Mitral valvuloplasty using real-time three-dimensional transesophageal echocardiography.

OBJECTIVE: This study aimed to investigate the structure of the mitral valve in patients undergoing mitral valvuloplasty (MVP) using real-time three-dimensional transesophageal echocardiography (RT-3D-TEE). The main objective was to study the relationship between intraoperative annuloplasty ring size and mitral valve structure dimensions, with a focus on exploring the application value of RT-3D-TEE in MVP. METHODS: A total of 28 patients with degenerative mitral regurgitation (DMR), who underwent MVP between February and September 2022, as well as 12 normal control cases, were enrolled in this study. The MV annulus and leaflets were quantitatively analyzed using MVN software. RESULTS: The DMR group exhibited significantly greater dimensions in various parameters of the mitral valve, including the anterolateral-to-posteromedial diameter (DAlPm ), anterior-to-posterior diameter (DAP ), annulus height (HA ), three-dimensional annulus circumference (CA3D ), two-dimensional annulus area (AA2D ), anterior leaflet area (Aant ), posterior leaflet area (Apost ), anterior leaflet length (Lant ), posterior leaflet length (Lpost ), and tenting volume (Vtent ) compared to the control group. CONCLUSION: Real-time three-dimensional transesophageal echocardiography provides valuable insights into the morphological structure of the mitral valve and lesion location. It can aid in surgical decision-making, validate the success of MVP, and potentially reduce mortality and complications associated with mitral valve repair procedures.

Minimally Invasive Direct Coronary Artery Bypass Versus Percutaneous Coronary Intervention for Isolated Left Anterior Descending Artery Stenosis: An Updated Meta-Analysis.

BACKGROUND: The optimal revascularization strategy for isolated left anterior descending (LAD) coronary artery lesion between minimally invasive direct coronary artery bypass (MIDCAB) and percutaneous coronary intervention (PCI) remains controversial. This updated meta-analysis aims to compare the long- and short-term outcomes of MIDCAB versus PCI for patients with isolated LAD coronary artery lesions. METHODS: The Pubmed, Web of Science, and Cochrane databases were searched for retrieving potential publications from 2002 to 2022. The primary outcome was long-term survival. Secondary outcomes were long-term target vessel revascularization (TVR), long-term major adverse cardiovascular events (MACEs), and short-term outcomes, including postoperative mortality, myocardial infarction (MI), TVR, and MACEs of any cause in-hospital or 30 days after the revascularization. RESULTS: Six randomized controlled trials (RCTs) and eight observational studies were included in this updated meta-analysis. In total, 1757 patients underwent MIDCAB and 15245 patients underwent PCI. No statistically significant difference was found between the two groups in the rates of long-term survival. MIDCAB had a lower long-term MACE rate compared with PCI. Besides, PCI resulted in an augmented risk of TVR. Postoperative mortality, MI, TVR, and MACEs were similar between the two groups. CONCLUSIONS: The updated meta-analysis presents the evidence that MIDCAB has a reduced risk of long-term TVR and MACEs, with no benefit in terms of long-term mortality and short-term results, in comparison with PCI. Large multicenter RCTs, including patients treated with newer techniques, are warranted in the future.

Lymphocyte-to-monocyte ratio associated with severe post-stenotic aortic dilation in a case-control study.

