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Atrial size atrial fibrillation and stroke.

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Atrial Size, Atrial Fibrdlation, and Stroke
L. R. Caplan, MD,* I. DCruz, MD,? D. B. Hier, MD,” H . Reddy, MD,? and S. Shah, MD?
~~
M-mode and two-dimensional echocardiographic images were reviewed retrospectively in 20 patients with atrial
fibrillation and ischemic stroke with no known valvular disease and in 20 patients with atrial fibrillation without
known stroke. Left atrial size was measured and analyzed without knowledge of patient grouping. Two-dimensional
echocardiography showed that !N%of the stroke patients had left atrial enlargement compared with only 20% in the
nonstroke group. This finding suggests that left atrial enlargement may convey additional stroke risk in patients with
atrial fibrillation.
Caplan LR, DCruz I, Hier DB, Reddy H, Shah S: Atrial size, atrial fibrillation, and stroke.
Ann Neurol 19:158-161, 1986
Atrial fibrillation (AF) is an important cause of cerebral infarction. Postmortem studies document a high
incidence of stroke among patients with AF, whether
or not the arrhythmia was accompanied by rheumatic
o r other valvular disease or by ischemic myocardial
damage 12, 101. Other reviews El, 6 , 11, 13, 20, 231
and our own data from the Harvard { l 6 } and Michael
Reese { 141 stroke registries document a higher stroke
frequency in patients with AF, regardless of cause.
In spite of this correlation, however, translating the
frequency data into therapeutic action is difficult for
several reasons. First, AF is common and increases
with advancing age. Moss 117) estimates that 5% of
patients over 70 years of age have AF. In the Framingham Study C24, 251, nonvalvular AF accounted for 9%
of strokes in the 5 5 to 64 age range, 18% of strokes
between the ages of 65 and 74, and 27% between the
ages of 75 and 84 years. Second, the risk of embolism
varies greatly among patients with AF and depends on
the presence, nature, and severity of the accompanying
heart disease. Third, the risk of cerebral embolism in
AF is chronic, averaging 20% per year during the 9
years of one study 1201. Finally, prospective studies
have been limited and have considered the chance that
a patient with AF and stroke will have a second stroke;
studies usually have not investigated the chance that a
patient with AF will have a first stroke. Anticoagulation with coumarin compounds is the most common
treatment proposed for the prophylactic prevention of
stroke caused by AF, but this therapy is hazardous
when used on a long-term basis and in geriatric patients. Physicians justifiably have been reluctant to
anticoagulate all patients with AF, as the benefidrisk
ratio of this treatment is unknown and the risk is predictably high.
If high-risk subgroups could be identified among the
larger population with AF, anticoagulation might be
more feasible for these patients. Especially at risk for
stroke are patients with onset of AF within the past 6
months {261 and patients with accompanying mitral
stenosis or prior embolism. Moss E17) noted that
“large atria are more likely to embolize than smaller
ones.” Although no convincing published data are
cited to corroborate this statement, Moss’s conclusion
does seem likely based on knowledge of the pathological characteristics of atrial-origin emboli 131.
Because echocardiography has become readily available and can measure atrial dimensions, we retrospectively reviewed atrial size as determined by Mmode and two-dimensional echocardiography in
patients with AF with and without known ischemic
stroke. Our premise was that if atrial size is an important predictor of embolism, echocardiographic determination of atrial size-along with the nature of coexistent cardiac disease, duration of fibrillation, and the
presence of a prior embolus-could be used to decide
whether to recommend anticoagulants for long-term
use in elderly patients with AF.
From the ‘Department of Neurology and the ?Department of Cardiology, Michael Reese Hospital and the University of Chicago
Pritzker School of Medicine, Chicago, IL 60616.
Received Mar 11, 1985, and in revised form May 4. Accepted for
publication July 11, 1985.
158
Methods
Patients
The Michael Reese Stroke Registry and the Stroke Data
Bank of the National Institute of Neurological Disorders
and Stroke were searched for Michael Reese Hospital patients who had AF, a history of stroke, and adequately
definitive echocardiographic studies. All stroke patients had
been included in the “cardiac-source embolism” (Subgroup
2) of previously reported patients [ 4 } or had met the Stroke
Data Bank criteria for “embolism from a cardiac source.”
Atrial size in these 20 patients was compared with that of 20
other patients with AF who had been referred to the echo-
Address reprint requests to Dr Caplan, Department of Neurology,
New England Medical Center, Boston, MA 021 11.
