Predictive value of lymphocyte-to-monocyte ratio in critically Ill patients with atrial fibrillation: A propensity score matching analysis.

BACKGROUND: Inflammation plays a key role in the initiation and progression of atrial fibrillation (AF). Lymphocyte-to-monocyte ratio (LMR) has been proved to be a reliable predictor of many inflammation-associated diseases, but little data are available on the relationship between LMR and AF. We aimed to evaluate the predictive value of LMR in predicting all-cause mortality among AF patients. METHODS: Data of patients diagnosed with AF were retrieved from the Medical Information Mart for Intensive Care-III (MIMIC-III) database. X-tile analysis was used to calculate the optimal cutoff value for LMR. The Cox regression model was used to assess the association of LMR and 28-day, 90-day, and 1-year mortality. Additionally, a propensity score matching (PSM) method was performed to minimize the impact of potential confounders. RESULTS: A total of 3567 patients hospitalized with AF were enrolled in this study. The X-tile software indicated that the optimal cutoff value of LMR was 2.67. A total of 1127 pairs were generated, and all the covariates were well balanced after PSM. The Cox proportional-hazards model showed that patients with the low LMR (≤2.67) had a higher 1-year all-cause mortality than those with the high LMR (>2.67) in the study cohort before PSM (HR = 1.640, 95% CI: 1.437-1.872, p < 0.001) and after PSM (HR = 1.279, 95% CI: 1.094-1.495, p = 0.002). The multivariable Cox regression analysis for 28-day and 90-day mortality yielded similar results. CONCLUSIONS: The lower LMR (≤2.67) was associated with a higher risk of 28-day, 90-day, and 1-year all-cause mortality, which might serve as an independent predictor in AF patients.

Role of Hydrogen Sulfide in Myocardial Ischemia-Reperfusion Injury.

ABSTRACT: Hydrogen sulfide (H2S), generally known as a new gas signal molecule after nitric oxide and carbon monoxide, has been found as an important endogenous gasotransmitter in the last few decades, and it plays a significant role in the cardiovascular system both pathologically and physiologically. In recent years, there is growing evidence that H2S provides myocardial protection against myocardial ischemia-reperfusion injury (MIRI), which resulted in an ongoing focus on the possible mechanisms of action accounting for the H2S cardioprotective effect. At present, lots of mechanisms of action have been verified through in vitro and in vivo models of I/R injury, such as S-sulfhydrated modification, antiapoptosis, effects on microRNA, bidirectional effect on autophagy, antioxidant stress, or interaction with NO and CO. With advances in understanding of the molecular pathogenesis of MIRI and pharmacology studies, the design, the development, and the pharmacological characterization of H2S donor drugs have made great important progress. This review summarizes the latest research progress on the role of H2S in MIRI, systematically explains the molecular mechanism of H2S affecting MIRI, and provides a new idea for the formulation of a myocardial protection strategy in the future.

Identification and characterization of circular RNAs in atrial appendage of patients with atrial fibrillation.

Circular RNAs (circRNAs) have emerged as a novel type of non-coding RNA (ncRNA) of interest in gene regulation, especially for its vital function underlying many diseases. Atrial fibrillation is the most common sustained arrythmia. However, the expression spectrum and function of circRNAs in atrial appendage of patients with atrial fibrillation (AF) has seldomly been investigated. Human atrial appendage tissues were acquired during cardiac surgery, which were divided into the AF group and the Sinus rhythm (SR) group. The expression characterization of circRNAs of two groups was revealed by high-throughput sequencing. The dysregulated circRNAs were identified and analyzed by bioinformatics methods, and further validated by realtime PCR. A total 18109 circRNAs in human atrial appendage tissues were targeted. Among them, 147 differentially expressed circRNAs (102 up-regulated and 45 down-regulated) were found between AF group and SR group. Gene ontology (GO) and KEGG pathway analysis indicated that many mRNAs transcribed from the host genes of altered circRNAs were implicated in regulation of sequence-specific DNA binding transcription factor activity, as well as nicotinate and nicotinamide metabolism pathways. Analysis of the association between differently expressed circRNA and miRNA were explored, which revealed an ample interaction. Our study firstly revealed the expression spectrum of circRNAs in both left and right atrial appendage of patients with or without AF. Differentially expressed circRNAs in the atrial appendage were also identified, analyzed and validated. The results of this study may provide novel biomarkers and potential therapeutic targets for AF.

