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.
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 mm(3), p < 0.001) and CKD4-5 (+9.8 mm(3), p < 0.001) despite anti-atherosclerotic treatment, whereas plaque regression occurred in CKD-1 (-5.4 mm(3), p = 0.002) and CKD-2 (-3.2 mm(3), 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 mm(3), p < 0.001) and CKD4-5 (+5.4 mm(3), p < 0.001), but decreased in CKD-2 (-2.7 mm(3), p < 0.05). Fibrotic plaque also increased in CKD4-5 (+3.4 mm(3), 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.
Second Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, 807-8555, Japan.
Kuninobu
K
Kashiyama
Shinjo
S
Sonoda
Yoshitaka
Y
Muraoka
Yoshiyuki
Y
Suzuki
Fumihiko
F
Kamezaki
Yuki
Y
Tsuda
Masaru
M
Araki
Masahito
M
Tamura
Masaaki
M
Takeuchi
Haruhiko
H
Abe
Masahiro
M
Okazaki
Yoshihisa
Y
Fujino
Yutaka
Y
Otsuji
D000368:Aged; D000369:Aged, 80 and over; D016009:Chi-Square Distribution; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging* / Q000378:metabolism / Q000628:therapy*; D003331:Coronary Vessels / Q000000981:diagnostic imaging* / Q000187:drug effects / Q000378:metabolism; D005260:Female; D005355:Fibrosis; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007090:Image Interpretation, Computer-Assisted; D016014:Linear Models; D008055:Lipids / Q000032:analysis; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016017:Odds Ratio; D062645:Percutaneous Coronary Intervention; D058226:Plaque, Atherosclerotic; D011237:Predictive Value of Tests; D051436:Renal Insufficiency, Chronic / Q000150:complications* / Q000175:diagnosis; D012189:Retrospective Studies; D012307:Risk Factors; D012542:Scattering, Radiation; D012720:Severity of Illness Index; D013997:Time Factors; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids