Impact of new allocation system on length of stay following heart transplantation in the United States.

BACKGROUND: United Network for Organ Sharing (UNOS) allocation criteria changed in 2018 to accommodate the increased prevalence of ventricular assist device use as a bridge to heart transplant, which consequently prioritized sicker patients. We aimed to assess the impact of this new allocation policy on the length of stay following heart transplantation. Secondary outcomes include other risk factors for prolonged hospitalization and its effect on mortality and postoperative complications. METHODS: The UNOS Registry was queried to identify patients who underwent isolated heart transplants in the United States between 2001 and 2023. Patients were divided into quartiles according to their respective length of stay. RESULTS: A total of 57 020 patients were included, 15 357 of which were allocated with the new system. The median hospital length of stay was 15 days (mean 22.7 days). Length of stay was longer in the new allocation era (25 ± 30 vs. 22 ± 27 days, p < .001). The longer length of stay was associated with increased 5-year mortality in the new allocation system (aHR: 1.18; 95% CI: 1.15, 1.20; p-value: < .001). CONCLUSION: Longer hospital stays and associated observed increased risk for mortality in the era after the allocation criteria change reflect the rationale of this shift which was to prioritize heart transplants for sicker patients. Further studies are needed to track the progress of surgical and perioperative management of these studies over time.

Pericardiectomy and Pericardial Window for the Treatment of Pericardial Disease in the Contemporary Era.

PURPOSE OF REVIEW: To summarize the contemporary practice of pericardiectomy and pericardial window. We discuss the indications, preoperative planning, procedural aspects, postprocedural management, and outcomes of each procedure. RECENT FINDINGS: Surgical approaches for the treatment of pericardial disease have been around even before the emergence of cardiopulmonary bypass. Since the forthcoming of cardiopulmonary bypass, there have been significant changes in the epidemiology and diagnostic approach of pericardial diseases as well as advancements in the surgical techniques and perioperative management used in the care of these patients. Pericardiectomy has an average mortality of almost 7% and is typically performed in patients with advanced symptoms from constrictive pericarditis and relatively few comorbidities. Pericardial window is a safe procedure for the treatment of pericardial effusion that can be performed with different approaches.

Human endothelial colony-forming cells provide trophic support for pluripotent stem cell-derived cardiomyocytes via distinctively high expression of neuregulin-1.

The search for a source of endothelial cells (ECs) with translational therapeutic potential remains crucial in regenerative medicine. Human blood-derived endothelial colony-forming cells (ECFCs) represent a promising source of autologous ECs due to their robust capacity to form vascular networks in vivo and their easy accessibility from peripheral blood. However, whether ECFCs have distinct characteristics with translational value compared to other ECs remains unclear. Here, we show that vascular networks generated with human ECFCs exhibited robust paracrine support for human pluripotent stem cell-derived cardiomyocytes (iCMs), significantly improving protection against drug-induced cardiac injury and enhancing engraftment at ectopic (subcutaneous) and orthotopic (cardiac) sites. In contrast, iCM support was notably absent in grafts with vessels lined by mature-ECs. This differential trophic ability was due to a unique high constitutive expression of the cardioprotective growth factor neuregulin-1 (NRG1). ECFCs, but not mature-ECs, were capable of actively releasing NRG1, which, in turn, reduced apoptosis and increased the proliferation of iCMs via the PI3K/Akt signaling pathway. Transcriptional silencing of NRG1 abrogated these cardioprotective effects. Our study suggests that ECFCs are uniquely suited to support human iCMs, making these progenitor cells ideal for cardiovascular regenerative medicine.

Staged ventricular recruitment and biventricular conversion following single-ventricle palliation in unbalanced atrioventricular canal defects.

Objective: Restoration of biventricular circulation is an alternative management strategy in unbalanced atrioventricular canal defects (uAVCDs), especially in patients with risk factors for single-ventricle palliation (SVP) failure. When ventricular volume is inadequate for biventricular circulation, recruitment procedures may accommodate its growth. In this study, we review our uAVCD experience with biventricular conversion (BIVC) after prior SVP. Methods: This is a single-institution, retrospective cohort study of uAVCD patients who underwent BIVC after SVP, with staged recruitment (staged) or primary BIVC (direct) between 2003 to 2018. Mortality, unplanned reinterventions, imaging, and catheterization data were analyzed. Results: Sixty-five patients underwent BIVC from SVP (17 stage 1, 42 bidirectional Glenn, and 6 Fontan). Decision for conversion was based on poor SVP candidacy (n = 43) or 2 adequately sized ventricles (n = 22). Of the 65 patients, 20 patients underwent recruitment before conversion. The staged group had more severe ventricular hypoplasia than the direct group, reflected in prestaging end-diastolic volume z scores (-4.0 vs -2.6; P < .01), which significantly improved after recruitment (-4.0 to -1.8; P < .01). Median follow-up time was 1.0 years. Survival and recatheterizations were similar between both groups (hazard ratio, 0.9; 95% CI, 0.2-3.7; P = .95 and hazard ratio, 1.9; 95% CI, 0.9-4.1; P = .09), but more reoperations occurred with staged approach (hazard ratio, 3.1; 95% CI, 1.3-7.1; P = .01). Conclusions: Biventricular conversion from SVP is an alternative strategy to manage uAVCD, particularly when risk factors for SVP failure are present. Severe forms of uAVCDs can be converted with staged BIVC with acceptable mortality, albeit increased reinterventions, when primary BIVC is not possible.

The Impact of Congenital Cardiac Surgery Fellowship on Training and Practice.

BACKGROUND: In 2007, congenital cardiac surgery became a recognized fellowship by the American Council of Graduate Medical Education (ACGME). Beginning in 2023, the fellowship transitioned from a 1-year to a 2-year program. Our objective is to provide current benchmarks by surveying current training programs and assessing characteristics contributing to career success. METHODS: This was a survey-based study in which tailored questionnaires were distributed to program directors (PDs) and graduates of the ACGME accredited training programs. Data collection included responses to multiple-choice and open-ended questions relevant to didactics, operative training, training center characteristics, mentorship, and employment characteristics. Results were analyzed using summary statistics and subgroup and multivariable analyses. RESULTS: The survey yielded responses from 13 of 15 PDs (86%) and 41 of 101 graduates (41%) from ACGME accredited programs. Perceptions among PDs and graduates were somewhat discordant, with PDs more optimistic than graduates. Of PDs, 77% (n = 10) believed current training adequately prepares fellows and is successful in securing employment for graduates. The responses from graduates demonstrated 30% (n = 12) were dissatisfied with operative experience and 24% (n = 10) with overall training. Being supported during the first 5 years of practice was significantly associated with retention in congenital cardiac surgery and greater practicing case volumes. CONCLUSIONS: Dichotomous views exist between graduates and PDs regarding success in training. Mentorship during the early career was associated with increased case volumes, career satisfaction, and retention in the congenital cardiac surgery field. Educational bodies should incorporate these elements during training and after graduation.

Photopolymerizable Hydrogel for Enhanced Intramyocardial Vascular Progenitor Cell Delivery and Post-Myocardial Infarction Healing.