Dynamic monitoring of cardiac foreign body by perioperative echocardiography: A case study.

Cardiac foreign bodies, especially those with sharp tips, may lead to unpredictable complications, such as penetrating cardiac injuries. Yet there have not been many reports of penetrating cardiac injuries caused by a needle that migrates from the neck to the heart. We herein present a review of such a case, focusing on the dynamic monitoring by perioperative echocardiography. The needle was represented on the monitor as a linear artifact that had penetrated through the ventricular wall and caused increasing pericardial effusion. Fortunately, the needle was successfully removed before it completely entered the right ventricular cavity. In this case, perioperative echocardiography played a significant role in clinical emergency decision making.

Glycemic control is associated with atrial structural remodeling in patients with type 2 diabetes.

BACKGROUND: Diabetes mellitus (DM) has been demonstrated to be a strong risk factor for development and perpetuation of atrial fibrillation (AF). However, how DM and glycemic control affect the pathogenesis of AF has not been sufficiently investigated, especially for the atrial structural remodeling. METHODS: A total of 86 patients undergoing coronary artery bypass graft surgery were enrolled in this study, with atrium sample collected in the operation. The patients were divided into the DM group (n = 40) and the control group (n = 46) accordingly. Demographics, clinical data were collected and compared. Echocardiography, Masson staining and Western blotting were conducted to evaluate atrial structural remodeling. RESULTS: There was no significant difference between the two groups in baseline characteristics (all P > 0.05). Fast blood glucose and HbA1c of DM group were significantly higher than the control group (P < 0.001). Echocardiography results demonstrated that the left atrium diameter (LAD) and left atrium volume index (LAVI) of DM group was significantly higher than the control group (P < 0.001). Masson staining showed that the collagen volume fraction (CVF), a quantitative indicator of fibrosis, was significantly higher in DM patients (P = 0.03). Western blot results indicated that the Collagen I of DM group was more expressed in the DM group than the control group (P < 0.001). Univariate linear regression revealed that the HbA1c level was significantly associated with both LAD (Y = 1.139X + 25.575, P < 0.001, R2 = 0.291) and CVF (Y = 0.444X + 29.648, P = 0.009, R2 = 0.078). CONCLUSIONS: DM was associated with atrial structural remodeling, including atrium enlargement and atrial fibrosis, which might be attributed to poor glycemic control.

Unusual Drug Fever Caused by Imipenem/Cilastatin and a Review of Literature.

INTRODUCTION: Drug fever is a febrile reaction caused by initiation of one drug or varieties of drugs and often disappears after cessation of the drug(s). Clinically, drug fever is frequently induced by antibiotics, anticonvulsants, and antineoplastics. There are few previous reports about drug fever caused by imipenem/cilastatin. CASE PRESENTATION: Here, we described a 66-year-old man undergoing the Ivor Lewis esophagectomy for esophageal carcinoma, who developed drug fever. The patient had a high temperature with shivering after administration of imipenem/cilastatin for 7 days. Furthermore, his temperature came down after discontinuing imipenem/cilastatin and receiving steroids. Body temperature increased rapidly 4 hours after intravenous readministration of imipenem/cilastatin and rapidly decreased to normal after discontinuing imipenem/cilastatin and administering steroids. CONCLUSION: Thorough history, blood tests, physical examination, and computed tomography (CT) did not reveal any evidence of fever. Drug fever caused by imipenem/cilastatin was considered. We also present a review of relevant literature and provide a point of reference for the clinical diagnosis and therapy of patients with drug fever.

Human Epicardial Adipose Tissue Activin A Expression Predicts Occurrence of Postoperative Atrial Fibrillation in Patients Receiving Cardiac Surgery.

