2.2 million Americans have
intermittent or sustained AF.1 The incidence of
AF increases with advancing age, with an annual incidence per 1000
person-years of about 3.1 cases in men and 1.9 cases in women 55 to 64
years of age, rising to 38.0 and 31.4 cases in men and women 85 to 94
years of age.2 The clinical risk factors for AF
include advancing age, diabetes, hypertension, congestive heart
failure, rheumatic and nonrheumatic valve disease, and myocardial
infarction.2 The
echocardiographic risk factors for nonrheumatic AF
include left atrial enlargement, increased left ventricular
wall thickness, and reduced left ventricular fractional
shortening.3 AF is an independent risk factor for
stroke, resulting in an approximate 3- to 5-fold excess
risk.4 Furthermore, whereas the attributable
risks for most stroke risk factors decline with advancing age, the
attributable risks for stroke associated with AF dramatically increase
with age, from 1.5% for those 50 to 59 years of age to 23.5% for
those 80 to 89 years of age.4
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Subjects
The Framingham Heart Study was begun in 1948 to explore risk
factors for and consequences of cardiovascular disease
in a longitudinal population-based cohort. At entry, 5209 residents of
Framingham, Mass, who were 28 to 62 years of age were enrolled. The
subjects have received biennial examinations with routine assessment of
medical history, physical examination, blood tests, and 12-lead ECGs.
The examination procedures were approved by the Investigational Review
Board of Boston Medical Center, and all subjects gave informed consent.
Previous reports have outlined the study design, response rates, and
completeness of follow-up.5 For the present
study, we analyzed 40 years of follow-up. Subjects were
excluded from analysis if they had AF at the first examination
(n=19). Analyses were restricted to subjects 55 to 94 years of
age at each biennial examination. AF was diagnosed if chronic or
paroxysmal AF or atrial flutter was present on ECG. ECGs were
obtained from the routine biennial Framingham Heart Study clinic
examination or from outside hospitals and
physicians.2
Hypertension was considered present if the systolic
blood pressure was at least 140 mm Hg or the
diastolic blood pressure was 
90 mm Hg on each of 2
successive readings obtained by the clinic physician or if the subject
was receiving antihypertensive medication.6
Diabetes was defined as a nonfasting blood glucose level 11.11
mmol/L (200 mg/dL) or the use of insulin or an oral hypoglycemic agent.
ECG left ventricular hypertrophy was diagnosed
if a subject had voltage criteria for left ventricular
hypertrophy accompanied by lateral repolarization
changes.7 Prevalent congestive heart failure and
myocardial infarction were determined by a panel of 3 physicians using
previously published criteria.8 Because
echocardiography was unavailable for the first 3
decades of the study, valvular heart disease was defined by
auscultation criteria as any diastolic murmur or a >2 over
6 systolic murmur on Framingham Heart Study examination.
The diagnosis of a stroke or transient ischemic attack was made
by a panel of 3 investigators, including a neurologist, after they
reviewed all records from relevant hospitalizations and
clinic-reported events. Subjects suspected of having a cerebrovascular
event were seen by a study neurologist in the hospital and in periodic
follow-up.9
The primary analysis examined the impact of AF on
mortality in men and women using pooled logistic regression
analysis.10 The pooled logistic
regression analysis is equivalent to a Cox time-dependent
regression analysis.10 The pooled
logistic regression analyses allowed the covariates in the
multivariate models to change over time, with the
clinical variables redefined at every biennial examination. Missing
data were imputed by substituting the most recent values as long as
they were obtained within the 2 preceding examination cycles.
