(Circulation. 1995;92:835-841.)
© 1995 American Heart Association, Inc.
Articles |
Left Atrial Size and the Risk of Stroke and Death
The Framingham Heart Study
From The Framingham Heart Study, Framingham, Mass (E.J.B., R.B.D., A.J.B., P.A.W., D.L.); the Departments of Cardiology (E.J.B.), Neurology (P.A.W.), and Preventive Medicine (E.J.B., P.A.W., D.L.), Boston (Mass) University School of Medicine; the Department of Mathematics, Boston (Mass) University (R.B.D., A.J.B.); the Division of Cardiology and Clinical Epidemiology, Beth Israel Hospital, Boston, Mass (D.L.); and the NHLBI, Bethesda, Md (D.L.).
Correspondence and reprint requests to Emelia J. Benjamin, MD, ScM, The Framingham Heart Study, 5 Thurber St, Framingham, MA 01701.
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Abstract |
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Background The medical literature contains conflicting reports on the association of left atrial (LA) enlargement with risk of stroke. The relation of LA size to risk of stroke and death in the general population remains largely unexplored.
Methods and Results Subjects 50 years of age and older from the Framingham Heart Study were studied to assess the relations between echocardiographic LA size and risk of stroke and death. During 8 years of follow-up, 64 of 1371 (4.7%) men and 73 of 1728 (4.2%) women sustained a stroke, and 296 (21.6%) men and 271 (15.7%) women died. Sex-specific Cox proportional-hazards models were adjusted for age, hypertension, diabetes, atrial fibrillation, smoking, ECG left ventricular (LV) hypertrophy, and congestive heart failure or myocardial infarction. After multivariable adjustment, for every 10-mm increase in LA size, the relative risk of stroke was 2.4 in men (95% CI, 1.6 to 3.7) and 1.4 in women (95% CI, 0.9 to 2.1); the relative risk of death was 1.3 in men (95% CI, 1.0 to 1.5) and 1.4 in women (95% CI, 1.1 to 1.7). Adjusting for ECG LV mass/height attenuated the relation of LA size to stroke and death.
Conclusions After multivariable adjustment, LA enlargement remained a significant predictor of stroke in men and death in both sexes. The relation of LA enlargement to stroke and death appears to be partially mediated by LV mass.
Key Words: echocardiography • cerebrovascular disorders • heart atrium • hypertrophy • risk factors • mortality
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Introduction |
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In the United States, stroke is the third leading cause of death1 and a leading cause of disability in the elderly. With the aging of the population,2 stroke will likely result in an even greater burden of disability and death in the future. Whether left atrial enlargement promotes stroke remains controversial. Disagreement about the importance of left atrial enlargement first emerged regarding patients with mitral valve disease3 4 5 6 7 8 9 10 and has continued in the nonrheumatic atrial fibrillation literature.11 12 13 14 15 16 17 18 19 20 21 22 23 The impact of left atrial dilation on the risk of stroke and death in the general population has not been explored previously.
The introduction of echocardiography into the Framingham Heart Study in 1979 provided an opportunity to investigate noninvasively the contribution of alterations of cardiac structure to the risk of stroke and death. Echocardiographic examination may aid in the identification of subjects at increased risk for stroke and death and may provide insights into the pathogenesis of stroke. The purpose of this investigation was to evaluate the contribution of left atrial size to risk of stroke and death in a longitudinal, population-based cohort of subjects.
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Methods |
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The Framingham Heart Study was initiated in 1948 to prospectively investigate risk factors for cardiovascular disease. A sample of 5209 residents of Framingham, Mass, was enrolled in the study and subsequently has received biennial examinations. The children (and their spouses) of the original cohort were recruited in the early 1970s and were examined 8, 12, and 16 years after their initial examinations. Previous reports detailed the study design.24 25 At each examination, a medical history, physical examination, and 12-lead ECG were routinely performed. Echocardiography became available at the Framingham Study at the 16th original cohort and second offspring examinations (1979 through 1983), the index examinations. At the index examinations, 3645 subjects 50 years of age and older were alive and attended the examinations; echocardiography was routinely performed on 3581 subjects. Subjects were excluded from analysis if they had prior stroke (n=91), mitral valve prosthesis, or mitral stenosis (by echocardiogram or physical examination, n=27) at or before the index examination; subjects also were excluded if they were lost to follow-up in the subsequent 8 years (n=50).