BACKGROUND: Activin A secreted by epicardial adipose tissue (EAT) plays a major role in the progress of atrial fibrosis. However, the potential of Activin A in predicting the occurrence of postoperative atrial fibrillation (POAF) has yet to be elucidated. We aimed to investigate the predicable value of Activin A expression in EAT on POAF. METHODS: A total of 89 patients receiving cardiac surgery without atrial fibrillation (AF) history were enrolled in this study, including 49 patients with valvular heart disease (VHD) and 40 patients with non-valvular heart disease (NVHD). Activin A expression in EAT was determined by quantitative polymerase chain reaction (qPCR), while the thickness of EAT (EATT) was estimated by echocardiography. New onset POAF before discharge was documented. RESULTS: Eventually 32 patients (36.0%) developed POAF, including 20 patients with VHD (40.8%) and 12 patients with NVHD (30.0%). Activin A expression was higher in POAF than sinus rhythm (SR) patients, whether for VHD or NVHD group (All p<0.001). In general, Activin A expression predicted the occurrence of POAF with a sensitivity of 65.6% and specificity of 91.2% (AUC: 0.795; 95%CI: 0.693-0.897, p<0.001). Subgroup analysis showed that EATT was not significant for the VHD group in predicting POAF (p=0.07), while Activin A expression demonstrated a sensitivity of 60.0% and specificity of 89.7% (AUC: 0.745; 95%CI: 0.601-0.889, p<0.001). Multivariate regression analysis showed that Activin A expression in EAT was an independent risk factor for POAF (OR: OR=1.067, 95%CI:1.002-1.136, p=0.042). CONCLUSIONS: Activin A expression in EAT is an independent risk factor for POAF, which can be used for prediction of POAF, especially for patients with VHD.

Synergistic Anticancer Activity of Combined Use of Caffeic Acid with Paclitaxel Enhances Apoptosis of Non-Small-Cell Lung Cancer H1299 Cells in Vivo and in Vitro.

BACKGROUND/AIMS: Caffeic acid (CA) is known to possess multiple biological activities including anti-cancer activities. However, the molecular mechanisms underlying these activities in non-small-cell lung cancer (NSCLC) cells are not fully understood. We attempted to clarify whether CA could enhance paclitaxel (PTX)-induced cytotoxicity in H1299 cells. METHODS: First, we tested the cytotoxic effects in both H1299 cells and normal human Bease-2b cells by cell proliferation experiments. Next, we use Annexin V/propidium iodide apoptosis analysis and flow cytometric analysis to investigate apoptosis and cell cycle arrest under the treatments mentioned above. To further pinpoint changes in apoptosis, we tested the caspase-associated apoptotic pathway, which involves the activities of caspase-3 and caspase-9. Moreover, apoptosis-related proteins and MAPK pathway proteins were examined by western blot. An H1299 xenograft nude mice model was used to further evaluate the tumor-suppressing effects of CA and PTX in vivo. RESULTS: Combination treatment with low-dose CA and PTX decreased the proliferation of NSCLC H1299 cells but not normal Beas-2b cells. Flow cytometry showed that H1299 cells were arrested in the sub-G1 phase and apoptosis was significantly increased in H1299 cells after CA treatment. Caspase-3 and caspase-9 activities were both increased after CA treatment. Furthermore, CA increased the PTX-induced activation of Bax, Bid, and downstream cleaved PARP, and phosphorylation of extracellular signal regulated kinase1/2 and c-Jun NH2-terminal protein kinase1/2. An in vivo tumor-suppression assay demonstrated that CA and PTX combined treatment exerted a more effective suppressive effect on tumor growth in H1299 xenografts without causing significant adverse effects. CONCLUSIONS: Our results indicated that CA inhibited NSCLC H1299 cell growth by inducing apoptosis and CA and PTX combined produced a synergistic anti-cancer effect in H1299 cells.

Activation of TGF-ß1/α-SMA/Col I Profibrotic Pathway in Fibroblasts by Galectin-3 Contributes to Atrial Fibrosis in Experimental Models and Patients.

