Download Cardioversion of "Common" Atrial

Thromboembolism Following
Cardioversion of "Common" Atrial
Flutter*
Risk Factors and Limitations of Transesophageal
Echocardiography
Davendra Mehta, MD, PhD; and Lawrence Baruch, MD
Based on multiple recent studies, anticoagulant therapy is recommended prior to elective cardio¬
version for patients with atrial fibrillation of more than 24 h duration. The value of anticoagulation
in patients with atrial flutter, however, is less well established. Published recommendations for
of atrial fibrillation often do not extend to patients with atrial
pericardioversion anticoagulation
flutter. We evaluated the risk of thromboembolism in our patient population undergoing cardio¬
version for atrial flutter. Over a period of 30 months, clinically indicated electrical cardioversions
were performed in 41 patients with "common" atrial flutter. Sixteen of these patients underwent
transesophageal echocardiograms
immediately prior to cardioversion to exclude a left atrial
thrombus. Three of the 41 patients with atrial flutter developed neurologic ischemic syndromes
within 48 h of elective cardioversion. All three patients who developed ischemic neurologic compli¬
cations had undergone transesophageal echocardiography immediately prior to cardioversion and
did not have any evidence of left atrial clot. One patient had cardiomyopathy and the other two had
left ventricular hypertrophy. Thus, electrical cardioversion without anticoagulation in patients with
atrial flutter and associated heart disease is associated with a risk of thromboembolic events. A nor¬
mal transesophageal echocardiogram is of doubtful value in prevention of thromboembolic
complications. (CHEST 1996; 110:1001-03)
Key words: atrial flutter; stroke; thromboembolism; transesophageal echocardiography
Abbreviations: bpm=beats per minute
prevent thromboembolism, patients with atrial
r|io
-*- fibrillation are treated with
for
anticoagulation
up
cardioversion.1
following
about the need for this
was performed immediately prior to cardioversion
phy
and showed no evidence of
intracardiac thrombi.
to several weeks prior to and
Scant data
available
approach patients with atrial flutter, in whom the
risk of embolic stroke is reportedly lower.1,2 Transe¬
sophageal echocardiography may be useful for identi¬
fication of thrombi in the left atrium or its appendage
in patients with recent-onset atrial flutter or fibrilla¬
tion; when thrombi are absent, anticoagulation may not
be necessary prior to cardioversion, according to recent
reports.3 We describe three patients who suffered
thromboembolic events shortly after elective directcurrent cardioversion of "common" atrial flutter with¬
out anticoagulant medication prior to the procedure.
In all three patients, transesophageal echocardiograare
in
*From The Cardiovascular Institute of The Mount Sinai Hospital
and The Bronx VA Medical Center, The Mount Sinai School of
Medicine of The City University of New York, New York.
Manuscript received
January 30, 1996; revision accepted June 3.
Reprint
requests: Dr. Mehta, Cardiovascular Institute, The Mount
Sinai Medical Center, One Gustave Levy Place, New York, NY
10029-6574
Materials
and
Methods
During the 30-month period for which complete retrospective
data were available, 135 patients underwent clinically indicated,
elective direct-current cardioversion of supraventricular tachyarrhythmias under our care at The Mount Sinai Hospital, New York,
and The VA Medical Center, Bronx, NY. Twelve-lead ECGs
obtained immediately prior to cardioversion were reviewed to de¬
fine the atrial tachyarrhythmia. For the purpose ofthe study, atrial
flutter was defined as persistent atrial rate of 250 to 300 beats/min
(bpm) with negative flutter waves in leads II, III, and aVF (com¬
mon or type 1 atrial flutter). Forty-one (30%) patients had classic/
common atrial flutter. As compared to patients with atrial fibrilla¬
tion, most of whom were anticoagulated prior to cardioversion for
periods of 3 to 8 weeks, anticoagulation was not routinely carried
out in cases of atrial flutter. In 16 ofthe 41 patients with atrial flut¬
ter, transesophageal echocardiography (Hewlett-Packard multi¬
plane probe: 5 and 3.5 MHz) was carried out to identify left atrial
thrombi. Seven of these 41 patients were receiving aspirin therapy
for coronary artery disease and another 2 were receiving oral anti¬
coagulant therapy for associated prosthetic heart valves. Electrical
cardioversion restored sinus rhythm in all patients with atrial flut¬
ter with up to three shocks. All patients were monitored in the
CHEST /110 / 4 / OCTOBER, 1996
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1001
The patient was treated with IV heparin followed by oral warfarin.
There was progressive improvement with minimal persistent residual
neurologic deficit. There was no recurrence of atrial arrhythmia.