Cell transplantation success for myocardial infarction (MI) treatment is often hindered by low engraftment due to washout effects during myocardial contraction. A clinically viable biomaterial that enhances cell retention can optimize intramyocardial cell delivery. In this study, a therapeutic cell delivery method is developed for MI treatment utilizing a photocrosslinkable gelatin methacryloyl (GelMA) hydrogel. Human vascular progenitor cells, capable of forming functional vasculatures upon transplantation, are combined with an in situ photopolymerization approach and injected into the infarcted zones of mouse hearts. This strategy substantially improves acute cell retention and promotes long-term post-MI cardiac healing, including stabilized cardiac functions, preserved viable myocardium, and reduced cardiac fibrosis. Additionally, engrafted vascular cells polarize recruited bone marrow-derived neutrophils toward a non-inflammatory phenotype via transforming growth factor beta (TGFß) signaling, fostering a pro-regenerative microenvironment. Neutrophil depletion negates the therapeutic benefits generated by cell delivery in ischemic hearts, highlighting the essential role of non-inflammatory, pro-regenerative neutrophils in cardiac remodeling. In conclusion, this GelMA hydrogel-based intramyocardial vascular cell delivery approach holds promise for enhancing the treatment of acute myocardial infarction.

The Ventricular Switch: An Alternative Strategy Toward Biventricular Repair in Moderately Hypoplastic Left Ventricles or Complex Connections.

Hypoplastic left heart complex (HLHC) constitutes a spectrum of left ventricular hypoplasia and valvar disease and can be associated with increased morbidity and mortality. Traditionally, management of these lesions involves single ventricle palliation (SVP). However, the SVP may be associated with substantial long-term consequences related to its physiology. Alternative management strategies have been employed to achieve biventricular circulation. We have proposed a novel technique, termed the "ventricular switch" procedure, in which the hypoplastic or unroutable left ventricle can be harnessed to function as the subpulmonic ventricle, and the right ventricle functions as the systemic ventricle. Herein, we describe our rationale for considering biventricular circulation and the ventricular switch procedure in HLHC and in other complex lesions.

Double Switch in Congenitally Corrected Transposition of the Great Arteries With Incomplete Atrioventricular Septal Defect, Ebsteinoid Tricuspid Valve, Ventricular Outflow Tract Obstructions, and Multiple VSDs.

We describe the management of a 2 month-old male (BSA 0.27 m2) with congenitally corrected transposition of the great arteries (CCTGA), left and right ventricular outflow tract obstruction, incomplete atrioventricular (AV) canal defect, Ebsteinoid left AV valve, and multiple VSDs. In short, the patient presented with respiratory failure, metabolic acidosis with worsening AV valve regurgitation, and acute decompensation from pulmonary overcirculation. We performed a complex double switch operation described below. Despite the unique anatomical complexities, the patient's successful course demonstrates the importance of multidisciplinary discourse, preoperative imaging and planning, and intraoperative decision making from patient selection to anatomic repair.

Major Aortopulmonary Collateral Arteries Requiring Percutaneous Intervention Following the Arterial Switch Operation: A Case Series and Systematic Review.

Background: Dextro transposition of the great arteries (d-TGA) is the most common critical congenital cardiac defect surgically treated in the neonatal period by arterial switch operation (ASO). Major aortopulmonary collaterals (MAPCAs) can be present in this population and may complicate the early postoperative period. Our aim was to review our institutional data and systematically review the available literature to provide further insight on the clinical significance of MAPCAs during the early postoperative course after ASO. Methods: This is a retrospective study of patients with simple d-TGA who underwent ASO between March 1998 and September 2020 at Boston Children's Hospital. The MEDLINE, Embase, and Cochrane databases were searched from inception to June 2020. Results: Of the 671 d-TGA patients who underwent ASO at our center, 13 (1.9%) were diagnosed with MAPCAs. Five were diagnosed before ASO, while eight were diagnosed after ASO. Of these, two patients required catheterization for MAPCAs coiling during the same hospitalization on the 2nd and 11th postoperative days. The systematic review retrieved a total of 34 articles after duplicates were removed. Finally, nine studies reporting on 23 patients were deemed eligible for our analysis. The average time to MAPCAs coiling was 12 days, while the mean hospital stay was 36 days. Conclusions: MAPCAs should be included in the differential diagnosis of ASO complicated by cardiac or respiratory failure, or pulmonary hemorrhage acutely postoperatively. Once managed, recovery of these patients is predictable, and mortality is low. Further studies investigating the diagnostic value of echocardiography and the long-term outcomes of these MAPCAs are necessary.

