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Updated: Jun 26, 2026
Myocardial Infarction by Percutaneous Embolization Coil Deployment in a Swine Model
Published on: November 4, 2021
Myocardial microinfarction after coronary microembolization in swine: MR imaging characterization
Marcus Carlsson1, Mark Wilson, Alastair J Martin
1Department of Radiology and Biomedical Imaging, University of California San Francisco, 513 Parnassus Ave, HSW 207B, San Francisco, CA 94134, USA.
Purpose:
To use first-pass perfusion and delayed-enhanced (DE) magnetic resonance (MR) imaging for the detection of the early effects of coronary microembolization on myocardial perfusion and viability.
Materials And Methods:
Approval was obtained from the institutional committee on animal research. A hybrid x-ray and MR imaging system was used to guide the endovascular catheter and quantify the left anterior descending coronary artery (LAD) perfusion territory before microembolization and ischemic myocardium and microinfarction after microembolization. The embolic agent was selectively delivered in the LAD in six pigs. First-pass perfusion MR imaging was performed 1 hour and 1 week after microembolization. Microinfarction was measured on DE MR images in beating and nonbeating hearts (high-spatial-resolution sequence) by using extracellular and blood pool MR contrast media and after death. The Wilcoxon signed rank test and correlation analysis were used.
Results:
The LAD perfusion territory was 35% of left ventricular (LV) mass +/- 2 (standard error of the mean). Microembolization caused perfusion deficit in 15.7% of LV mass +/- 2.6 compared with that of LAD territory (P = .03). At 1 week, perfusion parameters improved and the extent of hypoperfused territory declined (4.6% of LV mass +/- 1.4, P = .03). Microinfarction size expanded from 1.4% of LV mass +/- 0.2 at 1 hour to 7.5% of LV mass +/- 1.2 at 1 week. In nonbeating hearts and at triphenyltetrazolium chloride staining at 1 week, microinfarction size was 7.6% of LV mass +/- 1.4 and 7.2% of LV mass +/- 1.5, respectively. There was no correlation between the ejection fraction and the extents of microinfarction or hypoperfused territory. Histopathologic findings confirmed the presence of patchy microinfarction.
Conclusion:
Coronary microembolization caused persistent decline in myocardial perfusion at first-pass perfusion imaging. DE MR imaging has the potential to help reliably quantify subacute microinfarction. The magnitude of LV dysfunction is not related to the extents of microinfarction or hypoperfused territory.
