Transplantation Outcomes with Donor Hearts after Circulatory Death.

BACKGROUND: Data showing the efficacy and safety of the transplantation of hearts obtained from donors after circulatory death as compared with hearts obtained from donors after brain death are limited. METHODS: We conducted a randomized, noninferiority trial in which adult candidates for heart transplantation were assigned in a 3:1 ratio to receive a heart after the circulatory death of the donor or a heart from a donor after brain death if that heart was available first (circulatory-death group) or to receive only a heart that had been preserved with the use of traditional cold storage after the brain death of the donor (brain-death group). The primary end point was the risk-adjusted survival at 6 months in the as-treated circulatory-death group as compared with the brain-death group. The primary safety end point was serious adverse events associated with the heart graft at 30 days after transplantation. RESULTS: A total of 180 patients underwent transplantation; 90 (assigned to the circulatory-death group) received a heart donated after circulatory death and 90 (regardless of group assignment) received a heart donated after brain death. A total of 166 transplant recipients were included in the as-treated primary analysis (80 who received a heart from a circulatory-death donor and 86 who received a heart from a brain-death donor). The risk-adjusted 6-month survival in the as-treated population was 94% (95% confidence interval [CI], 88 to 99) among recipients of a heart from a circulatory-death donor, as compared with 90% (95% CI, 84 to 97) among recipients of a heart from a brain-death donor (least-squares mean difference, -3 percentage points; 90% CI, -10 to 3; P<0.001 for noninferiority [margin, 20 percentage points]). There were no substantial between-group differences in the mean per-patient number of serious adverse events associated with the heart graft at 30 days after transplantation. CONCLUSIONS: In this trial, risk-adjusted survival at 6 months after transplantation with a donor heart that had been reanimated and assessed with the use of extracorporeal nonischemic perfusion after circulatory death was not inferior to that after standard-care transplantation with a donor heart that had been preserved with the use of cold storage after brain death. (Funded by TransMedics; ClinicalTrials.gov number, NCT03831048.).

Trends in the Use of Recombinant Activated Factor VII and Prothrombin Complex Concentrate in Heart Transplant Patients in Virginia.

OBJECTIVES: To explore trends in intraoperative procoagulant factor concentrate use in patients undergoing heart transplantation (HTx) in Virginia. Secondarily, to evaluate their association with postoperative thrombosis. DESIGN: Patients who underwent HTx were identified using a statewide database. Trends in off-label recombinant activated factor VII (rFVIIa) use and on-label and off-label prothrombin complex concentrate (PCC) use were tested using the Mantel-Haenszel test. Multivariate logistic regression was used to test for an association between procoagulant factor concentrate administration and thrombosis. SETTING: Virginia hospitals performing HTx. PARTICIPANTS: Adults undergoing HTx between 2012 and 2022. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Among 899 patients who required HTx, 100 (11.1%) received off-label rFVIIa, 69 (7.7%) received on-label PCC, and 80 (8.9%) received off-label PCC. There was a downward trend in the use of rFVIIa over the 10-year period (p = 0.04). There was no trend in on-label PCC use (p = 0.12); however, there was an increase in off-label PCC use (p < 0.001). Patients who received rFVIIa were transfused more and had longer cardiopulmonary bypass time (p < 0.001). Receipt of rFVIIa was associated with increased thrombotic risk (odds ratio [OR] 1.92; 95% CI 1.12-3.29; p = 0.02), whereas on-label and off-label PCC use had no association with thrombosis (OR 0.98, 95% CI 0.49-1.96, p = 0.96 for on-label use; and OR 0.61, 95% CI 0.29-1.30, p = 0.20 for off-label use). CONCLUSIONS: Use of rFVIIa in HTx decreased over the past decade, whereas off-label PCC use increased. Receipt of rFVIIa was associated with thrombosis; however, patients who received rFVIIa were more severely ill, and risk adjustment may have been incomplete.

Influence of sex on global myocardial ischemia tolerance and mitochondrial function in circulatory death donor hearts.

