The traditional description of cardiac development involves progression from a cardiac crescent to a linear heart tube, which in the phase of transformation into a mature heart forms a cardiac loop and is divided with the septa into individual cavities. Cardiac morphogenesis involves numerous types of cells originating outside the initial cardiac crescent, including neural crest cells, cells of the second heart field origin, and epicardial progenitor cells. The development of the fetal heart and circulatory system is subject to regulatation by both genetic and environmental processes. The etiology for cases with congenital heart defects (CHDs) is largely unknown, but several genetic anomalies, some maternal illnesses, and prenatal exposures to specific therapeutic and non-therapeutic drugs are generally accepted as risk factors. New techniques for studying heart development have revealed many aspects of cardiac morphogenesis that are important in the development of CHDs, in particular transposition of the great arteries.

Aims Centrifugal continuous flow pumps are currently the state of the art in left ventricular assist device therapy. This study was conducted to compare the results after implantation of the HVAD® and the HeartMate 3®. Methods and results We retrospectively analysed preoperative and post‐operative patient data of all 106 patients, who received a HeartMate 3 (HM3) at our centre between 2014 and 2018. A total of 392 patients receiving a sintered HVAD® served as controls. Patient matching was performed for age, sex, Interagency Registry for Mechanically Assisted Circulatory Support level at the time of implant, perioperative right heart failure, and implantation strategy, that is, bridge to transplant or destination therapy, as well as preoperative renal function, that is, as indicated by serum creatinine levels. A total of 79 matched pairs could be identified. During a median follow‐up of 15.3 months (range: 0–30 months), 23 (29.1%) and 19 (24.1%) patients died in the HVAD and HM3 groups, respectively, with a hazard ratio for mortality of 0.84 [95% confidence interval (CI): 0.46–1.54; P = 0.568]. Freedom from cerebrovascular events did not differ significantly between study groups, with a hazard ratio of 0.57 (95% CI: 0.23–1.45; P = 0.241). The risk of driveline infection was significantly lower in the HM3 (n = 33) than in the HVAD (n = 55) group (hazard ratio = 0.54; 95% CI: 0.35–0.84; P = 0.006). Eight HVAD, but no HM3, patients developed a pump thrombosis during follow‐up (P = 0.148). Conclusions Performance of both currently used centrifugal left ventricular assist device systems is comparable in terms of short‐term patient survival and freedom from cerebrovascular events. In our single‐centre experience, HM3 patients less frequently develop driveline infections and no pump thrombosis, which requires further evaluation.

Mechanical circulatory support gained a significant value in the armamentarium of heart failure therapy because of the increased awareness of the prevalence of heart failure and the tremendous advances in the field of mechanical circulatory support during the last decades. Current device technologies already complement a heart transplant as the gold standard of treatment for patients with end-stage heart failure refractory to conservative medical therapy. This article reviews important aspects of mechanical circulatory support therapy and focuses on currently debated issues.

We report a case of severe outflow graft infection following left ventricular assist device (LVAD) implantation. A 51-year old male LVAD patient was readmitted to our hospital presenting signs of systemic infection. One year previously, LVAD implantation (HeartMate3, Abbott, Chicago, IL, USA) with concomitant patent foramen ovale closure had been performed in the context of end-stage heart failure due to dilative cardiomyopathy (INTERMACS III). The indication for LVAD-therapy was bridge-to-candidacy, since the patient did not instantly fulfill all criteria for cardiac transplantation. At admission, a PET-CT scan unveiled fluid accumulation, encircling the outflow-graft prosthesis (SUV_max 10.5) with contrast-enhancement involving the intrathoracic driveline (SUV_max 11.2). Since cardiac transplantation was not feasible, the patient underwent surgical revision. In the first step, redo sternotomy was performed with local debridement, including jet lavage. Intraoperative swabs confirmed bacterial infection with staphylococcus aureus. Following this, the patient underwent negative pressure wound therapy (NPWT) with instillation using the V.A.C. VERAFLO system (KCI-3M, San Antonio, TX, USA) for a total of 19 days. Due to the severity of infection, local bacteriophage application was performed within the wound closure. In order to concentrate phage therapy at the infection site, phages were applied using a novel semi-fluid galenic. After wound closure, the patient was discharged with an uneventful course. A control PET-CT scan 3 months after discharge showed a significant decrease in infection (outflow graft: SUV_max 7.2, intrathoracic driveline: SUV_max 3.0) correlated with contrast enhancement. Bacterial infection of intrathoracic VAD components represents a severe and potentially life-threatening complication. If cardiac transplantation is not feasible, complex wound management strategies are required. Local bacteriophage therapy might be a promising addition to already established therapeutical options. In order to improve bacteriophage retention at the wound site, application of a viscous galenic might be beneficial.

Background: The benefit of prophylactic left ventricular (LV) unloading during venoarterial extracorporeal membrane oxygenation (VA-ECMO) in selected patients at risk of developing LV distension remains unclear. Methods: We enrolled 136 patients treated with Impella pump decompression during VA-ECMO therapy for refractory cardiogenic shock. Patients were stratified by specific indication for LV unloading in the prophylactic vs. bail-out group. The bail-out unloading strategy was utilized to treat LV distension in VA-ECMO afterload-associated complications. The primary endpoint was all-cause 30-day mortality after VA-ECMO implantation. The secondary endpoint was successful myocardial recovery, transition to durable mechanical circulatory support (MCS), or heart transplantation. Results: After propensity score matching, prophylactic unloading was associated with a significantly lower 30-day mortality risk (risk ratio 0.38, 95% confidence interval 0.23–0.62, and p < 0.001) and a higher probability of myocardial recovery (risk ratio 2.9, 95% confidence interval 1.48–4.54, and p = 0.001) compared with the bail-out strategy. Heart transplantation or durable MCS did not differ significantly between groups. Conclusions: Prophylactic unloading compared with the bail-out strategy may improve clinical outcomes in selected patients on VA-ECMO. Nevertheless, randomized trials are needed to validate these results.