Two-dimensional guided M-mode echocardiograms were performed with subjects in the left lateral decubitus position from a parasternal window with a Hoffrel 201 ultrasound machine, an Aerotech 2.25-MHz transducer, and a Jason thermographic printer. M-mode measurements were made from paper strip charts by use of the American Society of Echocardiography leading-edge-to-leading-edge convention26 at the time of the index examinations. Left atrial dimension was measured at end systole. Standardized assessment of mitral annular calcification was available on the original cohort subjects only; it was considered present if an echo-dense band behind the mitral valve leaflet was visualized throughout the cardiac cycle.27 Left ventricular mass in grams was calculated with the Penn formula: {1.04[(LVID+VST+PWT)3-(LVID)3]}-13.6, where LVID is the left ventricular internal diameter, VST is the ventricular septal thickness, and PWT is the posterior wall thickness, corrected for height in meters.28
Clinical parameters entered into the multivariable models were obtained from the index examinations unless otherwise specified. Hypertension was considered present if systolic pressure was 160 mm Hg or diastolic pressure was 95 mm Hg on each of two successive readings obtained by the clinic physician or if the subject was receiving antihypertensive medication. Diabetes was defined as a nonfasting blood glucose level of 11.11 mmol/L (200 mg/dL) or the use of insulin or an oral hypoglycemic agent. Cigarette smoking was ascertained at the 15th examination of the original cohort and the index offspring examination. Prevalent atrial fibrillation was diagnosed if transient or chronic atrial fibrillation or atrial flutter was documented at any examination up to and including the index examination or from any prior hospital or outside physician records. Interim atrial fibrillation was diagnosed if it was documented in the interval between the index examination and the occurrence of stroke. If atrial fibrillation was initially found by ECG on hospitalization for stroke, the rhythm was considered interim atrial fibrillation. ECG left ventricular hypertrophy was diagnosed when a subject had voltage criteria for left ventricular hypertrophy with lateral repolarization changes.29 Prevalent congestive heart failure and myocardial infarction were determined by a panel of three physicians using previously published criteria.30 31
Stroke events were detected by three means: review of interim Framingham Heart Study examinations, surveillance of all admissions to the local hospital, and scrutiny of outside hospital records. If stroke was suspected, the subject was referred to the Framingham Heart Study for a neurologist-administered, detailed examination. The diagnosis of a cerebrovascular event was made by a panel of three investigators (including a neurologist) after they reviewed all records from relevant hospitalizations and clinic visits. Stroke events were categorized with previously published criteria as atherothrombotic brain infarction, cerebral embolus, intraparenchymal hemorrhage, or subarachnoid hemorrhage.30 31
Statistical Analyses
All analyses were age-adjusted because
age is related to
left atrial size, stroke, and death. For descriptive purposes, the data
were analyzed according to tertiles of left atrial size. The
analysis of tertiles divided the subjects into sex-specific
thirds based on the distribution of left atrial size observed in the
sample. The tertiles were slightly uneven because left atrial dimension
was measured to the nearest millimeter. Logistic regression was used to
calculate the age-adjusted prevalence of the dichotomous clinical risk
factors within sex-specific tertiles of left atrial size and to test
for trend across the tertiles of left atrial size. Linear regression
was used to calculate the age-adjusted mean left
ventricular mass/height for each tertile. The cumulative
incidences of stroke and death were computed by the
Kaplan-Meier32 technique and age-adjusted by the direct
method. The sex-specific 8-year incidences of stroke and death for each
tertile of left atrial size were computed and age-adjusted by the
direct method. For the principal analyses, Cox33
proportional-hazards models were used to explore the association of
left atrial size with outcomes in sex-specific multivariable
models, controlling for other known clinical risk factors for stroke
and death (age, hypertension, diabetes, smoking, atrial fibrillation,
ECG left ventricular hypertrophy, and
myocardial infarction or congestive heart failure). Results from these
regressions were expressed as relative risks with 95% CI per 10-mm
increments of left atrial size. Analyses were performed with
the SAS program.34
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Results |
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Characteristics of the Subjects
Of the 3413 eligible subjects, 314 (9.2%) were excluded because they had M-mode echocardiograms technically inadequate for measuring left atrial size, leaving 1371 men and 1728 women available for analysis. A sex-specific, age-adjusted comparison of subjects with and without measurable left atrial size disclosed no significant differences in the rates of stroke and death. The average age of the study population at the index examination of 63±9 years for men and 65±9 years for women (range, 50 to 90 years, both sexes). The mean left atrial size was 41±5 mm in men and 38±5 mm in women. The sample was divided into approximate sex-specific tertiles of left atrial size (Table 1
). Table 1 also lists the sex-specific,
age-adjusted characteristics of the sample by tertile of left atrial
size. In both sexes, increasing left atrial size was associated with
increasing age and echocardiographic left
ventricular mass and a higher prevalence of hypertension,
atrial fibrillation, congestive heart failure or myocardial infarction,
and mitral annular calcification; cigarette smoking was less common as
left atrial size increased. In women, diabetes was also more common
with increasing left atrial size.
