Point-of-Care Viscoelastic Hemostatic Assays in Cardiac Surgery Patients: Comparison of Thromboelastography 6S, Thromboelastometry Sigma, and Quantra.

OBJECTIVES: Viscoelastic tests allow a reduction in blood product transfusion. Three modern devices are currently available (rotational thromboelastometry [ROTEM] sigma, thromboelastography [TEG] 6S, and Quantra). No study has compared the performances of these 3 devices simultaneously. DESIGN: An observational, nonrandomized cohort study. SETTING: A single-center of cardiac surgery in a university hospital. PARTICIPANTS: A total of 30 consecutive measurements from at least 10 adult patients presenting significant bleeding in the intensive care unit after cardiac surgery INTERVENTION: Viscoelastic tests using ROTEM sigma, TEG 6S, and Quantra were performed concomitantly with conventional coagulation measurements MEASUREMENTS AND MAIN RESULTS: The authors included 16 patients with 31 blood samples. After the exclusion of missing values, 27 samples were analyzed. Correlation with platelet count was as follows: ROTEM, r = 0.84 [0.66-0.93], p < 0.0001; Quantra, r = 0.83 [0.64-0.92], p < 0.0001; TEG 6S, r = 0.64 [0.29-0.83], p = 0.001. Correlation with fibrinogen (Clauss assay) was as follows: ROTEM, r = 0.85 [0.68-0.93], p < 0.0001; Quantra, r = 0.88 [0.74-0.95], p < 0.0001; TEG 6S, r = 0.79 [0.55-0.91], p < 0.0001. No difference was observed for the detection of residual circulating heparin (anti-Xa activity >0.1), with 87% of correct identification for Quantra and 80% for both ROTEM and TEG 6S (p = 0.3). Time to first results after the beginning of the test was shorter for Quantra than ROTEM and TEG 6S (136 [126-152] seconds v 205 [176-221] seconds, p = 0.003 and v 450 [372-516] seconds, p < 0.0001 respectively). CONCLUSION: ROTEM sigma, TEG 6S, and Quantra performed similarly for exploring platelet count or residual circulating heparin. Thromboelastography 6S presented a weaker correlation with fibrinogen Clauss.

Effect of mechanical ventilation during cardiopulmonary bypass on end-expiratory lung volume in the perioperative period of cardiac surgery: an observational study.

BACKGROUND: Many studies explored the impact of ventilation during cardiopulmonary bypass (CPB) period with conflicting results. Functional residual capacity or End Expiratory Lung Volume (EELV) may be disturbed after cardiac surgery but the specific effects of CPB have not been studied. Our objective was to compare the effect of two ventilation strategies during CPB on EELV. METHODS: Observational single center study in a tertiary teaching hospital. Adult patients undergoing on-pump cardiac surgery by sternotomy were included. Maintenance of ventilation during CPB was left to the discretion of the medical team, with division between "ventilated" and "non-ventilated" groups afterwards. Iterative intra and postoperative measurements of EELV were carried out by nitrogen washin-washout technique. Main endpoint was EELV at the end of surgery. Secondary endpoints were EELV one hour after ICU admission, PaO2/FiO2 ratio, driving pressure, duration of mechanical ventilation and post-operative pulmonary complications. RESULTS: Forty consecutive patients were included, 20 in each group. EELV was not significantly different between the ventilated versus non-ventilated groups at the end of surgery (1796 ± 586 mL vs. 1844 ± 524 mL, p = 1) and one hour after ICU admission (2095 ± 562 vs. 2045 ± 476 mL, p = 1). No significant difference between the two groups was observed on PaO2/FiO2 ratio (end of surgery: 339 ± 149 vs. 304 ± 131, p = 0.8; one hour after ICU: 324 ± 115 vs. 329 ± 124, p = 1), driving pressure (end of surgery: 7 ± 1 vs. 8 ± 1 cmH2O, p = 0.3; one hour after ICU: 9 ± 3 vs. 9 ± 3 cmH2O), duration of mechanical ventilation (5.5 ± 4.8 vs 8.2 ± 10.0 h, p = 0.5), need postoperative respiratory support (2 vs. 1, p = 1), occurrence of pneumopathy (2 vs. 0, p = 0.5) and radiographic atelectasis (7 vs. 8, p = 1). CONCLUSION: No significant difference was observed in EELV after cardiac surgery between not ventilated and ventilated patients during CPB.

Reliability of the Minto model for target-controlled infusion of remifentanil during cardiac surgery with cardiopulmonary bypass.