BACKGROUND: Calcific aortic valve stenosis (CAVS) represents a serious health threat to elderly patients. Post-stenotic aortic dilation, a common feature in CAVS patients, might progress into aneurysm and even dissection, potential consequences of CAVS, and predicts a poor prognosis. This study sought to investigate the association of lymphocyte-to-monocyte ratio (LMR), an inflammatory biomarker, with severe post-stenotic aortic dilation in a case-control study in Chinese population. MATERIALS AND METHODS: 208 consecutive patients with CAVS were recruited retrospectively in a case-control study in Chinese population, from July 1, 2015 to June 31, 2018. LMR was statistically analyzed using the ROC curve and binary logistic regression analyses for its prognostic value in severe post-stenotic aortic dilation. RESULTS: LMR was significantly reduced in patients with severe post-stenotic aortic dilation (2.72 vs. 3.53, p = 0.002 < 0.05) compared to patients without severe post-stenotic aortic dilation. There was an inverse correlation observed between the maximal diameter of ascending aorta and LMR in the overall patients (r = - 0.217, p = 0.002 < 0.05). For post-stenotic aortic dilation, the prevalence of high-LMR group was statistically lower than that of low-LMR group (19.7% vs. 43.9%, p < 0.001). The maximal diameter of ascending aorta was significantly reduced in the high-LMR group (4.35 vs. 4.76, p = 0.003 < 0.05) compared to low-LMR group. Additionally, LMR was identified in the multivariate analysis independently associated with severe post-stenotic aortic dilation (AUC 0.743, 95% CI: [0.573-0.964], p = 0.025). CONCLUSIONS: This study provided the evidence of an inverse correlation between severe post-stenotic aortic dilation and LMR. LMR is potentially independently associated with severe post-stenotic aortic dilation.

Association of serum anion gap and risk of long-term mortality in patients following coronary artery bypass grafting: A propensity score matching study.

BACKGROUND: The present study aimed to explore the relationship between serum anion gap (AG) and long-term mortality in patients undergoing coronary artery bypass grafting (CABG). METHODS: Clinical variables were extracted among patients undergoing CABG from Medical Information Mart for Intensive Care III (MIMIC III) database. The primary outcome was 4-year mortality following CABG. An optimal cut-off value of AG was determined by the receiver operating characteristic (ROC) curve. The Kaplan-Meier (K-M) analysis and multivariate Cox hazard analysis were performed to investigate the prognostic value of AG in long-term mortality after CABG. To eliminate the bias between different groups, propensity score matching (PSM) was conducted to validate the findings. RESULTS: The optimal cut-off value of AG was 17.00 mmol/L. Then a total of 3162 eligible patients enrolled in this study were divided into a high AG group (≥17.00, n = 1022) and a low AG group (<17.00, n = 2,140). A lower survival rate was identified in the high AG group based on the K-M curve (p < .001). Compared with patients in the low AG group, patients in the high AG group had an increased risk of long-term mortality [1-year mortality: hazard ratio, HR: 2.309, 95% CI (1.672-3.187), p < .001; 2-year mortality: HR: 1.813, 95% CI (1.401-2.346), p < .001; 3- year mortality: HR: 1.667, 95% CI (1.341-2.097), p < .001; 4-year mortality: HR: 1.710, 95% CI (1.401-2.087), p < .001] according to multivariate Cox hazard analysis. And further validation of above results was consistent in the matched cohort after PSM. CONCLUSIONS: The AG is an independent predictive factor for long-term all-cause mortality in patients following CABG, where a high AG value is associated with an increased mortality.

Endothelial-to-Mesenchymal Transition in Calcific Aortic Valve Disease.

Calcific aortic valve disease (CAVD) represents a significant threat to cardiovascular health worldwide, and the incidence of this sclerocalcific valve disease has rapidly increased along with a rise in life expectancy. Compelling evidence has suggested that CAVD is an actively and finely regulated pathophysiological process even though it has been referred to as "degenerative" for decades. A striking similarity has been noted in the etiopathogenesis between CAVD and atherosclerosis, a classical proliferative sclerotic vascular disease.1 Nevertheless, pharmaceutical trials that attempted to target inflammation and dyslipidemia have produced disappointing results in CAVD. While senescence is a well-documented risk factor, the sophisticated regulatory networks have not been adequately explored underlying the aberrant calcification and osteogenesis in CAVD. Valvular endothelial cells (VECs), a type of resident effector cells in aortic leaflets, are crucial in maintaining valvular integrity and homeostasis, and dysfunctional VECs are a major contributor to disease initiation and progression. Accumulating evidence suggests that VECs undergo a phenotypic and functional transition to mesenchymal or fibroblast-like cells in CAVD, a process known as the endothelial-to-mesenchymal transition (EndMT) process. The relevance of this transition in CAVD has recently drawn great interest due to its importance in both valve genesis at an embryonic stage and CAVD development at an adult stage. Hence EndMT might be a valuable diagnostic and therapeutic target for disease prevention and treatment. This mini-review summarized the relevant literature that delineates the EndMT process and the underlying regulatory networks involved in CAVD.

