Successful treatment of a large intracoronary thrombus with urokinase and a chimerical monoclonal platelet aggregation inhibitor

History and clinical findings: 7 days after an operation for intervertebral disc prolapse a 43-year-old man was referred with the clinical and ECG signs of an acute posterior wall myocardial infarction. Investigations: Creatine kinase (CK) activity was raised to 204 U/l (myocardial-specific isoenzyme CKMB of 23.6 U/l, 11.6% of total) and glutamatic-oxalate transferase (GOT) activity to 37 U/l. Emergency cardiac catheterisation, performed 4 hours after renewed onset of precordial pain showed no abnormal findings in the right coronary artery, despite the ECG signs, but a definite filling defect in the anterior interventricular branch which on intravascular ultrasound was an echo-dense noncalcified structure. Treatment and course: After percutaneous transluminal coronary angioplasty in the area of the obstructing structure al free-floating mass was identified in the proximal part of the anterior interventricular branch, most likely a thrombus. Intercoronary thrombolysis was therefore undertaken with urokinase (bolus of 1 mill. IU) together with the chimerical mono-clonal antibody c7E3, which inhibits platelet aggregation by blocking the platelet glycoprotein surface receptor IIb/IIIa. Coronary angiography 12 hours later revealed almost complete dissolution of the previously obstructing mass. Conclusion: Combining the platelet aggregation inhibitor c7E3 with a thrombolytic agent is an alternative treatment to the current management of intracoronary thrombi. Intravascular ultrasound is a suitable method for demonstrating angiographically inconspicious or unclear but pathogenetically significant vessel changes.