Cardiovascular disease was defined as congestive heart
failure, myocardial infarction (recognized or unrecognized), and stroke
or transient ischemic attack; these events were redefined
between biennial examinations as long as they occurred at or before the
onset of AF. To assess the net effect of AF, we used
multivariate models that adjusted for age,
hypertension, smoking, diabetes, ECG left ventricular
hypertrophy, myocardial infarction, congestive heart
failure, valvular heart disease, and stroke or transient
ischemic attack unless otherwise specified.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
During up to 40 years of follow-up, 296 men (mean age, 73.7 years)
and 325 women (mean age, 76.4 years) developed AF. Table 1
displays the baseline characteristics
of the AF and the age-, sex-, and calendar year–matched subjects
without AF. Subjects with AF were significantly more likely than
subjects without AF to have cardiovascular disease risk
factors and preexisting disease at baseline, including hypertension,
smoking, left ventricular hypertrophy,
myocardial infarction, congestive heart failure, valvular heart
disease, and stroke or transient ischemic attack. In addition,
women with AF were more likely to be diabetic.
View this table:
[in a new window]
Table 1. Baseline Characteristics of Subjects With and
Matched Subjects Without AF (top, subjects 55 to 74 years of age at baseline;
bottom, subjects 75 to 94 years of age). For both the younger and older
age groups, the mortality of men and women with AF was substantially
greater than for the non-AF subjects (log rank test, all
P<0.0001). At 10 years of follow-up, in the subjects 55 to
74 years of age, 61.5% of men with AF had died compared with 30.0% of
men without AF; in women, 57.6% of those with AF had died compared
with 20.9% of women without AF. Table 2
details the mortality of AF and matched non-AF subjects by decade of
age and sex. The median survival of men 55 to 64 years of age with AF
was 12.6 years compared with 18.1 years in men without AF. Median
survival was 12.1 years in women with AF and 21.3 years in women
without AF. The excess mortality of the AF subjects was apparent within
the first 30 days and persisted throughout follow-up. Furthermore, the
excess mortality with AF was observed across all 4 decades of age
studied.
View larger version (24K):
[in a new window]
Figure 1. A, Kaplan-Meier mortality curves for subjects 55 to 74 years
of age. Vertical axis shows percent of subjects dead at follow-up (0%
to 80%); horizontal axis, up to 10 years of follow-up. Subjects
included men with AF (n=159), men without AF (n=318), women with AF
(n=133), and women without AF (n=266). Both men and women with AF had
significantly higher mortality than age-, sex-, and calendar
year–matched non-AF subjects. Log rank test for men gave
2=42.90 (P<0.0001); for women,
2=70.93 (P<0.0001). B, Kaplan-Meier
mortality curves for subjects 75 to 94 years of age. Vertical axis
shows percent of subjects dead at follow-up (0% to 80%); horizontal
axis, up to 5 years of follow-up. Results are shown for men with AF
(n=137), men without AF (n=274), women with AF (n=192), and women
without AF (n=384). Both men and women with AF had significantly higher
mortality than age-, sex-, and calendar year–matched non-AF subjects.
Log rank test for men gave 2=51.44
(P<0.0001); for women, 2=101.51
(P<0.0001).
View this table:
[in a new window]
Table 2. Kaplan-Meier Death Rates in Subjects With and
Matched Subjects Without AF ). For the pooled logistic regression
analyses, 2149 men and 2714 women met eligibility criteria for
inclusion at some point during follow-up. Age-adjusted ORs for death
with AF were 2.4 in men and 3.5 in women. After
multivariate adjustment, with risk factor status at
each biennial examination taken into account, AF remained significantly
associated with an increased risk of death; the OR with AF was 1.5 in
men (95% CI, 1.2 to 1.8) and 1.9 in women (95% CI, 1.5 to 2.2).
View this table:
[in a new window]
Table 3. Impact of AF on Mortality: Pooled Logistic
Regression Analyses 
). With subjects who died within the first 30
days of follow-up eliminated, AF remained significantly associated with
greater mortality in women (OR, 1.5) but not in men (OR, 1.1). Lastly,
in an analysis limited to subjects initially free of clinically
evident cardiovascular disease and valvular
heart disease, AF was associated with a doubling in mortality
(multivariate OR, 2.4 [95% CI, 1.8 to 3.3] in men
and 2.2 [95% CI, 1.6 to 3.1] in women).
