OBJECTIVES:. To determine the concordance between activated partial thromboplastin time (aPTT) and anti-factor-Xa (anti-Xa) in adults undergoing extracorporeal membrane oxygenation (ECMO) and to identify the factors associated with discordant paired aPTT/anti-Xa. DESIGN:. Pre-planned secondary analysis of the Low-Dose Heparin in Critically Ill Patients Undergoing Extracorporeal Membrane Oxygenation pilot randomized unblinded, parallel-group controlled trial. SETTING:. Two ICUs in two university hospitals. PATIENTS:. Thirty-two critically ill patients who underwent ECMO and who had at least one paired aPTT and anti-Xa assay performed at the same time. INTERVENTIONS:. We analyzed the concordance between aPTT and anti-Xa and identified factors associated with discordant paired aPTT/anti-Xa based on their respective therapeutic ranges. We also compared biological parameters between heparin resistance episode and no heparin resistance. MEASUREMENTS AND MAIN RESULTS:. Of the 32 patients who were included in this study, 24 (75%) had at least one discordant paired aPTT/anti-Xa. Of the 581 paired aPTT/anti-Xa that were analyzed, 202 were discordant. The aPTT was relatively lower than anti-Xa in 66 cases (32.7%) or relatively higher than anti-Xa in 136 cases (67.3%). Thirty-three heparin resistance episodes were identified in six patients (19%). CONCLUSIONS:. In these critically ill patients undergoing ECMO, one third of paired aPTT/anti-Xa measures was discordant. Coagulopathy and heparin resistance might be the reasons for discordance. Our results support the potential importance of routinely monitoring both tests in this setting.

OBJECTIVES:With the exception of 0.9% saline, little is known about factors that may contribute to increased serum chloride concentration (SCl-) in patients undergoing cardiac surgery. For the present study, the authors sought to characterize the association between administered chloride load from intravenous fluid and other perioperative variables, with peak perioperative SCl-. DESIGN:Secondary analysis of data from a previously published controlled clinical trial in which patients were assigned to a chloride-rich or chloride-limited perioperative fluid strategy (NCT02020538). SETTING:Academic medical center. PARTICIPANTS:The study comprised 1,056 adult patients with normal preoperative SCl- undergoing cardiac surgery. INTERVENTIONS:None MEASUREMENTS AND MAIN RESULTS: Peak perioperative SCl- and hyperchloremia, defined as peak SCl- >110 mmol/L, were selected as co-primary endpoints. Regression modeling identified factors independently associated with these endpoints. Mean (standard deviation) peak perioperative SCl- was 114 (5) mmol/L, and hyperchloremia occurred in 824 (78.0%) of the cohort. In addition to administered volume of 0.9% saline, multivariate linear and logistic regression modeling consistently associated preoperative SCl- (regression coefficient 0.5; 95% confidence interval [CI] 0.4-0.6 mmol/L; odds ratio 1.60; 95% CI 1.41-1.82 per 1 mmol/L increase) and cardiopulmonary bypass duration (regression coefficient 0.1; 95% CI 0.1-0.2 mmol/L; odds ratio 1.12; 95% CI 1.06-1.19 per 10 minutes) with both co-primary outcomes. Multivariate modeling only explained approximately 50% of variability in peak SCl-. CONCLUSIONS:The present study's data identified an association for both 0.9% saline administration and other nonfluid variables with peak perioperative SCl- and hyperchloremia. Stand-alone strategies to limit administration of chloride-rich intravenous fluid may have limited ability to prevent hyperchloremia in this setting.

The apnea test (AT) during clinical brain death (BD) testing does not account for different arterial gas tensions on venoarterial extracorporeal membrane oxygenation (V-A ECMO). We aimed to develop a protocol and now report our experience with three patients. The protocol was developed and implemented in 2015 at a quaternary center in Australia, measures both right radial and postoxygenator carbon dioxide (CO2) and oxygen (O-2) gas tensions during the AT, incorporates regular gas sampling and a gradual reduction in fresh gas flow to ensure patient oxygenation. Patient 1 remained apneic despite both right radial and postoxygenator CO2 gas tensions >60 mmHg. Patient 2, despite having CO2 levels in a right radial arterial sample high enough to diagnose BD, postoxygenator CO2 remained <60 mmHg. Patient 2 did not breathe but radiological tests confirmed BD. Patient 3 showed respiratory effort but only once CO2 levels rose high enough in both right radial and postoxygenator samples. No patient was hypoxic during the AT. Performance of a reliable AT on V-A ECMO requires measurement of both right radial and postoxygenator blood gases. A protocol, which measures both blood gas values, is feasible to implement, while being both safe and easy to perform.

