Vol 68, No 9 (2010)
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Published online: 2010-09-21

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Risk factors of asymptomatic restenosis in patients with first anterior ST elevation myocardial infarction treated by primary percutaneous coronary intervention

Krystian Wita, Leszek Kinasz, Artur Filipecki, Michał Lelek, Jan Szczogiel, Maciej Turski, Przemysław Węglarz, Marek Elżbieciak, Adam Staroń, Maria Trusz-Gluza
DOI: 10.33963/v.kp.79597
Kardiol Pol 2010;68(9):987-993.

Abstract


Background: The issue of predicting coronary artery restenosis, especially silent, in patients following primary percutaneous coronary intervention (PCI) has been extensively studied, however, risk factors have not been fully defined.
Aim: To asses the frequency of silent restenosis and its predictors in patients with anterior ST elevation myocardial infarction (STEMI) treated with primary PCI and implantation of bare metal stents (BMS).
Methods: We recruited a cohort of 114 patients with first anterior STEMI treated with primary PCI within 12 hours of the onset of symptoms, and with the left anterior descending coronary artery occlusion (TIMI 0) and successful flow restoration (TIMI 3). A 12-lead ECG was performed before and 60 minutes after PCI. Troponin I and CK-MB were measured on admission and after six, 12 and 24 hours. Transthoracic echocardiography (TTE) was performed at discharge. Resting TTE and coronary angiography were performed after a six month follow-up in asymptomatic patients.
Results: The frequency of silent restenosis in our study group was 23.9%. The best multivariate models in logistic regression of restenosis prediction were: lower end-systolic volume of the left ventricle assessed two days after infarction longer lesion and smaller reference diameter of the stented vessel.
Conclusions: Silent restenosis in patients with first anterior STEMI treated by primary PCI with the use of BMS is still frequent. The best ways to identify patients with silent restenosis at six month follow-up, apart from the lower end systolic volume in the echocardiographic study, are longer narrowing in the infarct-related artery and lower reference diameter of the treated vessel.
Kardiol Pol 2010; 68, 9: 987-993

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Polish Heart Journal (Kardiologia Polska)