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Electrocardiograms (lead II and Vi) prior to cardiover¬
patients 1, 2, and 3. Atrial rate is 270, 250, and 240 bpm,
Figure 1.
sion in
respectively, with a variable atrioventricular block.
coronary care unit or the telemetry unit. Monitoring was continued for
24 h in patients admitted to hospital and for 4 h for ambulatory patients.
Three patients with atrial flutter (ECGs prior to cardioversion shown
in Figure 1) developed acute neurologic ischemic syndromes within 48
h of
cardioversion. The clinical presentations were as follows.
Case 1
A 65-year-old
man with chronic alcoholic cardiomyopathy was
admitted to the hospital for congestive heart failure and acute pul¬
monary edema. Medications at admission included digoxin, captopril, aspirin, furosemide, folic acid, and thiamine. He had previous
episodes of classic atrial flutter. ECG, 4 weeks prior to hospital ad¬
mission, had shown normal sinus rhythm. On admission, the ECG
showed atrial flutter with ventricular rate of 80 bpm. Despite IV
furosemide, heart failure persisted. Cardioversion was undertaken
in an effort to improve hemodynamics. Transesophageal echocar¬
diography
performed immediately prior to cardioversion revealed
global left ventricular systolic dysfunction, moderate mitral and
tricuspid regurgitation,
pulmonary hypertension, and spontaneous
echo-contrast both in a dilated left atrium and in the proximal
aorta. There was no evidence of thrombus in the left atrium, atrial
appendage, or the ventricle. Direct-current cardioversion was
achieved at an energy level of 100 J. He was commenced on a reg¬
imen of oral amiodarone, 600 mg daily, to prevent recurrence of
atrial flutter. About 48 h after conversion, there was sudden devel¬
opment of central blindness and cerebellar ataxia. CT ofthe brain re¬
vealed findings suggestive of a right occipitoparietal infarction. Carotid
ultrasound examination showed no evidence ofatherosclerotic disease.
Case 2
An 83-year-old
man with long-standing hypertension and coro¬
nary artery disease was readmitted to the hospital 6 weeks follow¬
ing percutaneous coronary angioplasty because of increasing angina
and dyspnea. The ECG on admission showed sinus rhythm and is¬
chemic repolarization abnormalities in the anterolateral leads. He
was treated with IV heparin (partial thromboplastin time main¬
tained twice control) and nitroglycerin. On the day following hos¬
pital admission, the patient developed atrial flutter with a ventric¬
ular rate of 90 bpm. Attempt to restore sinus rhythm with oral
quinidine sulfate failed. Because of rapid ventricular rate contrib¬
uting to worsening angina, electrical cardioversion was performed
following transesophageal echocardiography; this revealed hypoki¬
nesis of the left ventricular apex and lateral wall with no thrombus,
mild mitral and tricuspid incompetence, and neither thrombus nor
spontaneous echo-contrast in the left atrium. Sinus rhythm was re¬
stored at an energy level of 100 J after failure of the first shock of
100 J. Heparin therapy was discontinued after 24 h as angina sub¬
sided after cardioversion. After 40 h while still in sinus rhythm, the
patient developed right hemiparesis and slurred speech. Although
at the time of onset of the neurologic event the patient was in si¬
nus rhythm, 2 h after the onset ofthe neurologic event, the patient
was in atrial fibrillation with well-controlled ventricular rate. Neu¬
rologic signs resolved after another 48 h. CT of the brain disclosed
a parieto-occipital infarction. Carotid ultrasound examination
showed bilateral intimal plaque formation without hemodynamically significant stenosis. Warfarin anticoagulation was imple¬
mented and continued long term.
Case 3
A 55-year old man with diabetes mellitus and hypertension was
admitted to the hospital for management of schizophrenia. ECG at
hospital admission showed sinus rhythm. There was no history of
atrial arrhythmias. Two days after hospitalization, he developed type
1 atrial flutter with rapid ventricular response that was not
controlled with IV diltiazem hydrochloride (Cardizem) and digoxin.
As onset of flutter was recent, it was decided to perform electrical
cardioversion following transesophageal echocardiography. This
revealed normal chamber dimensions and
ventricular function.
thrombus or echo-contrast in the left atrium or its
appendage or the left ventricle. There was a sessile plaque in the
ascending aorta. Sinus rhythm was restored with the third shock at
360 J (Table 1). Fourteen hours following cardioversion, the patient
developed altered sensorium and right hemiparesis. CT ofthe head
revealed a large hypodense area in the territory of the left middle
cerebral artery consistent with embolic infarction. Carotid ultra¬
sound studies showed no abnormalities. Following hospital admis¬
sion after the onset ofthe neurologic episode, the patient developed
a self-terminating episode of atrial fibrillation. Treatment included
IV heparin followed by oral warfarin. There was gradual neurologic
recovery with moderate persistent neurologic deficit.
