Cardioprotective effects of high-altitude adaptation in cardiac surgical patients: a retrospective cohort study with propensity score matching.

Background: The cardioprotective effect of remote ischemia preconditioning in clinical studies is inconsistent with experimental results. Adaptation to high-altitude hypoxia has been reported to be cardioprotective in animal experiments. However, the clinical significance of the cardioprotective effect of high-altitude adaptation has not been demonstrated. Methods: A retrospective cohort study with propensity score matching was designed to compare the outcomes of cardiac surgery between highlanders and lowlanders in a tertiary teaching hospital. The data of adult cardiac surgical patients from January 2013 to December 2022, were collected for analysis. Patients with cardiopulmonary bypass and cardioplegia were divided into a low-altitude group (<1,500 m) and a high-altitude group (≥1,500 m) based on the altitude of their place of residence. Results: Of 3,020 patients, the majority (87.5%) permanently lived in low-altitude regions [495 (435, 688) m], and there were 379 patients (12.5%) in the high-altitude group [2,552 (1,862, 3,478) m]. The 377 highlander patients were matched with lowlander patients at a ratio of 1:1. The high-altitude group exhibited a 44.5% reduction in the incidence of major adverse cardiovascular events (MACEs) compared with the low-altitude group (6.6% vs. 11.9%, P = 0.017). The patients in the moderate high-altitude subgroup (2,500-3,500 m) had the lowest incidence (5.6%) of MACEs among the subgroups. The level of creatinine kinase muscle-brain isoenzymes on the first postoperative morning was lower in the high-altitude group than in the low-altitude group (66.5 [47.9, 89.0] U/L vs. 69.5 [49.3, 96.8] U/L, P = 0.003). Conclusions: High-altitude adaptation exhibits clinically significant cardioprotection in cardiac surgical patients.

NLRP6 deficiency inhibits neuroinflammation and ameliorates brain injury in ischemic stroke by blocking NLRs inflammasomes activation through proteasomal degradation of pro-caspase-1.

Innate inflammation is crucial for ischemic stroke development. NLRP6, a nucleotide-binding and oligomerization domain-like receptors (NLRs) family member, regulates innate inflammation. Whether NLRP6 regulates neurological damage and neuroinflammation during ischemic stroke remains unclear. We report that NLRP6 is abundantly expressed in microglia and significantly upregulated in the ischemic brain. The brain injury severity was alleviated in NLRP6-deficient mice after ischemic stroke, as evidenced by reduced cerebral infarct volume, decreased neurological deficit scores, improved histopathological morphological changes, ameliorated neuronal denaturation, and relief of sensorimotor dysfunction. In the co-culture OGD/R model, NLRP6 deficiency prevented neuronal death and attenuated microglial cell injury. NLRP6 deficiency blocked several NLRs inflammasomes' activation and abrogated inflammasome-related cytokine production by decreasing the expression of the common effector pro-caspase-1. NLRP6 deficiency reduced pro-caspase-1's protein level by inducing proteasomal degradation. These findings confirm the neuroprotective role of NLRP6 deficiency in ischemic stroke and its underlying regulation mechanism in neuroinflammation and provide a potential therapeutic target for ischemic stroke.

A comparison of bilateral and unilateral cerebral perfusion for total arch replacement surgery for non-marfan, type A aortic dissection.