Yap overexpression attenuates septic cardiomyopathy by inhibiting DRP1-related mitochondrial fission and activating the ERK signaling pathway.

Context: Yes-associated protein (Yap) has been linked to several cardiovascular disorders, but the role of this protein in septic cardiomyocytes is not fully understood. Objective: The aim of our study was to explore the influence of Yap in septic cardiomyopathy in vivo and in vitro. Materials and methods: In the current study, Yap transgenic mice and Yap adenovirus-mediated gain-of-function assays were used in an LPS-established septic cardiomyopathy model. Mitochondrial function and mitochondrial fission were determined through western blotting, immunofluorescence analysis and ELISA. Results: Our results demonstrated that Yap expression was downregulated by LPS, whereas Yap overexpression sustained cardiac function and attenuated cardiomyocyte death. The functional exploration revealed that LPS treatment induced cardiomyocyte mitochondrial stress, as manifested by mitochondrial superoxide overproduction, cardiomyocyte ATP deprivation, and caspase-9 apoptosis activation. Furthermore, we demonstrated that LPS-mediated mitochondrial damage was controlled by mitochondrial fission. However, Yap overexpression reduced mitochondrial fission and therefore improved mitochondrial function. A molecular investigation revealed that Yap overexpression inhibited mitochondrial fission by reversing ERK activity, and the inhibition of the ERK pathway promoted DRP1 upregulation and thereby mediated mitochondrial fission activation in the presence of Yap overexpression. Conclusions: Overall, our results suggest that the cause of septic cardiomyopathy appears to be connected with Yap downregulation. The overexpression of Yap can attenuate myocardial inflammation injury through the reduction of DRP1-related mitochondrial fission in an ERK pathway activation-dependent manner.

Predictive Roles of Neutrophil-to-Lymphocyte Ratio and C-Reactive Protein in Patients with Calcific Aortic Valve Disease.

The neutrophil-to-lymphocyte ratio (NLR) and C-reactive protein (CRP) are emerging indirect blood markers to roughly reflect the inflammation level in our body while some pathological changes occurring in aortic valve tissue. Few recent studies demonstrated that NLR is related to calcific aortic valve disease (CAVD). However, the extent of the relationship between them and the impact of CRP on CAVD are not clear. This study aimed to investigate the diagnostic influence and surgical predictive effect of NLR and CRP on CAVD.A total of 278 consecutive patients with CAVD (123 patients with bicuspid aortic valve and others with tricuspid aortic valve) and 108 healthy individuals who were included in the control group were enrolled in the study. The NLR was calculated from the complete blood count, and the CRP was measured from peripheral blood samples. Echocardiography was used to evaluate the severity of aortic stenosis. Intraoperation/postoperation indicators were collected in 166 patients from the total consecutive patients who underwent aortic valve replacement (AVR) alone.Significantly higher NLR was measured in both the BAV group (1.96 ± 0.78 versus 0.97 ± 0.15, P < 0.001) and the TAV group (2.51 ± 2.03 versus 0.97 ± 0.15, P < 0.001) compared with the control group. Moreover, the NLR level was significantly higher (P < 0.001) and the CRP level was significantly lower (P = 0.007) of the TAV group than that of the BAV group; a significant positive correlation between the NLR and the maximum gradient of aortic valve was detected. Furthermore, there was a moderate correlation between the NLR and the postoperative mechanical ventilation time.Our results indicated that the NLR and CRP were novel and useful predictive factors in patients with CAVD, and these two potential factors have guiding significance for the prediction of different pathological typing (BAV or TAV). Higher NLR level will not extend the cardiopulmonary bypass time (CPB); however, it will prolong the operation time and the postoperative mechanical ventilation time.

Dissecting Molecular Mechanisms Underlying Pulmonary Vascular Smooth Muscle Cell Dedifferentiation in Pulmonary Hypertension: Role of Mutated Caveolin-1 (Cav1F92A)-Bone Marrow Mesenchymal Stem Cells.

BACKGROUND: Pulmonary arterial hypertension (PAH) is characterised by remodelling in vascular smooth muscles, and switching from contractile (differentiated) to synthetic (dedifferentiated) phenotype. This study aimed to investigate the effect of a mutated caveolin-1 (Cav1F92A) gene from bone marrow mesenchymal stem cells (rBMSCs) on phenotypic switching in the smooth muscle cells during PAH. METHODS: Human pulmonary smooth muscle cells (HPASMCs) were treated with monocrotaline (MCT,1µM), and co-cultured with Cav1F92A gene modified rBMSCs (rBMSCs/Cav1F92A). The nitric oxide (NO) production, cell adhesion, cell viability and inflammatory cytokines expression in rBMSCs was measured to evaluate the survival rate of rBMSCs and the changes of inflammatory cytokines. The concentration of NO/cGMP (nitric oxide/Guanosine-3',5'-cyclic monophosphate), the tumour necrosis factor-alpha (TNF-α), transforming growth factor-beta1 (TGF-ß1) mRNA, the expression of contractile smooth muscle cells (SMCs) phenotype markers (thrombospondin-1 and Matrix Gla protein, MGP), the synthetic SMCs phenotype markers (H-caldesmon and smooth muscle gene SM22 alpha, SM22α), cell migration and the morphological changes in rBMSCs/Cav1F92A co-cultured HPASMCs were investigated. RESULTS: Cav1F92A increased NO concentration, cell adhesion, cell viability, anti-inflammatory cytokines interleukin-4 (IL-4), and interleukin-10 (IL-10), but decreased the inflammatory cytokines interleukin-1α (IL-1α), interferon-γ (INF-γ) and TNF-α expression in rBMSCs. rBMSCs/Cav1F92A activated the NO/cGMP, down-regulated TNF-α, TGF-ß1, thrombospondin-1 and MGP expression, up-regulated SM22α and H-caldesmon expression, restored cell morphology, and inhibited cell migration in MCT treated HPASMCs. CONCLUSIONS: rBMSCs/Cav1F92A inhibits switching from contractile to synthetic phenotype in HPASMCs. It also inhibits migration and promotes morphological restoration of these cells. rBMSCs/Cav1F92A may be used as a therapeutic modality for PAH.

Functional SNP in the 3'UTR of PON1 is Associated with the Risk of Calcific Aortic Valve Stenosis via MiR-616.

BACKGROUND/AIMS: Previous studies have examined the associations between the single nucleotide polymorphism in the Paraoxonase 1 (PON1) gene and development of calcific aortic valve stenosis (CAVS). The association between functional SNP in 3'UTR of PON1 and the risk of CAVS, however, is unclear. In this study, we investigated the role of SNP in the regulation of PON1 expression via miR-616, as well as the association of SNP with the risk of CAVS. METHODS: Two hundred and sixteen patients with CAVS and 243 CAVS-free participants were recruited in this study.They all obtained transthoracic echocardiogram and the ejection fraction (EF) and aortic valve area were recorded and analyzed. The PON1 expression were measured by western blot, Quantitative Real-Time Polymerase Chain Reaction were used to examine the transcriptional activity of miR-616 and PON1. Differences between CVAS patients and controls in terms of genotype frequency distribution and the estimates of Hardy-Weinberg equilibrium were evaluated using chi-square tests. Logistic regression modeling was used to determine the association between the independent effect of rs3735590 SNP and the interaction between genotype, PON1 activity, and other covariates on lipids and CAVS risk. All statistical analyses were performed using SPSS, version 17.0.1 for Windows (SPSS Inc., Chicago, IL). A p value of < 0 .05 was considered significant for all analyses. RESULTS: This study confirmed that PON1 is a validated target gene of miR-616 in liver cells. The relative quantification representing the expression of PON1 mRNA and the serum level of PON1 protein was decreased in the TT genotype. Moreover, the expression of PON1 had a negative regulatory relationship with the expression of miR-616(r=-0.3959, P<0.05) in human tissues. The patients with CT OR TT genotype at loci rs3735590 had a lower risk of CAVS than patients with the CC genotype. CONCLUSIONS: Our results suggest that functional SNP in the 3'UTR of PON1 regulates the expression of PON1 via miR-616, and such SNP is associated with the risk of CAVS in human.