Table I . Age and
Le
,h Atrial Echocardiographic Measurements for Stroke and Nonstroke Groups"
~
~
Group
Variables
Stroke(n = 20)
Nonstroke (n = 20)
t Value
Age (yr)
Echocardiographic measurements
AP (M-mode)
AP (parasternal)
SI (four-chamber)
Transverse (four-chamber)
74.7 (10.4)
66.8 (15.0)
1.9
49.5 (7.0)
47.3 (8.6)
52.4 (10.5)
46.6 (10.3)
44.3 (8.4)
35.1 (7.7)
45.5 (10.3)
33.7 (6.1)
2.1h
4.7b
2.1b
4.@
"Values are group means (SD).
'Means differ, p < 0.05, dF = 38, two-tailed Student's t-rest
AP
=
anteroposterior;SI
=
superoinfesior.
.a
Table 2. Echocardiographic and Clinical Findings
in Stroke and Nonstroke Groups
Frequency
Findings
Echocardiographic findings
Mitral valve sclerosis
Mitral valve prolapse
Mitral valve stenosis
Aortic valve sclerosis
Mitral valve calcification
Left ventricular hypertrophy
Diffuse hypokinesia
Left ventricular aneurysm
Left ventricular dilatation
Clinical findings
Hypertension (by history)
Congestive heart failure
Cardiomy opathy
Pulmonary disease
Recent myocardial infarction
,;
(9%)
Nonstroke
Stroke Group Group
(n = 20)
(n = 20)
25
0
5
35
20
20
10
5
25
15
25
10
5
10
25
5
::.'.':....::::::
.......
. . ..,....,.;. :,
...
....._.
............__..
,.. ..,. . .
.....
......
............
APICAI
0
45
15
15
20
0
25
25
20
20
5
0
cardiographic laboratory at Michael Reese Hospital during
the same period and who had no history of stroke and no
known valvular disease.
Women constituted 60% of each study group. The mean
age of the stroke group was older than that of the nonstroke
group (74.7 years versus 66.8 years), but this difference was
not significant (Table 1). The frequency of valvular and left
ventricle abnormalities (Table 2) and the prevalence of hypertension, congestive heart failure, pulmonary disease, and
recent myocardial infarction were comparable in the two
groups.
Echocardiographic Methods
M-mode as well as two-dimensional echocardiographic studies were performed in all patients using Mark 3 Advanced
Technical Laboratories equipment. End-systolic measurements of left atrial dimensions were made on the M-mode
tracing by the technique recommended by the American
Society of Echocardiography [ 2 11. Two-dimensional echo-
LA
Method b~ which the lejit atrial dimensions were measured on the
two-dimensionalechocardiogram. In the parasternal long-axis
view (top), arrow A indicates the anteroposterior dimension of
the left atrium (LA). In the apical four-chamber view (bottom),
vertical arrow B indicates the superoinferior, or roof-to-base, dimension of the lejii atrium; horizontal arrow C represents the
transverse lejt atrial dimension. (Ao = aorta; LV = left ventricle; RV = right ventricle; RA = right atrium.)
cardiographic measurements were made on hard-copy images obtained from the calibrated videotape recording. Three
left atrial dimensions were measured (Fig 1): the maximum
anteroposterior dimension in the parasternal long-axis view,
the maximum superoinferior (base-to-roof) dimension in the
apical four-chamber view, and the maximum transverse dimension in the apical four-chamber view. These left atrial
dimensions were measured at end-systole (i.e., at the videoframe just preceding the opening of the mitral valve).
Statistical Methods
Group means were compared by the two-tailed Student's t
test. Two-by-two contingency tables were analyzed by the
Caplan et al: Atrial Size, Fibrillation, and Stroke
159
Table 3. intercorrelations between Left Atrial Echocardiographic Measurementsa
Echocardiographic View
AP (M-mode)
AP (parasternal)
SI (four-chamber)
Transverse (four-chamber)
AP
(M-mode)
-
AP
(parasternal)
SI
(four-chamber)
100
...
66
64
100
...
...
62
86
100
63
62
Transverse
(four-chamber)
...
...
...
100
"Numbers rounded to nearest whole numbers. All correlarions sighificant fp < 0.05, dF = 38), as determined by two-tailed Student's t-test.
AP = anteroposterior; SI = superoinferior.
Table 4. Increased Left Atrial Diametersa in Stroke and Nonstroke Group
Frequency (96)
~~
Stroke Group
Nonstroke Group
Echocardiographic View
(n
(n = 20)
X2
AP (M-mode)
AP (parasternal)
SI (four-chamber)
Transverse (four-chamber)
85
65
90
55
50
20
2.1
19.8''
5.2'
=
20)
20
10
7.6"
"Cutpoints for increased diameters: AP (M-mode), > 40 mm; AP (parasternal), > 38 mm; SI (four-chamberj, > 53 mm; transverse (fourchamber), > 46 mm.
hSignificant difference (p < 0.05) as determined by &square test (dF-2).
