ImagingLipid-core burden response to stent implantation assessed with near-infrared spectroscopy and intravascular ultrasound evaluation in patients with myocardial infarction

- Acute coronary syndromes mainly develop from rupture of a vulnerable.
- Vulnerable plaques have a thin fibrotic cap and a lipid-rich necrotic core that is highly thrombogenic.
- The lipid-core plaque can be identified and quantified in vivo by near-infrared spectroscopy.
- During percutaneous coronary intervention the lipid-core plaque may be compressed or redistributed longitudinally.

IntroductionNear-infrared spectroscopy (NIRS) is a new method to identify lipid core plaque (LCP). The LCP and vascular response were assessed with NIRS to examine whether LCP was compressed or redistributed during percutaneous coronary intervention with stent implantation.MethodsIn 25 patients with non-ST segment elevation myocardial infarction (NSTEMI) NIRS acquisition was performed after predilation, stent implantation with nominal pressure and high-pressure post-dilation with a non-compliant balloon. The intravascular ultrasound (IVUS) measures included volumes of external elastic membrane (EEM), lumen and plaque + media. The NIRS measures included lipid core burden index (LCBI) and maximum value of LCBI for any of the 4-mm segment (maxLCBI4mm).ResultsFrom predilation to stent implantation and post-dilation EEM volume increased from 337 ± 124 mm3 to 369 ± 136 mm3 and to 397 ± 144 mm3 (p < 0.001), while plaque volume decreased from 225 ± 84 mm3 to 202 ± 85 mm3 and to 192 ± 81 mm3 (p < 0.001). Plaque shift to the proximal reference segment was found in 40% of the lesions. The maxLCBI4mm decreased significantly from predilation to stent implantation (492 ± 235 to 208 ± 193 (p < 0.001), whereas post dilation did not cause any further significant reduction. Also LCBI decreased significantly from predilation to stent implantation (173 ± 103 to 68 ± 67, p < 0.001), without any further significant reduction during post-dilation. The LCBI did neither in the proximal nor in the distal reference segments change significantly during stent implantation or post-dilation.ConclusionLumen enlargement was caused by vessel expansion, plaque compression and longitudinally plaque redistribution. Lipid-core burden at the stented segment was decreased.