The Relationship Between the CASTLE (EUROCTO) Score and Contrast-Induced Nephropathy in Patients Undergoing Coronary Chronic Total Occlusion Interventions

Öz

Background: Contrast-induced nephropathy (CIN) is still recognized as a major complication in patients undergoing chronic total occlusion (CTO) interventions. The predictive value of CTO complexity scores for CIN remains unclear. The present study investigated whether the CASTLE (EuroCTO) score is associated with the development of CIN in patients treated with CTO-PCI. Methods: A total of 356 patients undergoing CTO-PCI were retrospectively analyzed and classified according to CIN development. Clinical, angiographic, and procedural characteristics were compared between groups. Missing data were handled using multiple imputation, and independent predictors of CIN were identified through multivariable logistic regression analysis. The predictive performance of CTO scoring systems was evaluated using receiver operating characteristic (ROC) curve analysis. Results: CIN was observed in 34 patients (9.5%). Individuals who developed CIN were generally older, more frequently diabetic, and had lower left ventricular ejection fraction values. Procedural complexity was greater in the CIN group, reflected by higher CASTLE and J-CTO scores, longer lesion length, and higher contrast volume. In multivariable analysis, the CASTLE score remained associated with CIN (OR: 1.838, 95% CI: 1.354–2.494, p<0.001), whereas the association with the J-CTO score was weaker, and the PROGRESS CTO score was not significant. ROC analysis demonstrated that the CASTLE score showed acceptable discriminative performance (AUC: 0.694, 95% CI: 0.643–0.742), with a cut-off >2 providing a reasonable balance between sensitivity (70.6%) and specificity (63.3%). Conclusion: The CASTLE (EuroCTO) score showed an association with CIN occurrence in patients treated with CTO-PCI and demonstrated acceptable predictive capability compared with other CTO scoring models. Although the score may contribute to preprocedural risk assessment, the results should be interpreted carefully.

Anahtar Kelimeler

• Coronary artery disease
• Chronic total occlusion
• CASTLE score; contrast-induced nephropathy
• percutaneous coronary intervention; acute kidney injury

Koroner Kronik Total Oklüzyon Girişimi Uygulanan Hastalarda CASTLE (EUROCTO) Skoru ile Kontrast Kaynaklı Nefropati Arasındaki İlişki

Öz

Amaç: Kontrastla indüklenen nefropati (KİN), kronik total tıkanıklık (KTO) müdahaleleri yapılan hastalarda hâlâ önemli bir komplikasyon olarak kabul edilmektedir. KİN için KTO karmaşıklık puanlarının öngörülebilir değeri belirsizdir. Mevcut çalışma, CTO-PCI ile tedavi edilen hastalarda CASTLE (EuroCTO) puanının KİN gelişimiyle ilişkili olup olmadığını incelemiştir. Yöntemler: KTO-PKG uygulanan toplam 356 hasta retrospektif olarak analiz edildi ve KİN gelişimine göre sınıflandırıldı. Klinik, anjiyografik ve prosedürel özellikler gruplar arasında karşılaştırıldı. Eksik veriler çoklu imputasyon yöntemiyle tamamlanırken, KİN’in bağımsız prediktörleri çok değişkenli lojistik regresyon analizi ile belirlendi. KTO skorlama sistemlerinin prediktif performansı receiver operating characteristic (ROC) eğrisi analizi kullanılarak değerlendirildi. Bulgular: KİN, 34 (%9,5) hastada gelişti. KİN gelişen hastalar daha ileri yaşta olup, diyabetes mellitus prevalansı daha yüksek ve sol ventrikül ejeksiyon fraksiyonu daha düşüktü. Prosedürel kompleksite KİN grubunda daha yüksek olup, bu durum daha yüksek CASTLE ve J-KTO skorları, daha uzun lezyon uzunluğu ve daha fazla kontrast kullanımı ile ilişkiliydi. Çok değişkenli analizde, CASTLE skoru KİN ile ilişkisini sürdürürken (OR: 1,838, %95 CI: 1,354–2,494, p<0,001), J-CTO skoru ile olan ilişki daha zayıftı ve PROGRESS CTO skoru anlamlı değildi. ROC analizi, CASTLE skorunun kabul edilebilir ayırt edici performans gösterdiğini ortaya koydu (AUC: 0,694, %95 CI: 0,643–0,742); >2 eşik değeri, duyarlılık (%70,6) ve özgüllük (%63,3) arasında makul bir denge sağladı. Sonuç: CASTLE (EuroCTO) skoru, KTO-PCI uygulanan hastalarda KİN gelişimi ile ilişkili bulundu ve diğer KTO skorlama modellerine kıyasla kabul edilebilir düzeyde prediktif performans gösterdi. Bu skor işlem öncesi risk değerlendirmesine katkı sağlayabilir; ancak elde edilen bulgular dikkatli yorumlanmalıdır.

Anahtar Kelimeler

• koroner arter hastalığı
• kronik total oklüzyon; CASTLE skoru
• kontrast ilişkili nefropati
• perkütan koroner girişim
• akut böbrek hasarı.