AP
=
anteroposterior; SI = superoinferior.
chi-square test. Linear correlation coefficients were calculated by standard methods C18J
Results
Group means for left atrial measurements are presented in Table 1. Correlations between the anteroposterior diameter of the left atrium in M-mode
and the diameter of the left atrium as measured in all
three views by two-dimensional echocardiography
were high (Table 3).
In the M-mode, 85% of the stroke patients and
65% of the nonstroke patients had an increased anteroposterior diameter of the left atrium (Table 4).
By two-dimensional echocardiography, a statistically
significant and impressive difference between the
groups was found in the frequency of left atrial enlargement (Table 4).
Discussion
Atrial enlargement is a common postmortem finding
in patients with AF documented during life. The
pathological findings in the atria in rheumatic heart
disease include atrial infarction and left atrial wall
calcification [3). Atrophy of the left atrial myocardium
in patients with AF leads to thinning of the atrial wall
and to fibrous tissue proliferation and replacement. Fibrous replacement of the left atrial wall also is common in patients with cardiomyopathy, ruptured chordae tendinae, and papillary muscle dysfunction [15}.
160 Annals of Neurology Vol 19 No 2
February 1986
Clots or loosely attached mural thrombi often are
found within the auricular appendages. In experimental animals, AF cannot be sustained unless the atria are
nonhomogeneous [3, 12, 15, 18, 21). Fibrillation leads
to ineffective atrial muscle contraction and to further
atrial dilatation {I, 12, 15, 19). A dilated left atrium
with irregularly distributed fibrous replacement of
muscle tissue would theoretically perpetuate AF and
potentially cause stasis and thrombus formation [3,
153.
Left atrial size also has been measured during life
and correlated with the cause of cardiac disease and the
response of AF to therapy 15, 7, 9, 14, 191. AF is
found in approximately 40% of patients with mitral
stenosis and in 75% of patients with mitral insufficiency 119, 22); the larger size of the left atrium in
mitral insufficiency may explain the difference in frequency. In one study C191, left atrial size was measured
by cineangiography in 135 patients with mitral stenosis. Increased left atrial size was correlated with age
(and presumably duration of illness) and was inversely
related to the residual size of the stenotic mitral orifice.
In another study of patients with mitral valve disease,
aortic valve disease, and septal hypertrophy (Idiopathic
hypertrophic subaortic stenosis) 191, AF correlated
well with the size of the left atrium measured echocardiographicdy and was rare when the left atrial diameter was less than 40 mm. Patients with left atrial diameters greater than 45 mm have much less chance of
converting to and sustaining normal sinus rhythm after
receiving antiarrhythmic drugs or electrical current
defibrillation than do patients with normal-sized atria
and AF [ 5 , 7, 7, 141.
We could find only one report that included measurements of left atrial size in stroke patients 181. In
that study, all patients had AF without accompanying
valvular disease, and M-mode echocardiography was
used. Among 56 patients with AF, 22 had echocardiography performed, and left atrial size averaged 45.3
mm in this group. Those with constant AF had an
average atrial size of 45.7 mm (n = 12), while patients
with intermittent AF had a mean left atrial size of 44.7
mm (n = 10). Thirty-five patients were thought to
have cerebral emboli explained by AF, and 13 were
considered to have a nonembolic cause of their ischemic stroke; in the remaining 8 patients, the cause of
stroke was uncertain. Atrial size was largest in patients
with a nonembolic cause (47.2 mm; n = 5 ) as compared to those with embolic (44.7 mm; n = 13) and
uncertain (44.3 mm; n = 4 ) mechanisms [22). Although the clinical material was excellent in that study,
the number of echocardiograms was small and only Mmode echocardiography was used.
We have compared atrial size as determined by Mmode and two-dimensional echocardiography in AF
patients with and without known stroke. By M-mode
echocardiography, the mean anteroposterior diameter
of the left atrium was significantly larger in the group
of AF patients with known stroke. By four-chamber
echocardiography, the mean left atrial diameters in
superoinferior and transverse dimensions were also
significantly larger in the AF patients with stroke.
These results suggest that echocardiography may be
useful in evaluating patients with chronic AF. However, the present study was retrospective, and the
stroke and nonstroke groups differed in age and probably in length of fibrillation history. If these results are
confirmed by prospective studies of comparable AF
patients with and without stroke, atrial size may prove
to be an important factor in evaluating stroke risk in
patients with this common arrhythmia.