Hetrombopag, a Thrombopoietin Receptor Agonist, Protects Cardiomyocyte Survival from Oxidative Stress Damage as an Enhancer of Stem Cells.

PURPOSE: Current human umbilical cord blood stem cell therapy faces the great challenges, because the stem cells are scarce and cannot survive for a long time. Here we describe how hetrombopag, an orally-active TPO receptor agonists, enhanced ex vivo expansion of human UCB stem cells, and protected cardiac myocytes from the damage caused by oxidative stress. METHODS: Ex vivo expansion of stem cells were performed in serum-free medium supplemented with rhSCF and rhFL plus hetrombopag for 7 days. The percentage and number of stem cell subsets were determined by flow cytometry. Rat cardiac myocytes, ex vivo expanded stem cells, or cardiac myocytes plus ex vivo expanded stem cells were serum starved for 24 hours, and were then subjected to H2O2, hetrombopag or both for 12 hours at the indicated concentrations. Cell viability assays, protein microarrays and western blots were then performed in each group. RESULTS: Our studies first revealed that the combination of hetrombopag and rhTPO manifested additive effect on ex vivo expansion of human UCB stem cells. Besides, hetrombopag dose-dependently enhanced the beneficial effects of ex vivo expanded human UCB MNCs in increasing the survival of injured cardiomyocytes during free oxygen radical stress. CONCLUSION: These data, for the first time, uncovered a novel function of non-peptide small molecular TPO receptor agonists as enhancers of stem cells in protecting cardiac myocyte survival from oxidative stress damage, which might provide a new therapeutic avenue for the treatment of oxidative stress-related cardiovascular disease. Graphical abstract ᅟ.

Peratrial Device Closure of a Congenital Coronary Artery Fistula through a Right Parasternal Approach: Innovative Use of Available Technology.

Current treatments for congenital coronary artery fistulas (CAFs) include surgical obliteration and transcatheter occlusion. However, surgical techniques involve significant trauma. Transcatheter occlusion is performed under fluoroscopy and angiography, in which radiation injury is inevitable. We present a patient, with a CAF from the left coronary artery to the right atrium, who underwent peratrial device closure of the CAF with a right parasternal approach under transesophageal echocardiography guidance. Complete occlusion was achieved by a symmetric ventricular septal occluder. We suggest that peratrial device closure of a congenital coronary artery fistula through a right parasternal approach may be a safe and effective option.

Congenital heart surgery in patients with ventricular noncompaction.

BACKGROUND: Noncompaction of the ventricular myocardium (NVM) is exceedingly rare and associated with a high morbidity and mortality. This pathology has been associated with other congenital heart diseases (CHDs). The efficacy of surgical treatment of patients with NVM and other CHDs is largely unknown. The aim of the present study was to describe surgical outcomes of 16 patients. METHODS AND RESULTS: Between April 2009 and October 2011, 16 patients with NVM and CHD were admitted to our hospital. Through a clinical chart review, we analyzed results of surgical treatment of NVM with other CHDs retrospectively. The median age was 3.9 years (range 2 m-11 y). The follow-up time was 23.93 months (range 3 m-36 m). Two patients (12.5%) died after the surgery, the remaining patients (87.5%) had an uneventful postoperative course. An additional patient died due to sudden death three months after surgery. Two patients developed recurrent heart failure after surgery. Congestive heart failure, severe arrhythmias, and the range of NVM may be risk factors for death. At 6 months after the operation, the NYHA functional class was significantly improved (2.38 ± 0.89 vs. 1.62 ± 0.65, p = 0.009). The cardiothoracic ratio was significantly reduced when compared to before the operation (p < 0.001). CONCLUSIONS: Surgery in patients with NVM and other CHDs can be effective in relieving heart failure, improving heart function, and decreasing heart size.

Coronary pseudoaneurysm with a superficial mass and accompanying Brucella infection.

