Download st-elevation myocardial infarction following thrombolysis for acute

The West London Medical Journal 2011 Vol 3 No 1 pp 7-13
ST-ELEVATION MYOCARDIAL INFARCTION
FOLLOWING THROMBOLYSIS FOR ACUTE
STROKE: A CASE REPORT
Bo Wang
Hitesh Patel*
Tom Snow
Ed Leatham
ABSTRACT
Diseases of the coronary and cerebral vasculature share common
aetiologies and hence are often linked. Whereas ischaemic stroke following an
acute myocardial infarction is relatively common, the converse is much rarer.
We present a case of a 69 year old patient with a ST-elevation myocardial
infarction three days after systemic thrombolysis for acute ischaemic stroke.
We discuss the possible underlying aetiologies and the necessary
investigations, and highlight the possibility of thrombosis as a paradoxical
complication of thrombolysis.
Keywords: ST elevation myocardial
Thrombolysis; Prothrombotic state.
infarction;
Acute
stroke;
KEY POINTS
ST elevation myocardial infarction following an acute stroke is not
commonly seen and an underlying aetiology should be investigated for
from several possible differentials.
A prothrombotic state exists after systemic thrombolysis that can
contribute to complications and impacts upon management.
Glycoprotein IIb/IIIa inhibitor can be considered in patients with
ischaemic cardiac chest pain despite recent thrombolysis for stroke.
CASE HISTORY
A 69 year old woman presented with a one hour history of right-sided
weakness and dysphasia and had clinical findings suggestive of a stroke.
Computed tomography (CT) scan of the head suggested a left middle cerebral
artery territory ischaemic stroke. She was thrombolysed in accordance with
the NINDS guidelines with 63mg of Alteplase, a recombinant tissue
*
Hitesh Patel, Royal Surrey County Hospital, Guildford GU2 7XX, UK. Email:[email protected]
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plasminogen activator, two hours after onset of symptoms. Admission
electrocardiogram showed normal sinus rhythm with left axis deviation only
(figure 1).[1]
Her past medical history included angina, for which she had a 3.5x12mm
bare metal coronary stent inserted into a dominant left circumflex artery 13
months ago. She also underwent open biological aortic valve replacement
with a 23mm Perimount valve for mixed aortic valve disease 2 months prior
to this admission. Other medical problems included bronchiectasis, anaemia
of unknown origin and depression. Her medications on admission consisted of
aspirin 75mg once a day, bisoprolol 1.25mg once a day, amiodarone 200mg
once a day (started after valve replacement to maintain sinus rhythm),
simvastatin 20mg once a day, ferrous sulphate 200mg three times a day,
omeprazole 40mg once a day.
The patient initially showed a good response with NIHSS (National
Institute of Health stroke scale) score improving from 10 to 7. On the third
day post stroke thrombolysis, she suddenly developed severe central chest
pain. ECG showed significant ST elevation in anterior and inferior leads
(figure 2). Whilst being assessed for chest pain, the patient arrested with an
underlying rhythm of ventricular fibrillation. This was promptly defibrillated
and the patient regained cardiac output within one cycle of cardio-pulmonary
resuscitation by which stage there was resolution of the ST segment changes
and chest pain.
The patient was admitted to the coronary care unit and was loaded with
300mg clopidogrel and was started on a Tirofiban (glycoprotein IIb/IIIa
inhibitor) infusion. Aspirin was continued at 75mg once a day. A lowmolecular-weight heparin was not given, despite the protocol for acute
coronary syndrome, due to the increased risk of intracerebral haemorrhage
with recent systemic thrombolysis. Troponin I at 12 hours was elevated at
18.41 and creatine kinase was 889. ECG four hours after the onset of chest
pain showed Q waves in inferior leads and deep T wave inversion in the
anterior leads (figure 3).
The patient was transferred to the local angioplasty referral hospital the
following morning. A coronary angiogram showed unobstructed coronary
arteries and a patent stent within a dominant left circumflex artery. Transoesophageal echocardiograghy (TOE) showed did not show any thrombus
within the cardiac chambers. Saline contrast (bubble) echocardiograghy with
Valsalva release did not reveal any intracardiac shunts.
The patient was transferred back to our hospital and eventually
rehabilitated well from both events and was discharged to the community.
Prior to discharge, she was anticoagulated with warfarin in addition to aspirin,
a combination on which she still remains.