OBJECTIVES: Acknowledging lacking of consensus exist in total aortic arch (TAA) surgery for acute type A aortic dissection (AAD), this study aimed to investigate the neurologic injury rate between bilateral and unilateral cerebrum perfusion on the specific population. METHODS: A total of 595 AAD patients other than Marfan syndrome receiving TAA surgery since March 2013 to March 2022 were included. Among them, 276 received unilateral cerebral perfusion (via right axillary artery, RCP) and 319 for bilateral cerebral perfusion (BCP). The primary outcome was neurologic injury rate. Secondary outcomes were 30-day mortality, serum inflammation response (high sensitivity C reaction protein, hs-CRP; Interleukin-6, IL-6; cold-inducible RNA binding protein, CIRBP) and neuroprotection (RNA-binding motif 3, RBM3) indexes. RESULTS: The BCP group reported a significantly lower permanent neurologic deficits [odds ratio: 0.481, Confidence interval (CI): 0.296-0.782, p = 0.003] and 30-day mortality (odds ratio: 0.353, CI: 0.194-0.640, p < 0.001) than those received RCP treatment. There were also lower inflammation cytokines (hr-CRP: 114 ± 17 vs. 101 ± 16 mg/L; IL-6: 130 [103,170] vs. 81 [69,99] pg/ml; CIRBP: 1076 [889, 1296] vs. 854 [774, 991] pg/ml, all p < 0.001), but a higher neuroprotective cytokine (RBM3: 4381 ± 1362 vs 2445 ± 1008 pg/mL, p < 0.001) at 24 h after procedure in BCP group. Meanwhile, BCP resulted in a significantly lower Acute Physiology, Age and Chronic Health Evaluation (APACHE) Ⅱscore (18 ± 6 vs 17 ± 6, p < 0.001) and short stay in intensive care unit (4 [3,5] vs. 3 [2,3] days, p < 0.001) and hospital (16 ± 4 vs 14 ± 3 days, p < 0.001). CONCLUSIONS: This present study indicated that BCP compared with RCP was associated with lower permanent neurologic deficits and 30-day mortality in AAD patients other than Marfan syndrome receiving TAA surgery.

Low-dose dexamethasone in combination with luteolin improves myocardial infarction recovery by activating the antioxidative response.

This study aimed to explore the effects of dexamethasone (DEX) and its combination with luteolin (LUT) on cardiac function during myocardial infarction (MI) in a mouse model. We evaluated whether the Keap1/Nrf2 pathway mediates the cardioprotective function of DEX both in vivo and in vitro. The MI mouse model was established by ligation of the left anterior descending coronary artery of wild-type (WT) and Nrf2 knockout mice. After recovery for 21 days, DEX or its combination with LUT was intraperitoneally administered at different doses to WT or Nrf2 knockout mice daily for 7 consecutive days. Mice treated with DEX at a low dose (50 µg/kg/day) showed better cardiac function, fewer cardiac lesions, and smaller infarct sizes compared with MI model mice. DEX (50 µg/kg/day) administration also significantly decreased the production of reactive oxygen species (ROS) and pro-inflammatory cytokines, increased the expression of antioxidative enzymes, and activated the Keap1/Nrf2/HO-1 pathway. However, in Nrf2 knockout mice, DEX treatment did not influence cardiac function, inflammation, the oxidative response, or Keap1/Nrf2/HO-1 activation. In the MI cell model, low concentrations of DEX attenuated the H2O2-induced decreases in cell viability and antioxidative enzyme levels and activated the Keap1/Nrf2/HO-1 pathway. Low doses of DEX exerted protective effects in MIR mice and MI cell models by improving cardiac function, eliminating ROS, inhibiting inflammatory responses, and activating antioxidative responses. The protective effects of DEX on myocardial tissues were mediated by the Keap1/Nrf2/HO-1 pathway.

The impact of medical insurance reimbursement on postoperative inflammation reaction in distinct cardiac surgery from a single center.

BACKGROUND: Evidences shows that socioeconomic status is reversely associated with the risk of morbidity and mortality for people with cardiovascular disease via pro-inflammation mechanism, but the population profile is not deeply defined on. We aimed to investigate the impact of medical insurance coverage on postoperative systemic inflammatory reaction in two kinds of disease populations undergoing distinct cardiac procedures. METHODS: A total of 515 patients receiving open mitral valve procedure with high-total expense from May 2013 through May 2021 in Sichuan Provincial People's Hospital were retrospectively collected and stratified according to medical insurance reimbursement: low coverage with high out-pocket (< 30%), medium coverage (≤ 60%, but ≥ 30%), and high coverage (> 60%). Another 118 cases undergoing atrium septum defect (ASD) or patent foramen ovale (PFO) occlusion and taking on consistent low-total expense and low-coverage (< 30%) were also classified according to their insured conditions. The postoperative systemic inflammatory response indexes were high sensitivity C-reactive protein (hs-CRP) and the neutrophil-lymphocyte ratio (NLR). RESULTS: Low insurance reimbursement population undergoing open mitral valve procedure had a higher level of hs-CRP and NLR but not troponin I protein or lactate within 48 h postoperatively, and higher thoracic drainage, longer ventilation use and stay in intensive care unit. No significant difference in inflammatory indexes existed among diverse medical insurance coverage in population undergoing ASD/PFO occlusion. CONCLUSIONS: Higher inflammatory reaction and weaker clinical recovery was associated with lower insurance coverage population undergoing open mitral valve procedure but not ASD/PFO interventional occlusion procedure.

