There is a great need for living valve replacements for patients of all ages. Such constructs could be built by tissue engineering, with perspective of the unique structure and biology of the aortic root. The aortic valve root is composed of several different tissues, and careful structural and functional consideration has to be given to each segment and component. Previous work has shown that immersion techniques are inadequate for whole-root decellularization, with the aortic wall segment being particularly resistant to decellularization. The aim of this study was to develop a differential pressure gradient perfusion system capable of being rigorous enough to decellularize the aortic root wall while gentle enough to preserve the integrity of the cusps. Fresh porcine aortic roots have been subjected to various regimens of perfusion decellularization using detergents and enzymes and results compared to immersion decellularized roots. Success criteria for evaluation of each root segment (cusp, muscle, sinus, wall) for decellularization completeness, tissue integrity, and valve functionality were defined using complementary methods of cell analysis (histology with nuclear and matrix stains and DNA analysis), biomechanics (biaxial and bending tests), and physiologic heart valve bioreactor testing (with advanced image analysis of open–close cycles and geometric orifice area measurement). Fully acellular porcine roots treated with the optimized method exhibited preserved macroscopic structures and microscopic matrix components, which translated into conserved anisotropic mechanical properties, including bending and excellent valve functionality when tested in aortic flow and pressure conditions. This study highlighted the importance of (1) adapting decellularization methods to specific target tissues, (2) combining several methods of cell analysis compared to relying solely on histology, (3) developing relevant valve-specific mechanical tests, and (4) in vitro testing of valve functionality.

This work aims to provide a comprehensive description of the characteristics of a group of acute aortic diseases that are all potentially life-threatening and are collectively referred to as acute aortic syndromes (AASs). There have been recent developments in the care and diagnostic plan for AAS. A substantial clinical index of suspicion is required to identify AASs before irreversible fatal consequences arise because of their indefinite symptoms and physical indicators. A methodical approach to the diagnosis of AAS is addressed. Timely and suitable therapy should be started immediately after diagnosis. Improving clinical outcomes requires centralising patients with AAS in high-volume centres with high-volume surgeons. Consequently, the management of these patients benefits from the increased use of aortic centres, multidisciplinary teams and an “aorta code”. Each acute aortic entity requires a different patient treatment strategy; these are outlined below. Finally, numerous preventive strategies for AAS are discussed. The keys to good results are early diagnosis, understanding the natural history of these disorders and, where necessary, prompt surgical intervention. It is important to keep in mind that chest pain does not necessarily correspond with coronary heart disease and to be alert to the possible existence of aortic diseases because once antiplatelet drugs are administered, a blocked coagulation system can complicate aortic surgery and affect prognosis. The management of AAS in “aortic centres” improves long-term outcomes and decreases mortality rates.

Introduction: Pediatric patients with cardiac congenital diseases require heart valve implants that can grow with their natural somatic increase in size. Current artificial valves perform poorly in children and cannot grow; thus, living-tissue-engineered valves capable of sustaining matrix homeostasis could overcome the current drawbacks of artificial prostheses and minimize the need for repeat surgeries.Materials and Methods: To prepare living-tissue-engineered valves, we produced completely acellular ovine pulmonary valves by perfusion. We then collected autologous adipose tissue, isolated stem cells, and differentiated them into fibroblasts and separately into endothelial cells. We seeded the fibroblasts in the cusp interstitium and onto the root adventitia and the endothelial cells inside the lumen, conditioned the living valves in dedicated pulmonary heart valve bioreactors, and pursued orthotopic implantation of autologous cell-seeded valves with 6 months follow-up. Unseeded valves served as controls.Results: Perfusion decellularization yielded acellular pulmonary valves that were stable, no degradable in vivo, cell friendly and biocompatible, had excellent hemodynamics, were not immunogenic or inflammatory, non thrombogenic, did not calcify in juvenile sheep, and served as substrates for cell repopulation. Autologous adipose-derived stem cells were easy to isolate and differentiate into fibroblasts and endothelial-like cells. Cell-seeded valves exhibited preserved viability after progressive bioreactor conditioning and functioned well in vivo for 6 months. At explantation, the implants and anastomoses were intact, and the valve root was well integrated into host tissues; valve leaflets were unchanged in size, non fibrotic, supple, and functional. Numerous cells positive for a-smooth muscle cell actin were found mostly in the sinus, base, and the fibrosa of the leaflets, and most surfaces were covered by endothelial cells, indicating a strong potential for repopulation of the scaffold.Conclusions: Tissue-engineered living valves can be generated in vitro using the approach described here. The technology is not trivial and can provide numerous challenges and opportunities, which are discussed in detail in this paper. Overall, we concluded that cell seeding did not negatively affect tissue-engineered heart valve (TEHV) performance as they exhibited as good hemodynamic performance as acellular valves in this model. Further understanding of cell fate after implantation and the timeline of repopulation of acellular scaffolds will help us evaluate the translational potential of this technology.

