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BackgroundCardiac physiology changes after heart transplant (HT), resulting in a restrictive physiology with an increase in both arterial elastance (Ea) and ventricular elastance (Ees). This leads to a higher susceptibility to develop afterload mismatch, although the early identification of this phenomenon has not yet been explored. The aim of this study is to identify the presence of afterload mismatch after HT, its determinants, and its impact on cardiac mortality.MethodsWe conducted an observational, single-centre study based on the historical cohort of patients who underwent HT from 1985 to 2015 at our institution. We included patients who had survived the first year after HT with left ventricular ejection fraction (LVEF) ≥ 50%, International Society of Heart and Lung Transplantation (ISHLT) cardiac allograft vasculopathy of grade 0–1, and ISHLT acute cellular rejection of grade 0–1R at 1 year after HT. Ea and Ees were calculated using a non-invasive method based on blood pressure and end-systolic volume and end-diastolic volume measured at transthoracic echocardiography. Patients were grouped in 3 categories according to the presence of increased afterload and afterload mismatch as follows: low afterload (LA - Ea lower the median), matched high afterload (MHA - Ea higher of equal than the median, Ees higher or equal than the median), afterload mismatch (AM - Ea higher or equal than the median, Ees lower than the median). The impact of AM on long-term outcome, defined as cardiac mortality, was investigated, as well as predictors of AM.ResultsThe study cohort consisted of 345 HT patients. The median of Ea and Ees were 4.0 mmHg/mL and 6.75 mmHg/mL, respectively. 49 patients (13%) developed AM, while LA and MHA groups accounted for 49% and 36% of the cohort, respectively. Patients with AM were mostly male (91%), with ischemic heart disease (45%) and a higher percentage of left ventricular assisted device prior to HT (8%). LVEF was lower in AM (57% vs 63% and 64% for LA and MHA respectively, p < 0.0001), while stroke volume was lower than LA and similar to MHA (27 ml vs 35 mL and 26 mL for LA and MHA respectively, p = 0.0001 ). Predictors of AM were male recipient from male donor (Mr/Md) (β 015, p = 0.0067) and Mr from female donor (Mr/Fd) (β 0.6, p = 0.0078). After a median of 11.3-year follow-up, 59 HT recipients died. Cardiac mortality was higher in AM than in the other groups (AM median survival 17.2 y vs 27.8 y and 24.1 y for LA and MHA respectively, log-rank p = 0.005). After adjusting for confounding variables, AM was a predictor of cardiac mortality (HR: 2.26; 95%CI 1.18 – 4.35), such as Mr/Fd (HR 2.94; 95%CI 1.18 – 4.35, p = 0.0358).ConclusionAM, in the context of a normal LVEF, is associated with male donor and sex mismatch, and negatively affects long-term outcome after HT.Abstract 144 Figure 1Cardiac mortality across the 3 groups of afterload conditionsAbstract 144 Figure 2Univariable and multivariable Cox proportional hazard modelConflict of InterestHeart Failure Unit

The United Network for Organ Sharing (UNOS) adopted new criteria for the heart allocation score on October 18, 2018 to reflect the changing trends of candidates’ mortality while awaiting transplant. We examined the impact of these policy changes on rates of left ventricular assist device (LVAD) implantation and outcomes after transplant from a relatively newer UNOS database. The UNOS registry was used to identify first-time adult heart recipients with LVAD at listing or transplant who underwent transplantation between January 1, 2016 and March 10, 2020. Survival data were collected through March 30, 2023. Those listed before October 18, 2018 but transplanted after were excluded. Patients were divided into before or after change groups. Demographics and clinical parameters were compared. Survival was analyzed with Kaplan–Meier curves and log-rank tests. A p <0.05 was considered significant. We identified 4,387 heart recipients with LVAD in the before (n = 3,606) and after (n = 781) score change eras. The after group had a lower rate of LVAD implantation while listed than the before group (20.4% vs 34.9%, p <0.0001), and were more likely to be female (25.1% vs 20.2%, p = 0.002); in both groups, most recipients (62.8%) were white. There was significantly farther distance from the donor hospital to transplant center in the after group (264.4 NM vs 144.2 NM, p <0.0001) and decreased waitlist days (84.9 ± 105.1 vs 369.2 ± 459.5, p <0.0001). Recipients in the after group were more likely to use extracorporeal membrane oxygenation (3.7% vs 0.5%, p <0.0001) and intravenous inotropes (19.1% vs 7.5%, p <0.0001) and receive a Centers for Disease Control and Prevention increased risk donor organ (37.9% vs 30.5%, p <0.0001). Survival at 3 years was comparable between the 2 groups. The allocation score change in 2018 yielded considerable changes in mechanical circulatory support device implantation strategy and outcomes. The rate of LVAD implantation decreased with increased utilization of temporary mechanical circulatory support devices.