Abstract This chapter is centred on a case study on acute heart failure. This topic is one of the key challenging areas in critical care medicine and one that all intensive care staff will encounter. The chapter is based on a detailed case history, ensuring clinical relevance, together with relevant images, making this easily relatable to daily practice in the critical care unit. The chapter is punctuated by evidence-based, up-to-date learning points, which highlight key information for the reader. Throughout the chapter, a topic expert provides contextual advice and commentary, adding practical expertise to the standard textbook approach and reinforcing key messages.

Objective: We sought to characterize the relationship between postoperative blood pressure on the day of surgery and metrics of bleeding. Methods: In a preplanned secondary analysis of prospectively collected data from the Limiting IV Chloride to Reduce AKI trial (NCT02020538), univariate and multivariable regression analyses explored the association between peak systolic blood pressure, peak mean arterial pressure, and peak central venous pressure recorded postoperatively on the day of surgery and multiple metrics of bleeding. Patients at increased bleeding risk due to specific criteria were excluded from analysis. The primary outcome was chest tube drainage (milliliters per hour) on the day of surgery. Secondary outcomes included red blood cell transfusion, surgical re-exploration for bleeding, and hospital mortality. Results: The study cohort comprised 793 patients. Mean +/- standard deviation peak systolic blood pressure, mean arterial pressure, and central venous pressure were 125 +/- 15 mm Hg, 83 +/- 9 mm Hg, and 12 +/- 4 mm Hg, respectively. Median (interquartile range) chest tube drainage on the day of surgery was 33 mL/hour (interquartile range, 23 mL/hour-51 mL/hour). Adjusted for prespecified variables, there was no positive association between peak systolic blood pressure and bleeding outcomes, including chest tube drainage (-2.2 mL/10 mm Hg; 95% confidence interval, -3.9 to -0.5 mL/h/10 mm Hg; P = .01) or volume of transfusion (-15 mL/10 mm Hg; 95% confidence interval, -29 to -1 mL/ h/10 mm Hg; P = .04). Results remained broadly consistent across multiple secondary outcomes and regardless of whether systolic blood pressure or mean arterial pressure was the explanatory variable. Conclusions: The lack of positive association between peak systolic blood pressure or peak mean arterial pressure with metrics of bleeding after cardiac surgery promotes equipoise for testing the influence of higher blood pressure targets during the early postoperative period.

Objectives: To determine whether randomization of patients undergoing extracorporeal membrane oxygenation to either therapeutic or a low-dose anticoagulation protocol results in a difference in activated partial thromboplastin time and anti-Xa. Design: Randomized, controlled, unblinded study. Setting: Two ICUs of two university hospitals. Patients: Patients admitted to the ICU, who required extracorporeal membrane oxygenation (venovenous or venoarterial) and who did not have a preexisting indication for therapeutic anticoagulation. Interventions: Therapeutic anticoagulation with heparin (target activated partial thromboplastin time between 50 and 70 s) or lower dose heparin (up to 12,000 U/24 hr aiming for activated partial thromboplastin time < 45 s). Measurements and Main Results: Thirty-two patients were randomized into two study groups that were not significantly different in demographics and extracorporeal membrane oxygenation characteristics. There was a significant difference in the daily geometric mean heparin dose (11,742 U [95% CI, 8,601-16,031 U] vs 20,710 U [95% CI, 15,343-27,954 U]; p = 0.004), daily geometric mean activated partial thromboplastin time (48.1 s [95% CI, 43.5-53.2 s] vs 55.5 s [95% CI, 50.4-61.2 s]; p = 0.04), and daily geometric mean anti-Xa (0.11 international units/mL [95% CI, 0.07-0.18] vs 0.27 [95% CI, 0.17-0.42]; p = 0.01). We found similar results when considering only venovenous extracorporeal membrane oxygenation episodes; however, no difference in daily geometric mean activated partial thromboplastin time between groups when considering only venoarterial extracorporeal membrane oxygenation episodes. Conclusions: Allocating patients on extracorporeal membrane oxygenation to two different anticoagulation protocols led to a significant difference in mean daily activated partial thromboplastin time and anti-Xa levels between groups. When considering subgroups analyses, these results were consistent in patients on venovenous extracorporeal membrane oxygenation. Our results support the feasibility of a larger trial in patients undergoing venovenous extracorporeal membrane oxygenation to compare different anticoagulation protocols; however, this study does not provide evidence on the optimal anticoagulation protocol for patients undergoing extracorporeal membrane oxygenation.

