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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.

Kashiyama K, Sonoda S, Muraoka Y, Suzuki Y, Kamezaki F, Tsuda Y, Araki M, Tamura M, Takeuchi M, Abe H, Okazaki M, Fujino Y, Otsuji Y - Int J Cardiovasc Imaging (2015)

Bottom Line: 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).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.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.

View Article: PubMed Central - PubMed

Affiliation: Second Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, 807-8555, Japan.

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 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.

No MeSH data available.


Related in: MedlinePlus

Correlations between the eGFR at baseline and plaque volume change
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Fig4: Correlations between the eGFR at baseline and plaque volume change

Mentions: Table 3 shows the volume data using conventional gray-scale IVUS. The EEM volume was significantly greater in CKD4–5 than the other groups at both baseline and follow-up. The lumen volume showed no significant differences among groups at baseline; however, at follow-up, it was significantly greater in CKD-1. The plaque volume was significantly greater in CKD4–5 than the other stages at both baseline and follow-up. The EEM volume significantly increased in CKD4–5, whereas it did not in the other groups. The lumen volume significantly decreased in CKD-3 and CKD4–5, but increased in CKD-1. The plaque volume significantly increased in CKD-3 and CKD4–5, whereas it significantly decreased in CKD-1 and CKD-2. Furthermore, in the ANCOVA models including age, gender, BMI, unstable angina pectoris, hypertension, hyperlipidemia, diabetes, follow-up LDL-cholesterol and HDL-cholesterol levels, ACE-I/ARB use, beta-blocker use, and statin use, did not change the results, reflected by still greater plaque progression in moderate to advanced CKD patients (Fig. 3). Univariate linear regression analysis showed the baseline eGFR correlated significantly with plaque volume change (R = 0.65, p < 0.0001) (Fig. 4). On univariate and multivariate logistic regression analyses, after considering CKD stage, confounding factors (age, gender, and unstable angina pectoris), coronary risk factors and medications, CKD stage 3–5 demonstrated the strongest association with plaque progression (Tables 4, 5).Table 3


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.

Kashiyama K, Sonoda S, Muraoka Y, Suzuki Y, Kamezaki F, Tsuda Y, Araki M, Tamura M, Takeuchi M, Abe H, Okazaki M, Fujino Y, Otsuji Y - Int J Cardiovasc Imaging (2015)

Correlations between the eGFR at baseline and plaque volume change
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4446522&req=5

Fig4: Correlations between the eGFR at baseline and plaque volume change
Mentions: Table 3 shows the volume data using conventional gray-scale IVUS. The EEM volume was significantly greater in CKD4–5 than the other groups at both baseline and follow-up. The lumen volume showed no significant differences among groups at baseline; however, at follow-up, it was significantly greater in CKD-1. The plaque volume was significantly greater in CKD4–5 than the other stages at both baseline and follow-up. The EEM volume significantly increased in CKD4–5, whereas it did not in the other groups. The lumen volume significantly decreased in CKD-3 and CKD4–5, but increased in CKD-1. The plaque volume significantly increased in CKD-3 and CKD4–5, whereas it significantly decreased in CKD-1 and CKD-2. Furthermore, in the ANCOVA models including age, gender, BMI, unstable angina pectoris, hypertension, hyperlipidemia, diabetes, follow-up LDL-cholesterol and HDL-cholesterol levels, ACE-I/ARB use, beta-blocker use, and statin use, did not change the results, reflected by still greater plaque progression in moderate to advanced CKD patients (Fig. 3). Univariate linear regression analysis showed the baseline eGFR correlated significantly with plaque volume change (R = 0.65, p < 0.0001) (Fig. 4). On univariate and multivariate logistic regression analyses, after considering CKD stage, confounding factors (age, gender, and unstable angina pectoris), coronary risk factors and medications, CKD stage 3–5 demonstrated the strongest association with plaque progression (Tables 4, 5).Table 3

Bottom Line: 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).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.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.

View Article: PubMed Central - PubMed

Affiliation: Second Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, 807-8555, Japan.

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 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.

No MeSH data available.


Related in: MedlinePlus