Donation after circulatory death (DCD) donor hearts are not routinely used for heart transplantation (HTx) because of ischemic damage, which is inherent to the DCD process. HTx outcomes are suboptimal in males who received female donor hearts. The exact mechanism for suboptimal outcomes from female donor hearts has not been defined. Differential susceptibility to ischemia tolerance, which would play a significant role in DCD donation, could be a reason but has not been studied. We studied the influence of sex on global myocardial ischemia tolerance and mitochondrial function. Sprague-Dawley rats of both sexes were assigned to DCD (n = 32) or control beating-heart donor (CBD, n = 28) groups. DCD hearts underwent 25 min of in vivo global myocardial ischemia and 90 min of ex vivo Krebs-Henseleit buffer perfusion at 37°C. CBD hearts were procured without ischemia. Infarct size was determined in hearts following 90 min of reperfusion, and in another set of hearts, mitochondrial function (oxidative-phosphorylation) was studied following 60 min of reperfusion. Infarct size was increased 3.3-fold in male and 3.1-fold in female DCD hearts compared with CBD hearts. However, infarct size (%) was comparable in female and male DCD hearts (male: 25.4 ± 3.7 vs. female 19.0 ± 3.3, P = NS). Oxidative phosphorylation was similarly decreased in male and female DCD hearts' mitochondria compared with CBD hearts' mitochondria. Thus, neither infarct size nor mitochondrial dysfunction was higher in female DCD hearts. These results suggest that the susceptibility to ischemia is not the reason for suboptimal HTx outcomes with female donor hearts.NEW & NOTEWORTHY The current study shows cardiac injury is not increased in female DCD hearts following global ischemia-reperfusion compared with male DCD hearts. In addition, mitochondrial dysfunction with DCD ischemia-reperfusion is comparable in both sexes. Sex-specific immune responses and hormone receptor modulation may contribute to suboptimal outcomes in male HTx recipients with female donor hearts.

Pulmonary Hypertension and Operative Risk in Mitral Valve and Coronary Surgery.

INTRODUCTION: Pulmonary hypertension (PHT) is a known risk factor for coronary artery bypass grafting (CABG), though less well understood for valve operations. We hypothesized PHT is associated with lower risk during mitral valve operations compared to CABG. METHODS: Patients undergoing isolated mitral valve or CABG operations (2011-2019) in a regional Society of Thoracic Surgeons (STS) database were stratified by pulmonary artery systolic pressure (PASP). The association of PASP by procedure type was assessed by hierarchical regression modeling, adjusting for STS predicted risk scores. RESULTS: Of the 2542 mitral and 11,059 CABG patients, the mitral population had higher mean STS risk of mortality (3.6% versus 2.4%, P < 0.0001) and median PASP (42 mmHg versus 32 mmHg, P < 0.0001). PASP was independently associated with operative mortality and major morbidity in both mitral and CABG patients. However, for mitral patients a 10-mmHg increase in PASP was associated with lower odds of morbidity (odds ratio: 1.06 versus 1.13), mortality (odds ratio: 1.11 versus 1.18) and intensive care unit time (4.3 versus 7.6 h) compared with CABG patients (interaction terms P < 0.0001). Among mitral patients, median PASP was higher in stenotic versus regurgitant disease (57 mmHg versus 40 mmHg, P < 0.0001). However, there was no differential association of PASP on morbidity or mortality (interaction terms P > 0.05). CONCLUSIONS: Although mitral surgery patients tend to have higher preoperative pulmonary artery pressures, PHT was associated with a lower risk for mitral outcomes compared with CABG. Further research on the management and optimization of patients with PHT perioperatively is needed to improve care for these patients.

Electron Transport Chain Inhibition to Decrease Injury in Transplanted Donation After Circulatory Death Rat Hearts.

ABSTRACT: Donation after circulatory death (DCD) donor hearts sustain ischemic damage and are not routinely used for heart transplantation. DCD heart injury, particularly reperfusion injury, is primarily mediated by releasing reactive oxygen species from the damaged mitochondria (complex I of the electron transport chain). Amobarbital (AMO) is a transient inhibitor of complex I and is known to reduce releasing reactive oxygen species generation. We studied the beneficial effects of AMO in transplanted DCD hearts. Sprague-Dawley rats were assigned to 4 groups-DCD or DCD + AMO donors and control beating-heart donors (CBD) or CBD + AMO donors (n = 6-8 each). Anesthetized rats were connected to a ventilator. The right carotid artery was cannulated, heparin and vecuronium were administered. The DCD process started by disconnecting the ventilator. DCD hearts were procured after 25 minutes of in-vivo ischemia, whereas CBD hearts were procured without ischemia. At procurement, all donor hearts received 10 mL of University of Wisconsin cardioplegia solution. The CBD + AMO and DCD + AMO groups received AMO (2 mM) dissolved in cardioplegia. Heterotopic heart transplantation was performed by anastomosing the donor aorta and pulmonary artery to the recipient's abdominal aorta and inferior vena cava. After 14 days, transplanted heart function was measured with a balloon tip catheter placed in the left ventricle. Compared with CBD hearts, DCD hearts had significantly lower developed pressure. AMO treatment significantly improved cardiac function in DCD hearts. Treatment of DCD hearts at the time of reperfusion with AMO resulted in an improvement of transplanted heart function that was comparable with the CBD hearts.