Long-term outcomes of truncus arteriosus repair: A modulated renewal competing risks analysis.

OBJECTIVE: In this study, we sought to identify independent risk factors for mortality and reintervention after early surgical correction of truncus arteriosus using a novel statistical method. METHODS: Patients undergoing neonatal/infant truncus arteriosus repair between January 1984 and December 2018 were reviewed retrospectively. An innovative statistical strategy was applied integrating competing risks analysis with modulated renewal for time-to-event modeling. RESULTS: A total of 204 patients were included in the study. Mortality occurred in 32 patients (15%). Smaller right ventricle to pulmonary artery conduit size and truncal valve insufficiency at birth were significantly associated with overall mortality (right ventricle to pulmonary artery conduit size: hazard ratio, 1.34; 95% confidence interval, 1.08-1.66, P = .008; truncal valve insufficiency: hazard ratio, 2.5; 95% confidence interval, 1.13-5.53, P = .024). truncal valve insufficiency at birth, truncal valve intervention at index repair, and number of cusps (4 vs 3) were associated with truncal valve reoperations (truncal valve insufficiency: hazard ratio, 2.38; 95%, confidence interval, 1.13-5.01, P = .02; cusp number: hazard ratio, 6.62; 95% confidence interval, 2.54-17.3, P < .001). Right ventricle to pulmonary artery conduit size 11 mm or less was associated with a higher risk of early catheter-based reintervention (hazard ratio, 1.54; 95% confidence interval, 1.04-2.28, P = .03) and reoperation (hazard ratio, 1.96; 95% confidence interval, 1.33-2.89, P = .001) on the right ventricle to pulmonary artery conduit. CONCLUSIONS: Smaller right ventricle to pulmonary artery conduit size and truncal valve insufficiency at birth were associated with overall mortality after truncus arteriosus repair. Quadricuspid truncal valve, the presence of truncal valve insufficiency at the time of diagnosis, and truncal valve intervention at index repair were associated with an increased risk of reoperation. The size of the right ventricle to pulmonary artery conduit at index surgery is the single most important factor for early reoperation and catheter-based reintervention on the conduit.

Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment.

Endocardial fibroelastosis (EFE) is defined by fibrotic tissue on the endocardium and forms partly through aberrant endothelial-to-mesenchymal transition. However, the pathologic triggers are still unknown. In this study, we showed that abnormal flow induces EFE partly through endothelial-to-mesenchymal transition in a rodent model, and that losartan can abrogate EFE development. Furthermore, we translated our findings to human endocardial endothelial cells, and showed that laminar flow promotes the suppression of genes associated with mesenchymal differentiation. These findings emphasize the role of flow in promoting EFE in endocardial endothelial cells and provide a novel potential therapy to treat this highly morbid condition.

An updated meta-analysis of MitraClip versus surgery for mitral regurgitation.

BACKGROUND: Although studies demonstrate its feasibility, there is ongoing debate on the short and long-term outcomes of MitraClip versus surgical repair or mitral valve replacement (MVR). The objective of this meta-analysis is to compare the safety, morbidity, mortality and long-term function following MitraClip compared to MVR. METHODS: Articles were searched in PubMed and Cochrane databases for studies comparing outcomes of MitraClip and surgery on December 1, 2019. Eligible prospective, retrospective, randomized and non-randomized studies were reviewed. RESULTS: A total of nine studies (n=1,873, MitraClip =533, MVR =644) were eligible for review. At baseline, MitraClip patients had more comorbidities than MVR patients, including myocardial infarction (P<0.001), chronic obstructive pulmonary disease (P=0.022) and chronic kidney disease (P<0.001). MitraClip was associated with shorter length of stay (-3.86 days; 95% CI, -4.73 to -2.99; P<0.01) with a similar safety profile. Residual moderate-to-severe mitral regurgitation was more frequent in MitraClip at discharge (OR, 2.81; 95% CI, 1.39-5.69; P<0.01) and at five years (OR, 2.46; 95% CI, 1.54-3.94; P<0.01), and there was a higher need for reoperation on the MitraClip group at latest follow-up (OR, 5.28; 95% CI, 3.43-8.11; P<0.01). The overall mortality was comparable between the two groups (HR, 2.06; 95% CI, 0.98-4.29; P=0.06) for a mean follow-up of 4.8 years. CONCLUSIONS: Compared to surgery, MitraClip demonstrates a similar safety profile and shorter length of stay in high-risk patients, at the expense of increased residual mitral regurgitation and higher reoperation rate. Despite this, long term mortality appears comparable between the two techniques, suggesting that a patient-tailored approach will lead to optimal results.