BACKGROUND/AIMS: This study aimed to evaluate whether galectin-3 (Gal-3) contributes actively to atrial fibrosis both in patients and experimental atrial fibrillation (AF) models. METHODS: Mouse HL-1 cardiomyocytes were subjected to rapid electrical stimulation (RES) to explore Gal-3 expression and secretion levels by western blotting (WB) and enzyme linked immunosorbent assay (ELISA). Neonatal rat cardiac fibroblasts were treated with conditioned culture medium and recombinant human Gal-3 to evaluate the activation of the transforming growth factor (TGF)-ß1/α-smooth muscle actin (SMA)/collagen I (Col I) profibrotic pathway (WB) and fibroblast proliferation with a Cell Counting Kit-8 (CCK-8). Furthermore, in the rapid atrial pacing (RAP) rabbit AF model, atrial Gal-3 expression and its effects on the profibrotic pathway were evaluated (WB and Masson's trichrome staining). Moreover, 44 consecutive patients who underwent single mitral valve repair/replacement were included, consisting of 28 patients with persistent AF (PeAF) and 16 with sinus rhythm (SR). Coronary sinus blood was also sampled to test circulating Gal-3 levels (ELISA), and atrial myocardium Gal-3 and its downstream TGF-ß1/α-SMA pathway were also measured by WB and immunohistochemical staining. RESULTS: Gal-3 expression in HL-1 cells and its secretion level in culture medium were greatly increased after 24 h RES. Treatment of neonatal rat cardiac fibroblasts with conditioned media collected from the RES group or recombinant human Gal-3 protein (10 and 30 µg/mL) for 72 h induced the activation of the TGF-ß1/α-SMA/Col I profibrotic pathway. RAP increased Gal-3 levels and activated the TGF-ß1/α-SMA/Col I pathway in rabbit left atria, while the Gal-3 inhibitor N-acetyllactosamine, injected at 4.5 mg/kg every 3 days, mitigated these adverse changes. Furthermore, Gal-3 levels in coronary sinus blood samples and myocardial Gal-3 expression levels were higher in the PeAF patients than in the SR patients, and higher level profibrotic pathway activation was also confirmed. CONCLUSIONS: Activation of Gal-3 expression in the atria can subsequently activate the TGF-ß1/α-SMA/Col I pathway in cardiac fibroblasts, which may enhance atrial fibrosis.

YKL-40 is highly expressed in the epicardial adipose tissue of patients with atrial fibrillation and associated with atrial fibrosis.

BACKGROUND: YKL-40 (CHI3L1) is a novel biomarker for inflammation, tissue remodeling, and fibrosis, as well as cardiovascular diseases. We investigated the association between YKL-40 expression in epicardial adipose tissue (EAT) and atrial fibrosis in patients with atrial fibrillation (AF). METHODS: Blood samples, subcutaneous adipose tissue (SAT), paracardial adipose tissue (PAT), EAT, and adjacent atrial myocardium were acquired from patients receiving coronary artery bypass grafts. The patients were divided into the AF group (n = 28) and the sinus rhythm (SR) group (n = 36). RESULTS: We did not detect a significant difference in the serum YKL-40 levels in the SR and AF groups (P = 0.145). Quantitative real-time PCR showed that YKL-40 (CHI3L1) mRNA levels in the EAT were significantly higher than in the SAT or PAT of AF patients, or the EAT of SR patients (All P < 0.001). We found similar results for YKL-40 protein levels by immunohistochemistry. Masson staining showed significantly more fibrosis in AF patients than in SR patients (P < 0.001). Western blotting indicated that AF patients had significantly higher expression of collagen I (P = 0.039). We found a linear relationship between YKL-40 mRNA expression and the collagen volume fraction of the atrial myocardium (y = 3.576x + 26.205, P < 0.001). Multivariate linear regression analysis revealed that body mass index is an independent risk factor for YKL-40 expression in EAT (ß = 0.328, P = 0.011). CONCLUSIONS: YKL-40, which is highly expressed in the EAT of patients with AF, is affected by body mass index and associated with atrial fibrosis, which may contribute to the development of AF.

Mechanical Valve Replacement for Congenital Heart Disease Complicated by Native Pulmonary Valve Endocarditis: A Case Report and Literature Review.

Congenital heart disease (CHD) is one of the most common risk factors for infective endocarditis. However, it is rare to find a CHD patient complicated by isolated pulmonary valve endocarditis. Here, we report an adult patient with congenital heart disease complicated by native pulmonary valve endocarditis who underwent a mechanical valve replacement. We also review previous literature to examine key points in the treatment of such patients.

Smoking as a Risk Factor for the Occurrence of Atrial Fibrillation in Men Versus Women: A Meta-Analysis of Prospective Cohort Studies.

