Ortotopowe przeszczepienie serca w leczeniu pierwotnego chłoniaka serca

We here describe the case of a patient diagnosed with primary lymphoma who underwent orthotopic heart transplantation.Postsurgically, the patient was treated with immunosuppressants and chemotherapy. Three months later, lesions were foundon the right side of the neck and the inferior vena cava; 12 months later, the lesion of the neck became smaller and the lesionof the inferior vena cava was not detected by positron emission tomography/computed tomography. The problems we encountered with this rare disease are discussed and compared to previous studies

Decreased adiponectin and increased inflammation expression in epicardial adipose tissue in coronary artery disease

<p>Abstract</p> <p>Background</p> <p>Disorders of endocrine substances in epicardial adipose tissue are known causes of coronary artery disease (CAD). Adiponectin is associated with cardiovascular disease. However, expression of adiponectin in epicardial adipose tissue and its function in CAD pathogenesis is unclear. This study investigates adiponectin expression in epicardial adipose tissue in CAD patients.</p> <p>Methods</p> <p>Vessels or adipose tissue samples collected from CAD patients and non-CAD controls were examined after immunochemical staining. Adiponectin, cytokines of interleukin-6 (IL-6) and necrosis factor-α (TNF-α) and toll-like receptor 4 (TLR4) expression level in adipose tissue were measured using real-time quantitative RT-PCR. Adiponectin concentrations in peripheral and coronary sinus vein plasma were measured with enzyme-linked immunosorbent assay. Peripheral vein plasma biochemistries were performed with routine laboratory techniques. Monocytes were collected from blood using lymphocyte separation medium. Expression level of cytokines and transcription factor NF-κB were measured to learn the effect of adiponectin on stearic acid-stimulated monocytes. Percentage of TLR4 positive monocytes was analyzed using flow cytometry.</p> <p>Results</p> <p>Histological examination revealed increased macrophage infiltration into epicardial adipose tissue of CAD patients. Decreased adiponectin displayed by real-time quantitative RT-PCR was associated with enhanced cytokines of IL-6 and TNF-α or TLR4 expression level in epicardial adipose tissue, suggesting decreased circulating adiponectin may be useful as a more sensitive predictor for coronary atherosclerosis than routine laboratory examinations. Adiponectin suppressed secretion of IL-6 and TNF-α in stimulated monocytes and TLR4 was expressed on cell surfaces.</p> <p>Conclusions</p> <p>Endocrine disorders in epicardial adipose tissue are strongly linked to CAD, and adiponectin has a protective effect by inhibiting macrophage-mediated inflammation.</p

Elevated serum albumin-to-creatinine ratio as a protective factor on outcomes after heart transplantation

BackgroundThe purpose of this study was to investigate the prognostic significance of serum albumin to creatinine ratio (ACR) in patients receiving heart transplantation of end-stage heart failure.MethodsFrom January 2015 to December 2020, a total of 460 patients who underwent heart transplantation were included in this retrospective analysis. According to the maximum Youden index, the optimal cut-off value was identified. Kaplan-Meier methods were used to describe survival rates, and multivariable analyses were conducted with Cox proportional hazard models. Meanwhile, logistic regression analysis was applied to evaluate predictors for postoperative complications. The accuracy of risk prediction was evaluated by using the concordance index (C-index) and calibration plots.ResultsThe optimal cut-off value was 37.54 for ACR. Univariable analysis indicated that recipient age, IABP, RAAS, BB, Hb, urea nitrogen, D-dimer, troponin, TG, and ACR were significant prognostic factors of overall survival (OS). Multivariate analysis showed that preoperative ACR (HR: 0.504, 95% = 0.352–0.722, P &lt; 0.001) was still an independent prognostic factor of OS. The nomogram for predicting 1-year and 5-year OS in patients who underwent heart transplantation without ACR (C-index = 0.631) and with ACR (C-index = 0.671). Besides, preoperative ACR level was a significant independent predictor of postoperative respiratory complications, renal complications, liver injury, infection and in-hospital death. Moreover, the calibration plot showed good consistency between the predictions by the nomogram for OS and the actual outcomes.ConclusionOur research showed that ACR is a favorable prognostic indicator in patients of heart transplantation

