CARDIOVASCULAR JOURNAL OF AFRICA • Vol 21, No 3, May/June 2010
AFRICA
157
compared with aspirin alone, there were five fewer deaths (
p
=
0.03) and three fewer recurrent infarctions (
p
=
0.04), at the
expense of three major bleeds (
p
=
0.001).
11
It is now clear that fibrinolysis recanalises thrombotic occlu-
sions associated with STEMI, restores coronary flow, reduces
infarct size and improves myocardial function and survival over
both the short and long term.
1,12,13
In patients receiving fibrinolysis
for STEMI, the overall incidence of haemorrhagic complications
is about 10%, and the incidence of intracranial haemorrhage is
about 0.8%. Atrial fibrillation predisposes to atrial thrombus,
and Crenshaw
et al
.
14
demonstrated an increased risk for throm-
botic strokes with atrial fibrillation in MI treated with TT.
In the present case, neurological signs were noted two hours
after TT. It was assumed that the patient had had an intracranial
haemorrhage. A cranial CT scan was immediately obtained, but
haemorrhage was excluded and no abnormality was detected.
In the second cranial CT scan, which was performed 12 hours
later, a left frontal embolic infarction was detected. This is a
rare condition. We continued to treat the STEMI and cerebral
infarction, together with a neurologist/neurosurgeon consultant.
On the follow up, the neurological problems progressed, conges-
tive heart failure developed, clinical deterioration occurred, and
subsequently the patient died.
In this case, although a thrombus was not detected during
echocardiographic examination, it is likely that the TT induced
lysis and fragmentation of an undetected microthrombus and
the subsequent dislodging and embolisation of pre-existing
cardiac microthrombi, which caused the cerebral infarction.
Distal embolisation secondary to lysis of arterial thrombi in an
aortic graft occlusion has been reported. It was speculated that
this complication occurred when a combination of fresh and
old thrombus was present.
15
Rapid lysis of the fresh clot, along
with arterial pulsations, may liberate older and more resistant
clot fragments. When peripheral embolisation occurs, TT can be
continued as long as the patient is clinically stable.
There is only one other case report in the literature describing
embolic cerebral infarction following TT for STEMI.
1
Conclusion
This case represents an extremely rare clinical condition, which
we report on to show the importance of the treatment of STEMI
with TT. We deduced that the fact that the patient was in AF was
a major contributing factor to her CVA. In conclusion, patients
receiving TT for the treatment of STEMI should have constant
neurological and cardiovascular re-evaluation and clinicians must
be prepared to handle such complications in a timely manner.
References
Chang MC, Lee AY, Chang WF, Chen TJ. Embolic cerebral infarction
1.
and gastrointestinal hemorrhage following thrombolytic therapy for
acute myocardial infarction.
Echocardiography
2002;
19
(2): 139–141.
Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA,
2.
et al.
ACC/AHA guidelines for the management of patients with ST-elevation
myocardial infarction: A report of the American College of Cardiology/
American Heart AssociationTask Force on practice guidelines. American
College of Cardiology website, 2006 (
stemi/index.pdf). Accessed 6/21/06.
Second International Study of Infarct Survival collaborative group.
3.
Randomised trial of intravenous streptokinase, oral aspirin, both, or
neither among 17,187 cases of suspected acute myocardial infarction:
ISIS-2.
Lancet
1988;
2
: 349–360.
Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardio
4.
(GISSI). Effectiveness of intravenous thrombolytic treatment in acute
myocardial infarction.
Lancet
1986;
1
: 397–401.
Marder VJ, Stewart D. Towards safer thrombolytic therapy.
5.
Semin
Hematol
2002;
39
(3): 206–216.
Boersma E, Mercado N, Poldermans D, Gardien M, Vos J, Simoons ML.
6.
Acute myocardial infarction.
Lancet
2003;
361
: 847–858.
Janousek S. Does streptokinase still have a role in the treatment of acute
7.
myocardial infarct?
V nitr Lek
2003;
49
(11): 880–884.
Weaver WD, Simes RJ, Betriu A, Grines CL, Zijlstra F, Garcia E,
8.
et al.
Comparison of primary angioplasty and intravenous thrombolytic therapy
for acute myocardial infarction.
J Am Med Assoc
1997;
278
: 2093–2098
Cohen M, Demers C, Gurfinkel EP, Turpie AGG, Fromell GJ, Goodman
9.
S,
et al.
for the Efficacy and Safety of Subcutaneous Enoxaparin in
Non-Q-Wave Coronary Events study group. A comparison of low-
molecular-weight heparin with unfractionated heparin for unstable coro-
nary artery disease.
N Engl J Med
1997;
337
: 447–452.
Antman EM, McCabe CH, Gurfinkel EP, Turpie AGG, Bernink PJLM,
10.
et al.
Enoxaparin prevents death and cardiac ischemic events in unstable
angina/non-Q-wave myocardial infarction: results of the Thrombolysis in
MyocardialInfarction(TIMI)11Btrial.
Circulation
1999;
100
:1593–1601.
Morrow DA. Heparin and low-molecular-weight heparin. In: Manson
11.
JE, Buring JE, Ridker PM, Gaziano JM. Clinical Trials in Heart Disease:
a Companion to Braunwald’s Heart Disease. 2nd edn. Philedelphia:
Elsevier Saunders, 2004: 45–65.
The international tPA/SK Mortality Trial study group. In hospital
12.
mortality and clinical course of 20,891 patients with suspected acute
myocardial infarction randomised between tissue plasminogen activator
or streptokinase with or without heparin.
Lancet
1990;
336
: 71–75.
Anderson JL, Marshall HW, Bray BE, Lutz JR, Frederick PR, Yanowitz
13.
FG,
et al.
A randomized trial of intracoronary streptokinase in the treat-
ment of acutemyocardial infarction.
NEngl JMed
1983;
308
: 1312–1318.
Crenshaw BS, Ward SR, Granger CB, Stebbins AL, Topol EJ,
14.
et al.
Atrial
fibrillation in the setting of acute myocardial infarction: the GUSTO-I
experience. Global Utilization of Streptokinase and TPA for Occluded
Coronary Arteries.
J Am Coll Cardiol
1997;
30
(2): 406–413.
Wood WA, Tisnado J, Cho SR. Visceral embolisation during low-dose
15.
fibrinolysis of aortic graft occlusion.
Am J Roentgenol
1983;
141
:
1055–1056.