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ACUTE STROKE
DISCUSSION
The incidence of acute ischaemic stroke after myocardial infarction (MI)
has been shown to be around 2%.[2] Amongst other shared risk factors such
as hypertension, diabetes mellitus and smoking, atrial fibrillation is the single
most important risk factor and it occurs in up to 20% of patients after a STelevation myocardial infarction (STEMI)[3]. Poor ventricular function after a
recent infarct with atrial fibrillation predispose to the formation of mural
thrombi, which then becomes a source of emboli to the cerebral vasculature.
The incidence of acute MI following a stroke is not known but there have
been other case reports[4,5,6]. The pathogenesis in all these cases was thought
to be disruption of a cardiac thrombus, which gave rise to an embolic stroke
and an embolic MI. 26% of patients presenting with acute stroke or transient
ischaemic attacks have intra-cardiac thrombus[7,8]. Embolic myocardial
infarction, although rare, has been described elsewhere in the context of atrial
myxoma, aortic valve endocarditis, dilated cardiomyopathy and atrial septal
defects (ASD)[4,6]. In this case however, no definitive evidence for such an
embolic aetiology was found. Therefore the authors had to consider several
possible differentials (Table I). In managing this patient, each differential had
to be considered and investigated for, accordingly.
De novo thrombus in this patient is raised in the context of recent systemic
thrombolysis. A paradoxical prothrombotic state exists after thrombolysis due
to the selective action of tissue-plasminogen activators on fibrin degradation,
leaving thrombin exposed and thus resulting in increased platelet
aggregation.[10] Studies have also shown a transient but significant increase
in total thrombin levels after thrombolysis, possibly via direct stimulation of
the coagulation cascade by plasminogen activators.[11] This may explain the
good evidence for early use of heparin and antiplatelets such as aspirin and
clopidogrel after thrombolysis for STEMI for preventing vessel
reocclusion.[12,13,14]
Management of patients after stroke thrombolysis is different from
patients after STEMI thrombolysis. Early anticoagulant and antiplatelet
therapy is not recommended after stroke thrombolysis due to the associated
risk of intracerebral haemorrhage. However, in stroke as in MI, there is a
significant reocclusion rate, estimated at 13%.[1] Recently, work has been
directed into evaluating any possible benefit of early antiplatelet therapy.
Some early trials have shown that patients taking aspirin long-term show
better outcomes when thrombolysed for acute stroke.[15] Further to this, a
large randomised controlled trial is currently being carried out looking at early
use of antiplatelet agents with stroke thrombolysis.[16]
We thought that out of the differential mechanisms discussed in table 1,
the most likely for our patient were: 1. Embolisation of existing thrombus
following thrombolysis ; 2. De novo thrombus formation in the pro-coagulant
state following thrombolysis. Neither of these theories could be proven
despite extensive investigations. On balance of probability we started
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anticoagulation with warfarin to reduce the risk of further potential
thromboembolic events.
CONCLUSION
Acute STEMI after a recently thrombolysed ischaemic stroke is not a
frequent event, but one that requires decisive treatment balancing the risk benefit of relieving a coronary obstruction to that of intracerebral
haemorrhage. We have reported a successful outcome following early use of a
glycoprotein IIb/IIIa inhibitor whilst awaiting transfer for urgent coronary
angiography. It is important to consider aetiological investigations in the
subsequent management of these patients including TOE and saline contrast
echocardiography as this would alter management.
Figure 1. ECG on admission
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ST-ELEVATION MYOCARDIAL INFARCTION FOLLOWING THROMBOLYSIS FOR
ACUTE STROKE
Figure 2. ECG at onset of chest pain
Figure 3. ECG at resolution of chest pain and after GpIIb/IIIa inhibitor
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Table I. Possible pathogenic mechanisms
Mechanism
For
Against
Mural thrombus leading to
embolic stroke then MI
Recent cardiac surgery ; postoperative atrial fibrillation
No thrombus seen on TOE
9
(95% sensitive )
De novo
thrombus
in
coronary artery following
thrombolysis
Pre-existing ischaemic heart
disease; prothrombotic state
after systemic thrombolysis
Normal coronary angiogram
Stent thrombosis following
thrombolysis
Bare metal stent thrombosis
likely; prothrombotic state
after systemic thrombolysis
Normal coronary angiogram;
ST elevation distribution not
in keeping with stent position
Paradoxical emboli through
an ASD causing stroke then
MI
Unlikely
No ASD seen on TOE/Bubble
echo
Coronary artery spasm
Spontaneous
resolution;
normal coronary angiogram
Persistent ischaemic changes
on ECG; cardiac-specific
markers elevated
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