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Musculoskeletal injuries are the most common reason for surgery in severely injured patients. In addition to direct cardiac damage after physical trauma, there is rising evidence that trauma induces secondary cardiac structural and functional damage. Previous research associates hip fractures with the appearance of coronary heart disease: As 25% of elderly patients developed a major adverse cardiac event after hip fracture. 20 male pigs underwent femur fracture with operative stabilization via nailing (unreamed, reamed, RIA I and a new RIA II; each group n = 5). Blood samples were collected 6 h after trauma and the concentration of troponin I and heart-type fatty acid binding protein (HFABP) as biomarkers for EMD were measured. At baseline and 6 h after trauma, transesophageal ECHO (TOE) was performed; and invasive arterial and left ventricular blood pressure were measured to evaluate the cardiac function after femur fracture. A systemic elevation of troponin I and HFABP indicate an early myocardial damage after femur fracture in pigs. Furthermore, various changes in systolic (ejection fraction and cardiac output) and diastolic (left ventricular end-diastolic pressure, mitral valve deceleration time and E/A ratio) parameters illustrate the functional impairment of the heart. These findings were accompanied by the development of valvular dysfunction (pulmonary and tricuspid valve). To the best of our knowledge, we described for the first time the development of functional impairment of the heart in the context of EMD after long bone fracture in pigs. Next to troponin and HFABP elevation, alterations in the systolic and diastolic function occurred and were accompanied by pulmonary and tricuspid valvular insufficiency. Regarding EMD, none of the fracture stabilization techniques (unreamed nailing, reaming, RIA I and RIA II) was superior.

Background: In vitro assessment is mandatory for artificial heart valve development. This study aims to investigate the effects of pulse duplicator features on valve responsiveness, conduct a sensitivity analysis across valve prosthesis types, and contribute on the development of versatile pulse duplicator systems able to perform reliable prosthetic aortic valve assessment under physiologic hemodynamic conditions. Methods: A reference pulse duplicator was established based on literature. Further optimization process led to new designs that underwent a parametric study, also involving different aortic valve prostheses. These designs were evaluated on criteria such as mean pressure differential and pulse pressure (assessed from high‐fidelity pressure measurements), valve opening and closing behavior, flow, and regurgitation. Finally, the resulting optimized setup was tested under five different hemodynamic settings simulating a range of physiologic and pathologic conditions. Results: The results show that both, pulse duplicator design and valve type significantly influence aortic and ventricular pressure, flow, and valve kinematic response. The optimal design comprised key features such as a compliance chamber and restrictor for diastolic pressure maintenance and narrow pulse pressure. Additionally, an atrial reservoir was included to prevent atrial–aortic interference, and a bioprosthetic valve was used in mitral position to avoid delayed valve closing effects. Conclusion: This study showed that individual pulse duplicator features can have a significant effect on valve's responsiveness. The optimized versatile pulse duplicator replicated physiologic and pathologic aortic valve hemodynamic conditions, serving as a reliable characterization tool for assessing and optimizing aortic valve performance. [ABSTRACT FROM AUTHOR]

This article discusses a study that evaluated the potential use of small extracellular vesicles (sEVs) derived from human cardiac progenitor cells (CPCs) for the treatment of acute myocardial infarction (AMI). The study compared the delivery of sEVs through intramyocardial (IM) and intracoronary (IC) routes in a porcine model of AMI. The results showed that IC delivery of sEVs was more effective in reducing scar size, improving heart function, promoting blood vessel growth, and reducing myocardial fibrosis. The study suggests that IC delivery of clinical-grade sEVs could be a promising treatment option for AMI patients, but further research is needed to validate these findings. [Extracted from the article]

Microvascular obstruction (MVO) often occurs in ST-elevation myocardial infarction (STEMI) patients after percutaneous coronary intervention (PCI). Diagnosis and treatment of MVO lack appropriate and established procedures. This study focused on two major points by using an in vitro multiscale flow model, which comprised an aortic root model with physiological blood flow and a microfluidic model of the microcirculation with vessel diameters down to 50 µm. First, the influence of porcine microthrombi (MT), injected into the fluidic microchip, on perfusion was investigated. We found that only 43% of all injected MT were fully occlusive. Second, it could also be shown that the maximal concentration of a dye (representing therapeutic agent) during intracoronary infusion could be increased on average by 58%, when proximally occluding the coronary artery by a balloon during drug infusion. The obtained results and insights enhance the understanding of perfusion in MVO-affected microcirculation and could lead to improved treatment methods for MVO patients. [ABSTRACT FROM AUTHOR]

Open in new tab Download slide OBJECTIVES Despite the success of coronary artery bypass graft (CABG) surgery using autologous saphenous vein grafts (SVGs), nearly 50% of patients experience vein graft disease within 10 years of surgery. One contributing factor to early vein graft disease is endothelial damage during short-term storage of SVGs in inappropriate solutions. Our aim was to evaluate the effects of a novel endothelial damage inhibitor (EDI) on SVGs from patients undergoing elective CABG surgery and on venous endothelial cells (VECs) derived from these SVGs. METHODS SVGs from 11 patients participating in an ongoing clinical registry (NCT02922088) were included in this study, and incubated with both full electrolyte solution (FES) or EDI for 1 h and then examined histologically. In 8 of 11 patients, VECs were isolated from untreated grafts, incubated with both FES and EDI for 2 h under hypothermic stress conditions and then analysed for activation of an inflammatory phenotype, cell damage and cytotoxicity, as well as endothelial integrity and barrier function. RESULTS The EDI was superior to FES in protecting the endothelium in SVGs (74 ± 8% versus 56 ± 8%, P  < 0.001). Besides confirming that the EDI prevents apoptosis in SVG-derived VECs, we also showed that the EDI temporarily reduces adherens junctions in VECs while protecting focal adhesions compared to FES. CONCLUSIONS The EDI protects the connectivity and function of the SVG endothelium. Our data suggest that the EDI can preserve focal adhesions in VECs during short-term storage after graft harvesting. This might explain the superiority of the EDI in maintaining most of the endothelium in venous CABG surgery conduits. [ABSTRACT FROM AUTHOR]

Mitral valve prolapse (MVP) is common among heart valve disease patients, causing severe mitral regurgitation (MR). Although complications such as cardiac arrhythmias and sudden cardiac death are rare, the high prevalence of the condition leads to a significant number of such events. Through next-generation gene sequencing approaches, predisposing genetic components have been shown to play a crucial role in the development of MVP. After the discovery of the X-linked inheritance of filamin A, autosomal inherited genes were identified. In addition, the study of sporadic MVP identified several genes, including DZIP1, TNS1, LMCD1, GLIS1, PTPRJ, FLYWCH, and MMP2. The early screening of these genetic predispositions may help to determine the patient population at risk for severe complications of MVP and impact the timing of reconstructive surgery. Surgical mitral valve repair is an effective treatment option for MVP, resulting in excellent short- and long-term outcomes. Repair rates in excess of 95% and low complication rates have been consistently reported for minimally invasive mitral valve repair performed in high-volume centers. We therefore conceptualize a potential preventive surgical strategy for the treatment of MVP in patients with genetic predisposition, which is currently not considered in guideline recommendations. Further genetic studies on MVP pathology and large prospective clinical trials will be required to support such an approach. [ABSTRACT FROM AUTHOR]