There was
no
Table 1.Clinical Presentations*
Cardiac
Patient
No./Age, yr
1/65
2/83
3/55
Disease
CMY
CAD
Normal heart
LVEF,
18
35
50
Duration of
Atrial Flutter
2-3 wk
>24h
48 h
Energy Used
for CV, J
Time, h,
CV to Stroke
100
48
40
16
100, 100
100, 100, 360
*CAD=coronary artery disease; CMY=dilated cardiomyopathy with normal coronary arteries; CV=cardioversion;
LVEF=left ventricular
fraction.
1002
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Clinical
ejection
Investigations
nism.6,7 This phenomenon has been likened to atrial
Discussion
Patients with atrial fibrillation
are
conventionally
treated with anticoagulants for periods of 3 to 4 weeks
prior to and following elective cardioversion, particu¬
larly when associated organic heart disease increases
the risk of thromboembolic complications.1"4 The ap¬
proach to patients with atrial flutter, however, is less
well established, and the risk of stroke is considered
much lower.1,2 Arnold, et al2 reported no embolic
events among 122 patients with atrial flutter undergo¬
ing cardioversion, and no anticoagulation was given in
75% of the cases. Absence of thromboembolic events
in their patients was probably related to the difference
in patient population, as a large proportion of their pa¬
tients had atrial flutter immediately following cardiac
surgery. Other studies addressing the use of anticoagu¬
lant therapy for patients undergoing cardioversion have
included relatively few cases of atrial flutter. Whereas in
patients with atrial fibrillation the risk of stroke is
attributed to stasis of blood in the left atrium, more or¬
electrical activity during atrial flutter is
ganized atrial
preservation of atrial mechanical
thought towithreflect
a reduced risk of thrombus formation.1
transport
Two of the three patients who had complications,
successful cardioversion, on postcardiover¬
following
sion monitoring, had transient atrial fibrillation. Al¬
atrial flutter might be the presenting arrhyth¬
thoughatrial
fibrillation can present intermittently and
mia,
thus be missed. These patients probably have the same
thromboembolic risk as patients with atrial fibrillation.
Furthermore, occurrence of atrial fibrillation following
successful cardioversion in patients who were moni¬
tored for a longer time, despite no previous documen¬
tation, shows interchangeability of the two rhythms.
In the three patients described herein, acute cere¬
bral ischemic events developed within 1 to 2 days of
successful restoration of sinus rhythm by direct-current
cardioversion, and the results of brain imaging studies
were suggestive of cardiogenic thromboembolism. Two
of these patients had received no prior anticoagulation
therapy and all three had undergone transesophageal
prior to rhythm cor¬
immediately
echocardiography
of
intracardiac
thrombi. The
rection without evidence
mechanism of stroke in these patients cannot be
established with certainty, but carotid atherosclerotic
lesions were not demonstrated on ultrasound studies.
In one patient, there was spontaneous echo-contrast in
the left atrium, considered a marker of stasis and a
prethrombotic state,5 inandthein another there was an
atherosclerotic lesion
ascending aorta. ob¬
Transesophageal
echocardiographic
imaging
tained during electrical cardioversion for atrial fibril¬
lation and flutter has shown that a period of mechan¬
ical quiescence occurs during which there is atrial
asystole despite restoration of electrical sinus mecha¬
"stunning/' or "electromechanical dissociation" during
which the process of thrombus formation may be en¬
hanced. Transmitral blood flow velocity may be de¬
for weeks after cardioversion, and this has
pressed
been cited to explain the delayed appearance of clin¬
ical thromboembolic sequelae.8,9 Similar sequence of
events may occur in patients undergoing cardioversion
of atrial flutter, and anticoagulation should be consid¬
ered during and following cardioversion. Although the
for which anticoagulation is continued follow¬
period
ing cardioversion is debatable, it could be guided by the
duration of atrial systole.
All three patients who had embolic events had ev¬
idence of heart disease: cardiomyopathy in the first
patient and left ventricular hypertrophy in the second
and third. It is likely that patients with atrial flutter who
have associated cardiac involvement such as enlarged
left atrium from any cause, left ventricular hypertro¬
or impaired left ventricular function have risk of
phy,
thromboembolic complications. Based on these obser¬
vations, it appears that a decision about anticoagulation
should be made on the basis of the underlying heart
disease and not on the basis ofthe rate and type ofatrial
Furthermore, the absence of throm¬
tachyarrhythmia.
bus on precardioversion transesophageal echocardio¬
gram in this group does not seem to be associated with
a reduced risk of thromboembolic complications.
References
Dunn
Albers
G,
M, et al. Antithrombotic therapy in
A,
Laupacis
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