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Stroke
During 8 years of follow-up, 64 men (4.7%) and 73
women (4.2%)
had strokes. Fig 1 displays the 8-year, age-adjusted
cumulative incidence of stroke by tertile of left atrial size. Table
2 delineates the distribution of stroke events by
tertile of left atrial size. Men in the lowest and highest tertiles of
left atrial size had age-adjusted stroke rates of 3.1 and 9.4 per 1000
person-years, respectively. Corresponding rates in women were 3.0 and
5.9 strokes per 1000 person-years.
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Table 3 gives the
results of age-adjusted and
multivariable analyses. For every 10-mm increment in left
atrial size, the age-adjusted relative risk of stroke was 2.2 in men
and 2.0 in women. After adjustment for traditional stroke risk factors
(age, hypertension, diabetes, smoking, ECG left ventricular
hypertrophy, prevalent atrial fibrillation, and prevalent
congestive heart failure or myocardial infarction), the relative risk
of stroke in men was 2.4 (95% CI, 1.6 to 3.7), whereas the risk of
stroke was 1.4 in women (95% CI, 0.9 to 2.1). The variables most
responsible for diminishing the relative risk of stroke in women from
2.0 in the age-adjusted model to 1.4 per 10 mm of left atrial size in
the multivariable model were prevalent atrial fibrillation and
prevalent congestive heart failure or myocardial infarction.
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Additional
analyses were performed to clarify whether the
stroke–left atrial size relation was restricted to particular subsets
of subjects or altered by other stroke risk factors (Table 3
).
The risk
associated with increasing left atrial size was not restricted to
subjects with atrial fibrillation at baseline; eliminating subjects
with prevalent atrial fibrillation did not alter the left atrial
size–stroke relation. Adjusting for atrial fibrillation at any time
before stroke (ie, both prevalent and interim atrial fibrillation)
modestly diminished the stroke–left atrial size relation in both
sexes, but left atrial size remained predictive of stroke in men
(relative risk of stroke was 2.0 in men and 1.2 in women per 10-mm
increment in left atrial size).
Mitral annular calcification assessment
was available only in the
original cohort subjects. After adjustment for mitral annular
calcification27 and the traditional stroke risk factors
listed above, the stroke–left atrial size relation remained
essentially unaltered (Table 3). To explore whether the
deleterious
impact of left atrial enlargement was limited to subjects with
structural heart disease, the data were reanalyzed. After
exclusion of subjects with congestive heart failure or myocardial
infarction at baseline,35 the relative risk of stroke per
10-mm increment in left atrial size was 2.8 in men and 1.6 in women.
Finally, we examined whether left ventricular mass
contributed to the risk of stroke with left atrial dilation. After
adjustment for left ventricular mass/height, the
multivariable relative risk of stroke was 1.8 in men and 0.9 in
women per 10-mm increment in left atrial size (Table 3).
