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Arteria mesenterica superior pseudoaneurysm is a rare disease that may be caused by iatrogenic damage to the superior mesenteric artery pseudoaneurysm in pancreaticoduodenal surgeries, trauma, inflammatory processes in the abdominal cavity. The paper presents a case report of surgical treatment for arteria mesenterica superior pseudoaneurysm. Surgical resection of superior mesenteric artery pseudoaneurysm was performed. The patient’s postoperative course was complicated by arteria mesenterica superior occlusion; arterial reconstruction was performed :iliaco-mesenteric bypass using the great saphenous vein with subsequent segmental resection of the jejunum. A research case study indicated the complexity of the pathology such as visceral artery pseudoaneurysm at the stage of diagnosing as well as at the stage of selecting treatment tactics. Visceral organ ischemia is one of the severest complications in the postoperative period which can make the diagnosis difficult as well as complicating the selection of treatment tactics. [ABSTRACT FROM AUTHOR]

Ventricular septal defect (VSD) is a known complication after myocardial infarction associated with high mortality. Extracorporeal membrane oxygenation (ECMO) is being successfully used in patients with VSD as a bridge to definitive surgical repair. Although often the only possibility to stabilize hemodynamics and oxygenation, ECMO has many potential complications, carrying significant morbidity and mortality. Here, the patient presented with a postinfarct VSD on peripheral venoarterial ECMO who developed a dissection of the common iliac artery (CIA) on the 5th day after ECMO implantation. As a result, a sudden drop in ECMO flow has become evident along with high pressures in the arterial cannula. After a definitive diagnosis of a CIA lesion obstructing the blood flow was made, trans-ECMO endovascular repair of CIA was performed. Four days after endovascular repair, we encountered the same problem of decreased blood flow associated with stent kinking and were approached with another endovascular repair to re-establishing full ECMO flow. [ABSTRACT FROM AUTHOR]

[Display omitted] • ADM, GADD45G, IL6, TM4SF1 and CDKN1A in blood is affected by ischemic brain stroke. • Carotid endarterectomy may activate ischemic stroke tolerance as post-conditioning. • ADM andGADD45G genes are potential diagnostic markers of ischemic brain stroke. A brain stroke is a serious disease and the second leading cause of death in the European Union. Carotid stenosis accounts for 15% of all ischemic cerebral strokes. However, there is currently no effective screening for carotid disease. Analysis of the DNA from peripheral blood is increasingly being used for several disease diagnoses. The potentially beneficial therapeutic method of inducing tissue tolerance to ischemia has so far been studied mainly in animal models. The aim of this study is to investigate changes in the gene expression of selected markers of brain ischemia during carotid endarterectomy, considered in this study as an activator of ischemic tolerance. During the carotid endarterectomy, there is a short-term occlusion of the internal carotid artery. Using the RT-qPCR method, we detected changes in the early identified gene markers of brain ischemia (ADM, CDKN1A, GADD45G, IL6, TM4SF1) in peripheral blood during sub lethal cerebral ischemia caused by carotid endarterectomy. Patients underwenting surgical procedure were divided into three groups: asymptomatic, symptomatic, and those who underwent carotid endarterectomy after an acute stroke. The results were compared to a negative/control group. Carotid endarterectomy had an impact on the expression of all monitored biomarkers. We observed statistically significant changes (p value 0.05–0.001) when comparing the groups among themselves, as well as the presence of ischemic tolerance of brain tissue to ischemic attacks. In conclusion, ADM, GADD45G, and TM4SF1 were affected in symptomatic patients, GADD45G and IL6 in acute patients, and CDKN1A and ADM in asymptomatic group after application of carotid endarterectomy. [ABSTRACT FROM AUTHOR]

Introduction: Many studies have highlighted the important role of PCSK9 in the development of cardiometabolic changes and its possible function as a biomarker of myocardial infarction or ischemic heart disease. This study aimed to determine the relationship between circulating PCSK9 levels and subclinical vascular changes in the group of low risk patients without manifest cardiovascular diseases. Methods: In this study, 120 healthy patients, free of manifest cardiovascular diseases, diabetes mellitus, and without lipid-lowering therapy, were divided into three groups based on BMI: normal weight ( N = 50), overweight ( N = 30), and obese ( N = 40). Biochemical parameters, including basic lipid and non-lipid ones, were analyzed. PCSK9 levels were measured by ELISA, vascular changes were quantified by carotid ultrasound (carotid artery intima-media thickness, cIMT), and arterial stiffness parameters (pulse wave velocity, PWV; augmentation index, AI; stiffness parameter, β) were measured by an echo-tracking method. Results: Plasma levels of PCSK9 significantly increased in obese (172.78 ± 51.67 ng/mL) in comparison with overweight (120.14 ± 37.64, p < 0.001) and normal weight groups (114.92 ± 35.87, p < 0.001). Differences between the overweight and normal weight groups were not significant ( p = 0.85). The level of PCSK9 significantly correlated with values of BMI ( p < 0.001, r = 0.38). In addition to increase in laboratory parameters associated with moderate metabolic changes, significant increase in cIMT and parameters of vascular changes ( β, AI, PWV) were detected in groups with elevated BMI. Significant positive linear correlation of PCSK9 concentrations and cIMT ( p < 0.001, r = 0.39), PWV ( p < 0.001, r = 0.31), and β ( p < 0.001, r = 0.3) were found. In multivariable regression analysis after adjusting for gender, age, BMI, and LDL, the impact of PCSK9 on cIMT, β, and PWV remained significant ( p = 0.006, 0.03, and 0.002, respectively). Conclusion: PCSK9 plasma levels significantly correlated with subclinical vascular changes and their values were significantly elevated in obese subjects. We assume that PCSK9 could be used as a predictor of early vascular involvement, prior to the existence of manifest atherosclerosis. These results also highlight the role of anti-PCSK9 treatment in primary prevention. [ABSTRACT FROM AUTHOR]