Modifying strategies for SDF-1/CXCR4 interaction during mesenchymal stem cell transplantation.

Mesenchymal stem cell (MSC) transplantation is regarded as a promising candidate for the treatment of ischaemic heart disease. The major hurdles for successful clinical translation of MSC therapy are poor survival, retention, and engraftment in the infarcted heart. Stromal cell-derived factor-1/chemokine receptor 4 (SDF-1/CXCR4) constitutes one of the most efficient chemokine/chemokine receptor pairs regarding cell homing. In this review, we mainly focused on previous studies on how to regulate the SDF-1/CXCR4 interaction through various priming strategies to maximize the efficacy of mesenchymal stem cell transplantation on ischaemic hearts or to facilitate the required effects. The strengthened measures for enhancing the therapeutic efficacy of the SDF-1/CXCR4 interaction for mesenchymal stem cell transplantation included the combination of chemokines and cytokines, hormones and drugs, biomaterials, gene engineering, and hypoxia. The priming strategies on recipients for stem cell transplantation included ischaemic conditioning and device techniques.

Multiple left ventricular myxomas combined with severe rheumatic valvular lesions: A case report.

BACKGROUND: Primary cardiac tumors are uncommon, of which cardiac myxoma accounts for 50%-80%. Left ventricular myxoma has been rarely reported, accounting for only 3%-4% of all cardiac myxomas. Multiple left ventricular myxomas are, relatively, even rarer. CASE SUMMARY: In this report, we present a case of multiple left ventricular myxomas combined with severe rheumatic valve lesions. Symptomatically, the patient presented with fatigue, shortness of breath, and palpitation after activities. The patient underwent complete surgical resection of multiple left ventricular myxomas combined with mechanical replacement of the mitral and aortic valves, tricuspid valvuloplasty. The patient recovered well after the operation, with no obvious related complications. CONCLUSION: Multiple left ventricular myxomas may coexist with severe rheumatic valve disease. Operation is an effective treatment.

Long-Term High-Altitude Exposure Does Not Increase the Incidence of Atrial Fibrillation Associated with Organic Heart Diseases.

Wang, Man, Mengxue Liu, Jia Huang, Dan Fan, Shengzhong Liu, Tao Yu, Keli Huang, Xinchuan Wei, and Qian Lei. Long-term high-altitude exposure does not increase the incidence of atrial fibrillation associated with organic heart diseases. High Alt Med Biol. 22:285-292, 2021. Background: Atrial fibrillation (AF) is one of the most common arrhythmias and is associated with several complications following cardiac surgery. However, the differences in the incidence of AF associated with organic heart diseases between highland and lowland populations have not been comprehensively studied. Methods: In this retrospective study, a total of 2,316 highland and lowland patients who underwent cardiac surgery between January 2013 and December 2018 in a single center were enrolled. According to the altitude of residence, patients were divided into high-altitude (>1,500 m) and low-altitude (<1,500 m) groups. A propensity score matching analysis was performed to estimate the association of lifetime high-altitude exposure with AF. Results: Among the enrolled patients, 239 (10.9%) were from a high-altitude plateau, while 1,946 (89.1%) were from a low-altitude area. There were statistical differences in age, gender, European System for Cardiac Operative Risk Evaluation, and other factors, between the two groups (p < 0.05). According to the propensity score, 237 patients in the high-altitude group were successfully matched to 237 patients in the low-altitude group without significant difference in baseline data (p > 0.05). Among the matched patients, 125 patients (26.4%) suffered from AF, with 66 (27.8%) in the high-altitude group and 59 (24.9%) in the low-altitude group. The incidence of AF was statistically similar between the two groups and not significantly influenced by long-term high-altitude exposure (odds ratio 1.07; 95% confidence interval 0.71-1.60, p > 0.05). Conclusion: Long-term high-altitude exposure did not significantly increase the occurrence of AF in patients with organic heart diseases. Clinical Trial No. ChiCTR1900028612.

