Paul Yock, MD

Publication Details

  • Serial intravascular ultrasonic study of outcomes of coronary culprit lesions with plaque rupture following bare metal stent implantation in patients with angina pectoris AMERICAN JOURNAL OF CARDIOLOGY Hur, S., Hassan, A. H., Rekhi, R., Ako, J., Shimada, Y., Nakamura, M., Yamasaki, M., Bonneau, H. N., Sudhir, K., Yock, P. G., Honda, Y., Fitzgerald, P. J. 2007; 99 (10): 1394-1398


    Coronary culprit lesions with plaque rupture (PR) have been treated with different coronary interventions. However, it is unknown whether the presence of PR affects the restenotic process after coronary intervention. One hundred forty-two patients undergoing coronary bare metal stent implantation were enrolled in the present retrospective analysis. Case selection was based on availability of intravascular ultrasound (IVUS) and quantitative coronary angiographic examinations at baseline (before and after intervention) and at follow-up. Serial comparative analyses included qualitative and quantitative features of the culprit lesion and reference segments. PR was defined as an intraplaque cavity in communication with the lumen in the presence of a residual, disrupted cap. Patients were categorized according to the presence/absence of PR. Pre-interventional IVUS detected PR in 54 patients (38%). Baseline patient demographics were similar between the +PR and -PR groups. Quantitative IVUS analysis showed higher rates of positive remodeling and larger vessel and plaque areas in the +PR compared with -PR lesions (p <0.001 for all). At follow-up (7.2 +/- 2.6 months), no statistically significant difference was observed between the 2 groups in quantitative coronary angiographic or IVUS measurements. In conclusion, culprit lesions with PR exhibited larger plaque mass and higher rates of positive remodeling at preintervention IVUS examination. However, when treated with bare metal stents, the absence/presence of preintervention PR was not found to affect the rate or severity of in-stent restenosis in these culprit lesions.

    View details for DOI 10.1016/j.amjcard.2006.12.067

    View details for Web of Science ID 000246715900010

    View details for PubMedID 17493467

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