We present 38-years male patient. He has suffered from muscle weakness since 5 years. Arrhythmias appeared at the age of 32. In 37 years he had sick sinus syndrome, transient AV block II degree, paroxysmal atrial fibrillation, atrial flutter, ventricular arrhythmias. At this time, dilated cardiomyopathy was also detected. The evaluation revealed knees and elbows contractures, increased level of creatine kinase. The genetic testing revealed a frame shift deletion c.del619C in the emerin (EMD) gene and c.IVS4-13T> A in the lamin (LMNA) gene, and c.del619C deletion in the heterozygous state in a patient`s mother. Radiofrequency ablation of cavotricuspid isthmus, implantable cardioverter-defibrillator (ICD) implantation were performed. Heart transplantation was performed nine months later, due to severe heart failure and electrical storm. A morphological evaluation revealed sclerosis, atrophy and hypertrophy of cardiomyocytes. He underwent an induction therapy with (basiliximab) methylprednisolone, tacrolimus, mycophenolate after heart transplantation. During 40 months after transplantation, patient`s condition is satisfactory. heart failure in Emery-Dreifuss muscular dystrophy can progress quickly unless the previously stable condition. The use of correct regimens of immunosuppression therapy provides good long-term results of the heart transplantation.

Myocardial remodeling is an inevitable risk factor for cardiac arrhythmias and can potentially be corrected with cell therapy. Although the generation of cardiac cells ex vivo is possible, specific approaches to cell replacement therapy remain unclear. On the one hand, adhesive myocyte cells must be viable and conjugated with the electromechanical syncytium of the recipient tissue, which is unattainable without an external scaffold substrate. On the other hand, the outer scaffold may hinder cell delivery, for example, making intramyocardial injection difficult. To resolve this contradiction, we developed molecular vehicles that combine a wrapped (rather than outer) polymer scaffold that is enveloped by the cell and provides excitability restoration (lost when cells were harvested) before engraftment. It also provides a coating with human fibronectin, which initiates the process of graft adhesion into the recipient tissue and can carry fluorescent markers for the external control of the non-invasive cell position. In this work, we used a type of scaffold that allowed us to use the advantages of a scaffold-free cell suspension for cell delivery. Fragmented nanofibers (0.85 µm ± 0.18 µm in diameter) with fluorescent labels were used, with solitary cells seeded on them. Cell implantation experiments were performed in vivo. The proposed molecular vehicles made it possible to establish rapid (30 min) electromechanical contact between excitable grafts and the recipient heart. Excitable grafts were visualized with optical mapping on a rat heart with Langendorff perfusion at a 0.72 ± 0.32 Hz heart rate. Thus, the pre-restored grafts’ excitability (with the help of a wrapped polymer scaffold) allowed rapid electromechanical coupling with the recipient tissue. This information could provide a basis for the reduction of engraftment arrhythmias in the first days after cell therapy.

электронный журнал: Клиническая и экспериментальная морфология

Mandibular arteriovenous malformation (AVM) is a rare lesion, but it often can be presented with life-threatening bleedings. Endovascular treatment of mandibular AVMs has multiple approaches including transarterial embolization, transvenous embolization, direct puncture, and sclerotherapy. In this case study, we present a patient with mandibular AVM complicated by hemorrhage. The patient was treated with transarterial embolization, followed by transvenous sclerotherapy with balloon occlusion of venous outflow. But radical occlusion of AVM was achieved only by transvenous embolization of AVM with Onyx via double lumen balloon, which occluded the venous outflow.

Background: The systemic inflammatory response to coronary artery bypass grafting (CABG) is highly variable and a key driver of complications. We hypothesised that a pre-existing pro-inflammatory immune state, characterised by a skewed monocyte profile, ‘primes’ patients for an exaggerated response. This pilot prospective study aimed to test this hypothesis and to evaluate the Neutrophil-to-Albumin Ratio (NAR) as an integrated biomarker of this response, comparing it against the established Neutrophil-to-Lymphocyte Ratio (NLR). Methods: In this pilot prospective, single-centre pilot study, we enrolled 34 patients with multivessel coronary artery disease (CAD) scheduled for off-pump CABG and 20 control subjects. Preoperatively, peripheral blood monocyte subsets were quantified by flow cytometry. Neutrophil, lymphocyte, and albumin levels were measured before and after surgery to calculate NAR and NLR. Multivariable linear regression was used to test for independent predictors of the inflammatory response. Results: Preoperatively, CAD patients exhibited a reduced percentage of the classical monocyte subpopulation (p < 0.001), with a skew toward intermediate and non-classical subpopulations. Postoperatively, both NAR and NLR increased significantly (p < 0.001) and performed comparably in discriminating the postoperative state (AUC: 0.89 vs. 0.86, p > 0.05). Critically, in multivariable linear regression analysis, the preoperative percentage of classical monocytes remained a significant and independent predictor of the magnitude of the postoperative NAR surge (β = −0.028, p = 0.007), after adjusting for clinical confounders including atherosclerotic burden. Conclusion: A patient’s preoperative immune profile, specifically the degree of monocyte skew, is an independent predictor of the acute inflammatory response to CABG. This finding supports a ‘priming’ mechanism in high-risk patients. While NAR and NLR perform similarly as monitoring tools, the independent link between the underlying immunology and the postoperative outcome suggests that combining preoperative immunophenotyping with simple biomarker monitoring could offer a powerful new strategy for personalised risk stratification in cardiac surgery.