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. 1993 Mar 1;21(3):622-7.
doi: 10.1016/0735-1097(93)90093-g.

Thrombosis of a flexible coil coronary stent: frequency, predictors and clinical outcome

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Free article

Thrombosis of a flexible coil coronary stent: frequency, predictors and clinical outcome

F C Nath et al. J Am Coll Cardiol. .
Free article

Abstract

Objectives: The aim of this study was to evaluate the predictors and clinical sequelae of stent thrombosis.

Background: Although coronary artery stenting is being increasingly applied, the major unique complication of stent thrombosis is not well characterized.

Methods: We studied 145 patients who underwent coronary artery stenting with the Gianturco-Roubin flexible coil design for abrupt vessel closure or to prevent restenosis. There were 17 stented vessel closures (11.7%), 7 as a result of acute (< 24 h) and 10 of subacute (days 1 to 21) thrombosis.

Results: In seven patients successful coronary recanalization was achieved with thrombolytic agents and balloon angioplasty. Creatine kinase was significantly elevated in 13 patients, with a Q wave myocardial infarction in 11 and emergency coronary artery bypass grafting in 8. Comparisons (multivariate analysis) with a control cohort (n = 33) of patients without thrombosis matched for age, gender and vessel stented revealed lesion eccentricity (p = 0.003), unstable angina (p = 0.048) and indication for stent implantation (abrupt closure versus restenosis) (p = 0.002), as predictors of thrombotic occlusion of stented vessels. Subtherapeutic anticoagulation (activated partial thromboplastin time < 2 times control value, prothrombin time < 1.4 control value) occurred at least once during the hospital stay in all 10 patients with subacute thrombosis and in 20 of 33 control patients (p = 0.047). In 2 patients with subacute thrombosis and 11 control subjects, subtherapeutic anticoagulation was necessitated by bleeding.

Conclusions: Early thrombosis after coronary stenting was relatively common (> 10%), occurring predominantly in eccentric lesions and in patients with unstable angina pectoris. This complication is associated with significant adverse clinical outcomes and may be reduced by more intensive anticoagulation yet, in a delicate balance, can be precipitated by inadequate heparin therapy.

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