Coronary plaque progression of non-culprit lesions after culprit percutaneous coronary intervention in patients with moderate to advanced chronic kidney disease: intravascular ultrasound and integrated backscatter intravascular ultrasound study

Abstract

Previous studies have suggested that the deterioration of renal function increases the risk of major adverse clinical events not only in culprit lesions but also in non-culprit lesions (NCLs) after percutaneous coronary intervention (PCI). This study evaluated serial coronary plaque change of NCL in patients with different stages of chronic kidney disease (CKD) using intravascular ultrasound (IVUS) and integrated backscatter IVUS (IB-IVUS). In 113 patients (113 NCLs) underwent both IVUS-guided PCI and follow-up IVUS, volumetric IVUS analyses were performed at proximal reference NCLs in de novo target vessels post PCI and at 8-month follow-up. NCLs were divided into 4 groups based on baseline CKD stage: CKD-1, n = 18; CKD-2, n = 42; CKD-3, n = 29; and CKD4–5, n = 24. We compared serial changes of plaque burden and composition among groups under statin treatment. Plaque progression occurred in CKD-3 (+4.6 mm3, p < 0.001) and CKD4–5 (+9.8 mm3, p < 0.001) despite anti-atherosclerotic treatment, whereas plaque regression occurred in CKD-1 (−5.4 mm3, p = 0.002) and CKD-2 (−3.2 mm3, p = 0.001) mainly due to initiate statin treatment after PCI. Plaque volume change was correlated with eGFR (p < 0.0001). Multivariate analysis showed CKD stage 3–5 was an independent predictor of plaque progression. Regarding IB-IVUS analyses, lipid plaque increased in CKD-3 (+4.6 mm3, p < 0.001) and CKD4–5 (+5.4 mm3, p < 0.001), but decreased in CKD-2 (−2.7 mm3, p < 0.05). Fibrotic plaque also increased in CKD4–5 (+3.4 mm3, p < 0.001). Moderate to advanced CKD was associated with coronary plaque progression characterized by greater lipid and fibrotic plaque volumes in NCL under statin treatment after culprit PCI.