Zero balance ultrafiltration to correct metabolic alkalosis occurring during veno-arterial extracorporeal membrane oxygenation.

INTRODUCTION: We describe a case report of metabolic alkalosis that occurred during veno-arterial extracorporeal membrane oxygenation (VA ECMO) that was corrected during cardiopulmonary bypass (CPB) using zero balance ultrafiltration with normal saline (NS) 0.9%. CASE REPORT: A 67-year-old male received a heart transplant 6 days after being placed on VA ECMO. During VA ECMO the patient developed metabolic alkalosis. During CPB, zero balance ultrafiltration with NS 0.9% was used to correct metabolic alkalosis. DISCUSSION: Metabolic alkalosis during CPB is rare. To our knowledge, this is the first reported case of the use of zero balance ultrafiltration to effectively correct metabolic alkalosis. CONCLUSION: Metabolic alkalosis during CPB may be corrected using zero balance ultrafiltration with NS 0.9%.

Percutaneous approach to left ventricular assist device decommissioning.

OBJECTIVE: To assess the outcomes of a single-center experience with percutaneous left ventricular assist device (LVAD) decommissioning. BACKGROUND: Patients with LVADs may eventually require their removal, either due to recovery of left ventricular function or recurrent complications. Traditionally, withdrawal of LVAD support has been managed with surgical device explantation, which carries significant procedural risks. Transcatheter LVAD decommissioning, with outflow graft occlusion and driveline transection, has recently been described as an alternative to surgical removal. METHODS: Here, we report on a retrospective cohort of five consecutive cases treated with transcatheter LVAD decommissioning. RESULTS: The procedure was effective in all cases, and no patient experienced procedure-related complications. At midterm follow-up, the three patients who had myocardial function recovery were alive and had not experienced heart failure-related symptoms or complications. CONCLUSION: Percutaneous LVAD decommissioning appears to be a safe and effective approach to LVAD treatment discontinuation.

Access to Left Ventricular Assist Device: Travel Time Does Not Tell The Whole Story.

BACKGROUND: Negative health effects of traveling longer distances for surgical services have been reported. Given the high complexity of multidisciplinary care required for management of Left Ventricular Assist Device (LVAD) implantation, only 4 of 18 centers in our state perform these operations. Given the limited access we hypothesized increased travel time would adversely affect postoperative outcomes and 30-d mortality. METHODS: A statewide Society of Thoracic Surgeons database was queried to identify patients undergoing Heartmate II/III and HVAD implantation, and 725 patients were identified. Travel time was calculated by zip code. Patients were stratified into regional and distant groups by the upper quartile of travel time (1-h). Preoperative variables and outcomes were compared between the groups. Multivariate analysis was performed to evaluate the impact of travel time in risk-adjusted models of 30-d mortality. RESULTS: Median patient travel time to their LVAD center in our state is 32 min (mean 53 ± 65 min, 46 ± 71 miles). Patients in the distant group (n = 191) had lower median incomes, higher self-pay status, higher rates of medical comorbid disease. Despite these differences there was no difference between the groups in ICU and/or hospital length of stay, readmission, postoperative complications, or 30-d mortality. Multivariate regression demonstrated insurance status, age, and prior surgery predicted 30-d mortality, but not travel time. CONCLUSIONS: Despite only four centers in the state performing LVAD implantation, travel time was strongly associated with preoperative risk, and socioeconomic status but not postoperative outcomes or 30-d mortality. Therefore, increasing access should focus on insurance, and patient characteristics not travel time.

Modulation of Mitochondrial Respiration During Early Reperfusion Reduces Cardiac Injury in Donation After Circulatory Death Hearts.

