Culprit lesion vessel size and risk of reperfusion injury in ST-segment elevation myocardial infarction – A cardiac magnetic resonance imaging study

Ivan Lechner (Innsbruck)1, M. Reindl (Innsbruck)1, C. Tiller (Innsbruck)1, M. Holzknecht (Innsbruck)1, F. Oberhollenzer (Innsbruck)1, S. Von der Emde (Innsbruck)1, A. Mayr (Innsbruck)2, A. Bauer (Innsbruck)1, B. Metzler (Innsbruck)1, S. J. Reinstadler (Innsbruck)1

1Medizinische Universität Innsbruck Universitätsklinik für Innere Medizin III - Kardiologie und Angiologie Innsbruck, Österreich; 2Medizinische Universität Innsbruck Universitätsklinik für Radiologie Innsbruck, Österreich


Background: Microvascular obstruction (MVO) and intramyocardial hemorrhage (IMH) are well-established imaging biomarkers of failed myocardial tissue reperfusion in patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI). MVO and IMH are associated with an increased risk of death and heart failure independent of infarct size, but whether the size of the culprit lesion vessel plays a role in the occurrence and severity of reperfusion injury is currently unknown.

Objective: The goal of this study was to evaluate the association between culprit lesion vessel size and the occurrence and severity of reperfusion injury as determined by cardiac magnetic resonance (CMR) imaging-based tissue characterization.

Methods: Patients (n=516) with first-time STEMI treated with primary PCI underwent evaluation with CMR imaging at 4 (3-5) days after infarction. A comprehensive imaging protocol including late gadolinium enhancement imaging for MVO assessment and T2* mapping for IMH assessment was used. Vessel dimensions were determined by direct measurement using the catheter as reference.

Results: Median culprit lesion vessel size was 3.1 (2.7-3.6) mm. MVO and IMH were found in 299 (58%) and 182 (35%) patients. Culprit lesion vessel size was associated with body surface area, diabetes mellitus and infarct size. There was no association between vessel size and MVO or IMH in univariable as well as multivariable analysis (p>0.05). These findings were replicated in the subgroups of patients with LAD (n=226) and non-LAD (=290) infarction as well as in patients with Thrombolysis in Myocardial Infarction 3 flow after PCI (n=464). 

Conclusion: Comprehensive characterization of myocardial tissue reperfusion injury by CMR revealed no association between culprit lesion vessel size and the occurrence of MVO and IMH in patients treated with primary PCI for STEMI.

Diese Seite teilen