BACKGROUND: Although smoking is known to be associated with cardiovascular diseases, the number of large-scale cohort studies on the association between smoking and atrial fibrillation (AF) is limited and the results obtained are also inconsistent, and even fewer studies have addressed the difference between the male and female genders. The present study was intended to clarify and quantify the association between smoking and the risk of AF in men versus women. METHODS: Using AF- and smoking-related keywords, a comprehensive literature search on PubMed, Embase and Web of Science was conducted with a time limit until December 2016, which was followed by manual screening, quality assessment and data extraction. The pooled relative risk (RR) of the included studies was estimated by using the random-effects model. Subgroup, heterogeneity and sensitivity analyses were also conducted. RESULTS: A total of 14 prospective studies and 222,159 individuals were included in this meta-analysis, and the pooled RR of the 14 studies was 1.24 (95% CI, 1.12-1.36; p<0.0001) for the occurrence of AF in smoking populations. The pooled RR in men was 1.38 (95% CI, 1.21-1.57 p<0.0001) versus 1.28 in women (95% CI, 0.93-1.76; p=0.1356). The male-to-female ratio of relative risk (RRR) was 1.17 (95% CI, 0.84-1.63; p=0.3418) of smoking versus non-smoking individuals. CONCLUSION: Smoking is a risk factor for the occurrence of AF. Compared with women, male smokers are more likely to develop AF.

[Discussion on the standard of clinical genetic testing report and the consensus of gene testing industry].

The widespread application of next generation sequencing (NGS) in clinical settings has enabled testing, diagnosis, treatment and prevention of genetic diseases. However, many issues have arisen in the meanwhile. One of the most pressing issues is the lack of standards for reporting genetic test results across different service providers. The First Forum on Standards and Specifications for Clinical Genetic Testing was held to address the issue in Shenzhen, China, on October 28, 2017. Participants, including geneticists, clinicians, and representatives of genetic testing service providers, discussed problems of clinical genetic testing services across in China and shared opinions on principles, challenges, and standards for reporting clinical genetic test results. Here we summarize expert opinions presented at the seminar and report the consensus, which will serve as a basis for the development of standards and guidelines for reporting of clinical genetic testing results, in order to promote the standardization and regulation of genetic testing services in China.

Hydrogen Sulfide Protects Cardiomyocytes against Apoptosis in Ischemia/Reperfusion through MiR-1-Regulated Histone Deacetylase 4 Pathway.

BACKGROUND/AIMS: Hydrogen sulfide (H₂S) is a powerful inhibitor of cardiomyocytes apoptosis following ischemia/reperfusion (IR) injury, but the underlying mechanism remains unclear. Our previous study showed that microRNA-1 (miR-1) was upregulated by 2.21 fold in the IR group compared with that in the H₂S preconditioned group. MiR-206 affected the process of cardiomyocytes hypertrophy by regulating histone deacetylase 4 (HDAC4). HDAC4 is also known to play an anti-apoptotic role in tumor cells, but its role in the myocardium has not been reported. The aim of this study was to test whether H₂S could inhibit apoptosis of cardiomyocytes through HDAC4 regulation by miR-1 in IR. METHODS: Cardiomyocytes of neonatal rats were subjected to hypoxia/reoxygenation (HR) injury with or without H₂S pretreatment to simulate IR injury Cardiomyocytes were transfected with miR-1 mimic or HDAC4 siRNA to evaluate whether the miR-1-HDAC4 signaling pathway was involved in the protective effect of H₂S. RESULTS: HR increased cell apoptosis and caspase-3 cleavage, upregulated miR-1, and downregulated HDAC4. H₂S preconditioning attenuated the apoptosis of cardiomyocytes, caspase-3 cleavage and LDH release, and enhanced cell viability In addition, H₂S downregulated miR-1, and preserved HDAC4 expression. HDAC4 protein was down-regulated by miR-1 mimic. Transfection of cardiomyocytes with miR-1 mimic partially reduced the protective effect of H₂S. Meanwhile, transfection of cardiomyocytes with siRNA to HDAC4 partially abrogated the protective effect of H₂S. CONCLUSIONS: The miR-1-HDAC4 signaling pathway is involved in the protective effect of H₂S against the apoptosis of cardiomyocytes during the IR injury process.

PI3K/SGK1/GSK3ß signaling pathway is involved in inhibition of autophagy in neonatal rat cardiomyocytes exposed to hypoxia/reoxygenation by hydrogen sulfide.