BACKGROUND AND AIMS: To our knowledge, no previously reported clinical data of a coronary artery fistula forming a pseudoaneurysm and presenting as a anterior chest wall lump. We reported a rare case of Coronary pseudoaneurysm with a superficial mass and accompanying Brucella infection. The patient was successfully treated with surgery. MATERIALS AND METHODS: The patient case data was extracted from hospital records. RESULTS: A 64-year-old male presented with a history of paroxysmal left-sided chest pain and painful anterior chest wall lump. Coronary computed tomography (CT) angiography revealed the RCA pseudoaneurysm that showed a peripherally calcified soft-tissue mass in the anterior mediastinum and communicated with the chest wall lump through intercostal spaces. The patient underwent the resection of chest lump and RCA pseudoaneurysm under cardiopulmonary bypass, along with a combined antimicrobial therapy. The patient was discharged successfully after the surgery. DISCUSSION AND CONCLUSION: We report this rare case and highlight the possible origin of the anterior mediastinal mass and anterior chest wall lump as a pseudoaneurysm formed by a coronary artery fistula.

Interaction between nitric oxide and superoxide in the macula densa in aldosterone-induced alterations of tubuloglomerular feedback.

Tubuloglomerular feedback (TGF)-mediated constriction of the afferent arteriole is modulated by a balance between release of superoxide (O(2)(-)) and nitric oxide (NO) in macula densa (MD) cells. Aldosterone activates mineralocorticoid receptors that are expressed in the MD and induces both NO and O(2)(-) generation. We hypothesize that aldosterone enhances O(2)(-) production in the MD mediated by protein kinase C (PKC), which buffers the effect of NO in control of TGF response. Studies were performed in microdissected and perfused MD and in a MD cell line, MMDD1 cells. Aldosterone significantly enhanced O(2)(-) generation both in perfused MD and in MMDD1 cells. When aldosterone (10(-7) mol/l) was added in the tubular perfusate, TGF response was reduced from 2.4 ± 0.3 µm to 1.4 ± 0.2 µm in isolated perfused MD. In the presence of tempol, a O(2)(-) scavenger, TGF response was 1.5 ± 0.2 µm. In the presence of both tempol and aldosterone in the tubular perfusate, TGF response was further reduced to 0.4 ± 0.2 µm. To determine if PKC is involved in aldosterone-induced O(2)(-) production, we exposed the O(2)(-) cells to a nonselective PKC inhibitor chelerythrine chloride, a specific PKCα inhibitor Go6976, or a PKCα siRNA, and the aldosterone-induced increase in O(2)(-) production was blocked. These data indicate that aldosterone-stimulated O(2)(-) production in the MD buffers the effect of NO in control of TGF response, an effect that was mediated by PKCα.

Effects of high-dose ulinastatin on inflammatory response and pulmonary function in patients with type-A aortic dissection after cardiopulmonary bypass under deep hypothermic circulatory arrest.

OBJECTIVES: To investigate effects of high-dose ulinastatin on the release of proinflammatory cytokines and lung injury in patients with aortic dissection after cardiopulmonary bypass (CPB) under deep hypothermic circulatory arrest (DHCA). DESIGN: A prospective, randomized and double-blinded study. SETTING: A teaching hospital. PARTICIPANTS: Thirty-six patients with acute type-A aortic dissection undergoing cardiac surgery using CPB under DHCA. INTERVENTIONS: These patients randomly were selected to received total doses of 20,000 units/kg of ulinastatin (n = 18) or 0.9% saline (control, n = 18) at 3 time points (after anesthetic induction, before aortic cross-clamp, and after aortic cross-clamp release). MEASUREMENTS AND MAIN RESULTS: Tumor necrosis factor-alpha, interleukin 6, interleukin 8 and polymorphonuclear neutrophil elastase (PMNE) were measured after anesthetic induction (T0), 30 minutes (T1) after aortic cross-clamp, 3 (T2), 6 (T3) and 9 (T4) hours after weaning from CPB. Except for T1, pulmonary data, such as alveolar-arterial oxygen pressure difference, physiologic deadspace, peak inspiratory pressure, plateau pressure, static compliance and dynamic compliance, were obtained at the same time points. Concentrations of cytokines and PMNE were significantly lower in the ulinastatin group than the control group from T1 to T4, and peaked at T2 between the 2 groups. Compared with the pulmonary data of the control group at T2~T4, postoperative alveolar-arterial oxygen pressure difference, physiologic deadspace, peak inspiratory pressure, and plateau pressure significantly were lower, and static compliance and dynamic compliance higher in the ulinastatin group. Significantly shorter intubation time and intensive care unit stay were found in the ulinastatin group. CONCLUSIONS: High-dose ulinastatin attenuates the elevation of cytokines and PMNE, reduces the pulmonary injury and improves the pulmonary function after CPB under DHCA. Consequently, it shortens the time of intubation and intensive care unit stay.