Kaynakça

1. 1.Brilakis ES, Sandoval Y, Azzalini L, et al. Chronictotal occlusion percutaneous coronary intervention:present and future. Circ Cardiovasc Interv.2025;18:e014801.
2. 2.Morino Y, Abe M, Morimoto T, et al. Predictingsuccessful guidewire crossing through chronic totalocclusion of native coronary lesions within 30minutes: the J-CTO (Multicenter CTO Registry inJapan) score as a difficulty grading and timeassessment tool. JACC Cardiovasc Interv.2011;4:213-21.
3. 3.Szijgyarto Z, Rampat R, Werner GS, et al.Derivation and validation of a chronic total coronary occlusion intervention procedural success scorefrom the 20,000-patient EuroCTO Registry: theEuroCTO (CASTLE) score. JACC Cardiovasc Interv.2019;12:335-42.
4. 4.Christopoulos G, Kandzari DE, Jaffer FA, et al.Development and validation of a novel scoringsystem for predicting technical success of chronictotal occlusion percutaneous coronaryinterventions: the PROGRESS CTO score. JACCCardiovasc Interv. 2016;9:1-9.
5. 5.Nombela-Franco L, Urena M, Jerez-Valero M, et al.Validation of the J-chronic total occlusion score forchronic total occlusion percutaneous coronaryintervention in an independent contemporarycohort. Circ Cardiovasc Interv. 2013;6:635-43.
6. 6.Fähling M, Seeliger E, Patzak A, Persson PB.Understanding and preventing contrast-inducedacute kidney injury. Nat Rev Nephrol. 2017;13:169-80.
7. 7.Tepel M, Aspelin P, Lameire N. Contrast-inducednephropathy: a clinical and evidence-basedapproach. Circulation. 2006;113:1799-806.
8. 8.Azzalini L. The clinical significance andmanagement implications of chronic total occlusionassociated with surgical coronary arteryrevascularization. Can J Cardiol. 2016;32:1286-9.

9. 9.Ybarra LF, Rinfret S, Brilakis ES, et al. Definitionsand clinical trial design principles for coronaryartery chronic total occlusion therapies: CTO-ARCconsensus recommendations. Circulation.2021;143:479-500.
10. 10.TIMI Study Group. The thrombolysis inmyocardial infarction (TIMI) trial. Phase I findings.N Engl J Med. 1985;312:932-6. 11.Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improveoutcomes in acute kidney injury. Crit Care.2007;11:R31.
11. 12.Li SY, Chen JY, Yang WC, Chuang CL. Acute kidneyinjury network classification predicts in-hospitaland long-term mortality in patients undergoingelective coronary artery bypass grafting surgery.Eur J Cardiothorac Surg. 2011;39:323-8.
12. 13.Levine GN, Bates ER, Blankenship JC, et al. 2011ACCF/AHA/SCAI guideline for percutaneouscoronary intervention: a report of the AmericanCollege of Cardiology Foundation/American HeartAssociation Task Force on Practice Guidelines andthe Society for Cardiovascular Angiography andInterventions. Circulation. 2011;124:e574-651.
13. 14.Mehran R, Dangas GD, Weisbord SD. Contrast-associated acute kidney injury. N Engl J Med.2019;380:2146-55.
14. 15.Murphy SW, Barrett BJ, Parfrey PS. Contrastnephropathy. J Am Soc Nephrol. 2000;11:177-82.
15. 16.Fishbane S, Durham JH, Marzo K, Rudnick M. N-acetylcysteine in the prevention of radiocontrast-induced nephropathy. J Am Soc Nephrol.2004;15:251-60.
16. 17.Gleeson TG, Bulugahapitiya S. Contrast-inducednephropathy. AJR Am J Roentgenol. 2004;183:1673-89.
17. 18.Maeder M, Klein M, Fehr T, Rickli H. Contrastnephropathy: review focusing on prevention. J AmColl Cardiol. 2004;44:1763-71.
18. 19.Goldenberg I, Matetzky S. Nephropathy inducedby contrast media: pathogenesis, risk factors andpreventive strategies. CMAJ. 2005;172:1461-71.
19. 20.Wu MY, Lo WC, Wu YC, et al. The incidence ofcontrast-induced nephropathy and the need ofdialysis in patients receiving angiography: asystematic review and meta-analysis. Front Med.2022;9:862534.
20. 21. Heyman SN, Rosenberger C, Rosen S, Khamaisi M. Why is diabetes mellitus a risk factor for contrast-induced nephropathy? Biomed Res Int.2013;2013:123589.
21. 22.Aurelio A, Durante A. Contrast-inducednephropathy in percutaneous coronary interventions: pathogenesis, risk factors, outcome, prevention and treatment. Cardiology. 2014;128:62-72.
22. 23.Hamidi MHM, Zakaria AF, Asis AM, et al.Contrast-induced nephropathy after percutaneouscoronary intervention in a Northern Kuala Lumpurtertiary cardiac center. Int J Cardiol. 2021;345:24.
23. 24.Rosenstock JL, Gilles E, Geller AB, et al. Impact ofheart failure on the incidence of contrast-inducednephropathy in patients with chronic kidneydisease. Int Urol Nephrol. 2010;42:1049-54.
24. 25.Heyman SN, Evans RG, Rosen S, Rosenberger C.Cellular adaptive changes in AKI: mitigating renalhypoxic injury. Nephrol Dial Transplant.2012;27:1721-8.
25. 26.Agmon Y, Peleg H, Greenfeld Z, Rosen S, Brezis M.Nitric oxide and prostanoids protect the renal outermedulla from radiocontrast toxicity in the rat. J ClinInvest. 1994;94:1069-75.
26. 27.Sendeski MM, Persson AB, Liu ZZ, et al. Iodinatedcontrast media cause endothelial damage leading tovasoconstriction of human and rat vasa recta. Am JPhysiol Renal Physiol. 2012;303:F1592-8.
27. 28.Nguyen TV, Quang NT, Liu W, Kim Trinh NT,Nguyen TN. Assessing contrast-inducednephropathy risk in older adults undergoingcoronary angiography and intervention: the CV/GFR ratio versus Mehran score. SAGE Open Med.2024;12:20503121241275419.