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

Q: What is the clinical evidence from this study?

Study design: Observational. Population: Chronic kidney disease and coronary artery disease (n=113). Intervention: Moderate to advanced chronic kidney disease (CKD stage 3-5) vs. Normal to mild chronic kidney disease (CKD stage 1-2). Primary outcome: Coronary plaque progression in non-culprit lesions (OR 13.56, 95% CI 2.85-64.44, p=0.001).

Kuninobu Kashiyama; Shinjo Sonoda; Yoshitaka Muraoka; Yoshiyuki Suzuki; Fumihiko Kamezaki; Yuki Tsuda; Masaru Araki; Masahito Tamura; Masaaki Takeuchi; Haruhiko Abe; Masahiro Okazaki; Yoshihisa Fujino; Yutaka Otsuji

doi:10.1007/s10554-015-0633-y

February 27, 2015International journal of cardiac imagingOpen Access

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

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Key result

Moderate to advanced chronic kidney disease (stage 3-5) was an independent predictor of coronary plaque progression in non-culprit lesions (OR 13.56) despite statin treatment after culprit PCI.

Why the study?

Does moderate to advanced CKD affect coronary plaque progression in non-culprit lesions under statin treatment after PCI?

Study Design

Type

Observational (n=113)

Multicenter

No

Structured PICO

Does moderate to advanced CKD affect coronary plaque progression in non-culprit lesions under statin treatment after PCI?

P

Population

113 patients with varying stages of chronic kidney disease who underwent IVUS-guided PCI, followed for 8 months to evaluate serial coronary plaque changes in non-culprit lesions.

E

Exposure

Standard medical treatment including statin therapy (rosuvastatin, atorvastatin, pitavastatin, or pravastatin) for 8 months after PCI.

C

Comparator

Comparison among 4 groups based on baseline CKD stage: CKD-1 (eGFR ≥90, n=18), CKD-2 (eGFR 60-89, n=42), CKD-3 (eGFR 30-59, n=29), and CKD4-5 (eGFR <30, n=24).

O

Outcome

Serial coronary plaque volume change of non-culprit lesions at 8-month follow-up measured by intravascular ultrasound (IVUS).surrogate

Main Result

Odds Ratio: 13.56 (95% CI 2.85–64.44)

p-value: p=0.001

Moderate to advanced chronic kidney disease is an independent predictor of coronary plaque progression, characterized by increased lipid and fibrotic volumes, in non-culprit lesions despite statin therapy after PCI.

Limitations

Relatively small number of patients at a single center, raising the possibility of selection bias
Excluded patients with acute myocardial infarction
Defined a non-culprit lesion as a 5-mm lesion proximal to the PCI target vessel, which comprises only a small part of the entire coronary artery
IVUS examinations were performed only in patients with established angiographic CAD
Plaque instability depends not only on increased lipid volume but also on thinness of the cap, which is better assessed by OCT
Medications were not fixed during the study period
Unclear whether intensive statin treatment was administered
Relatively small number of patients at a single center (selection bias)
Exclusion of patients with acute myocardial infarction
Non-culprit lesion defined as a 5-mm lesion proximal to the PCI target vessel, which may not reflect the entire coronary arterial tree

Implication

Serial IVUS tracks NCL plaque across CKD stages; leaves open whether renal decline independently accelerates vulnerability post-PCI.

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.

Discussion

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Cite This Study

Kashiyama et al. (2015) conducted an observational in Chronic kidney disease and coronary artery disease (n=113). Moderate to advanced chronic kidney disease (CKD stage 3-5) vs. Normal to mild chronic kidney disease (CKD stage 1-2) was evaluated on Coronary plaque progression in non-culprit lesions (OR 13.56, 95% CI 2.85-64.44, p=0.001). Moderate to advanced chronic kidney disease (stage 3-5) was an independent predictor of coronary plaque progression in non-culprit lesions (OR 13.56) despite statin treatment after culprit PCI.

synapsesocial.com/papers/6aa03a16bdf28614dc2d26ee https://doi.org/10.1007/s10554-015-0633-y