The genetic associations linking the chromosome 9 p21 (chr9p21) locus with cardiovascular diseases, such as aneurysm and coronary artery disease, are well characterised. However, the underlying molecular mechanism remains unclear. The chr9p21 locus is also associated with traits such as arterial stiffness, implicating a role in vascular cell biology. We investigated whether the risk variants affect vascular smooth muscle cell (VSMC) responses to inflammation. Methods We used recently developed and well characterised methods to differentiate VSMC from induced pluripotent stem cells (iPS) and compared the responses of risk and non-risk genotype iPS-VSMC to a range of IL-1 and TLR agonists. Results Risk and non-risk genotype iPS differentiated equally well to iPS-VSMC. However, the chr9p21 risk genotype conferred increased sensitivity to stimulation with IL-1alpha, IL-1beta and selective TLR agonists, due to increased expression of interleukin-1 receptor-associated kinase 4 (IRAK4). IRAK4-independent inflammatory responses remained unaffected by the risk genotype. IRAK4 expression was increased in risk iPS-VSMC as a consequence of altered epigenetic remodelling, including DNA methylation, of the IRAK4 promoter. Abstract 128 Figure 1 Conclusions Our study establishes a mechanistic link between the chr9p21 locus, inflammation and susceptibility to cardiovascular diseases, and provides support for the targeted use of therapies that inhibit IRAK4-dependent pathways, such as IL-1 signalling, in individuals of chr9p21 risk genotype.

Despite the benefits of mechanical circulatory and respiratory support (MCS), patients undergoing extracorporeal membrane oxygenation (ECMO) and the implantation of ventricular assist devices (VADs) continue to experience high rates of serious and life-threatening complications. These include bleeding, thrombosis, sepsis, multiorgan dysfunction, and death. These complications may be caused by the mechanical support or the underlying critical illness that necessitates its use. Reducing MCS complications remains an important goal for the future uptake of this technology.

Force-dependent binding of platelet glycoprotein Ib (GPIb) receptors to plasma von Willebrand factor (VWF) plays a key role in hemostasis and thrombosis. Previous studies have suggested that VWF activation requires force-induced exposure of the GPIb binding site in the A1 domain that is autoinhibited by the neighboring A2 domain. However, the biochemical basis of this “mechanopresentation” remains elusive. From a combination of protein chemical, biophysical, and functional studies, we find that the autoinhibition is controlled by the redox state of an unusual disulfide bond near the carboxyl terminus of the A2 domain that links adjacent cysteine residues to form an eight-membered ring. Only when the bond is cleaved does the A2 domain bind to the A1 domain and block platelet GPIb binding. Molecular dynamics simulations indicate that cleavage of the disulfide bond modifies the structure and molecular stresses of the A2 domain in a long-range allosteric manner, which provides a structural explanation for redox control of the autoinhibition. Significantly, the A2 disulfide bond is cleaved in ~75% of VWF subunits in healthy human donor plasma but in just ~25% of plasma VWF subunits from heart failure patients who have received extracorporeal membrane oxygenation support. This suggests that the majority of plasma VWF binding sites for platelet GPIb are autoinhibited in healthy donors but are mostly available in heart failure patients. These findings demonstrate that a disulfide bond switch regulates mechanopresentation of VWF.

