CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 4, September/October 2023 AFRICA 199 of postoperative AKI among adults operated on for CABG with CPB.12 Fanning et al. reported urinary NGAL, measured 24 hours after the initiation of CPB, to be a better predictor of postoperative AKI.13 Recently, neutrophil–lymphocyte ratio (NLR) and platelet– lymphocyte ratio (PLR) have been investigated as prognostic factors for cardiovascular disease, and their mutual role together with endothelial inflammation appeared as optimal predictors for major cardiovascular events and prognostic factors of postprocedural results.14 Parlar et al. reported that postoperative NLR in the first four days after CABG was a useful biomarker to predict AKI during in-hospital follow up.15 Elevated NLR and PLR in the pre- and postoperative periods of CABG were reported as independent biomarkers directly associated with early postoperative AKI.16 Cross-sectional studies on the general population showed an inversely proportional relationship between renal function and CIMT.6 Zhang et al. reported significantly higher levels of CIMT in patients with early-stage chronic kidney disease.17 There have been very few studies in the recent literature that examined the relationship between early postoperative AKI following isolated CABG and CIMT as an inflammatory marker. The case–control study by Onk et al. reported that common carotid artery IMT (CCA-IMT) measurements prior to CABG were significantly higher in patients with postoperative AKI.18 This study aimed to analyse markers of inflammation together with CIMT, search for associated risk factors of early postoperative AKI, and supply a base for clinical prevention and reduction of AKI following CABG. Methods Retrospective data were analysed of 289 patients, operated on for isolated CABG with CPB in the same centre by the same team between June 2014 and December 2020, whose carotid artery systems were normal on Doppler ultrasonography and CIMT was measured in the pre-operative period. Among these, we enrolled 237 patients who were diagnosed with critical coronary artery disease (≥ 75% narrowing) and operated on for CABG with CPB, and who had a pre-operative serum creatinine level < 1.5 mg/dl. A diagnosis of AKI was made by comparing baseline and postoperative serum creatinine (sCr) levels to determine the predefined significant change based on the Kidney Disease Improving Global Outcomes (KDIGO) definition (increase in sCr level by ≥ 0.3 mg/dl within 48 hours of surgery or increase in sCr to ≥ 1.5 times baseline within three days of cardiac surgery).19 AKI diagnosis was based on the highest sCr concentration measured during the first three postoperative days compared with the baseline sCr concentration, defined as the last concentration before surgery. Urine output, affected by diuretics administered during anaesthesia and CPB, was not used to define AKI. Patients who developed AKI in the early postoperative period were classified as group 1 (n = 63) and those with normal postoperative renal function as group 2 (n = 174). We excluded patients previously diagnosed with end-stage renal disease and on dialysis. We also excluded patients who had peripheral or carotid arterial disease, valvular heart disease, chronic obstructive pulmonary disease, malignancy, endocrinological disorders, advanced age (> 75 years), systemic inflammatory diseases, left ventricular ejection fraction (LVEF) ≤ 30%, decompensated congestive heart failure, congenital cardiac disease, severely overweight (body mass index > 30 kg/m2), renal impairment (sCr > 1.5 mg/dl), haematological proliferative diseases, low pre-operative haemoglobin (≤ 10 g/dl), on steroid or non-steroidal anti-inflammatory drugs, pre-operative immunosuppressive drug treatment within the last two weeks, the presence of signs of clinical infection [fever > 37.5°C, C-reactive protein (CRP) ≥ 5 mg/dl, erythrocyte sedimentation rate (ESR) > 20 mm/h or leukocyte count > 11 000 cells/μl] pre-operatively, patients with acute myocardial infarction and percutaneous coronary intervention in the last 30 pre-operative days, emergent operations, re-operations due to haemodynamic instability or bleeding, intra-aortic balloon pump requirement, operations on a beating heart or redo CABG. Proximal aortic anastomosis sites were examined by palpation, since we did not perform routine pre-operative computed tomography. Patients ineligible for side clamping, whose proximal anastomoses were done in a single ACC period, were excluded. Patients with missing data such as sCr level or urine output and whose cardiac catheterisations were performed within the last 15 pre-operative days were also excluded. Carotid artery ultrasonography and CIMT measurements were performed using the M Turbo ultrasonography device with a 5–12-MHz superficial probe. Carotid imaging was performed in the supine position with an approximate contralateral neck angle of 20°. Different measurements of CIMT were obtained from the common carotid arteries, bifurcations and the first 2 cm of the internal carotid arteries bilaterally, and the posterior walls were only evaluated. These measurements were performed with B-mode on the longitudinal axis from the level between the luminal and media/adventitia echogenities. The average of CIMT measured three times on both carotid arteries was calculated.20 The demographic and clinical data of the patients were obtained from the hospital software system. Age, gender, smoking status, diabetes, hypertension, hyperlipidaemia, LVEF, laboratory parameters, operation information, the number of grafts used, duration of CPB and ACC, use of blood products and length of ICU and hospital stays were recorded. PLR was calculated by dividing the number of platelets by the number of lymphocytes. NLR was calculated by dividing the number of neutrophils by the number of lymphocytes. This study complied with the Declaration of Helsinki and was carried out following approval of the Ethics Committee for Clinical Trials of Kocaeli Derince Training and Research Hospital of Health Sciences University (Approval date no: 28.01.2021- 2021/19). All patients were operated on with a median sternotomy under general anaesthesia. Standard CPB was established with aortic and venous cannulations, and systemic heparin (300 IU/ kg) with the maintenance of activated clotting time (ACT) > 450 seconds. Hyperkalaemic cold blood cardioplegia was applied for cardiac arrest. Surgery was performed under moderate hypothermia (28–30ºC). CPB flow was maintained at 2.2–2.5 l/ min/m2, mean perfusion pressure between 50 and 80 mmHg, and haematocrit level between 20 and 25%. All distal anastomoses were done during the ACC period and the proximal anastomoses onto the ascending aorta on a beating heart. All patients were extubated following the onset of spontaneous breathing,
RkJQdWJsaXNoZXIy NDIzNzc=