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From the Cardiac Catheterization Unit, Rabin Medical Center, Beilinson
Campus, Tel Aviv University Sackler School of Medicine, Israel.
Correspondence to Dr Eldad Rechavia, Cardiac Catheterization Unit, Rabin Medical Center, Beilinson Campus, Petach Tikva 49100, Israel.
Several reports
have recently opened a new therapeutic window for the use of
platelet glycoprotein (GP) IIb/IIIa receptor blockade
as an adjunct to thrombolytic therapy in acute
myocardial infarction.1 2 Because of the
different protocols and the different agents that were used, as well as
the relatively small number of patients included in these studies, one
cannot draw any definitive conclusions about the efficacy of
platelet GP IIb/IIIa receptor blockers as an adjunct to
thrombolysis. Nevertheless, one could also make a case
for the use of GP IIb/IIIa receptor blockers even as a monotherapy for
acute myocardial infarction, as in the following case.
A 36-year-old, previously healthy male who was a heavy smoker was
admitted with intermittent chest pain of 4 hours' duration and ECG
findings compatible with an acute anterior wall myocardial infarction
(Figure 1
Footnotes
The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke's Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.
Circulation encourages readers to submit cardiovascular images to Dr Hugh A. McAllister, Jr, St Luke's Episcopal Hospital and Texas Heart Institute, 6720 Bertner Ave, MC1–267, Houston, TX 77030.
References
© 1998 American Heart Association, Inc.
Images in Cardiovascular Medicine
Platelet Glycoprotein IIb/IIIa Receptor Blockade in Acute Myocardial Infarction Associated With Thrombotic Occlusion of the Left Main Coronary Artery
). The patient was treated with
aspirin (325 mg) and underwent emergency coronary angiography.
This demonstrated multiple filling defects consistent with
thrombotic occlusions involving the left main (Figures 2 and 3), the proximal left anterior
descending, and the right (Figure 4) coronary arteries. At
this stage, intravenous heparin (5000 U) was administered,
achieving an activated clotting time of 265 seconds.
Standard-dose, weight-adjusted abciximab was administered as a bolus,
and continuous infusion was subsequently started for 12 hours, together
with heparin, maintaining an activated partial
thromboplastin time between 60 and 80 seconds. A few minutes after
abciximab bolus injection, chest pain was relieved and gradual
resolution of ST-segment elevation was apparent. Over the following 4
days, the patient remained asymptomatic. He developed a
non–Q-wave myocardial infarction (Figure 5), with an increase in creatine kinase
to 579 IU/L and 18% MB fraction. Echocardiography
demonstrated mild septoapical hypokinesis. Repeat angiography on day 5
revealed normal coronary arteries with no evidence of residual
thrombus or coronary narrowing (Figures 6 and 7).
Laboratory workup revealed that the patient is heterozygous for a
mutation in factor V known as activated protein C resistance
(APCR), a mutation that results in an abnormal resistance to
degradation by APC (frequently called factor V Leiden) and an increased
tendency to thrombosis, particularly in patients who are homozygous for
this mutation.3 This was detected and confirmed
by a polymerase chain reaction–based test. The patient was discharged
on oral therapy with aspirin and warfarin and remained symptom-free for
the next 4 months.
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Figure 1. ECG taken on admission showing ST-segment
elevation in leads V2 to V6, I, and aVL with
reciprocal changes in leads III and aVF.
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Figure 2. Cine frame in right anterior oblique cranial
projection showing a conglomerate of thrombus-containing lesions
involving left main coronary artery.
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Figure 3. Cine frame in right anterior oblique and more
cranial angulation with same findings as in Figure 2 
.
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Figure 4. Right coronary angiography (right anterior
oblique projection) reveals a filling defect (arrow) suggestive of
thrombus with 70% luminal narrowing.
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Figure 5. ECG tracing recorded 12 hours after admission
showing inverted T waves in leads V2 to V6, I,
and aVL, changes compatible with non–Q-wave myocardial
infarction.
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Figure 6. Follow-up angiography 4 days after abciximab
administration demonstrating no evidence for residual thrombus of left
main coronary artery. Note smooth angiographic appearance of
artery.
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Figure 7. Normal angiographic appearance of right
coronary artery on repeat angiography.
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