Application of decellularized vascular matrix in small-diameter vascular grafts

Coronary artery bypass grafting (CABG) remains the most common procedure used in cardiovascular surgery for the treatment of severe coronary atherosclerotic heart disease. In coronary artery bypass grafting, small-diameter vascular grafts can potentially replace the vessels of the patient. The complete retention of the extracellular matrix, superior biocompatibility, and non-immunogenicity of the decellularized vascular matrix are unique advantages of small-diameter tissue-engineered vascular grafts. However, after vascular implantation, the decellularized vascular matrix is also subject to thrombosis and neoplastic endothelial hyperplasia, the two major problems that hinder its clinical application. The keys to improving the long-term patency of the decellularized matrix as vascular grafts include facilitating early endothelialization and avoiding intravascular thrombosis. This review article sequentially introduces six aspects of the decellularized vascular matrix as follows: design criteria of vascular grafts, components of the decellularized vascular matrix, the changing sources of the decellularized vascular matrix, the advantages and shortcomings of decellularization technologies, modification methods and the commercialization progress as well as the application prospects in small-diameter vascular grafts

Concomitant valve surgery is associated with worse outcomes in surgical treatments of post-infarction ventricular aneurysm

ObjectiveTo evaluate the impact of concomitant valve surgery on the prognosis of patients who experienced coronary artery bypass graft (CABG) with/without ventricular reconstruction for the ventricular aneurysm.MethodsIn our department, 354 patients underwent CABG with/without ventricular reconstruction for a ventricular aneurysm from July 23rd, 2000 to December 23rd, 2022. A total of 77 patients received concomitant valve surgery, 37 of whom underwent replacement, and 40 of whom underwent repair. The baseline characteristics, prognostic, and follow-up information were statically analyzed. Univariate and multivariate Cox regression analyses were applied to identify the risk factors of long-term outcomes.ResultsCompared with patients who did not undergo valvular surgery, patients who experienced concomitant valve surgical treatments had a significantly lower survival rate (p = 0.00022) and a longer total mechanical ventilation time. Subgroup analysis indicated that the options of repair or replacement exhibited no statistically significant difference in postoperative mortality (p = 0.44) and prognosis. The multivariate Cox regression analysis suggested that the pre-operative cholesterol level (HR = 1.68), postoperative IABP (HR = 6.29), NYHA level (HR = 2.84), and pre-operative triglyceride level (HR = 1.09) were independent and significant predictors for overall all-cause mortality after surgery.ConclusionConcomitant valve surgery was considerably related to a higher risk of postoperative mortality in patients with post-infarction ventricle aneurysms who underwent surgical treatments. No significant difference in the prognosis outcomes was observed between the operating methods of repair or replacement valve surgery

Anthraquinone Emodin Inhibits Tumor Necrosis Factor Alpha-Induced Calcification of Human Aortic Valve Interstitial Cells via the NF-κB Pathway

Exploring effective therapies for delaying calcific heart valve disease (CHVD) is the focus of current cardiovascular clinical and scientific research. In this study, human aortic valve interstitial cells (hVICs) were isolated from patients with CHVD. After expansion, cultured hVICs were induced with the tumor necrosis factor-alpha (TNF-α) with or without anthraquinone emodin (EMD) treatments. Cytotoxicity and flow cytometric analysis were used to assess cell growth, while Alizarin Red S staining was used to detect hVICs calcification. Furthermore, RNA-sequencing analysis was utilized to investigate changes in mRNA profiles of cells cultured in TNF-α conditioned medium with or without EMD. Western blotting and qRT-PCR analyses were used for the verification of key selected genes. Our results indicated that EMD had limited influence on hVIC morphology, whereas in a dose-dependent fashion, EMD interfered with hVIC growth under TNF-α conditioned cell culture. Additionally, hVICs treated with TNF-α plus EMD, presented a gradual decrease of positive Alizarin Red S staining, when compared with cells treated with TNF-α only. Notably, cells treated with TNF-α plus EMD showed 1874 differential expression genes (DEGs), among them, 1131 were upregulated and 743 were downregulated. These DEGs displayed an enrichment of biological functions and signaling pathways, among them, BMP2, RELA, TNF, and TRAF1, were found to be significantly suppressed by EMD and selected given their role in mediating hVIC calcification. In conclusion, our study shows that EMD inhibits TNF-α-induced calcification and phenotypical transformation of hVICs via the NF-κB signaling pathway, thereby preventing calcification events stimulated during acute inflammatory responses

