Circulating and Urinary miR-210 and miR-16 Increase during Cardiac Surgery Using Cardiopulmonary Bypass - A Pilot Study.

A pilot study to measure and compare blood and urine microRNAs miR-210 and miR-16 in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB) and off-pump coronary artery bypass grafting surgery. Frequent serial blood and urine samples were taken from patients undergoing cardiac surgery with CPB (n = 10) and undergoing off-pump cardiac surgery (n = 5) before, during, and after surgery. Circulating miR-210 and miR-16 levels were determined by relative quantification real-time polymerase chain reaction. Levels of plasma-free haemoglobin (fHb), troponin-T, creatine kinase, and creatinine were measured. Perioperative serum miR-210 and miR-16 were elevated significantly compared to preoperative levels in patients undergoing cardiac surgery with CPB (CPB vs. Pre Op and Rewarm vs. Pre Op; p < .05 for both). There were increases of greater than 200% in miR-210 levels during rewarming and immediately postoperatively and a 3,000% increase in miR-16 levels immediately postoperatively in urine normalized to urinary creatinine concentration. Serum levels of miR-16 were relatively constant during off-pump surgery. miR-210 levels increased significantly in off-pump patients perioperatively (p < .05 Octopus on vs. Pre Op); however, the release was less marked when compared to cardiac surgery with CPB. A significant association was observed between both miR-16 and miR-210 and plasma fHb when CPB was used (r = -.549, p < .0001 and r = -.463, p < .0001 respectively). Serum and urine concentrations of hypoxically regulated miR-210 and hemolysis-associated miR-16 increased in cardiac surgery using CPB compared to off-pump surgery. These molecules may have utility in indicating severity of cardiac, red cell, and renal injury during cardiac surgery.

Mending a broken heart but breaking the kidney.

The incidence of acute kidney injury (AKI) is a frequent and serious complication of cardiac surgery. In 2013, 95% of cardiac surgical procedures performed in Australia and New Zealand used cardiopulmonary bypass (CPB). AKI following CPB is well known, yet the perioperative factors contributing to its development are incompletely understood. AKI following CPB has significant implications on both short-term and long-term outcomes. The techniques for conducting CPB have evolved, moving towards evidence-based practice; however, there is still no generally accepted definition of optimal perfusion and its conduct. This review examines the current incidence of AKI following cardiac surgery and the short-term and longer-term effects of AKI on morbidity and mortality. The purpose of this review is to discuss the perioperative risk factors related to CPB and their contribution to the development of AKI. This review will also discuss outcomes in regard to off-pump cardiac surgery, the role of remote ischaemic preconditioning on AKI and outcomes in patients with chronic renal failure undergoing cardiac surgery.

Should Air Bubble Detectors Be Used to Quantify Microbubble Activity during Cardiopulmonary Bypass?

Air bubble detectors (ABDs) are utilized during cardiopulmonary bypass (CPB) to protect against massive air embolism. Stockert (Munich, Germany) ABD quantify microbubbles >300 µm; however, their reliability has not been reported. The aim of this study was to assess the reliability of the microbubble data from the ABD with the SIII and S5 heart-lung machines. Microbubble counts from the ABD with the SIII (SIII ABD) and S5 (S5 ABD) were measured simultaneously with the emboli detection and classification (EDAC) quantifier in 12 CPB procedures using two EDAC detectors and two ABDs in series in the arterial line. Reliability was assessed by the Spearman correlation co-efficient (r) between measurements for each detector type, and between each ABD and EDAC detector for counts >300 µm. No correlation was found between the SIII ABD (r = .008, p = .793). A weak negative correlation was found with the S5 ABD (r = -.16, p < .001). A strong correlation was found between the EDAC detectors (SIII; r = .958, p < .001), (S5; r = .908, p < .001). With counts >300 µm, the SIII ABDs showed a correlation of small-medium effect size between EDAC detectors and ABD1 (r = .286, p < .001 [EDAC1], r = .347, p < .001 [EDAC2]). There was no correlation found between ABD2 and either EDAC detector (r = .003, p = .925 (EDAC1), r = .003, p = .929 [EDAC2]). A correlation between EDAC and the S5 ABD, was not able to be determined due to the low bubble count detected by the EDAC >300 µm. Both SIII ABD and S5 ABD were found to be unreliable for quantification of microbubble activity during CPB in comparison with the EDAC. These results highlight the importance of ensuring that data included in the CPB report is accurate and clinically relevant, and suggests that microbubble counts from devices such as the SIII ABD and S5 ABD should not be reported.

Rewarming Temperature During Cardiopulmonary Bypass and Acute Kidney Injury: A Multicenter Analysis.

BACKGROUND: Acute kidney injury (AKI) after cardiopulmonary bypass (CPB) is associated with a requirement for dialysis, a longer stay in the intensive care unit, a longer hospital length of stay, and mortality. An oxygenator arterial outlet temperature greater than 37°C has been reported to be associated with AKI; however, the influence of other rewarming temperatures is unclear. Using multicenter registry data, this study aimed to evaluate the role of CPB rewarming temperatures on AKI. METHODS: Data from 8,407 adult patients undergoing coronary artery bypass grafting (CABG) or valve repair or replacement, or a combination, were collected using the Perfusion Downunder Collaborative Database. Primary variables of interest were rewarming temperatures, defined as cumulative time the oxygenator arterial outlet temperature was greater than 36°C, greater than 36.5°C, or greater than 37°C. Propensity scores were calculated to determine the predicted probability of hyperthermic perfusion (rewarming temperature >37°C). The influence of temperature on AKI was determined using separate multivariate models adjusting for propensity score in the entire cohort (n = 6,904) and in propensity-matched patients (n = 2,044). RESULTS: Overall, 11.8% of patients acquired AKI. The duration of rewarming temperature greater than 36°C or 36.5°C was not associated with AKI. The duration of rewarming temperature greater than 37°C (hyperthermic perfusion) was independently associated with RIFLE (Risk, Injury, Failure, Loss, End-stage renal disease) risk classification or greater (odds ratio [OR], 1.42; 95% confidence interval [CI], 1.09-1.77; p = 0.012) and injury classification or greater AKI (OR, 1.52; 95% CI, 1.09-1.97; p = 0.016) in the entire cohort, and injury classification or greater AKI (OR, 1.51; 95% CI, 1.15-1.90; p = 0.006) in propensity-matched patients. CONCLUSIONS: The duration of hyperthermic perfusion-rewarming temperature greater than 37°C-was an independent predictor of AKI. Avoidance of hyperthermic perfusion may be more beneficial in reducing AKI than avoidance of rewarming.