Macrophage-mediated regulation of catecholamines in sympathetic neural remodeling after myocardial infarction.

Sympathetic neural remodeling, which involves the inflammatory response, plays an important role in ventricular arrhythmias (VAs) after myocardial infarction (MI). Adrenergic receptors on macrophages potentially modulate the inflammatory response. We hypothesized that the increased level of catecholamines activates macrophages and regulates sympathetic neural remodeling after MI. We treated MI mice with either clodronate or metoprolol for 5 days following coronary artery ligation. Mice without treatment after MI and sham-operation mice served as the positive control and negative control, respectively. The norepinephrine levels in plasma and the peri-infarct myocardium increased by almost two-fold in the MI mice compared with the sham-operation mice. Both in vivo and ex vivo electrophysiology examinations showed that the vulnerability to VAs induced by MI was alleviated by macrophage depletion with clodronate and ß1-adrenergic blockade with metoprolol, which was in line with circulating and peri-infarct norepinephrine levels, sympathetic reinnervation, and the expression of nerve growth factor (NGF) 7 days after surgery. To further verify the interaction between catecholamines and macrophages, we preconditioned lipopolysaccharide-stimulated RAW 264.7 cells using epinephrine or epinephrine with selective adrenergic antagonists. The expression and release of inflammatory factors including NGF were enhanced by epinephrine. This effect was inhibited by metoprolol but not by other subtype antagonists. Our data suggested that the increased level of catecholamines, traditionally known as positive inotropes secreted from sympathetic nerve endings, might regulate cardiac sympathetic neural remodeling through ß1-adrenergic receptors on macrophages, subsequently inducing VAs after MI.

[The Regulation of AMPKα1/Nrf2/ HO-1 Pathway Mediated by Galantamine Hydrobromide Lycoremine in Myocardial Ischemia Reperfusion Rats].

OBJECTIVE: To investigate the effects of AMPKα1/Nrf2/heme oxygenase-1 (HO-1) pathway mediated by galantamine hydrobromide lycoremine (Gal) on endoplasmic reticulum stress apoptosis, myocardial apoptosis and fibrosis in rats with myocardial ischemia reperfusion (I/R). METHODS: A myocardial ischemia reperfusion injury rat model was established, and the rats were randomly divided into 5 groups: Control group, I/R model group, Gal 1 mg/kg group, Gal 2 mg/kg group and Gal 4 mg/kg group. Left ventricular ejection fraction (LVEF), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular wall thickness (LVWT), and left ventricular short-axis shortening rate (FS) were detected by doppler ultrasound. Hematoxylin eosin staining was used to detect the pathological damage of myocardial tissue. The expression of Caspase-3 was detected by immunohistochemistry. Protein expression levels of CCAAT/enhancer-binding protein homologous protein (CHOP), cleaved Caspase-12, growth arrest and DNA damageinducible protein 34 (GADD34), immunoglobulin heavy-chain-binding protein (BiP), α-smooth muscle actin (α-SMA), Collagen Ⅰ, AMPKα1, Nrf2, and HO-1 were measured by western blot, and AMPK inhibitor Compound C was added for verification. RESULTS: Compared with the I/R model group, the grade of pathological damage of myocardial tissue in each group of Gal was improved, and cleaved Caspase-3 positive expression rate and Caspase-3 mRNA level were significantly reduced ( P<0.05) as well. The results showed that LVWT, FS and LVEF in Gal 2 mg/kg and Gal 4 mg/kg groups were significantly increased ( P<0.05), LVEDV and LVESV were significantly reduced ( P<0.05) compared with I/R model group. CHOP, cleaved Caspase-12, α-SMA, Collagen Ⅰ, AMPKα1, Nrf2, HO-1 protein levels were significantly reduced ( P<0.05), and GADD34 and BiP protein levels were significantly increased ( P<0.05) in Gal 2 mg/kg and Gal 4 mg/kg groups. CONCLUSION: The regulation of AMPKα1/Nrf2/HO-1 pathway mediated by Gal on endoplasmic reticulum stress apoptosis, myocardial apoptosis and fibrosis in myocardial ischemia reperfusion rats.