ABSTRACT: Donation after circulatory death (DCD) donors are a potential source for heart transplantation. The DCD process has unavoidable ischemia and reperfusion (I/R) injury, primarily mediated through mitochondria, which limits routine utilization of hearts for transplantation. Amobarbital (AMO), a transient inhibitor of the electron transport chain, is known to decrease cardiac injury following ex vivo I/R. We studied whether AMO treatment during reperfusion can decrease injury in DCD hearts. Sprague Dawley rat hearts subjected to 25 minutes of in vivo ischemia (DCD hearts), or control beating donor hearts, were treated with AMO or vehicle for the first 5 minutes of reperfusion, followed by Krebs-Henseleit buffer reperfusion for 55 minutes (for mitochondrial isolation) or 85 minutes (for infarct size determination). Compared with vehicle, AMO treatment led to decreased infarct size (25.2% ± 1.5% vs. 31.5% ± 1.5%; P ≤ 0.05) and troponin I release (4.5 ± 0.05 ng/mL vs. 9.3 ± 0.24 ng/mL, P ≤ 0.05). AMO treatment decreased H 2 O 2 generation with glutamate as complex I substrate in both subsarcolemmal mitochondria (SSM) (37 ± 3.7 pmol·mg -1 ·min -1 vs. 56.9 ± 4.1 pmol·mg -1 ·min -1 ; P ≤ 0.05), and interfibrillar mitochondria (IFM) (31.8 ± 2.8 pmol·mg -1 ·min -1 vs. 46 ± 4.8 pmol·mg -1 ·min -1 ; P ≤ 0.05) and improved calcium retention capacity in SSM (360 ±17.2 nmol/mg vs. 277 ± 13 nmol/mg; P ≤ 0.05), and IFM (483 ± 20 nmol/mg vs. 377± 19 nmol/mg; P ≤ 0.05) compared with vehicle treatment. SSM and IFM retained more cytochrome c with AMO treatment compared with vehicle. In conclusion, brief inhibition of mitochondrial respiration during reperfusion using amobarbital is a promising approach to decrease injury in DCD hearts.

Assessment of machine perfusion conditions for the donation after circulatory death heart preservation.

BACKGROUND: Donation after circulatory death (DCD) hearts requires machine perfusion preservation, the conditions of which are not well defined. METHODS: To achieve this, rat hearts were procured following a DCD or control beating-heart donation (CBD) model, and perfused for 60 min with one of three machine perfusion solutions-St. Thomas (ST), University of Wisconsin (UW), or Polyethylene Glycol-20k (PEG)-at one of two temperatures, 4°C or 15°C. At 15-min intervals, perfusion pressure was measured as a marker of vascular resistance. Colored microspheres were added to capture the distribution of perfusate into the metabolically active sub-endocardium, and the eluate was collected for troponin assays. Analyses compared groups using Wilcoxon rank-sum and ANOVA. RESULTS: Perfusion pressure was significantly higher for DCD than CBD hearts at 15°C regardless of solutions. The lowest rise in perfusion pressure over time was observed with PEG at 15°C. Except for PEG at 15°C, ST and UW solutions at 4 or 15°C had decreased sub-endocardial perfusion in DCD hearts. Troponin release from DCD hearts with UW and PEG solutions was comparable to CBD hearts but was significantly higher with ST solution at 15°C. CONCLUSIONS: Optimal preservation conditions for DCD hearts were observed with PEG machine perfusion solution at 15°C.

Contemporary prevalence and outcomes of rheumatic mitral valve surgery.

OBJECTIVE: Rheumatic mitral valve disease is often viewed as a historic disease in North America with limited contemporary data. We hypothesized that rheumatic pathology remains common and has worse short-term outcomes and higher resource utilization compared to other mitral valve pathologies. METHOD: All patients undergoing mitral valve repair or replacement (2011-2019) were extracted from a regional Society of Thoracic Surgeons database. Resource utilization metrics included inflation-adjusted hospital costs. Patients were stratified by mitral valve pathology for univariate analysis. RESULT: Out of the 6625 mitral valve procedures, 835 (12.6%) were from rheumatic disease, a proportion that incrementally increased over time (+0.39% per year, p = .032). Among 19 hospitals, there was high variability in number of rheumatic mitral operations (median: 22, interquartile range [IQR]: 5-80) and rate of rheumatic repairs (median: 3%, IQR: 0%-6%). Rheumatic patients were younger (62 vs. 65, p < .0001), more often female (75% vs. 43%, p < .001) and with greater burden of heart failure, multi-valve disease, and lung disease, but less coronary disease. There were no differences in operative mortality (5.2% vs. 5.0%, p = .85) or major morbidity (22.2% vs. 21.8%, p = .83). However, resource utilization was higher for rheumatic patients, including more frequent transfusions (43% vs. 39%, p = .012), longer ICU (73 vs. 64 h, p < .0001) and postoperative length of stay (8 vs. 7 days, p < .0001). CONCLUSIONS: Rheumatic mitral disease accounts for a meaningful (12%) and rising percentage of mitral valve operations in the region, with high variability among hospitals. Rheumatic mitral surgery yielded similar short-term outcomes compared to nonrheumatic pathology, but required greater resource utilization.

