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Objectives Patients with congenital heart disease frequently require surgical or percutaneous interventional valve replacement after initial congenital heart defect (CHD) repair. In some of these patients, simultaneous replacement of both semilunar valves is necessary, resulting in increased procedural complexity, morbidity, and mortality. In this study, we analyze the outcomes of simultaneous aortic and pulmonary valve replacements following multiple surgical interventions for CHD. Methods This was a retrospective study of 24 patients who after initial repair of CHD underwent single-stage aortic and pulmonary valve replacement at our institution between 2003 and 2021. Results The mean age of the patients was 28 ± 13 years; the mean time since the last surgery was 15 ± 11 years. Decellularized valved homografts (DVHs) were used in nine patients, and mechanical valves were implanted in seven others. In eight patients, DVHs, biological, and mechanical valves were implanted in various combinations. The mean cardiopulmonary bypass time was 303 ± 104 minutes, and aortic cross-clamp time was 152 ± 73 minutes. Two patients died at 12 and 16 days postoperatively. At a maximum follow-up time of 17 years (mean 7 ± 5 years), 95% of the surviving patients were categorized as New York Heart Association heart failure class I. Conclusion Single-stage aortic and pulmonary valve replacement after initial repair of CHD remains challenging with substantial perioperative mortality (8.3%). Nevertheless, long-term survival and clinical status at the latest follow-up were excellent. The valve type had no relevant impact on the postoperative course. The selection of the valves for implantation should take into account operation-specific factors—in particular reoperability—as well as the patients' wishes. [ABSTRACT FROM AUTHOR]

Immune rejection remains the major obstacle to long-term survival of allogeneic lung transplants. The expression of major histocompatibility complex molecules and minor histocompatibility antigens triggers allogeneic immune responses that can lead to allograft rejection. Transplant outcomes therefore depend on long-term immunosuppression, which is associated with severe side effects. To address this problem, we investigated the effect of genetically engineered transplants with permanently down-regulated swine leukocyte antigen (SLA) expression to prevent rejection in a porcine allogeneic lung transplantation (LTx) model. Minipig donor lungs with unmodified SLA expression (control group, n = 7) or with modified SLA expression (treatment group, n = 7) were used to evaluate the effects of SLA knockdown on allograft survival and on the nature and strength of immune responses after terminating an initial 4-week period of immunosuppression after LTx. Genetic engineering to down-regulate SLA expression was achieved during ex vivo lung perfusion by lentiviral transduction of short hairpin RNAs targeting mRNAs encoding β2-microglobulin and class II transactivator. Whereas all grafts in the control group were rejected within 3 months, five of seven animals in the treatment group maintained graft survival without immunosuppression during the 2-year monitoring period. Compared with controls, SLA-silenced lung recipients had lower donor-specific antibodies and proinflammatory cytokine concentrations in the serum. Together, these data demonstrate a survival benefit of SLA–down-regulated lung transplants in the absence of immunosuppression. Editor's summary: Solid organ transplants have saved the lives of many with late-stage organ failure. However, the need to match major histocompatibility complex (MHC) molecules reduces the number of donor-recipient pairs and results in long waits for donor organs. A strategy to avoid the need for MHC matching is to knock down MHC expression in the transplanted organ altogether. Here, Figueiredo et al. transplanted lungs that underwent gene engineering to knock down MHC expression in recipient pigs. This approach, which relied on lentiviral vectors carrying shRNAs against B2M and CIITA, effectively hid the donor lungs from the immune system, enabling long-term graft survival. Together, these results suggest that MHC knockdown may be a feasible strategy to improve graft survival after solid organ transplantation. —Courtney Malo [ABSTRACT FROM AUTHOR]