BACKGROUND: Atherosclerotic cardiovascular disease (heart attacks and strokes) is the major cause of death globally and is caused by the buildup of a plaque in the arterial wall. Genomic data showed that the B cell-activating factor (BAFF) receptor pathway, which is specifically essential for the survival of conventional B lymphocytes (B-2 cells), is a key driver of coronary heart disease. Deletion or antibody-mediated blockade of BAFF receptor ablates B-2 cells and decreases experimental atherosclerosis. Anti-BAFF immunotherapy is approved for treatment of autoimmune systemic lupus erythematosus, and can therefore be expected to limit their associated cardiovascular risk. However, direct effects of anti-BAFF immunotherapy on atherosclerosis remain unknown. METHODS: To investigate the effect of BAFF neutralization in atherosclerosis, the authors treated Apoe(-/-) and Ldlr(-/-) mice with a well-characterized blocking anti-BAFF antibody. Moreover, to investigate the mechanism by which BAFF impacts atherosclerosis, the authors studied atherosclerosis-prone mice that lack the alternative receptor for BAFF: transmembrane activator and calcium modulator and cyclophilin ligand interactor. RESULTS: The authors demonstrate here that anti-BAFF antibody treatment increased atherosclerosis in mice, despite efficient depletion of mature B-2 cells, suggesting a unique mechanism of action. Indeed, myeloid cell-specific deletion of transmembrane activator and calcium modulator and cyclophilin ligand interactor also results in increased atherosclerosis, while B cell-specific transmembrane activator and calcium modulator and cyclophilin ligand interactor deletion had no effect. Mechanistically, BAFF-transmembrane activator and calcium modulator and cyclophilin ligand interactor signaling represses macrophage IRF7-dependent (but not NF-kappa B-dependent) Toll-like receptor 9 responses including proatherogenic CXCL10 production. CONCLUSIONS: These data identify a novel B cell-independent anti-inflammatory role for BAFF in atherosclerosis and may have important clinical implications.

The administration of chloride-rich intravenous (IV) fluid and hyperchloraemia have been associated with perioperative renal injury. The aim of this study was to determine whether a comprehensive perioperative protocol for the administration of chloride-limited IV fluid would reduce perioperative renal injury in adults undergoing cardiac surgery.

Antibodies binding oxidised epitopes on apoptotic cells and oxidised forms of LDL form an important protective barrier slowing the development of atherosclerosis. However, not all B cell functions or subsets are protective since adaptive B2 cell depletion is atheroprotective and autoimmunity is associated with accelerated atherosclerosis. The inhibitory IgG receptor FcγRIIb is the only IgG receptor found on B cells and also counteracts pro-inflammatory signalling from activating Fcγ receptors in macrophages and dendritic cells. Studies on FcγRIIb knockout mice demonstrate significant regulation of atherosclerosis but contrasting effects depending on the genetic background, suggesting the need for alternative approaches. We have analysed the effects of B cell-specific over-expression of FcγRIIb using a previously characterised transgenic mouse strain. FcγRIIb over-expression was confirmed to be specific for B cells and was equal between genders. There was only minor impacts on mature B cell levels, but FcγRIIb over-expression significantly attenuated plasma cell levels and serum antibody titres. Female, but not male, FcγRIIb-B cell transgenic mice on the ApoE-/- background develop significantly enhanced atherosclerosis after 6 weeks high fat diet compared to non-transgenic littermates. Females but not males had significantly decreased oxidised epitope-specific IgM levels and B1a cells in spleen and peritoneal lavage. In vitro, B1 cells from female ApoE-/- mice were more susceptible to FcγRIIb-induced apoptosis. Overall, our study highlights a potential difference in B1 cell biology between males and females, and supports the investigation of gender specific effects of autoimmune-linked FcγRIIb polymorphisms on human cardiovascular disease.

Essentials Relationship of acquired von Willebrand disease (VWD) and platelet dysfunction is explored. Patients with ventricular assist devices and on extracorporeal membrane oxygenation are investigated. Acquired VWD and platelet receptor shedding is demonstrated in the majority of patients. Loss of platelet adhesion receptors glycoprotein (GP) Ibα and GPVI may increase bleeding risk.