References
Abdon NJ, Zettervall 0,Carlson J, et al: Is occult atrial disorder
a frequent cause of non-hemorrhagic stroke? Long-term ECG in
86 patients. Stroke 13:832-837, 1982
Aberg H : Atrial fibrillation. Acta Med Scand 185:373-379,
1969
Bailey G , Braniff B, Hancock E, Cohn K: Relation of left atrial
pathology to atrial fibrillation in mitral valvular disease. Ann
Intern Med 69:13-20, 1968
Caplan L, Hier D, DCruz I: Cerebral embolism in the Michael
Reese Stroke Registry. Stroke 14:530-540, 1983
5. Ewy G. Ulfers R, Hager W, et al: Response of atrial fibrillation
to therapy: role of etiology and left atrial diameter. J Electrocardiol 13:119-124, 1980
6. Fisher C: Reducing risks of cerebral embolism. Geriatrics
34~59-66, 1979
7. Goldman M: The management of chronic atrial fibrillation: indications for and method of conversion to sinus rhythm. Prog
Cardiovasc Dis 2:465-484, 1960
8. Hart R, Cod1 B, Hart D: Early recurrent embolism associated
with nonvalvular atrial fibrillation: a retrospective study. Stroke
14:688-693, 1983
9. Henry W, Morganroth J, Pearlman A, et al: Relation between
echocardiographically determined left atrial size and atrial
fibrillation. Circulation 53:273-279, 1976
10. Hinton R, Kistler J, Fallon J, et d.Influence of etiology of atrial
fibrillation on incidence of systemic embolism. Am J Cardiol
401509-513, 1977
11. Kannel W, Abbott R, Savage D, McNamara P: Epidemiologic
features of chronic atrial fibrillation: the Framingham Study. N
Engl J Med 306:1018-1022, 1982
12. Katz L, Pick A: Current status of theories of mechanisms of
atrial tachycardias, flutter, and fibrillation. Prog Cardiovasc Dis
2:650-662, 1960
13. Kelley RE, Berger JR, Alter M, Kovacs AG: Cerebral ischemia
and atrial fibrillation: a prospective study. Neurology (NY)
34:1285-1291, 1984
14. Mancini GB, Goldberger A L Cardioversion of atrial fibrillation:
consideration of embolization, anticoagulation, prophylactic
pacemaker and long-term success. Am Heart J 104:617-621,
1982
15. Moe G, Abildskov J: Atrial fibrillation as a self-sustaining arrhythmia independent of focal discharge. Am Heart J 58:59-70,
1959
16. Mohr JP, Caplan LR, Melski JW, et al: The Harvard Cooperative Stroke Registry: a prospective registry. Neurology (Minneap) 28:754-762, 1978
17. MOSSAJ: Atrial fibrillation and cerebral embolism [editorial].
Arch Neurol41:707, 1984
18. Pollard JH: A Handbook of Numerical and Statistical Techniques. Cambridge, Cambridge University Press, 1977
19. Probst P, Goldschlager N, Selzer A: Left atrial size and atrial
fibrillation in mitral stenosis. Circulation 48: 1282- 1287, 1983
20. Sage J, Van Uitert R: Risk of recurrent stroke in patients with
atrial fibrillation and non-valvular heart disease. Stroke 14:537540, 1983
21. Sahn DJ, DeMaria A, Kisslo J, Weyman A: Recommendations
regarding quantitation in M-mode echocardiography: results of
a survey of echocardiographic measurements. Circulation
58x1072-1083, 1978
22. Selzer A, Katayama F Mitral regurgitation: clinical patterns,
pathophysiology and natural history. Medicine 5 1:337-366,
1972
23. Sherman D, Goldman L, Whiting R, et al: Thromboembolism in
patients with atrial fibrillation. Arch Neurol41:708-7 10, 1984
24. Wolf PA, Dawber TR, Thomas HE Jr, b n n e l WB:
Epidemiologic assessment of chronic atrial fibrillation and risk
of stroke: the Framingham Study. Neurology (Minneap)
28:973-977, 1978
25. Wolf PA, Kannel WB, Abbott RD: Atrial fibrillation and stroke
in the elderly: the Framingham Study [abstract). Stroke 16:138,
1985
26. Wolf PA, Kannel WB, McGee DL, et al: Duration of atrial
fibrillation and imminence of stroke: the Framingham Study.
Stroke 14:664-667, 1983
Caplan et al: Atrial Size, Fibrillation, and Stroke
161
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