An interventional approach to left ventricular assist device outflow graft obstruction.

BACKGROUND: LVADs provide life-sustaining treatment for patients with heart failure, but their complexity allows for complications. One complication, LVAD outflow graft obstruction, may be misdiagnosed as intraluminal thrombus, when more often it is extraluminal compression from biodebris accumulation. It can often be treated endovascularly with stenting. This case series describes diagnostic and procedural techniques for the treatment of left ventricular assist device (LVAD) outflow graft obstruction. METHODS: We present four patients with LVADs who developed LVAD outflow graft obstruction within the bend relief-covered segment. All were initially diagnosed with computed tomographic angiography (CTA). All underwent invasive evaluation with intravascular ultrasound (IVUS), then were treated with stenting. After misdiagnosing a twist, we developed the technique of balloon "graftoplasty" to ensure suitability for stent delivery in subsequent cases. RESULTS: All patients presented with low-flow alarms and symptoms of low output, and were diagnosed with outflow graft obstruction by CTA. In all four, IVUS confirmed an extraluminal etiology. Patient 1 was treated with stenting and had a good outcome. Patient 2's obstruction was from twisting, rather than biodebris accumulation, and had sub-optimal stent expansion and ultimately required surgery. Balloon "graftoplasty" was used in subsequent cases to ensure subsequent stent expansion. Patients 3 and 4 were successfully stented. All improved after treatment. CONCLUSIONS: In patients with LVAD outflow graft obstruction, IVUS can distinguish intraluminal thrombus from extraluminal compression. Balloon "graftoplasty" can ensure that the outflow graft will respond to stenting. Many cases of LVAD outflow graft obstruction should be amenable to endovascular treatment.

Modulation of Interleukin-1 and -18 Mediated Injury in Donation after Circulatory Death Mouse Hearts.

BACKGROUND: Donation after circulatory death donors (DCD) can expand the donor pool for heart transplantation, which primarily depends on brain death donors. Ischemia and reperfusion injury are inherent to the DCD process. We hypothesize that pharmacologic inhibition of interleukin-1 (IL-1) and/or IL-18 is protective to DCD hearts. MATERIALS AND METHODS: Following clinical protocol, in-situ ischemia time in control beating-heart donor (CBD) and DCD groups was less than 5 and 40 min, respectively. Wild type (WT) C57Bl6/j, IL-1 receptor type I knockout (IL-1RI-KO), and IL-18 KO mice were used. Hearts were reanimated for 90 min on a Langendorff system with Krebs-Henseleit buffer at 37°C, to assess physiologic parameters. Recombinant IL-1 receptor antagonist (IL-1Ra) and/or IL-18 binding protein (IL-18BP) were added to the Krebs-Henseleit buffer to inhibit IL-1 and/or the IL-18 signaling, respectively. RESULTS: Developed pressure and ± dP/dt were significantly impaired in the DCD-WT group compared to CBD-WT (P ≤ 0.05). Troponin release was higher in DCD-WT groups. Functional parameters were preserved, and troponin release was significantly less in the DCD knockout groups. Heart function was improved in DCD groups treated with IL-1Ra or IL-18BP compared to the DCD-WT group. CONCLUSIONS: Heart function was significantly impaired in the DCD-WT group compared to CBD-WT. Genetic deletion or pharmacologic blockade of IL-1 or IL-18 was protective to DCD hearts.

Outcomes of surgical mitral valve replacement: A benchmark to assess transcatheter technologies.