Totally thoracoscopic surgical treatment for atrial septal defect: mid-term follow-up results in 45 consecutive patients.

BACKGROUND: Totally thoracoscopic operation provides minimally invasive alternative for patients with atrial septal defect. In this study, we report the mid-term follow-up results of 45 patients with atrial septal defect who underwent totally thoracoscopic operation and discuss the feasibility and safety of this new technique. METHODS: From January 2010 to February 2012, 45 patients with atrial septal defect underwent totally thoracoscopic closure as an alternative to traditional median sternotomy surgery. The mean age of the patients was 33.2±12.5 years (range 6.3-61.5 years), and mean weight was 55.7±11.1 kg (range 30.5-80 kg). Based on echocardiography the mean size of the atrial septal defect was 16.0±10.8mm (range 13-39 mm). RESULTS: All patients underwent totally thoracoscopic repair. Twenty-five patients with a pericardial patch and 20 patients were sutured directly. Five patients underwent concomitant tricuspid valvuloplasty with Kay technique. No death, reoperation or complete atrioventricular block occurred. The mean time of cardiopulmonary bypass was 70.5±20.6 min (range 31.0-153.0 min), the mean time of aortic cross-clamp was 28.8±13.3 min (range 0.0-80.0 min) and the mean time of operation was 155.8±36.8 min (range 65.0-300.0 min). Postoperative mechanical ventilation averaged 5.1±2.8h (range 3.6-12.6h), and the duration of intensive care unit stay 20.0±5.6h (range 16.2-25 h). The mean volume of blood drainage was 156±36 ml (range 51-800 ml). No death, residual shunt, lung atelectasis or moderate tricuspid regurgitation was found at three-month follow-up. CONCLUSION: Totally thoracoscopic repair is feasible and safe for patients with ASD, even with or without tricuspid regurgitation however more clinical data is needed in the future study.

The role of carotid artery stenosis in predicting stroke after coronary artery bypass grafting in a Chinese cohort study.

Current guidelines give priority to surgical treatment of carotid artery stenosis (CAS) before coronary artery bypass grafting (CABG), especially in symptomatic patients. Carotid artery stenting is an alternative treatment for narrowing of the carotid arteries. This study sought to demonstrate the role of severe CAS in predicting stroke after CABG and assess the efficacy of carotid artery stenting in preventing postoperative stroke in a Chinese cohort. From 2015 to 2021, 1799 consecutive patients undergoing isolated CABG surgery were retrospectively recruited in a Chinese cohort. The predictive value of severe CAS in postoperative stroke and carotid stenting in preventing postoperative stroke was statistically analyzed. The incidence of postoperative stroke was 1.67%. The incidence of CAS with stenosis ≥ 50% and ≥ 70% was 19.2% and 6.9%. After propensity matching, the incidence of stroke was 8.0% in the severe CAS group and 0% in the non-severe CAS group. We successfully established an optimal predictive nomogram for predicting severe CAS in patients undergoing CABG. Carotid artery stenting was found ineffective in preventing postoperative stroke. The present study provides the incidence of CAS and postoperative stroke in a Chinese cohort, identifies severe CAS as an independent risk factor for postoperative stroke after CABG, constructs a nomogram predicting the incidence of severe CAS, and evaluates the effectiveness of carotid artery stenting in preventing postoperative stroke after CABG.

Transplantation of microencapsulated Schwann cells and mesenchymal stem cells augment angiogenesis and improve heart function.