Mkk4 is a negative regulator of the transforming growth factor beta 1 signaling associated with atrial remodeling and arrhythmogenesis with age.

BACKGROUND: Atrial fibrillation (AF), often associated with structural, fibrotic change in cardiac tissues involving regulatory signaling mediators, becomes increasingly common with age. In the present study, we explored the role of mitogen-activated protein kinase kinase 4 (Mkk4), a critical component of the stress-activated mitogen-activated protein kinase family, in age-associated AF. METHODS AND RESULTS: We developed a novel mouse model with a selective inactivation of atrial cardiomyocyte Mkk4 (Mkk4(ACKO)). We characterized and compared electrophysiological, histological, and molecular features of young (3- to 4-month), adult (6-month), and old (1-year) Mkk4(ACKO) mice with age-matched control littermates (Mkk4(F/F)). Aging Mkk4(ACKO) mice were more susceptible to atrial tachyarrhythmias than the corresponding Mkk4(F/F) mice, showing characteristic slow and dispersed atrial conduction, for which modeling studies demonstrated potential arrhythmic effects. These differences paralleled increased interstitial fibrosis, upregulated transforming growth factor beta 1 (TGF-β1) signaling and dysregulation of matrix metalloproteinases in Mkk4(ACKO), compared to Mkk4(F/F), atria. Mkk4 inactivation increased the sensitivity of cultured cardiomyocytes to angiotensin II-induced activation of TGF-β1 signaling. This, in turn, enhanced expression of profibrotic molecules in cultured cardiac fibroblasts, suggesting cross-talk between these two cell types in profibrotic signaling. Finally, human atrial tissues in AF showed a Mkk4 downregulation associated with increased production of profibrotic molecules, compared to findings in tissue from control subjects in sinus rhythm. CONCLUSIONS: These findings together demonstrate, for the first time, that Mkk4 is a negative regulator of the TGF-β1 signaling associated with atrial remodeling and arrhythmogenesis with age, establishing Mkk4 as a new potential therapeutic target for treating AF

Matricellular protein CCN3 mitigates abdominal aortic aneurysm

Abdominal aortic aneurysm (AAA) is a major cause of morbidity and mortality; however, the mechanisms that are involved in disease initiation and progression are incompletely understood. Extracellular matrix proteins play an integral role in modulating vascular homeostasis in health and disease. Here, we determined that the expression of the matricellular protein CCN3 is strongly reduced in rodent AAA models, including angiotensin II-induced AAA and elastase perfusion-stimulated AAA. CCN3 levels were also reduced in human AAA biopsies compared with those in controls. In murine models of induced AAA, germline deletion of Ccn3 resulted in severe phenotypes characterized by elastin fragmentation, vessel dilation, vascular inflammation, dissection, heightened ROS generation, and smooth muscle cell loss. Conversely, overexpression of CCN3 mitigated both elastase- and angiotensin II-induced AAA formation in mice. BM transplantation experiments suggested that the AAA phenotype of CCN3-deficient mice is intrinsic to the vasculature, as AAA was not exacerbated in WT animals that received CCN3-deficient BM and WT BM did not reduce AAA severity in CCN3-deficient mice. Genetic and pharmacological approaches implicated the ERK1/2 pathway as a critical regulator of CCN3-dependent AAA development. Together, these results demonstrate that CCN3 is a nodal regulator in AAA biology and identify CCN3 as a potential therapeutic target for vascular disease