Postoperative Physician Phone Calls as a Method to Decrease Urgent Care and Emergency Department Returns After Ambulatory General Surgery.

Unplanned returns after ambulatory surgery pose a burden to patients and health care providers alike. We hypothesized that a postoperative phone call by a physician would decrease avoidable returns to urgent care (UC) or the emergency department (ED) in the week after anorectal (AR), laparoscopic cholecystectomy (LC), inguinal hernia repair (IHR), and umbilical hernia repair (UHR) operations. A retrospective analysis from 1/2011 to 12/2015 across 14 Kaiser hospitals was conducted to determine baseline UC/ED return rates of patients pre-call. Between 10/2017 and 06/2019, physicians placed phone calls to patients within postoperative days (PODs) 1-4. The cohorts were compared using chi-squared analysis with significance determined at P < .05. In total, 276 patients received a call, with the majority placed on PODs 1-3. There were no statistically significant differences in return rates between the pre- and post-call groups. All of the AR, 50.0% of LC, 66.7% of IHR, and 50.0% of UHR patients returned prior to phone call placement. Our data indicate that a physician phone call does not help in decreasing UC/ED returns. However, it is noteworthy that many of the returns occurred pre-call placement. Future directions should be aimed at placing earlier postoperative phone calls.

Plasmacytoid Dendritic Cell-driven Induction of Treg Is Strain Specific and Correlates With Spontaneous Acceptance of Kidney Allografts.

BACKGROUND: DBA/2J kidney allografts, but not heart allografts, are spontaneously accepted indefinitely in C57BL/6 (B6) mice, through regulatory tolerance mechanism dependent on Foxp3 cells. In contrast, B6 kidneys are rejected within a week in DBA/2J recipients. We hypothesized that the tolerogenic difference of the kidneys might be due to differences in number or function of plasmacytoid dendritic cells (pDCs), because these cells are potent inducers of Foxp3 cells. METHODS: pDCs from murine bone marrow, native kidneys, and spontaneously accepted kidney allografts were analyzed using flow cytometry and immunohistochemical staining. Naive T cells were cocultured with pDCs in specific strain combinations and analyzed for FoxP3 induction and functionality. MEK/ERK and NFκB inhibitors were used to assess the regulatory T-cell induction pathways. pDCs and T-cell cultures were adoptively transferred before heterotopic heart transplantation to assess allograft survival. RESULTS: DBA/2J pDCs were more potent in inducing Foxp3 in B6 T cells than the reverse combination, correlating with survival of the kidney allografts. Foxp3 induction by pDCs in vitro was dependent on pDC viability, immaturity, and class II MHC mismatch and blocked by MEK/ERK and NFκB inhibition. pDC-induced Foxp3 T cells suppressed proliferation of B6 T cells in vitro, and adoptive transfer into B6 recipients 2 weeks before heterotopic DBA/2J heart transplantation resulted in prolonged allograft survival. CONCLUSIONS: These data suggest that pDC-induced regulatory T cells are dependent on downstream signaling effects and on strain-dependent, MHC class II disparity with naive T cells, which may explain organ- and strain-specific differences in spontaneous tolerance.