Because of their plasticity and availability, bone-marrow-derived mesenchymal stem cells (MSC) are a potential cell source for treating ischemic heart disease. Schwann cells (SC) play a critical role in neural remodeling and angiogenesis because of their secretion of cytokines such as vascular endothelial growth factor (VEGF). Cell microencapsulation, surrounding cells with a semipermeable polymeric membrane, is a promising tool to shelter cells from the recipient's immune system. We investigated whether transplantation of microencapsulated SC (MC-SC) and MSC together could improve heart function by augmenting angiogenesis in acute myocardial infarction (AMI). Sprague-Dawley rats with ligation of the left anterior descending artery to induce AMI were randomly divided for cell transplantation into four groups-MC-SC+MSC, MC+MSC, MSC, MC-SC, and controls. Echocardiography was performed at 3 days and 2 and 4 weeks after AMI. Rat hearts were harvested on day 28 after transplantation and examined by immunohistochemistry and western blot analysis. Echocardiography revealed differences among the groups in fractional shortening and end-systolic and end-diastolic dimensions (P < 0.05). The number of BrdU-positive cells was greater with MC-SC+MSC transplantation than the other groups (P < 0.01). The vessel density and VEGF level in the infarcted zone was significantly increased with MC-SC+MSC transplantation (P < 0.05). These results show that transplanting a combination of MC-SC and MSC could augment angiogenesis and improve heart function in AMI.

Evaluation of the pharmacological function of ulinastatin in experimental animals.

Organ protection is a routine therapy in severe injuries. Our aim was to evaluate the beneficial effects of ulinastatin in experimental rats. Rats were randomly divided into a sham control, a model control and an ulinastatin-treated group. Malondialdehyde (MDA) and superoxide dismutase (SOD) levels were determined. Serum amylase, serum aspartate aminotransaminase (AST), lactate dehydrogenase (LDH) and creatine kinase isoenzyme (CKMD) activities, interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), nitric oxide (NO) and cardiac troponin I (nTnl) levels were examined. Results showed that ulinastatin decreased MDA levels and ameliorated the down-regulation of SOD activity. In addition, ulinastatin pretreatment may decrease serum AST, LDH and CKMD activities, IL-8, TNF-α, and nTnl levels, and enhance NO level. Our results demonstrated that oxidative injury occurred after IR and that ulinastatin exhibits significant protective effects against these effects.

Influence of verapamil on pressure overload-induced ventricular arrhythmias by regulating gene-expression profiles.

BACKGROUND: Life-threatening ventricular arrhythmias can lead to sudden cardiac death in patients. This study aimed to investigate the changes in gene profiles involved when verapamil (VRP) affects increased wall stress (pressure overload)-induced ventricular arrhythmias, thus revealing the potential causative molecular mechanisms and therapeutic targets through gene-expression identification and functional analysis. METHODS: Animal models with wall stress-induced ventricular arrhythmias were established. Low (0.5 mg/kg) and high (1 mg/kg) doses of VRP were administered intravenously 10 minutes before transverse aortic constriction, and average ventricular arrhythmia scores were calculated. Next, we evaluated the molecular role of VRP by characterising differential gene-expression profiles between VRP-pretreated (1 mg/kg) and control groups using RNA-sequencing technology. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were used to reveal molecular function. A protein-protein interaction (PPI) network was then developed. RESULTS: VRP exerted its anti-arrhythmic effects in response to increases in left ventricular (LV) afterload. We detected differentially expressed genes (DEGs), of which 36 were upregulated and 1 397 downregulated, between the VRP-pretreated and model groups during acute increases in LV wall stress. GO analysis demonstrated that the DEGs were associated with cytoskeletal protein binding. KEGG analysis showed that enriched pathways were mainly distributed in adherens junctions, actin cytoskeleton regulation and the MAPK signalling pathway. Centralities analysis of the PPI identified Rac1, Grb2, Rbm8a and Mapk1 as hub genes. CONCLUSIONS: VRP prevented acute pressure overload-induced ventricular arrhythmias, possibly through the hub genes Rac1, Grb2, Rbm8a and Mapk1 as potential targets of VRP.