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Extended left ventricular septal myectomy remains the gold standard for the treatment of hypertrophic obstructive cardiomyopathy (HOCM) with refractory symptoms. On the basis of traditional modified transaortic Morrow myectomy, we innovatively performed a minimally invasive, video-assisted single-port thoracotomy through the right infra-axillary region. Our procedure can provide good visualization of the left ventricular outflow tract and hypertrophic ventricular septum for accurate resection. It also ensures optimal exposure of the mitral valve in the presence of complex mitral subvalvular structures.

Background Lower limb venous varicosities (VVs) are clinically common; however, their molecular underpinnings are far from well elucidated. Previous studies have demonstrated that the phenotypic transition of vascular smooth muscle cells (VSMCs) plays a critical role in VV pathogenesis and that c-fos is upregulated in VSMCs from VVs. The present study investigated the histologic and cytologic changes in VVs and the correlation between c-fos upregulation and VSMC phenotypic switching. Methods Thirty-four patients with VVs (VV group) and 13 patients undergoing coronary artery bypass using autologous great saphenous vein segments (normal vein [NV] group) were enrolled in the present study. The great saphenous veins of both groups were harvested for subsequent experiments. Hematoxylin and eosin staining was performed for vein morphologic analysis. Real-time quantitative polymerase chain reaction, immunohistochemistry, and Western blot assays were used to assess mRNA and protein expression of c-fos, α-smooth muscle actin (α-SMA), and osteopontin (OPN). Simple linear regression was used to evaluate the correlation between c-fos and OPN/α-SMA. Primary VSMCs were isolated from both groups and cultured in vitro. A cell counting kit-8 assay and scratch-wound assay were used to analyze the proliferation and migration abilities of the cells, respectively. Results The mean age of the patients in the NV and VV groups was 61.4 ± 3.8 years and 59.5 ± 10.4 years, respectively. The vein cavities of the VV group were dilated, and the arrangement of the cells was disordered. The tunica media of the VV group was thicker than that of the NV group owing to the accumulation and proliferation of VSMCs. Significantly elevated mRNA levels of c-fos and OPN were observed in the VV group compared with the NV group, and a positive correlation was further demonstrated between the mRNA levels of c-fos and OPN/α-SMA (R2, 0.5524; P Conclusions Both mRNA and protein expression of c-fos were upregulated in VV specimens, and the phenotypic biomarkers (OPN/α-SMA) were altered concurrently. VSMCs derived from VVs showed increased proliferation and migration abilities. Upregulation of c-fos might play a role in the phenotypic switching of VSMCs and subsequently participate in the pathogenesis of VVs. Clinical Relevance C-fos is an immediate early gene owing to the transient and rapid change in its expression in response to stimuli. It is involved in the regulation of cell proliferation, cell growth, and cell movement. In the present study, varicose vein specimens showed increased mRNA and protein expression of c-fos, accompanied by altered phenotypic biomarkers. The upregulation of the c-fos gene in smooth muscle cells cultured from varicose vein specimens might be associated with phenotypic switching and functional disturbance. These results could contribute to the exploration of the molecular mechanisms underlying the pathogenesis of varicose veins and the development of new therapeutic strategies.

Background The incidence and mortality of thoracic aortic dissection(TAD) are increasing. In clinicopathological studies, macrophage, T lymphocytes and dendritic cells were found infiltrating in the aortic middle layer. Acetaldehyde dehydrogenase 2(ALDH2) gene polymorphism is associated with high incidence of hypertension in Asian populations. However, there is no clear evidence of the relationship between ALDH2 and TAD in Asians. The aim of this study was to investigate the incidence of aortic dissection in different ALDH2 genotypes and explore changes in the vascular wall. Materials and methods Three-week-old male mice were administered by freshly prepared β-aminopropionitrile(BAPN) solution dissolved in drinking water(1 g/kg/d) for 28 days to induce TAD. The animal ultrasound imaging system was used to observe the formation of arterial dissection. Subsequently, mice were killed by cervical dislocation. The aortic were fixed for HE staining and EVG staining to observe the aortic elastic fiber tears and pseudoluma formation under the microscope. Results Knockout(KO) of ALDH2 mitigated BAPN-induced TAD formation in animal studies. Ultrasound results showed that ALDH2 knockout reduced the degree of ascending aortic widening and the incidence of aortic dissection rupture. Pathological sections of multiple aortic segments showed that the protective effect of ALDH2 knockout included not only the ascending aorta but also the aortic arch and descending aorta. The expressions of NK CD56bright cells, Th17 cells, T cells and T helper cells were decreased in the ALDH2 KO mice treated with BAPN for 28 days. Conclusions ALDH2 knockout played a protective role in the aorta dissection by altering inflammatory response, immune response and protecting elastic fibers.

