Factors leading to subacute stent thrombosis after percutaneous coronary intervention (PCI) have not been well established. We assessed the pre- and post-PCI intravascular ultrasound (IVUS) characteristics of subacute stent thrombosis.
Methods and Results—
We analyzed 7484 consecutive patients without acute myocardial infarction who were treated with PCI and stenting and underwent IVUS imaging during the intervention. Twenty-seven (0.4%) had angiographically documented subacute closure <1 week after PCI (median time to subacute closure, 24 hours). Subacute closure lesions were compared with a control group (selected to be 3 times the abrupt closer group) matched by procedure date (within 6 months), age, gender, stable or unstable angina, lesion location, and additional treatment (balloon angioplasty or atherectomy). Postintervention IVUS did not identify a cause in 22% and did identify at least 1 cause for abrupt closure in 78% of patients (versus 33% in matched lesions,
=0.0002). In 48% of the patients, there were multiple causes in 48% (versus 3% in matched lesions,
<0.0001). Causes included dissection (17%), thrombus (4%), and tissue protrusion within the stent struts leading to lumen compromise lumen (4%). A total of 83% of patients with >1 of these abnormal morphologies also had reduced lumen dimensions post-PCI (final lumen <80% reference lumen). Preprocedural lesion characteristics were not different from matched lesions.
Subacute stent thrombosis is infrequently related to the preintervention lesion characteristics. Inadequate postprocedure lumen dimensions, alone or in combination with other procedurally related abnormal lesion morphologies (dissection, thrombus, or tissue prolapse), contribute to this phenomenon.