The mortality rate in the first 30 days and 1 year for the AF
subjects and matched subjects without AF are listed in Table 4. The excess mortality observed with AF
appeared early; about 15% of subjects with AF died within 30 days of
diagnosis. The cause-specific mortality at 1 year suggests that the
distribution of the causes of death for the AF subjects was similar to
that of the matched subjects without AF (Table 4). However, compared
with matched subjects without AF, for each of the causes of death, a
higher percentage of the AF subjects died in the first year after AF
was diagnosed.
View this table:
[in a new window]
Table 4. Cause-Specific 1 Year Mortality in Subjects by AF
Status
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
These population-based data indicate that subjects with AF have
markedly reduced survival compared with subjects without AF, with risk
factor–adjusted ORs for death of 1.5 and 1.9 in men and women,
respectively. The multivariate analyses suggest
that the greater mortality probably was attributable to AF, rather than
reflecting the greater burden of risk factors and
cardiovascular disease of AF subjects.
Although few would consider AF a benign condition, it has remained
unclear whether AF is associated with mortality independent of the
coexisting conditions with which it is often observed. The risk of
subsets of AF subjects with cardiovascular disease
remains controversial. For example, some investigators have reported
that after myocardial infarction, AF is associated with excess
mortality,14 15 whereas others have not found an
independent effect of AF on post–myocardial infarction
mortality.16 17 Similarly, whether AF is an
independent predictor of mortality in subjects with heart failure or
stroke is also unclear, with some investigators
reporting18 19 20 and others
refuting21 22 23 an independent contribution of AF
to mortality.
The Framingham Heart Study, by virtue of its longitudinal
population-based design, has several advantages. The selection bias
inherent in hospital-based series, prevalent AF series, or
retrospective series was minimized. In the present series, ECGs
were systematically ascertained on all subjects at each biennial
examination and by review of outside hospital and physician
records. Furthermore, the large number of subjects with AF
contained in this series allowed us to analyze the mortality of
AF over a broad age range and enabled the separate evaluation of the
risk of death in men and women. To the best of our knowledge, the
present investigation is the first to examine the relation between
sex and AF mortality. We observed a significant interaction between AF
mortality and sex, so that AF diminished the typical advantage women
enjoy in survival. In addition, the routine collection of clinical
history, physical examination, ECGs, and outside hospital records
allowed multivariate adjustment for other factors,
which may have contributed to the excess mortality seen with AF. A
strength of the present study was that pooled logistic regression
models were used so that the covariates in the
multivariate model were updated at each biennial
examination.
Several observations suggest that the burden of AF might be
expected to rise. The population is aging, and the incidence of AF
increases with advancing age.2 Furthermore,
recently published data suggest that the prevalence of AF in the
population is increasing even after accounting for
age.39 AF is known to result in substantial
morbidity, with a risk factor–adjusted 2.6- to 4.5-fold risk of
stroke.4 The present study demonstrates that
AF is independently associated with a 50% to 90% increase in the risk
of death. The increased mortality was seen in men and women and was
consistent across the 4 decades of age studied. Our
investigation supports the contention that AF is associated with excess
mortality, which persists after adjustment for coexisting
cardiovascular conditions.