The Role of BRAF V600E in Reducing AUS/FLUS Diagnosis in Thyroid Fine Needle Aspiration.

BRAF V600E mutations are common in papillary thyroid carcinoma (PTC) and some de-differentiated thyroid cancers. In this study, we summarize AUS/FLUS diagnosed cases from thyroid fine needle aspirations in our center from 2015 to 2017 to explore the impact of BRAF V600E detection on the cytopathological diagnosis of PTC. BRAF V600E detection could significantly reduce the AUS/FLUS diagnosis rates from 11.59 to 8.42% when all BRAF V600E-mutated AUS/FLUS cases were diagnosed as conforming to PTC (20.01 to 19.13% in 2016 and 10.92 to 7.93% in 2017, respectively). The AUS/M rates decreased from 0.67 to 0.64 in 2016 and from 0.33 to 0.23 in 2017. We further discuss a case with a single BRAF V600E cytological mutant lacking a postoperative PTC diagnosis and discuss the limitations of BRAF V600E detection using puncture elution fluid. Our findings support the notion that BRAF V600E detection can effectively reduce the diagnostic rates of AUS/FLUS and help clinicians decide both treatment strategies and patient prognosis.

Debulking and three-dimensional reconstruction of a rare case of right atrium-ventricular angiosarcoma.

A 48-year-old man presented with chest pain and ischemic manifestations according to an electrocardiogram due to coronary artery compression from a cardiac mass and was admitted to the emergency room and underwent extensive debulking followed by right atrium and ventricular three-dimensional reconstruction with concomitant tricuspid valve remodeling. He recovered a normal sinus rhythm and was discharged from the hospital a week later with a diagnosis of cardiac malignant angiosarcoma according to the pathological examination. He survived and had a normal cardiac structure and function performance, but vertebral metastasis was suspected after more than 4 months of follow-up after the procedure.

Analysis of potential roles of combinatorial microRNA regulation in occurrence of valvular heart disease with atrial fibrillation based on computational evidences.

BACKGROUND: Atrial fibrillation (AF) is the most common arrhythmia. Patients with valvular heart disease (VHD) frequently have AF. Growing evidence demonstrates that a specifically altered pattern of microRNA (miRNA) expression is related to valvular heart disease with atrial fibrillation (AF-VHD) processes. However, the combinatorial regulation by multiple miRNAs in inducing AF-VHD remains largely unknown. METHODS: The work identified AF-VHD-specific miRNAs and their combinations through mapping miRNA expression profile into differential co-expression network. The expressions of some dysregulated miRNAs were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The regulations of signaling pathways by the combinatorial miRNAs were predicted by enrichment analysis tools. RESULTS: Thirty-two differentially expressed (DE) miRNAs were identified to be AF-VHD-specific, some of which were new findings. These miRNAs interacted to form 5 combinations. qRT-PCR confirmed the different expression of several identified miRNAs, which illustrated the reliability and biomarker potentials of 32 dysregulation miRNAs. The biological characteristics of combinatorial miRNAs related to AF-VHD were highlighted. Twelve signaling pathways regulated by combinatorial miRNAs were predicted to be possibly associated with AF-VHD. CONCLUSIONS: The AF-VHD-related signaling pathways regulated by combinatorial miRNAs may play an important role in the occurrence of AF-VHD. The work brings new insights into biomarkers and miRNA combination regulation mechanism in AF-VHD as well as further biological experiments.