Introduction: Acute type A aortic dissection (ATAAD) is one of the most critical emergencies in cardiovascular surgery. Additional complications such as organ malperfusion can significantly decrease the chances of survival. Despite promptly performed surgical treatment, impaired organ perfusion may persist, thus close postoperative monitoring is recommended. But, is there a surgical consequence due to the existence of a preoperatively known malperfusion and is there a correlation between pre-, peri- and postoperative levels of serum lactate and proven malperfusion? Methods: Between 2011 and 2018, 200 patients (66% male; median age: 62.5 years; interquartile range: +/−12.4 years) that received surgical treatment at our institution for an acute dissection DeBakey type I were enrolled in this study. The cohort was divided into two groups according to the preoperative existence of malperfusion and non-malperfusion. At least one kind of malperfusion occurred in 74 patients (Group A: 37%), while 126 patients (Group B: 63%) showed no evidence of malperfusion. Furthermore, lactate levels of both cohorts were differentiated into four periods: preoperative, intraoperative, 24 hours after surgery, and 2–4 days after surgery. Results: The patients' status differed significantly prior to surgery. Group A (malperfusion) showed an elevated requirement for mechanical resuscitation (A: 10.8%; B: 5.6%; p : 0.173), were significantly more often admitted in an intubated state (A: 14.9%; B: 2.4%; p : 0.001) and showed higher incidences of stroke (A: 18.9% (n = 149); B: 3.2% (n = 4); p : 0.001). Levels of serum lactate from the preoperative period until days 2–4 were significantly increased in the malperfusion cohort at all times. Conclusions: Preexisting malperfusion due to ATAAD may significantly increase the chance of early mortality in patients with ATAAD. Serum lactate levels were a reliable marker for inadequate perfusion from admission until day 4 after surgery. Despite this, early intervention survival in this cohort remains limited. [ABSTRACT FROM AUTHOR]

The pathophysiology of pulmonary hypertension (PH) is not fully understood. Here, we tested the hypothesis that hypoxic perfusion of the vasa vasorum of the pulmonary arterial (PA) wall causes PH. Young adult pig lungs were explanted and placed into a modified ex vivo lung perfusion unit (organ care system, OCS) allowing the separate adjustment of parameters for mechanical ventilation, as well as PA perfusion and bronchial arterial (BA) perfusion. The PA vasa vasorum are branches of the BA. The lungs were used either as the control group ( n = 3) or the intervention group ( n = 8). The protocol for the intervention group was as follows: normoxic ventilation and perfusion (steady state), hypoxic BA perfusion, steady state, and hypoxic BA perfusion. During hypoxic BA perfusion, ventilation and PA perfusion maintained normal. Control lungs were kept under steady-state conditions for 105 min. During the experiments, PA pressure (PAP) and blood gas analysis were frequently monitored. Hypoxic perfusion of the BA resulted in an increase in systolic and mean PAP, a reaction that was reversible upon normoxic BA perfusion. The PAP increase was reproducible during the second hypoxic BA perfusion. Under control conditions, the PAP stayed constant until about 80 min of the experiment. In conclusion, the results of the current study prove that hypoxic perfusion of the vasa vasorum of the PA directly increases PAP in an ex situ lung perfusion setup, suggesting that PA vasa vasorum function and wall ischemia may contribute to the development of PH. NEW & NOTEWORTHY Hypoxic perfusion of the vasa vasorum of the pulmonary artery directly increased pulmonary arterial pressure in an ex vivo lung perfusion setup. This suggests that the function of pulmonary arterial vasa vasorum and wall ischemia may contribute to the development of pulmonary hypertension.

Objectives: Decellularized aortic homografts (DAH) were introduced as a new option for aortic valve replacement for young patients., Methods: A prospective, EU-funded, single-arm, multicentre study in 8 centres evaluating non-cryopreserved DAH for aortic valve replacement., Results: A total of 144 patients (99 male) were prospectively enrolled in the ARISE Trial between October 2015 and October 2018 with a median age of 30.4 years [interquartile range (IQR) 15.9-55.1]; 45% had undergone previous cardiac operations, with 19% having 2 or more previous procedures. The mean implanted DAH diameter was 22.6 mm (standard deviation 2.4). The median operation duration was 312 min (IQR 234-417), the median cardiopulmonary bypass time was 154 min (IQR 118-212) and the median cross-clamp time 121 min (IQR 93-150). No postoperative bypass grafting or renal replacement therapy were required. Two early deaths occurred, 1 due to a LCA thrombus on day 3 and 1 due ventricular arrhythmia 5 h postoperation. There were 3 late deaths, 1 death due to endocarditis 4 months postoperatively and 2 unrelated deaths after 5 and 7 years due to cancer and Morbus Wegener resulting in a total mortality of 3.47%. After a median follow-up of 5.9 years [IQR 5.1-6.4, mean 5.5 years. (standard deviation 1.3) max. 7.6 years], the primary efficacy end-points peak gradient with median 11.0 mmHg (IQR 7.8-17.6) and regurgitation of median 0.5 (IQR 0-0.5) of grade 0-3 were excellent. At 5 years, freedom from death/reoperation/endocarditis/bleeding/thromboembolism were 97.9%/93.5%/96.4%/99.2%/99.3%, respectively., Conclusions: The 5-year results of the prospective multicentre ARISE trial continue to show DAH to be safe for aortic valve replacement with excellent haemodynamics., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery.)