Excessive autophagy aggravates myocardial ischemia/reperfusion (IR) injury. Hydrogen sulfide (H2S) has been shown to possess a strong cardioprotective effect due to its anti-necrosis, anti-apoptosis, anti-oxidant and anti-inflammatory properties. Our previous study showed that H2S could also protect the myocardium against IR injury through its anti-autophagy effect in vivo, but the underlying mechanism remains unclear. The aim of the present study was to determine whether PI3K/SGK1/GSK3ß signaling pathway was involved in the anti-autophagy effect of H2S against myocardial hypoxia/reoxygenation (HR) injury in vitro. Autophagy was significantly increased in cardiomyocytes subjected to HR, but it was down-regulated by H2S (NaHS donor). Blocking PI3K by LY294002 (a PI3K inhibitor) or knocking down SGK1 by SGK1 siRNA augmented autophagy and attenuated the anti-autophagy effect of H2S. However, blocking GSK3ß by tws119 (a GSK3ß inhibitor) produced an opposite effect. In addition, while treatment of neonatal rat cardiomyocytes with HR reduced cell viability and augmented cell injury, H2S significantly reversed it. Blocking PI3K or knocking down SGK1 aggravated HR injury and weakened the protective effect of H2S, while blocking GSK3ß produced an opposite effect. In conclusion, H2S can inhibit autophagy in neonatal rat cardiomyocytes exposed to H/R and exert a cardioprotective effect at least partly by regulating PI3K/SGK1/GSK3ß signaling pathway.

Entry-Level Forward Surgical Team Training in 5th Grade Students of Second Military Medical University of the Chinese People's Liberation Army.

BACKGROUND: Forward surgical team (FST) is a highly mobile team for surgical missions in battlefield. FST training has been well held in many western countries. However, such training in Chinese army is far from satisfaction. METHODS AND RESULTS: Relying on Second Military Medical University and its affiliated hospitals, we are launching an entry-level training program for 5th grade students, in order to improve their understandings on basic concepts of FST, as well as their abilities to complete surgical missions on battlefield. CONCLUSIONS: In this article, we are going to introduce our training facilities as well as our training methods in our training program.

Effects of MIAVS on Early Postoperative ELWI and Respiratory Mechanics.

BACKGROUND: The effects of minimally invasive aortic valve surgery (MIAVS) on the early postoperative extravascular lung water index (ELWI) and respiratory mechanics have rarely been studied. MATERIAL/METHODS: A total of 90 patients were divided into 3 groups: a conventional full sternotomy (CS) group (n=30), an upper ministernotomy (US) group (n=30), and a right anterior thoracotomy (RT) group (n=30). Hemodynamic and respiratory mechanics parameters were recorded at perioperative time points, including before skin incision (T(-1)); at sternum closing (T0); and 4 h (T4), 8 h (T8), 12 h (T12), and 24 h (T24) after the operation. The ventilator support time, ICU length of stay, and postoperative hospitalization time, as well as the thoracic drainage volume and blood transfusion volume, were recorded. RESULTS: The ELWI and pulmonary vascular permeability index (PVPI) increased at T4, and the values were significantly lower in the US group than in the RT group and CS group (P<0.05). At T8, the ELWI and PVPI in the US group and RT group were significantly lower than in the CS group. At T12, there were no significant differences among the 3 groups. In addition, at T4 static lung compliance decreased, plateau airway pressure increased, and airway resistance changed non-significantly. There were no significant differences between the US group and the RT group, but both groups showed better results than the CS group did. CONCLUSIONS: The ELWI and PVPI may transiently increase after aortic valve surgery with cardiopulmonary bypass. Compared with the 12 h required to recover from a conventional sternotomy operation, it may only take 8 h to recover from MIAVS.

An Adjusted Calculation Model of Reduced Heparin Doses in Cardiopulmonary Bypass Surgery in a Chinese Population.