Intraoperative Implantation of Temporary Endocardial Pacing Catheter During Thoracoscopic Redo Tricuspid Surgery.

BACKGROUND: The placement of a temporary epicardial pacing wire is a challenge during a minimally invasive redo cardiac operation. The aim of this study is to assess the application of temporary endocardial pacing in patients who underwent minimally invasive redo tricuspid surgery. METHODS: Perioperative data of consecutive patients who underwent thoracoscopic redo tricuspid surgery were collected. All the tricuspid surgeries and combined procedures were performed under peripheral cardiopulmonary bypass without aortic cross-clamping. A sheath was introduced into the right jugular vein beside the percutaneous superior vena cava cannula and a temporary endocardial pacing catheter was guided into the right ventricle via the sheath prior to the right atrial closure. The pacemaker was connected and run as needed during or after operation. RESULTS: A total of 33 patients who underwent thoracoscopic redo tricuspid surgery were enrolled. Symptomatic tricuspid valve regurgitation (93.9%) and tricuspid valvular prosthesis obstruction (6.1%) after previous cardiac operations were noted as indications for a redo surgery. The mean time from previous cardiac operation to this time redo surgery was 13.3±6.4years. Isolated tricuspid valve replacement was performed in 18 patients (54.5%) and tricuspid valve plasty combined with or without mitral valve replacement was performed in 15 patients (45.5%). A temporary endocardial pacing catheter was successfully placed in the right ventricle for all patients with good sensing and pacing. No temporary pacing related complications occurred from insertion to removal of pacing catheter in the patients. CONCLUSIONS: This application of temporary endocardial pacing provided a safe and effective substitute for epicardial pacing in patients who underwent minimally invasive redo tricuspid surgery.

Comparison of two radiofrequency ablation devices for atrial fibrillation concomitant with a rheumatic valve procedure.

BACKGROUND: Perioperative and median-term follow-up outcomes have not been compared among procedures using radiofrequency ablation devices for permanent atrial fibrillation with concomitant rheumatic valve disease. We compared the sinus rhythm restoration efficacy of "non-irrigation" ablation forceps and an "irrigation" ablation device in patients with rheumatic valve disease undergoing a modified Cox maze radiofrequency ablation procedure due to permanent atrial fibrillation. METHODS: Data of 278 patients with rheumatic valve disease from the Cardiac Surgery Department of Sichuan Provincial People's Hospital who underwent the modified Cox maze radiofrequency ablation procedure between May 2013 and May 2017 were reviewed. The procedure was performed using "non-irrigation" ablation forceps (AtriCure, group A) in 149 patients and an "irrigation" ablation device (Medtronic, group M) in 129 patients. Data were collected prospectively, and follow-up was documented and compared between the groups. RESULTS: The radiofrequency procedure duration was 28.9 ±â€Š3.8 min in group A and 29.5 ±â€Š2.8 min in group M (t = 1.623, P = 0.106). The predicted radiofrequency time to the left atrium diameter was (Ya = 0.4964 X + 0.3762, R = 0.74) in group A and (Ym = 0.4331 X + 4.3563, R = 0.8435) in group M. The sinus rhythm (SR) conversion rate without use of anti-arrhythmic drugs was similarly good in groups A and M, with 75.2%, 72.5%, and 70.5% vs. 73.6%, 71.3%, and 69.8% at discharge, 6 and 12 months, respectively (F = 0.084, F = 0.046, F = 0.046, P > 0.05, respectively). CONCLUSION: Two types of radiofrequency ablation devices characteristic of "non-irrigation" and "irrigation" bipolar ablation forceps were similarly efficient at SR restoration.

LncRNA-MIAT Increased in Patients with Coronary Atherosclerotic Heart Disease.