Death
During 8 years of follow-up, 296 (21.6%) men and 271
(15.7%)
women died. Fig 2 shows the age-adjusted cumulative
incidence of death by tertile of left atrial size. As opposed to the
relation of left atrial size to stroke, which was graded across the
tertiles, the excess risk for mortality appeared to reside largely in
the highest tertile of left atrial size. It should be noted, however,
that the narrow range of left atrial size in the second tertile (4 mm
in both sexes) may have accounted for the lack of difference in
mortality compared with the first tertile. The age-adjusted death rates
for men in the lowest and highest tertiles of left atrial size were
23.3 and 30.8 per 1000 person-years, respectively. The corresponding
death rates for women were 13.9 and 22.7 per 1000 person-years,
respectively (Table 2). The age-adjusted relative risk of death
for
every 10-mm increment in left atrial size was 1.3 in men and 1.7 in
women (Table 4). In the multivariable model adjusted
for clinical risk factors (Table 4), left atrial size remained
a
significant predictor of death in both sexes, with a relative risk of
1.3 in men (95% CI, 1.0 to 1.5) and 1.4 in women (95% CI, 1.1 to 1.7)
per 10-mm increment in left atrial size. When subjects with myocardial
infarction or congestive heart failure at baseline were eliminated,
left atrial size remained a significant predictor of death in men, with
a relative risk of 1.4, and was marginally predictive of death in
women, with a relative risk of 1.3. Adjusting for left
ventricular mass/height diminished the left atrial
size–mortality relation in the multivariable model (Table
4); the
relative risk of death was 1.2 per 10-mm increment of left atrial size
in both sexes.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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In this population-based cohort, left atrial size was significantly associated with the age-adjusted risk for stroke and for death in both sexes. Left atrial size was associated with many risk factors for stroke and death, however, underscoring the need for multivariable analyses. After adjustment for age, hypertension, diabetes, smoking, ECG left ventricular hypertrophy, prevalent atrial fibrillation, and prevalent congestive heart failure or myocardial infarction, left atrial size remained a significant predictor of stroke in men (relative risk, 2.4 per 10-mm increment) and death in both sexes (relative risk, 1.3 in men and 1.4 in women).
Mechanisms of Risk
The mechanisms of the increased risk of
stroke and death in
subjects with left atrial enlargement are incompletely understood. Left
atrial dilation promotes stasis of blood, which in turn predisposes to
thrombus formation and the potential for embolization. The
thrombogenicity of left atrial dilation is supported by
transesophageal echocardiography
studies that found that left atrial dilation was associated with
spontaneous echocardiographic contrast, left atrial
thrombus, and embolic events.36 37 38 It
seems less likely
that left atrial size predisposed to nonstroke death in a causal
fashion.
Another possible mechanism is that left atrial dilation may serve as a marker for other risk factors for stroke and death such as atrial fibrillation, structural heart disease, hypertension, or increased left ventricular mass. Left atrial enlargement may function as an indicator for more severe cases of congestive heart failure or myocardial infarction. Nevertheless, it is noteworthy that the relation between left atrial enlargement and stroke and death persisted when subjects with congestive heart failure or myocardial infarction were excluded. In addition, left atrial enlargement is a powerful echocardiographic predictor of nonrheumatic atrial fibrillation risk39 ; in turn, atrial fibrillation is a leading stroke risk factor40 and is associated with a doubling of all-cause mortality.41 Eliminating subjects with prevalent atrial fibrillation at baseline, however, had little impact on the relation of left atrial size to stroke. The possibility remains that left atrial enlargement promoted the development of interim atrial fibrillation, which in turn predisposed to stroke. In the multivariable model adjusted for atrial fibrillation at anytime before stroke, the risk of stroke continued to double for every 10-mm increment in left atrial size in men. In women, in contrast, adjusting for atrial fibrillation at anytime before stroke further diminished the stroke–left atrial size relation, suggesting that the relation in women may be mediated in part by atrial fibrillation.
Left atrial enlargement and left ventricular hypertrophy are both manifestations of cardiac target organ damage in established hypertension.42 43 44 Left atrial enlargement also is significantly related to left ventricular mass.44 Other Framingham Heart Study analyses have found that increased left ventricular mass predicts stroke45 and death.46 After adjustment for left ventricular mass and other stroke risk factors, the left atrial size–stroke relation remained marginally significant in men (P=.05), suggesting that the association is not totally accounted for by blood pressure and left ventricular mass. In contrast, adjusting for left ventricular mass eliminated the relation between left atrial size and stroke in women and attenuated the relation with death in both sexes, partially because left atrial size and left ventricular mass are collinear. Of note, the inclusion of left ventricular mass in the model diminished the number of subjects by 22% and the number of stroke and death end points by 33% and 36%, respectively. Even if left atrial size is merely a biological marker for hypertensive heart disease, given the greater difficulty of measuring left ventricular mass, left atrial size may serve as a useful clinical predictor. Finally, left atrial enlargement may serve as a surrogate for other unidentified risk factors for stroke and death.
