Cerebral Aneurysm Rupture after
r-TPA Thrombolysis for Acute
Myocardial Infarction
A. Lagares,* P.A. Go ´ mez,* R.D. Lobato,* J.F. Ale ´n,* J. Campollo,** and J. Benito–Leo ´n†
*Neurosurgical Service and **Neuroradiological Service, Hospital 12 de Octubre, Madrid,
Spain, †Neurological Service, Hospital General de Mo ´stoles, Madrid, Spain
Lagares A, Go ´ mez PA, Lobato RD, Ale ´n JF, Campollo J, Benito–
Leo ´ n J. Cerebral aneurysm rupture after r-TPA thrombolysis for
acute myocardial infarction. Surg Neurol 1999;52:623– 6.
BACKGROUND
Intracranial hemorrhage is the most dreaded risk of
thrombolytic therapy for acute myocardial infarction be-
cause of the high mortality and disability rates associated
with this complication. Brain structural lesions may pre-
dispose a patient to bleeding. To date, aneurysm rupture
has not been described as a complication of such
therapy.
CASE DESCRIPTION
A 66-year-old hypertensive woman was admitted because
of chest pain. Myocardial infarction was diagnosed and
fibrinolytic therapy with recombinant tissue plasminogen
activator (r-TPA) was initiated. Eight hours after admis-
sion she became unconscious. Brain computed tomogra-
phy scan showed subarachnoid hemorrhage, and a cere-
bral arteriography showed an anterior communicating
artery aneurysm. Because of her poor clinical condition
treatment was postponed. Death occurred 7 days later
because of multiorgan failure.
CONCLUSIONS
Cerebral aneurysms should be considered as a possible
contributing factor to intracranial bleeding after throm-
bolytic therapy. © 1999 by Elsevier Science Inc.
KEY WORDS
Thrombolysis, myocardial infarction, cerebral aneurysm,
subarachnoid hemorrhage.
M
yocardial infarction, for which thrombolysis
has proved to be a very effective treatment,
diminishing death rates and improving patients’ re-
covery, is one of the leading causes of death in
developed countries. Intracranial hemorrhage is
the most dreaded risk of thrombolytic therapy for
acute myocardial infarction because of the high
mortality and disability rates associated with this
complication. Several factors such as age, gender,
hypertension, or previous central nervous system
disease [3–5,10,11] have been related to an in-
creased bleeding risk after thrombolytic therapy.
On the other hand, brain structural lesions may
also predispose a patient to bleeding. Amyloid an-
giopathy and arteriovenous malformations [9,11]
are the only structural lesions that have been re-
ported in association with this complication. To our
knowledge cerebral aneurysm rupture has not been
previously described as a complication of r-TPA
thrombolysis. We present a case of a patient who
suffered rupture of an anterior communicating ar-
tery aneurysm during r-TPA thrombolysis.
Case Report
A 66-year-old hypertensive woman was admitted to
another hospital because 4 hours before she had
noticed central chest pain radiating to the inter-
scapular area, neck, and left arm, accompanied by
nausea and vomiting. On examination, pulse rate
was 60 and blood pressure 105/60 mmHg. An ECG
was compatible with a posterior myocardial infarc-
tion. She was given 100 mg of recombinant tissue
plasminogen activator (r-TPA) and heparin perfu-
sion was initiated. Eight hours after admission she
suddenly became unconscious. The patient was intu-
bated and heparin was withdrawn. A brain computed
tomography (CT) scan showed massive subarach-
noid hemorrhage (Fisher grade III), intraventricular
hemorrhage, and a frontobasal interhemispheric
hematoma (Figure 1). With the suspicion of a rup-
tured anterior communicating artery aneurysm the
patient was transferred to the ICU at our hospital.
On admission, the patient was comatose but re-
sponded to pain; the pupils were reactive and equal.
A four-vessel cerebral angiogram demonstrated an
Address reprint requests to: Dr Go ´ mez, Hospital 12 de Octubre, Car-
retera de Andalucı ´a km. 5.400, 28041 Madrid, Spain.
Received June 7, 1999; accepted June 29, 1999.
© 1999 by Elsevier Science Inc. 0090-3019/99/$–see front matter
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