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Plaque and blood vulnerability in ST segment elevation myocardial infarction patients: association between lesion
Karlis Trusinskis1, Dace Juhnevica, Karlis Strenge
1aLatvian Centre of Cardiology, Pauls Stradins Clinical University Hospital bFaculty of Medicine, Riga Stradins University cFaculty of Medicine, University of Latvia, Riga, Latvia.
Aim:
The purpose of the study was to evaluate associations between iMap intravascular ultrasound tissue characterization of culprit and nonculprit lesions in infarct-related artery and plasma biomarkers during ST segment elevation myocardial infarction (STEMI) and at 10-month follow-up.
Methods And Results:
Sixty-three STEMI patients at the time of index hospitalization and 10-month follow-up underwent coronary angiography and intravascular ultrasound with iMap tissue characterization of the culprit artery. Proximal and culprit segments were analyzed. A higher percentage of necrotic tissue in the nonculprit segment was found in patients in the top soluble intercellular adhesion molecule 1 (sICAM-1) quartile compared with the other three quartiles (34.3±10.9 vs. 26.3±11.6%, P=0.041) in the acute setting. At 10-month follow-up the top quartile of sICAM-1 in both the acute and stable setting was associated with a lower percentage of fibrotic tissue, but a higher percentage of lipidic and necrotic tissue in the nonculprit segment. In the top quartile of plasminogen activator inhibitor 1 during STEMI, a lower percentage of fibrotic tissue (53.0±13.9 vs. 63.0±13.3%, P=0.014), higher percentage of lipidic tissue (11.7±3.1 vs. 9.4±2.4%, P=0.004), and higher percentage of necrotic tissue (33.4±11.6 vs. 25.7±11.3%, P=0.025) were found in the nonculprit segment.
Conclusion:
Nonculprit plaque vulnerability characteristics were associated with elevated plasma biomarkers for sICAM-1 and plasminogen activator inhibitor 1.
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