BACKGROUND: To study the expression and clinical significance of long noncoding RNA- (lncRNA-) MIAT in patients with coronary atherosclerotic heart disease (CAD). METHODS: Serum MIAT, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in 106 CAD patients and 89 healthy donors were detected. Correlations between serum MIAT and serum IL-6 and TNF-α were analyzed. Risk factors for patients with CAD were analyzed by multiple factor analysis. RESULTS: Compared with healthy donors, serum lncRNA-MIAT was significantly increased in CAD patients. Serum MIAT was positively correlated with serum IL-6 and TNF-α in CAD. Multivariate analysis found that hypertension (OR (95% CI) = 3.471 (2.180-4.091), P=0.011), diabetes (OR (95% CI) = 3.682 (1.698-4.897), P=0.003), HDL-C (OR (95% CI) = 3.372 (1.760-6.920), P=0.001), and serum MIAT expression (OR (95% CI) = 2.687 (1.683-7.468), P=0.001) were independent risk factors for CAD. CONCLUSIONS: Serum lncRNA-MIAT in CAD patients was significantly increased, which may be a potential marker for diagnosis and prognosis of CAD.

Remote ischaemic preconditioning ameliorates sinus rhythm restoration rate through Cox maze radiofrequency procedure associated with inflammation reaction reduction.

Remote ischaemic preconditioning (RIPC) as adjuvant to selective heart surgery attenuates cardiac injury and atrial fibrillation (AF) occurrence. We investigated its effect on sinus rhythm (SR) restoration rate in permanent AF patients undergoing Cox maze (CM) radiofrequency ablation with concomitant mitral valve surgery. From May 2013 to May 2017, 206 patients with rheumatic valve disease concomitant with permanent AF were randomized to receive prosthesis valve replacement and CM radiofrequency ablation procedure with (n = 104) or without (n = 102) RIPC (intermittent arm ischaemia through three cycles of 5-min inflation, followed by 5-min deflation of a blood pressure cuff). The primary end point of the study was freedom from cumulative AF without using antiarrhythmic drugs 1 year after operation; the secondary end points included inflammation reaction index over 48 h postoperatively and clinical outcomes. Baseline characteristics and preoperative data did not differ between groups. The SR restoration rates were significantly higher in the RIPC group, 85.6%, 83.7%, and 82.7%, than those in the control group, 72.5%, 70.6%, and 69.6%, at discharge, 6 months and 12 months, respectively, after the radiofrequency ablation procedure (P < 0.05). The serum concentration of high sensitivity C-reactive protein and neutrophil-lymphocyte ratio were significantly decreased at 12 h, 24 h, and 48 h postoperatively in the RIPC group compared to those in the control group (P < 0.05). RIPC induced by brief ischaemia and reperfusion of the arm ameliorated SR restoration rate in patients with permanent AF through CM radiofrequency ablation procedure and was associated with reduction of postoperative systemic inflammation reaction index.

Preoperative proteinuria and clinical outcomes in type B aortic dissection after thoracic endovascular aortic repair.

Background Proteinuria is a marker of poor outcomes in several diseases; however, few studies have been conducted to explore the prognostic value of proteinuria, assessed by urine dipstick test, for clinical outcomes in patients with type B acute aortic dissection (TBAD) undergoing thoracic endovascular aortic repair (TEVAR). Methods Consecutive patients with TBAD undergoing TEVAR were enrolled from January 2010 to July 2015. Proteinuria was defined as trace or higher, according to the results of urine dipstick testing. Associations among proteinuria and adverse events were evaluated. Results In total, 671 patients with a mean age of 44±15 years were included in the analysis. Proteinuria was detected in 281 patients (41.9%) before TEVAR. Multivariate logistic regression analysis showed that C-reactive protein and impaired renal function were independent predictors for proteinuria. During hospitalization, 21 patients died. In-hospital mortality was higher in patients with proteinuria (1.5% vs. 5.3%, p=0.005). After a median 3.4 years follow up, the post-TEVAR death rate was 10.4% (85 patients were lost to follow-up). The long-term cumulative mortality was significantly higher in patients with proteinuria (17.2% vs. 8.2%, log-rank=11.36, p=0.001). Multivariate Cox survival modeling indicated that proteinuria was significantly associated with long-term death, after adjustment for potential confounding risk factors (HR=1.92, p=0.012). Conclusions Pre-TEVAR proteinuria was identified as a prognostic marker in patients with TBAD and has potential for application as a convenient and simple risk assessment method before TEVAR.

