CARDIOVASCULAR JOURNAL OF AFRICA • Vol 21, No 3, May/June 2010
AFRICA
155
Case Report
Cerebral embolism following thrombolytic therapy for
acute myocardial infarction: the second reported case
MEHMET BOSTAN, AYHAN KANAT, MURAT SEN, HIZIR KAZDAL, HABIB BOSTAN
Summary
ST-elevation myocardial infarction (STEMI), caused by acute
occlusion of the infarct-related coronary artery, is an emer-
gency condition. The primary therapy is restoration of full
antegrade flow by either percutaneus coronary intervention
(PCI) or thrombolytic therapy (TT). Although primary PCI
is superior to TT in patients with STEMI, there are many
limitations in clinical practice. TT decreases mortality in
STEMI patients, but as experience with thrombolytic agents
grows, the potential risks of serious side effects become more
apparent. The major complications are bleeding, hypotension
and skin rash.
We report on a case of cerebrovascular accident (CVA)
caused by cerebral emboli following TT. We concluded that
the fact that the patient was in arterial fibrillation (AF) was
a major contributing factor to her CVA. This is an extremely
rare condition, and our case appears to be the second one
reported on in the literature.
Keywords:
acute myocardial infarction, thrombolytic therapy,
cerebral emboli
Submitted 23/4/09, accepted 21/8/09
Cardiovasc J Afr
2010;
21
: 155–157
One case of cerebrovascular accident due to cerebral embo-
li following thrombolytic therapy (TT) has previously been
published.
1
ST-elevation myocardial infarction (STEMI) is
caused by complete occlusion of the coronary artery. The gold-
standard therapy for STEMI is recanalisation of the infarct-
related coronary artery as soon as possible by pharmacological
or mechanical means.
2
Indications for this are STEMI or new left
bundle branch block (LBBB) presenting within 12 hours of the
onset of symptoms.
2
Primary percutaneus coronary intervention (PCI) is superior
to TT but there are many limitations to PCI. TT is therefore an
effective treatment of choice in STEMI, as it is easy to perform
anywhere and at any time.
All thrombolytic agents share a common mechanism of
activating plasminogen into plasmin, which in turn activates the
fibrin degradation pathway. The efficacy and safety of various
thrombolytic agents have been well documented in large clinical
trials.
3-5
The most feared complication of fibrinolytic treatment is
intracranial haemorrhage. Risk factors for haemorrhagic compli-
cations include increasing age, elevated pulse pressure, uncon-
trolled hypertension, recent stroke or surgery, the presence of a
bleeding diathesis, and severe congestive heart failure. Although
the haemorrhagic complications of TT are well documented, this
type of embolic cerebral infarction has not been documented in
the literature. Hence we report on our case.
Case report
An 80-year-old female patient presented to the emergency
department with severe chest pain. The duration between the
onset of pain and presentation to hospital was 60 minutes.
Electrocardiography revealed atrial fibrillation (AF) and
ST-segment elevation in leads D2, D3 and AVF (Fig. 1). Physical
examination of the patient in the orthopneic position revealed
shortness of breath and her blood pressure was 135/83 mmHg.
Primary PCI would not therefore have been appropriate for this
patient and we decided to use TT.
Laboratory findings were as follows: creatinine kinase-MB:
25 ng/ml, troponin I: 18 ng/ml, and normal liver function tests.
The patient had been seeing a cardiologist (MB) with regular
outpatient visits. The patient had left ventricular (LV) failure and
the last cardiac echocardiograph had been performed one month
earlier. In that evaluation, no trombus was detected. The chest
pain was very severe on admission, but a new echocardiograph
could not be done before TT. Her orthopnoeic breathing was
assumed to be due to her LV failure.
Acute inferior myocardial infarction was diagnosed and
she was hospitalised in the coronary care unit for intravenous
TT. Streptokinase 1 500 000 U was administered over 60 min
in the fourth hour of chest pain. Two-dimensional echocardio-
graphic examination at the bedside (Vivid 3 Pro) was performed
following the therapy. It revealed left ventricular, left atrial and
right-sided dilatations, third-degree mitral and second-degree
Department of Cardiology, Rize University Medical School,
Rize, Turkey
MEHMET BOSTAN, MD,
Department of Neurosurgery, Rize University Medical
School, Rize, Turkey
AYHAN KANAT, MD
Department of Neurology, Education and Research Hospital,
Rize, Turkey
MURAT SEN, MD
Department of Anesthesiology and Reanimation, Rize
University Medical School, Rize, Turkey
IR KAZDAL, MD
HABIB BOSTAN, MD