Extra corporeal membrane oxygenation (ECMO) is a rescue therapy for reversible cardiac and/or respiratory failure. Despite improvement in management of patients undergoing ECMO, mortality remains high. Due to thrombosis risk, which includes arterial and venous thrombosis as well as in the extracorporeal circuit and components, variable intensity systemic anticoagulation with unfractionated heparin is routinely used. However, bleeding is one of the most frequent complications, can be severe and is independently associated with worse outcomes. Optimal anticoagulation to prevent thrombosis whilst minimising bleeding in adults on ECMO remains unknown. Before conducting a large randomised controlled trial to determine whether lower anticoagulation intensity is safe and effective compared with therapeutic anticoagulation, we aimed to determine the feasibility of randomising ECMO patients to these anticoagulation protocols. Methods: The HELP-ECMO pilot study (ACTRN12613001324707) is a randomised, controlled, unblinded trial at two Australian intensive care units (ICUs). Inclusion criteria were ICU patients who required ECMO (venous-venous [VV] or venous-arterial [VA]). Patients who did not meet any exclusion criteria were randomised to receive either therapeutic anticoagulation with heparin (target activated partial thromboplastin time [aPTT] between 50 and 70 seconds) or low dose heparin (12000 units/24 hours aiming for aPTT Results: Between May 2014 and March 2016, 31 patients who underwent ECMO (9 (29%) VA and 22 (71%) VV) were enrolled; 16 were randomised to low dose and 15 to therapeutic dose heparin. The groups were similar in age (mean 41 years [SD 16.8] vs 43 [SD 17.6] p=0.75), gender (68% vs 80% male, p=0.47), type of ECMO (31% vs 27% VA, p=0.78) and Acute Physiology and Chronic Health Evaluation III illness severity score (mean 65.4 [SD 23.5] vs 61.8 [SD 30.1], p=0.72) and sepsis-related organ failure assessment score (mean 10 [SD 3.6] vs 10 [SD 3.3], p=1.0). The mean duration of ECMO support was 9.33 days (SD 5.97) in the low dose and 9.79 days (SD 4.77) in the therapeutic dose group (p=0.82). For the primary outcomes, there was a significant difference in the daily mean aPTT (48.1 [95% CI 43.5-53.3] vs 56.2 [95% CI 50.7-62.3], p=0.03), daily mean anti-Xa (0.11 [95% CI 0.07-0.18] vs 0.30 [IQR 0.19-0.46], p=0.003) and daily mean heparin dose (11784 units [95% CI 8693-15972] vs 22050 [IQR 16262-29899], p=0.004) in the low dose compared to therapeutic group. There was no difference in thrombotic complications with regard to DVT (2 [12.5%] vs 3 [20%], p=0.57), PE (1 [6.3%] vs 0 [0%], p=0.33), stroke (no events), intracardiac thrombus (1 [6.3%] vs 2 [13.3%], p=0.51), acute pump (1 [6.3%] vs 1[6.7%], p=0.96) and distal perfusion cannula thrombosis (2 [12.5%] vs 0 [0%], p=0.16) in low dose compared with therapeutic group, respectively. With regard to bleeding, there was no difference in intracranial haemorrhage (ICH) (0 [0%] vs 1 [6.7%], p=0.29), retroperitoneal bleeding (1 [6.3%] vs 1 [6.7%], p=0.96), gastrointestinal bleeding (0 [0%] vs 2 [13.3%] , p=0.13), or haemoptysis (1 [6.5%] vs 1 [6.7%], p=0.96) in low dose compared with therapeutic group, respectively. Conclusion: In this pilot trial, administration of a low dose heparin protocol was feasible, and resulted in a significant difference in mean heparin dose administered and daily aPTT and anti-Xa levels between groups. Low dose heparin was not associated with an increase in thrombotic events nor a decrease in bleeding events; however the study was not powered for these outcomes. Our findings support the feasibility of a larger phase III study to evaluate the safety and efficacy of low-dose anticoagulation compared with therapeutic heparin with regard to thrombotic and bleeding events in patients receiving ECMO. Disclosures No relevant conflicts of interest to declare.

Bleeding is the most frequent complication associated with extracorporeal membrane oxygenation (ECMO) support in critically ill patients. Nonetheless, risk factors for bleeding have been poorly described especially those associated with coagulation anomalies and anticoagulant therapy during ECMO support. The aim of this study is to describe bleeding complications in critically ill patients undergoing ECMO and to identify risk factors for bleeding events.

In patients requiring left ventricular assist device (LVAD) support, it can be difficult to ascertain suitability for long-term mechanical support with LVAD and eventual transplantation. LVAD implantation in a shocked patient is associated with increased morbidity and mortality. Interest is growing in the utilization of extracorporeal life support (ECLS) as a bridge-to-bridge support for these critically unwell patients. Here, we reviewed our experience with ECLS double bridging. We hypothesized that ECLS double bridging would stabilize end-organ dysfunction and reduce ventricular assist device (VAD) implant perioperative mortality. We conducted a retrospective review of prospectively collected data for 58 consecutive patients implanted with a continuous-flow LVAD between January 2010 and December 2013 at The Alfred Hospital, Melbourne, Victoria, Australia. Twenty-three patients required ECLS support pre-LVAD while 35 patients underwent LVAD implantation without an ECLS bridge. Preoperative morbidity in the ECLS bridge group was reflected by increased postoperative intensive care duration, blood loss, blood product use, and postoperative renal failure, but without negative impact upon survival when compared with the no ECLS group. ECLS stabilization improved end-organ function pre-VAD implant with significant improvements in hepatic and renal dysfunction. This series demonstrates that the use of ECLS bridge to VAD stabilizes end-organ dysfunction and reduces VAD implant perioperative mortality from that traditionally reported in these "crash and burn" patients.