BACKGROUND: Clinical trials are underway to evaluate the safety and efficacy of transcatheter mitral valve replacement in intermediate and high surgical risk patients. We analyzed outcomes of surgical mitral valve replacement in a regional consortium to provide benchmark data for emerging alternative therapies. METHODS: All patients undergoing mitral replacement with a Society of Thoracic Surgeons predicted risk of mortality (STS PROM) in a regional consortium from 2001 to 2017 were analyzed. Patients with endocarditis were excluded. Patients were stratified by STS PROM into low (<4%), moderate (4%-8%), and high risk (>8%) cohorts. Mortality, postoperative complications, and resource utilization were evaluated for each group. RESULTS: A total of 1611 patients were analyzed including 927 (58%) low, 370 (23%) moderate, and 314 (20%) high-risk patients. The mean STS PROM was 2%, 5.6%, and 15.4% for each group. Mortality was adequately predicted for all groups while the most common complications included prolonged ventilation, reoperation, and renal failure. Higher risk patients had longer intensive care unit and hospital lengths of stay (2 vs. 3 vs. 5 days, p < .0001 and 7 vs. 8 vs. 10 days, p < .0001) and higher total hospital costs ($38,029 vs. $45,075 vs. $59,171 p < .0001). CONCLUSIONS: Mitral valve replacement is associated with acceptable morbidity and mortality, particularly for low and intermediate-risk patients. These outcomes also serve as a benchmark with which to compare forthcoming results of transcatheter mitral valve replacement trials.

Donation after circulatory death: opportunities on the horizon.

PURPOSE OF REVIEW: Organ transplantation remains the gold standard therapy for many end-organ diseases. The demand for donor organs continues to grow to far exceed supply. This review summarizes recent protocols, procedures, and ethics surrounding the increased utilization of donors after circulatory death for transplantation. RECENT FINDINGS: An increasing number of centers are utilizing donation after circulatory death, and outcomes are improving. Although outcomes from donors after brain death continue to be the primary source of donation, circulatory death outcomes continue to improve approaching the level of brain death donors. SUMMARY: Donation after circulatory death offers a real opportunity to narrow the supply and demand issue with organ donation. Outcomes are improving, and protocols continue to evolve.

Predictors of Renal Failure in Patients Treated With the Total Artificial Heart.

BACKGROUND: The incidence of hemodialysis (HD)-dependent renal failure after total artificial heart (TAH) implantation is high. We sought to determine the preoperative predictors of HD after TAH implantation. METHODS AND RESULTS: We studied 87 patients after TAH implantation at our institution between April 2006 and March 2017. Baseline clinical data were obtained from the medical records, and patients were followed until death or heart transplantation. We performed logistic regression analysis to identify predictors of HD after TAH implantation. Of the patients, 24 (28%) required postimplantation HD. Those requiring HD were more likely to have histories of coronary artery disease (58% vs 29%; P = 0.01), required preoperative membrane oxygenation (33% vs 4.8%; P = 0.001) and had lower baseline estimated glomerular filtration rates (54 ± 29 vs 67 ± 24 mL/min/1.73m2; P = 0.04). Patients requiring HD were at a higher risk of death on device at 1 year (33% vs 5%, P = 0.001; log rank test: P =0.001, hazard ratio 6.6 [95% CI:1.8-23], P = 0.003). CONCLUSIONS: The incidence of postimplantation HD is high and is associated with increased likelihood of mortality. Lower baseline estimated glomerular filtration rates, histories of coronary artery disease and preoperative membrane oxygenation support are predictors of postimplantation requirement of HD. These data may help to identify patients at risk for adverse outcomes after TAH implantation.

Concomitant Left Atrial Appendage Closure Outcomes and Cost: A Multi-institutional Cohort Analysis.

BACKGROUND: Left atrial appendage closure (LAAC) is frequently performed during cardiac operations, but the impact of LAAC on patient outcomes is not fully known. We hypothesized that the addition of LAAC would increase morbidity and resource utilization. METHODS: All patients undergoing cardiac surgery from a multi-institutional Society of Thoracic Surgeons database from 2011 to 2016 were stratified by LAAC. The effect of LAAC on risk-adjusted outcomes was assessed by hierarchical regression modeling accounting for preoperative risk factors, planned surgical procedure, hospital, and year. RESULTS: Concomitant LAAC was performed on 2384 of 28,311 patients (9.3%), who were older, with a greater burden of preoperative atrial fibrillation and heart failure. Although the addition of LAAC increased the risk of new-onset postoperative atrial fibrillation (OR 1.69, P < 0.01), it did not increase rates of major morbidity (OR 1.00, P = 0.970), stroke (OR 0.92, P = 0.787), or mortality (OR 0.93, P = 0.684). Although cardiopulmonary bypass time was not significantly increased by LAAC, patients' total hospitalization costs were $3035 higher (P = 0.018). CONCLUSIONS: Although concomitant LAAC was not associated with major complications, there were higher risk-adjusted rates of new-onset postoperative atrial fibrillation. Furthermore, LAAC added approximately $3000 to a patient's total hospital cost. These short-term risks and costs should be weighed against potential long-term benefits of left atrial appendage closure.