Osthole down-regulates miR-30a and promotes autophagy to protect rats against myocardial ischemia/reperfusion injury.

BACKGROUND: This study aims to investigate the changes in miR-30a expression and myocardial autophagy following osthole treatment in a myocardial ischemia/reperfusion injury model. METHODS: Thirty male Wistar rats (weighing 170 to 220 g, aged 8 weeks) were randomly divided into three groups as control (sham) group, ischemia/reperfusion (model) group, and ischemia/ reperfusion + osthole post-treatment (osthole) group. Masson"s trichrome staining was used to detect myocardial collagen changes. Apoptotic cardiomyocytes in the ischemic area were labeled in situ by terminal deoxynucleotidyl transferase-mediated dUTP (2'-deoxyuridine 5'-triphosphate) nick end labeling assay. Levels of autophagy markers light chain 3 beta (LC3b) and Beclin-1 in myocardial tissue were detected by western blotting. Expression of miR-30a was detected by quantitative reverse transcriptionpolymerase chain reaction. RESULTS: Compared with the sham group, ischemia/reperfusion significantly increased collagen contents. Osthole significantly inhibited the ischemia/reperfusion-increased collagen contents. Osthole inhibited the ischemia/reperfusion-increased myocardial fibrosis, myocardial swelling, necrosis, and myocardial atrophy. Osthole also significantly inhibited the ischemia/reperfusionincreased apoptosis of myocardial cells. Moreover, the conversion of LC3b-I to LC3b-II and the Beclin-1 expression were significantly inhibited by ischemia/reperfusion. Osthole treatment significantly increased the conversion of LC3b-I to LC3b-II and Beclin-1 expression in ischemia/reperfusion rats. Finally, the expression of miR-30a was significantly increased in ischemia/reperfusion rats, while Osthole suppressed the expression of miR-30a. CONCLUSION: Osthole promoted autophagy, thereby alleviating myocardial ischemia/reperfusion injury. Osthole protects the myocardium during autophagy by down-regulating miR-30a expression.

Feasibility, safety, and short-term outcome of totally thoracoscopic mitral valve procedure.

BACKGROUND: The totally thoracoscopic procedure for mitral valve (MV) disease is a minimally invasive method. We investigated the procedure's feasibility, safety and effectiveness when it was performed by an experienced operator. METHODS: We retrospectively analysed 53 consecutive patients with MV disease treated between December 2014 and April 2017 by minimally invasive procedures. The procedures were performed on femoral artery-vein bypass through three 2-4 cm incisions, with one additional penetrating point on the right chest wall under totally thoracoscopic visual guidance and surveillance of transoesophageal echocardiography. RESULTS: Two patients who underwent intraoperative conversion to sternotomy were excluded due to indivisible pleural cavity adhesion. Of the others (38 female patients, average age, 49 ± 14 years, left ventricular ejection fraction, 59 ± 7%), 34 received MV replacement for rheumatic mitral lesions, which was redone for one patient after the discovery of serious paravalvular leakage, 17 received MV repair for mitral regurgitation (with 4 secondary to atrial septum defect, 2 diagnosed with left atrial myxoma, and 2 redone for mitral valve replacement due to repair failure), 28 received additional tricuspid valvuloplasty, and one patient received a Warden procedure. The cardiopulmonary bypass and aortic cross clamp times were 144 ± 39 min and 80 ± 22 min, respectively. Postoperational chest tube drainage in the first 48 h was 346 ± 316 ml. The ventilation time and intensive care unit stay length were 11 ± 11 h and 23 ± 2 h, respectively. One patient died of disseminated intravascular coagulation and prosthesis thrombosis with fear of anticoagulation-related bleeding. CONCLUSIONS: The totally thoracoscopic procedure on mitral valves by an experienced surgeon is technically feasible, safe, effective and worthy of widespread adoption in clinical practice.