The incidence and mortality of aortic dissection (AD) are increasing. In pathological studies, macrophages, T lymphocytes and dendritic cells were found in the tunica media of the aorta. Acetaldehyde dehydrogenase 2 (ALDHThree-week-old male mice were administered freshly prepared β-aminopropionitrile solution dissolved in drinking water (1 g/kg/d) for 28 days to induce TAD. An animal ultrasound imaging system was used to observe the formation of arterial dissection and changes in cardiac function. Subsequently, mice were euthanized by cervical dislocation. The aortas were fixed for HE staining and EVG staining to observe aortic elastic fiber tears and pseudoluma formation under a microscope.Knockout of ALDHALDH

Background: Cardiac resident macrophages are self-maintaining and originate from embryonic hematopoiesis. After myocardial infarction, cardiac resident macrophages are responsible for the efficient clearance and degradation of apoptotic cardiomyocytes (efferocytosis). This process is required for inflammation resolution and tissue repair; however, the underlying molecular mechanisms remain unknown. Therefore, we aimed to identify the mechanisms of the continued clearance and degradation of phagolysosomal cargo by cardiac resident macrophages during myocardial infarction. Methods: Multiple transgenic mice such as Lgmn −/− , Lgmn F/F ; LysM Cre , Lgmn F/F ; Cx3cr1 CreER , Lgmn F/F ; Lyve Cre , and cardiac macrophage Lgmn overexpression by adenovirus gene transfer were used to determine the functional significance of Lgmn in myocardial infarction. Immune cell filtration and inflammation were examined by flow cytometry and quantitative real-time polymerase chain reaction. Moreover, legumain (Lgmn) expression was analyzed by immunohistochemistry and quantitative real-time polymerase chain reaction in the cardiac tissues of patients with ischemic cardiomyopathy and healthy control subjects. Results: We identified Lgmn as a gene specifically expressed by cardiac resident macrophages. Lgmn deficiency resulted in a considerable exacerbation in cardiac function, accompanied by the accumulation of apoptotic cardiomyocytes and a reduced index of in vivo efferocytosis in the border area. It also led to decreased cytosolic calcium attributable to defective intracellular calcium mobilization. Furthermore, the formation of LC3-II–dependent phagosome around secondary-encountered apoptotic cardiomyocytes was disabled. In addition, Lgmn deficiency increased infiltration of MHC-II high CCR2 + macrophages and the enhanced recruitment of MHC-II low CCR2 + monocytes with downregulation of the anti-inflammatory mediators, interleukin-10, and transforming growth factor-β and upregulationof the proinflammatory mediators interleukin-1β, tumor necrosis factor-α, interleukin-6, and interferon-γ. Conclusions: Our results directly link efferocytosis to wound healing in the heart and identify Lgmn as a significant link between acute inflammation resolution and organ function.

Objective To evaluate the efficacy of intravenous iron sucrose (IS) in the perioperative period of a second thoracotomy after open-heart surgery. Methods This study enrolled patients that underwent a second thoracotomy after previous open-heart surgery. Propensity-score matching was used to match patients that received oral iron therapy with those that received IS after admission. The baseline demographic and clinical characteristics, perioperative data and adverse outcomes were compared between these two matched groups. Results The study enrolled 447 patients: of these, 148 received oral iron therapy and effective dietary guidance; and 299 patients received 300 mg IS per week. After matching the propensity scores, there were no significant differences between the two groups in terms of age, sex, smoking history, incidence of major cardiac adverse events, Euro-score, time between the two thoracotomies, application of recombinant erythropoietin, haemoglobin (Hb) on admission and red blood cell (RBC) count on admission. The differences between the two groups after propensity-score matching in terms of the amount of RBC input and Hb after the operation were significant. Conclusion The administration of IS might be useful for improving postoperative Hb levels and reducing intraoperative RBC input in patients undergoing a second thoracotomy.

Supplemental material, IMR902912 Supplemental Material1 for Intravenous transfusion of iron sucrose reduces blood transfusions and improves postoperative anaemia after a second thoracotomy: a propensity-score matching study by Chentao Luo, Yunqing Shi, Yi Lin, Runhua Ma, Qi Xia and Wenjun Ding in Journal of International Medical Research