Comparison With Previous Studies
Despite extensive
literature, it remains uncertain
whether3 4 8 9 11 12 13 14 15 16
or
not5 6 7 10 17 18 19 20 21 22 23
left
atrial enlargement is a risk factor for stroke. Most studies were
restricted to subjects with mitral valve
disease3 4 5 6 7 8 9 10
or
atrial
fibrillation.11 12 13 14 15 16 17 18 19 20 21 22 23
Subjects with mitral
stenosis or prosthesis were excluded from the current
study because we lacked sufficient power to explore the stroke–left
atrial enlargement relation in this subset of subjects. The most
thorough studies to examine the left atrial size–stroke relation were
the randomized trials of anticoagulation in atrial fibrillation. The
Stroke Prevention in Atrial Fibrillation Study supported an association
between stroke and left atrial enlargement,16 while the
other two cohort trials to examine the issue rejected such a
relation.22 23 Many of the studies in subjects with
atrial
fibrillation were hampered by small sample size or small numbers of
stroke,11 12 13 14 18 19 20 21 22
nonroutine or referral ascertainment of
echocardiograms,11 15 17 18 20 21
and
echocardiographic interpretations in which the
patient's stroke status was not explicitly stated to be blinded to the
readers.11 12 13 14 17 18 20 21
Furthermore, the majority of
prior studies used a case-control
design11 12 13 14 17 18 19 20
and
retrospective or cross-sectional
analyses.11 12 13 14 17 18 19 20 21
The majority of studies
performed only
univariate11 14 18 19 20 22
or
partial multivariable analyses and failed to control for
several important potential
confounders.12 13 15 17 21
Finally, to the best of our knowledge, prior studies did not
analyze men and women separately, did not examine subjects
without atrial fibrillation or mitral valve disease, and did not
investigate the relation of left atrial size to death.
Strengths and Limitations
The potential for bias was
minimized by routine ascertainment of
echocardiograms, which were read blinded to subject characteristics,
and by the longitudinal population-based cohort design. In addition,
the relatively large sample size and routine collection of antecedent
risk factor information provided the opportunity to perform
sex-specific and multivariable analyses. Additional study
is required to determine whether the relation between left atrial size
and death is continuous or whether there is a threshold of left atrial
dilation above which excess mortality is observed. Further
investigation is also necessary to determine whether the results are
generalizable to other races or ages because the current sample was
white and 50 years of age or older.
The echocardiographic examination was limited to M-mode technology, which may have resulted in some misclassification of left atrial size.47 In addition, we and other investigators48 have noted that subtypes of ischemic stroke are subject to misclassification because of clinical difficulties in distinguishing between atherothrombotic and cardioembolic stroke. Finally, the study lacked sufficient power to analyze the relation of left atrial size to specific stroke subtypes.
Clinical Implications
The current study demonstrated that
left atrial size was
significantly related to the risk of stroke in men and death in both
sexes; this association was attenuated by adjustment for
echocardiographic left ventricular mass.
The mechanisms of the increased risk are not fully understood and may
be multifactorial. However, our analyses suggest that left
ventricular mass partially mediates the excess risk of
stroke and death in the setting of left atrial dilation. Strategies for
the prevention of stroke and death in the setting of left atrial
enlargement remain to be determined. Nevertheless,
echocardiographic left atrial enlargement has
prognostic value in identifying a subset of persons at increased risk
for stroke and death.
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Acknowledgments |
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The Framingham Study is supported in part through NIH/NHLBI contract NO1-HC-38038 and by NINDS grant 2-R01-NS-17950-11. We would like to thank David M. Pollak for editorial assistance; Jonathan Plehn, MD, for contributions to the preliminary analyses; Martin Larson, ScD, for assistance in analyzing the prior literature and reviewing the manuscript; and Sonya Vaziri, MD, for insights into the determinants of left atrial size.
Received December 12, 1994; revision received January 30, 1995; accepted February 10, 1995.
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