Acknowledgments
The Framingham Heart Study is supported in part through
NIH/NHLBI contract NO1-HC-38038 and by NIH/NINDS grant
5-R01-NS-17950–16. We would like to thank David M. Pollak for
editorial assistance and Mary Healy, Karen Mutalik, Lois Abel, Lynne
McDonald, Kathy Ryder, MD, and Colleen Sam, MD, for assistance in the
collection of AF cases.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
This article has been cited by other articles:
 |
|
 |
|
  H. Grubitzsch, C. Grabow, H. Orawa, and W. Konertz Factors predicting the time until atrial fibrillation recurrence after concomitant left atrial ablation. Eur. J. Cardiothorac. Surg., July 1, 2008; 34(1): 67 - 72. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Matyal Newly Appreciated Pathophysiology of Ischemic Heart Disease in Women Mandates Changes in Perioperative Management: A Core Review Anesth. Analg., July 1, 2008; 107(1): 37 - 50. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Hippisley-Cox, C. Coupland, Y. Vinogradova, J. Robson, R. Minhas, A. Sheikh, and P. Brindle Predicting cardiovascular risk in England and Wales: prospective derivation and validation of QRISK2 BMJ, June 28, 2008; 336(7659): 1475 - 1482. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Roy, M. Talajic, S. Nattel, D. G. Wyse, P. Dorian, K. L. Lee, M. G. Bourassa, J. M. O. Arnold, A. E. Buxton, A. J. Camm, et al. Rhythm Control versus Rate Control for Atrial Fibrillation and Heart Failure N. Engl. J. Med., June 19, 2008; 358(25): 2667 - 2677. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Hertervig, O. Kongstad, E. Ljungstrom, B. Olsson, and S. Yuan Pulmonary vein potentials in patients with and without atrial fibrillation Europace, June 1, 2008; 10(6): 692 - 697. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. D. Vagaonescu, A. C. Wilson, and J. B. Kostis Atrial Fibrillation and Isolated Systolic Hypertension: The Systolic Hypertension in the Elderly Program and Systolic Hypertension in the Elderly Program-Extension Study Hypertension, June 1, 2008; 51(6): 1552 - 1556. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G.-R. Li, H.-B. Wang, G.-W. Qin, M.-W. Jin, Q. Tang, H.-Y. Sun, X.-L. Du, X.-L. Deng, X.-H. Zhang, J.-B. Chen, et al. Acacetin, a Natural Flavone, Selectively Inhibits Human Atrial Repolarization Potassium Currents and Prevents Atrial Fibrillation in Dogs Circulation, May 13, 2008; 117(19): 2449 - 2457. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Nieuwlaat, M. H. Prins, J.-Y. Le Heuzey, P. E. Vardas, E. Aliot, M. Santini, S. M. Cobbe, J. W.M.G. Widdershoven, L. H. Baur, S. Levy, et al. Prognosis, disease progression, and treatment of atrial fibrillation patients during 1 year: follow-up of the Euro Heart Survey on Atrial Fibrillation Eur. Heart J., May 1, 2008; 29(9): 1181 - 1189. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Freestone, F. Gustafsson, A. Y. Chong, P. Corell, C. Kistorp, P. Hildebrandt, and G. Y. H. Lip Influence of Atrial Fibrillation on Plasma Von Willebrand Factor, Soluble E-Selectin, and N-Terminal Pro B-type Natriuretic Peptide Levels in Systolic Heart Failure Chest, May 1, 2008; 133(5): 1203 - 1208. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. A. Lutomsky, T. Rostock, A. Koops, D. Steven, K. Mullerleile, H. Servatius, I. Drewitz, D. Ueberschar, T. Plagemann, R. Ventura, et al. Catheter ablation of paroxysmal atrial fibrillation improves cardiac function: a prospective study on the impact of atrial fibrillation ablation on left ventricular function assessed by magnetic resonance imaging Europace, May 1, 2008; 10(5): 593 - 599. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G Y H Lip and C J Boos Antithrombotic treatment in atrial fibrillation Postgrad. Med. J., May 1, 2008; 84(991): 252 - 258. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Darbar, P. J. Kannankeril, B. S. Donahue, G. Kucera, T. Stubblefield, J. L. Haines, A. L. George Jr, and D. M. Roden Cardiac Sodium Channel (SCN5A) Variants Associated with Atrial Fibrillation Circulation, April 15, 2008; 117(15): 1927 - 1935. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Q. Cui, L. B. Sun, Y. Li, C. L. Xu, J. Han, H. Li, and X. Meng Intraoperative Modified Cox Mini-Maze Procedure for Long-Standing Persistent Atrial Fibrillation Ann. Thorac. Surg., April 1, 2008; 85(4): 1283 - 1289. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Asbach, M. Olschewski, T. S. Faber, M. Zehender, C. Bode, and M. Brunner Mortality in patients with atrial fibrillation has significantly decreased during the last three decades: 35 years of follow-up in 1627 pacemaker patients Europace, April 1, 2008; 10(4): 391 - 394. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. S. Taggar, F. Marin, and G. Y.H. Lip Mortality in patients with atrial fibrillation: improving or not? Europace, April 1, 2008; 10(4): 389 - 390. [Full Text] [PDF]
|
|
|
|
 |
|
 M. Sakabe, A. Shiroshita-Takeshita, A. Maguy, B. J.J.M. Brundel, A. Fujiki, H. Inoue, and S. Nattel Effects of a heat shock protein inducer on the atrial fibrillation substrate caused by acute atrial ischaemia Cardiovasc Res, April 1, 2008; 78(1): 63 - 70. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Darbar, A. Hardy, J. L. Haines, and D. M. Roden Prolonged signal-averaged P-wave duration as an intermediate phenotype for familial atrial fibrillation. J. Am. Coll. Cardiol., March 18, 2008; 51(11): 1083 - 1089. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Watanabe, N. Tanabe, T. Watanabe, D. Darbar, D. M. Roden, S. Sasaki, and Y. Aizawa Metabolic Syndrome and Risk of Development of Atrial Fibrillation: The Niigata Preventive Medicine Study Circulation, March 11, 2008; 117(10): 1255 - 1260. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Soran, N. Younis, P. Currie, J. Silas, I.R. Jones, and G. Gill Influence of diabetes on the maintenance of sinus rhythm after a successful direct current cardioversion in patients with atrial fibrillation QJM, March 1, 2008; 101(3): 181 - 187. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. Taimur and S. Hussaini Atrial fibrillation in a commercial diver Occup. Med., March 1, 2008; 58(2): 144 - 146. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Grubitzsch, A. Menes, D. Modersohn, and W. Konertz The Role of Atrial Remodeling for Ablation of Atrial Fibrillation Ann. Thorac. Surg., February 1, 2008; 85(2): 474 - 480. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Mont, D. Tamborero, R. Elosua, I. Molina, B. Coll-Vinent, M. Sitges, B. Vidal, A. Scalise, A. Tejeira, A. Berruezo, et al. Physical activity, height, and left atrial size are independent risk factors for lone atrial fibrillation in middle-aged healthy individuals Europace, January 4, 2008; (2008) eum263v1. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Arriagada, A. Berruezo, L. Mont, D. Tamborero, I. Molina, B. Coll-Vinent, B. Vidal, M. Sitges, P. Berne, J. Brugada, et al. Predictors of arrhythmia recurrence in patients with lone atrial fibrillation Europace, January 1, 2008; 10(1): 9 - 14. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. K. Voeller, R. B. Schuessler, and R. J. Damiano Jr. Surgical Treatment of Atrial Fibrillation Card. Surg. Adult, January 1, 2008; 3(2008): 1375 - 1394. [Full Text]
|
|
|
|
|
|
F. G. Cosio, E. Aliot, G. L. Botto, H. Heidbuchel, C. J. Geller, P. Kirchhof, J.-C. De Haro, R. Frank, J. P. Villacastin, J. Vijgen, et al. Delayed rhythm control of atrial fibrillation may be a cause of failure to prevent recurrences: reasons for change to active antiarrhythmic treatment at the time of the first detected episode Europace, January 1, 2008; 10(1): 21 - 27. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Ferro, L. Loffredo, L. Polimeni, F. Fimognari, P. Villari, P. Pignatelli, V. Fuster, and F. Violi Soluble CD40 Ligand Predicts Ischemic Stroke and Myocardial Infarction in Patients With Nonvalvular Atrial Fibrillation Arterioscler. Thromb. Vasc. Biol., December 1, 2007; 27(12): 2763 - 2768. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
|