Platelet Glycoprotein ibb/llla receptor blockade in acute coronary artery syndrome – A ReviewA 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⇓). 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 the 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.
Figure 1.
ECG has taken on admission showing ST-segment elevation in leads V2 to V6, I, and aVL with reciprocal changes in leads III and IVF.
Cine frame in right anterior oblique cranial projection showing a conglomerate of thrombus-containing lesions involving left main coronary artery.
Figure 2.
Cine frame in right anterior oblique cranial projection showing a conglomerate of thrombus-containing lesions involving left main coronary artery.
Cine frame in right anterior oblique and more cranial angulation with same findings as in Figure 2.
Figure 3.
Cine frame in right anterior oblique and more cranial angulation with same findings as in Figure 2⇑.
Right coronary angiography (right anterior oblique projection) reveals a filling defect (arrow) suggestive of thrombus with 70% luminal narrowing.
Figure 4.
Right coronary angiography (right anterior oblique projection) reveals a filling defect (arrow) suggestive of thrombus with 70% luminal narrowing.
ECG tracing recorded 12 hours after admission showed inverted T waves in leads V2 to V6, I, and aVL, changes compatible with non–Q-wave myocardial infarction.
Figure 5.
ECG tracing recorded 12 hours after admission showed inverted T waves in leads V2 to V6, I, and aVL, changes compatible with non–Q-wave myocardial infarction.
Follow-up angiography 4 days after abciximab administration demonstrating no evidence for residual thrombus of the left main coronary artery. Note the smooth angiographic appearance of the artery.
Figure 6.
Follow-up angiography 4 days after abciximab administration demonstrating no evidence for residual thrombus of the left main coronary artery. Note the smooth angiographic appearance of the artery.
The normal angiographic appearance of the right coronary artery on repeat angiography.
Figure 7.
The normal angiographic appearance of the right coronary artery on repeat angiography.
H.K. Bali, Sunip Banerjee, M. Bhargava. Platelet Glycoprotein IBB/Ella receptor blockade in acute coronary artery syndrome – A Review. Bull PGI 2001; 35:4-10. |
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