Background and aim Extensive studies have revealed an important protective function for IgM antibodies from B1a cells in atherosclerosis, whereas the role of B2 cells and IgG antibodies is uncertain, with both pro- and anti-atherogenic actions reported. The aim of this study was to specifically target antibodies but not other B cell functions and determine the effect on mouse atherosclerosis. Methods We created MB1-Cre x XBP1 fl/fl mice that have B cell specific deficiency in the unfolded protein response transcription factor XBP1, previously reported to result in a specific antibody secretion defect. Specific antibody responses were assessed by ELISA and ELISpot after immunisation with NP-chicken gamma globulin. Chimeric Ldlr -/– mice with bone marrow from MB1-Cre x XBP1 fl/fl or control mice were fed a western diet for 8 weeks. Results B cell XBP1 deficiency led to significantly attenuated antibody secretion after NP-CGG immunisation. Analysis of ldlr –/– chimeric mice revealed enhanced atherosclerosis progression in MB1-Cre x XBP1 fl/fl recipients. These mice displayed severely attenuated serum IgM, IgG and IgE levels, but intact spleen, lymph node and peritoneal B cells. There were no differences in total cholesterol levels. Antibody deficiency was associated with enhanced pro-atherogenic Th1 CD4 + T cell immunity. Conclusions Antibodies have an overall protective effect on atherosclerosis and B2 cell antibodies are not responsible for enhanced atherosclerosis in IgM-deficient mice. Other B cell functions may be pathogenic in atherosclerosis.

Introduction: Right ventricular (RV) failure post LVAD insertion is a common, yet highly morbid complication associated with poor outcomes. The ability to predict this complication is important in allowing early intervention and in improving outcomes for these patients. Methods: Data from 101 consecutive patients implanted with third-generation continuous-flow LVAD between 2003 and 2013 at a single institution were analysed. After a thorough literature review, four studies were found to have developed predictive models for RV failure post LVAD suitable for validation in our population. These were applied to our data set. Results: The groups were well matched demographically. Bilirubin was noted to be significantly higher in the RV failure group (p=0.05). There was a trend towards higher creatinine in RV failure patients (135 μmol/L vs 108 μmol/L, p=0.06). Pre-operative systolic blood pressure was lower in the RV failure group (94.8 mmHg vs 100 mmHg, p=0.05). The overall incidence of RV dysfunction pre-operatively was not different. However, RV systolic pressure and tricuspid regurgitation were both found to be statistically significantly higher (p=0.041 and p=0.0019). TAPSE also trended towards being lower in the RV failure group (p=0.06). 63 patients (62.4%) developed RV failure. There was increased incidence of mortality pre-explantation in patients who developed RV failure (31.7% vs 10.5%, p=0.015), with a significant portion of these patients dying within 30 days (11% vs 0%, p=0.043). Mortality overall was also statistically significantly higher in the RV failure group (41.3% vs 15.8%, p=0.008)Tabled 1Mean ± SD score from established RV failure risk modelsRV Failure (n=63)No RV failure (n=38)Matthews(4)8.05 ± 2.237.46 ± 1.14p = 0.15Drakos(5)5.27 ± 2.544.85 ± 2.48p = 0.43Fitzpatrick(3)34.49 ± 15.3324.8 ± 10.3p = 0.003Alturi(6)1.632 ± 0.2111.33 ± 1.12p = 0.021 Open table in a new tab All of the models showed at least a weak trend in the relationship between their predictions and our actual outcomes. Matthews’ and Drakos’ predictive models were not able to achieve significant difference in our population (p=0.15 and p=0.43 respectively. The remaining models (Fitzpatrick and Atluri) achieved difference (p = 0.003 and p=0.021 respectively). Discussion Despite advances in technology and management, RV failure remains a highly morbid complication associated with a significantly increased risk of mortality. It appears that the patients who develop RV failure post LVAD implantation, in our experience, are already showing a degree of RV dysfunction pre-operatively. Existing models in the literature predicting this outcome appear to be valid in our population, albeit requiring re-calibration.