OBJECTIVE: To investigate the safety and efficacy of an adjusted regimen of heparin infusion in cardiopulmonary bypass (CPB) surgery in a Chinese population. DESIGN: Prospective, single-center, observational study. SETTING: University teaching hospital. PARTICIPANTS: Patients having cardiac surgery with CPB were selected for this study using the following criteria: 18 to 75 years of age, undergoing first-time cardiac surgery with conventional median sternotomy, aortic clamping time between 40 and 120 minutes, and preoperative routine blood tests showing normal liver, renal, and coagulation functions. The exclusion criteria include salvage cases, a history of coagulopathy in the family, and long-term use of anticoagulation or antiplatelet drugs. INTERVENTIONS: Sixty patients were divided randomly into a control group (n = 30) receiving a traditional heparin regimen and an experimental group (n = 30) receiving an adjusted regimen. MEASUREMENTS AND MAIN RESULTS: Activated coagulation time (ACT) was monitored at different time points, ACT>480 seconds was set as the safety threshold of CPB. Heparin doses (initial dose, added dose, and total dose), protamine doses (initial dose, added dose, and total dose), CPB time, aortic clamping time, assisted circulation time, sternal closure time, blood transfusion volume, and drainage volume 24 hours after surgery were recorded. There was no significant difference in achieving target ACT after the initial dose of heparin between the 2 groups; CPB time, aortic clamping time, assisted circulation time, postoperative complication rate, and drainage volume between the 2 groups were not significantly different (p>0.05). However, initial and total dosage of heparin, initial and total dosage of protamine, sternal closure time, and intraoperative blood transfusion volume in the experimental group were significantly lower (p< 0.05). CONCLUSIONS: Adjusted regimen of heparin infusion could be used safely and effectively in Chinese CPB patients, which might reduce the initial and total dosage of heparin and protamine as well as sternal closure time and intraoperative blood transfusion volume.

Hydrogen Sulfide Attenuates Myocardial Hypoxia-Reoxygenation Injury by Inhibiting Autophagy via mTOR Activation.

BACKGROUND: Autophagy plays a significant role in myocardial ischemia reperfusion (IR) injury. Hydrogen sulfide (H2S) has been demonstrated to protect cardiomyocytes against IR injury, while whether it has anti-autophagy effect has not been known. The aim of this study was to investigate whether H2S regulates autophagy during IR injury and its possible mechanism. METHODS AND RESULTS: The cardiomyocytes of neonatal rats were randomized into Con, hypoxia-reoxygenation (HR) and H2S protection groups. The severity of cell injury was evaluated by cell vitality (MTT) and lactate dehydrogenase (LDH) release assays, and autophagy level was evaluated by flow cytometry and the assessment of autophagy-related gene (Atg) expression, such as that of Beclin1 and LC3-II. In response to H2S, Beclin1 and LC3-II protein were found to be down-regulated and p-mTOR protein was found to be up-regulated, together with an increase in cell vitality and a decrease in LDH. Furthermore, to find out whether mTOR was involved in the protective effect of H2S, rapamycin, inhibiter of mTOR, was used with or without applying NaHS and HR. It was found that rapamycin attenuated the myocardiocyte protective effect of H2S. To demonstrate the effect of autophagy during HR injury, the cardiomyocytes were pre-treated with 3-MA, which is an autophagy inhibitor, cell injury was attenuated by 3-MA. CONCLUSIONS: H2S plays a myocardial protective role against IR injury by regulating autophagy via mTOR activation.

Risk factors for embolism in cardiac myxoma: a retrospective analysis.

BACKGROUND: Myxomas are the most common primary heart tumors and are closely associated with embolic events. Cardiac myxomas typically arise from the interatrial septum at the border of the fossa ovalis in the left atrium. Any other location is considered atypical. Embolism, one of the complications of myxoma, is associated with high morbidity and mortality. The aim of this study was to investigate the risk factors for embolism in patients with cardiac myxoma. MATERIAL AND METHODS: In this retrospective study, a cohort of 162 patients with cardiac myxomas was surgically treated between January 1998 and June 2014 at 3 cardiac centers in China. Preoperative data, including platelet count, sex, age, and the tumor (size, location, surface, and attachment), were compared between embolic and non-embolic groups of patients. RESULTS: No significant differences in vascular risk factors were seen between the 2 groups. However, the percentage of higher platelet count (>300 × 10(9)/L) and mean platelet volume in the embolic group were significantly higher than in the non-embolic group (P=0.0356, and 0.0113, respectively). Irregular surface and atypical location of the myxomas were also independently associated with increased risk of embolic complications. CONCLUSIONS: Tumor location, macroscopic appearance, mean platelet volume, and high platelet count are strong risk factors for embolic events in patients with cardiac myxomas.