BACKGROUND: The Minto pharmacokinetic model is used for target-controlled infusion of remifentanil. The reliability of this model has never been evaluated during normothermic cardiac surgery with cardiopulmonary bypass (CPB). The aim of this study was to assess the predictive performance of the model during CPB to determine its reliability during cardiac surgery. METHODS: This was a single-centre observational study. Arterial blood samples were drawn at five time points: T1, after tracheal intubation; T2, immediately before CPB; T3, 10 min after starting CPB; T4, 45 min after starting CPB; T5, 10 min after weaning off CPB. Prediction error (PE) and absolute prediction error (APE) were calculated for each sample and used to determine median prediction error (MDPE) and median absolute prediction error (MDAPE) per patient. Risk factors for APE >30% were assessed using multivariable analysis. Results are presented as medians with inter-quartile ranges. RESULTS: Fifty-eight patients with 283 blood samples (110 during CPB) were included. In the pre-CPB period, MDPE and MDAPE were -17.3 [-32.9 to 2.3] and 24.6 [12-37.7]%, whereas during CPB, they were -1.8 [-15.6 to 11.1] and 14.0 [6.74-27.1]%, respectively. There was no statistically significant difference between measured and predicted remifentanil plasma concentrations during CPB. Age, preoperative albumin concentrations, temperature, and haemodilution were not independently associated with MDAPE >30%. CONCLUSIONS: The Minto model accurately predicts plasma remifentanil concentrations during cardiac surgery with CPB. CLINICAL TRIAL REGISTRATION: 2017-A03153-50.

Left atrial unloading with an 8 mm septal cutting balloon to treat postcapillary pulmonary hypertension: a case report.

We report the case of a 58-year-old female with severe postcapillary pulmonary hypertension (averaged mean pulmonary arterial pressure was 49 mmHg, pulmonary arterial wedge pressure 29 mmHg, and right atrial pressure 8 mmHg) due to heart failure with preserved ejection fraction. A left-to-right atrial shunt was created using an 8 mm cutting balloon, under transesophageal echocardiography guidance. Both pulmonary arterial and wedge pressure dramatically decreased after the procedure. Symptoms immediately improved and benefits were sustained at 6 months of follow-up. This case suggests that iatrogenic septal defect using a cutting balloon could be an option to treat symptomatic postcapillary pulmonary hypertension.

Association between vasoactive peptide urotensin II in plasma and cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a potential therapeutic target.

OBJECTIVECerebral vasospasm (VS) is a severe complication of aneurysmal subarachnoid hemorrhage (SAH). Urotensin II (UII) is a potent vasoactive peptide activating the urotensin (UT) receptor, potentially involved in brain vascular pathologies. The authors hypothesized that UII/UT system antagonism with the UT receptor antagonist/biased ligand urantide may be associated with post-SAH VS. The objectives of this study were 2-fold: 1) to leverage an experimental mouse model of SAH with VS in order to study the effect of urotensinergic system antagonism on neurological outcome, and 2) to investigate the association between plasma UII level and symptomatic VS after SAH in human patients.METHODSA mouse model of SAH was used to study the impacts of UII and the UT receptor antagonist/biased ligand urantide on VS and neurological outcome. Then a clinical study was conducted in the setting of a neurosurgical intensive care unit. Plasma UII levels were measured in SAH patients daily for 9 days, starting on the 1st day of hospitalization, and were compared with plasma UII levels in healthy volunteers.RESULTSIn the mouse model, urantide prevented VS as well as SAH-related fine motor coordination impairment. Seventeen patients with SAH and external ventricular drainage were included in the clinical study. The median plasma UII level was 43 pg/ml (IQR 14-80 pg/ml). There was no significant variation in the daily median plasma UII level (median value for the 17 patients) from day 0 to day 8. The median level of plasma UII during the 9 first days post-SAH was higher in patients with symptomatic VS than in patients without VS (77 pg/ml [IQR 33.5-111.5 pg/ml] vs 37 pg/ml [IQR 21-46 pg/ml], p < 0.05). Concerning daily measures of plasma UII levels in VS, non-VS patients, and healthy volunteers, we found a significant difference between SAH patients with VS (median 66 pg/ml [IQR 30-110 pg/ml]) and SAH patients without VS (27 pg/ml [IQR 15-46 pg/ml], p < 0.001) but no significant difference between VS patients and healthy volunteers (44 pg/ml [IQR 27-51 pg/ml]) or between non-VS patients and healthy volunteers.CONCLUSIONSThe results of this study suggest that UT receptor antagonism with urantide prevents VS and improves neurological outcome after SAH in mice and that an increase in plasma UII is associated with cerebral VS subsequent to SAH in humans. The causality link between circulating UII and VS after SAH remains to be established, but according to our data the UT receptor is a potential therapeutic target in SAH.