Targeting the NLRP3 inflammasome to reduce warm ischemic injury in donation after circulatory death heart.

While the donation after circulatory death (DCD) heart transplantation is an emerging clinical practice, the primary source of donor hearts for transplantation remains donation after brain death (DBD) donors. DCD process induces formation of NOD-like receptor family pyrin domain containing-3 (NLRP3) inflammasome, a key mediator of inflammation-driven damage to heart. Inhibition of NLRP3 inflammasome formation could be protective to DCD hearts. Five groups (n = 8 each) of mice were studied-control beating heart donor (CBD) wild-type (WT), DCD WT, CBD NLRP3 knockout (KO), DCD NLRP3 KO, and DCD WT NLRP3 inhibitor group. Hearts were procured and reanimated on a Langendorff system to assess physiologic parameters and then for molecular assays. NLRP3 inhibitor (50 µmol/L) was administered to the DCD-NLRP3 inhibitor group at reanimation. Tissue NLRP3 levels were 80% higher in the DCD WT group compared with the CBD-WT group. Caspase-1 activity was significantly elevated in DCD WT but not in KO or NLRP3 inhibitor groups. The developed pressures and ±dP/dt were significantly impaired in the DCD WT group compared with the CBD-WT group, P < .05, but were well preserved in DCD-NLRP3 inhibitor group. The DCD process activates the NLRP3 inflammasome, contributing to myocardial damage and dysfunction. NLRP3 inflammasome inhibition limits myocardial injury and preserves DCD heart function.

Heart transplantation from donation after circulatory death donors: Present and future.

The first successful human heart transplantation was reported on 3 December 1967, by Christiaan Barnard in South Africa. Since then this life-saving procedure has been performed in over 120 000 patients. A limitation to the performance of this procedure is the availability of donor hearts with as many as 20% of patients dying before a donor's heart is available for transplant. Today, hearts for transplantation are procured from individuals experiencing donation after brain death (DBD). Interestingly, this, however, was not always the case as the first heart transplants occurred after circulatory death. Revisiting the availability of hearts for transplant from those experiencing donation after circulatory death (DCD) could further expand the number of hearts suitable for transplantation. There are several considerations pertinent to transplanting hearts from those undergoing circulatory death. In this review, we summarize the main distinctions between DBD and DCD heart donation and discuss the research relevant to increasing the number of hearts available for transplantation by including individual's hearts that experience circulatory death.

Impact of renal function recovery utilizing left ventricular assist device support.

BACKGROUND: In heart failure (HF) patients with renal insufficiency (RI), we hypothesize that mechanical circulatory support (MCS) with the left ventricular assist device (LVAD) will promote renal function recovery (RR). We sought to quantify RR with LVAD support over 6 months of follow-up. METHODS: RR data at 30, 90, and 180 days were analyzed for all LVAD patients with RI at the time of surgery. RI was defined as either the use of hemodialysis (HD) or a glomerular filtration rate (GFR) less than 60 mL/min/1.73 m2 . RESULTS: Between January 2008 and December 2013, 47 of 127 (37%) LVAD recipients had RI at the time of surgery. The mean preoperative GFR was 48 ± 7. We observed RR at each follow-up, with 30-, 90-, and 180-day mean GFRs of 79 ± 33, 71 ± 31, and 63 ± 21, respectively. The absolute increase in GFR at 30, 90, and 180 days was 34 ± 31, 26 ± 29, and 19 ± 20, respectively (All with P < .001). Four patients (8.5%) with RI required HD preoperatively. Of these, three recovered renal function, the fourth patient died. An additional 13 patients (30.2%) that were previously non-HD-dependent required HD postoperatively. Six of these 13 (46%) recovered renal function during the study period, four (30.7%) remain on HD and three (23%) died. CONCLUSIONS: RI improves significantly with LVAD support. Improvements in GFR are marked in the first 30 days. Among those patients requiring either pre- or post-operative HD, a majority recovered renal function.