From January 2016 to November 2017, we consecutively admitted 239 patients with CTO lesions diagnosed by coronary angiography (CAG) in our hospital. Baseline serum creatinine was determined upon admission. The serum creatinine level was monitored for 72 h after the procedure to determine the occurrence of CIN. Exclusion criteria included patients who underwent haemodialysis or those with glomerular filtration rate (GFR) < 15 mL/min/1.73 m², severe heart failure [New York Heart Association (NYHA) IV], pulmonary oedema, recent (past 2 days) use of contrast, and the use of potential nephrotoxic drugs within 72 h prior to the procedure and 72 h after the catheterization. PCI was performed among patients with angina or silent ischaemia with viable myocardium in the occluded coronary artery using the myocardial nuclear scan, stress dobutamine echocardiography, or cardiac magnetic resonance imaging.

All patients were prescribed a loading dose of aspirin 300 mg and clopidogrel 300 mg prior to the procedure. The CAG was performed via the radial artery approach, and bilateral CAG was performed when necessary. We attempted to open the CTO lesion using antegrade crossing techniques. The femoral artery path was used during vasospasm or vascular tortuosity or based on the operator’s decision. Retrograde crossing techniques were used if the antegrade crossing techniques failed and the patient had a good collateral circulation. Heparin 100 U/kg was administered as an anticoagulant. The use of glycoprotein IIb/IIIa receptor inhibitor and the type of stents were based on the physician’s discretion. All patients signed an informed consent.

Iopromide [for patients with estimated GFR (eGFR) ≥40 mL/min/1.73 m²] and iodixanol (for patients with eGFR < 40 mL/min/1.73 m²) were used during the procedure. Patients with a baseline eGFR < 40 mL/min/1.73 m² received intravenous hydration with a standard normal saline at a rate of 1 mL/kg/h (or 0.5 mL/kg/h in patients with heart failure) for at least 12 h before and after the cardiac catheterization. Potential nephrotoxic drugs were withdrawn for at least 72 h before and after the catheterization.

CTO is defined as an obstruction of the coronary arteries with Thrombolysis In Myocardial Infarction (TIMI) flow grade 0 with an estimated duration of at least 3 months [1, 10]. CIN was defined as a creatinine increase of at least 0.5 mg/dL or ≥ 25% from the baseline within 72 h following cardiac catheterization [11]. The Cockroft-Gault formula and modification of diet in renal disease equation were used to determine the baseline eGFR [12, 13]. Severe renal dysfunction (SRD) was defined as acute renal failure requiring dialysis or at least 2.0 mg/dL or ≥ 50% of creatinine elevation from the baseline within 24 h after the procedure [14]. Angiographic success was defined as residual stenosis ≤30% by visual analysis in the presence of TIMI flow grade 2–3.

The primary end point was the occurrence of CIN whereas the secondary end point was severe renal dysfunction requiring haemodialysis.

The mean age of our study population was 59.4 ± 9.9 years, and the mean CVRS was 2.3 ± 1.3. The patients’ demographic and clinical characteristics were compared among the 3 groups (Table 1). Data on the age, female gender, and the incidence of hypertension, pulse pressure, diabetes mellitus, stroke, and NYHA II–III on admission were higher in the group with CVRS ≥4. The patients in the high-risk group had higher pulse pressure, total contrast volume, total procedure time, rate of intra-aortic balloon pump (IABP) insertion, and number of stent implantation and lower eGFR and diastolic blood pressure. The overall rate of CIN was 16.3%, and a significant difference was noted in the high-risk group compared to the low-risk and intermediate-risk groups (6.3% VS 14.8% VS 37.5%, P < 0.001).

The incidence of CIN was 16.3%. Table 2 demonstrates that patients diagnosed with CIN were older and required longer procedure time. A significant difference was observed in the age, female, systolic and diastolic blood pressure, pulse pressure, and incidence of diabetes mellitus, hypertension, and stroke history between the 2 groups. Furthermore, patients with CIN had higher LDL-C, fasting glucose, uric acid, total contrast volume, rate of glycoprotein IIb/IIIa receptor inhibitor, and CVRS than those without CIN (3.1 ± 1.2 VS 2.1 ± 1.1; P < 0.001). The ROC curve analysis revealed that the area under the curve for predicting CIN was 0.742 (sensitivity, 69.2%; specificity, 78.0%; 95% CI, 0.682–0.797; P < 0.001) for CVRS ≥3 (Fig. 1). The incidence of CIN increased as the risk score increased. Multivariate analysis showed that higher pulse pressure [odds ratio (OR), 1.042; 95% CI, 1.012–1.197; P = 0.004] and contrast volume (OR, 1.772; 95% CI, 1.342–2.128; P = 0.039), lower baseline eGFR (OR, 0.662; 95% CI, 0.521–0.789; P = 0.012), and CVRS ≥3 (OR, 6.679; 95% CI, 3.169–15.531; P < 0.001) were independent predictors of CIN pre-procedure in CTO patients (Table 3).

This study had some limitations. First, consecutive cases of patients with CTO who underwent PCI were enrolled in the study; however, some patients were excluded because they were unsuitable for PCI or for other reasons (e.g. GFR < 15 mL/min/1.73 m², severe heart failure, absence of creatinine within 72 h after the procedure), which may have led to some bias in this study. Second, this is a single-centre study; therefore, a large-scale multi-centre study is needed to further confirm these results. Finally, some risk factors of CIN, such as proteinuria, were not included in this study.