Heart failure is a serious and challenging medical condition characterized by the inability of the heart to pump blood effectively, leading to reduced blood flow to organs and tissues. Several underlying causes may be linked to this, including coronary artery disease, hypertension, or previous heart attacks. Therefore, it is a chronic condition that requires ongoing management and medical attention. HF affects >64 million individuals worldwide. Heart transplantation remains the gold standard of treatment for patients with end-stage cardiomyopathy. The recruitment of marginal donors may be considered an asset at the age of cardiac donor organ shortage. Primary graft dysfunction (PGD) is becoming increasingly common in the new era of heart transplantations. PGD is the most common cause of death within 30 days of cardiac transplantation. Mechanical Circulatory Support (MCS), particularly venoarterial extracorporeal membrane oxygenation (V-A ECMO), is the only effective treatment for severe PGD. VA-ECMO support ensures organ perfusion and provides the transplanted heart with adequate rest and recovery. In the new era of heart transplantation, early use allows for increased patient survival and careful management reduces complications.

Recurrence of cardiac sarcoidosis (CS) and giant cell myocarditis (GCM) after heart transplant is rare, with rates of 5% in CS and 8% in GCM. We aim to identify all reported cases of recurrence in the literature and to assess clinical course, treatments, and outcomes to improve understanding of the conditions. A systematic review, utilizing Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) guidelines, was conducted by searching MEDLINE/PubMed and Embase of all available literature describing post-transplant recurrent granulomatous myocarditis, CS, or GCM. Data on demographics, transplant, recurrence, management, and outcomes data were collected from each publication. Comparison between the 2 groups were made using standard statistical approaches. Post-transplant GM recurrence was identified in 39 patients in 33 total publications. Reported cases included 24 GCM, 12 CS, and 3 suspected cases. Case reports were the most frequent form of publication. Mean age of patients experiencing recurrence was 42 years for GCM and 48 years for CS and favored males (62%). Time to recurrence ranged from 2 weeks to 9 years post-transplant, occurring earlier in GCM (mean 1.8 vs 3.0 years). Endomyocardial biopsies (89%) were the most utilized diagnostic method over cardiac magnetic resonance and positron emission tomography. Recurrence treatment regimens involved only steroids in 40% of CS, whereas other immunomodulatory regimens were utilized in 70% of GCM. In conclusion, GCM and CS recurrence after cardiac transplantation holds associated risks including concurrent acute cellular rejection, a higher therapeutic demand for GCM recurrence compared with CS, and mortality. New noninvasive screening techniques may help modify post-transplant monitoring regimens to increase both early detection and treatment of recurrence.

Alcoholic-dilated Cardiomyopathy (ACM) is the most prevalent form of ethanol-induced heart damage. Ethanol induces ACM in a dose-dependent manner, independently of nutrition, vitamin, or electrolyte disturbances. It has synergistic effects with other heart risk factors. ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias. Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular [Ca2+] transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms. The final process of ACM is the result of dosage and individual predisposition. The ACM prognosis depends on the degree of persistent ethanol intake. Abstinence is the preferred goal, although controlled drinking may still improve cardiac function. New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage. Growth factors and cardiomyokines are relevant molecules that may modify this process. Cardiac transplantation is the final measure in end-stage ACM but is limited to those subjects able to achieve abstinence.

Partial heart transplantation (PHT) is a novel surgical approach that involves transplantation of only the part of the heart containing a valve. The rationale for this approach is to deliver growing heart valve implants that reduce the need for future re-operations in children. However, prior to clinical application of this approach, it was important to assess it in a preclinical model. To investigate PHT short-term outcomes and safety, we performed PHT in a piglet model. Yorkshire piglets (n = 14) were used for PHT of the pulmonary valve. Donor and recipient pairs were matched based on blood types. The piglets underwent PHT at an average age of 44 days (range 34–53). Post-operatively, the piglets were monitored for a period of two months. Of the 7 recipient piglets, one mortality occurred secondary to anesthesia complications while undergoing a routine echocardiogram on post-operative day 19. All piglets had appropriate weight gain and laboratory findings throughout the post-operative period indicating a general state of good health and rehabilitation after undergoing PHT. We conclude that PHT has good short-term survival in the swine model. PHT appears to be safe for clinical application.

Post-transplant lymphoproliferative disorders (PTLD) are heterogenous lymphoproliferative disorders that develop as a consequence of immunosuppression in transplant recipients. We sought to determine if subtypes of PTLD correlated with different outcomes. We performed a retrospective review of PTLD occurring in pediatric heart transplant recipients. A total of 558 children and infants underwent cardiac transplantation at our institution between 1985 and 2019 and were followed until March 2021. Forty-nine of 558 patients developed PTLD (8.8%). As compared to older children (>one year of age), infant recipients (

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