Background: Brugada syndrome (BrS) has been associated with sudden cardiac death in otherwise healthy subjects, and drug‐induced BrS accounts for 55% to 70% of all patients with BrS. This study aims to develop a deep convolutional neural network and evaluate its performance in recognizing and predicting BrS diagnosis. Methods and Results: Consecutive patients who underwent ajmaline testing for BrS following a standardized protocol were included. ECG tracings from baseline and during ajmaline were transformed using wavelet analysis and a deep convolutional neural network was separately trained to (1) recognize and (2) predict BrS type I pattern. The resultant networks are referred to as BrS‐Net. A total of 1188 patients were included, of which 361 (30.3%) patients developed BrS type I pattern during ajmaline infusion. When trained and evaluated on ECG tracings during ajmaline, BrS‐Net recognized a BrS type I pattern with an AUC‐ROC of 0.945 (0.921–0.969) and an AUC‐PR of 0.892 (0.815–0.939). When trained and evaluated on ECG tracings at baseline, BrS‐Net predicted a BrS type I pattern during ajmaline with an AUC‐ROC of 0.805 (0.845–0.736) and an AUC‐PR of 0.605 (0.460–0.664). Conclusions: BrS‐Net, a deep convolutional neural network, can identify BrS type I pattern with high performance. BrS‐Net can predict from baseline ECG the development of a BrS type I pattern after ajmaline with good performance in an unselected population.

The race for an ideal cardioplegic solution has remained enthusiastic since the beginning of the modern cardiac surgery era. The Bretschneider solution, belonging to the “intracellular cardioplegic” group, is safe and practical in myocardial protection during ischemic time. Over time, some particular concerns have arisen regarding the effects on cardiac metabolism and postoperative myocardial functioning. This paper reviews the most important standpoints in terms of theoretical and practical analyses.

Background/Objectives: In recent decades, the advantages of minimizing surgical trauma have led to the development of minimally invasive surgical procedures. While the benefits often outweigh the risks, several challenges are encountered that are not present in conventional surgical approaches. Unilateral pulmonary edema (UPE) after mitral interventions performed through a right-sided approach is a rare but potentially life-threatening event. Methods: We present the case of a 49-year-old patient who underwent endoscopic mitral valve repair. Immediately following ICU admission, the patient’s oxygen saturation suddenly dropped, and serous discharge was exteriorized from the endotracheal tube, with a thoracic X-ray revealing right-sided unilateral pulmonary edema. Results: The therapeutical course was complex. The patient developed hemodynamic instability, leading to cardiac arrest, which required cardiopulmonary resuscitation and the initiation of peripheral veno-arterial extracorporeal membrane oxygenation (VA-ECMO). The endotracheal cannula was replaced with a right-sided double-lumen cannula, and the patient was placed on two ventilators operating independently. The patient was weaned off extracorporeal membrane oxygenation (ECMO) on the fifth day and extubated on the sixth postoperative day. Conclusions: We successfully treated this patient using ECMO and independent lung ventilation. Several cases have been described in the literature, but the pathogenesis and risk factors of UPE remain unclear. Management depends on the severity of UPE, but a deeper understanding of its underlying mechanisms could provide cardiac surgeons with enhanced strategies for preventing UPE and implementing timely interventions.