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[Treatment of a large intracoronary thrombus with urokinase and a chimeric monoclonal platelet aggregation inhibitor].

作者信息

Eick B, Haude M, Altmann C, Liu F, Caspari G, Leischik R, Erbel R

机构信息

Abteilung für Kardiologie, Universität Essen.

出版信息

Dtsch Med Wochenschr. 1997 May 30;122(22):709-15. doi: 10.1055/s-2008-1047678.

DOI:10.1055/s-2008-1047678
PMID:9213535
Abstract

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/I (myocardial-specific isoenzyme CKMB of 23.6 U/I, 11.6% of total) and glutamic-oxalate transferase (GOT) activity to 37 U/I. 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 a 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 chimeric monoclonal 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 inconspicuous or unclear but pathogenetically significant vessel changes.

摘要

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