Gut microbiota might mediate the benefits of high-fiber/acetate diet to cardiac hypertrophy mice

Continuously prolonged cardiac hypertrophy results in maladaptive myocardial remodeling, which affects cardiac function and can eventually lead to heart failure. Short-chain fatty acids (SCFAs), including acetate, propionate, and butyrate, have been reported to be associated with cardiovascular diseases (CVD). Gut microbiota may mediate between dietary fiber and SCFA effects on cardiac hypertrophy. The mice model of isoproterenol (ISO)-induced cardiac hypertrophy was constructed and verified for physiological, functional, and fibrotic alterations in this study. Both high-fiber and acetate diet improved physiological indexes, ameliorated cardiac functions, and relieved fibrotic alterations in model mice hearts; collectively, cardiac hypertrophy in mice receiving both high-fiber and acetate diet improved. Following 16s rDNA sequencing and integrative bioinformatics, analyses indicated that both high-fiber and acetate diet caused alterations in mice gut microbiota compared with the ISO group, including OTU composition and abundance. In conclusion, high-fiber and acetate diet improve the physiological status, cardiac functions, and fibrotic alterations in ISO-induced hypertrophic mice. Besides, considering the alterations in mice gut microbiota in response to single ISO, both high-fiber and acetate diet treatment, gut microbiota might mediate the favorable benefits of both high-fiber and acetate diet on cardiac hypertrophy. (AU)

Gut microbiota might mediate the benefits of high-fiber/acetate diet to cardiac hypertrophy mice.

Continuously prolonged cardiac hypertrophy results in maladaptive myocardial remodeling, which affects cardiac function and can eventually lead to heart failure. Short-chain fatty acids (SCFAs), including acetate, propionate, and butyrate, have been reported to be associated with cardiovascular diseases (CVD). Gut microbiota may mediate between dietary fiber and SCFA effects on cardiac hypertrophy. The mice model of isoproterenol (ISO)-induced cardiac hypertrophy was constructed and verified for physiological, functional, and fibrotic alterations in this study. Both high-fiber and acetate diet improved physiological indexes, ameliorated cardiac functions, and relieved fibrotic alterations in model mice hearts; collectively, cardiac hypertrophy in mice receiving both high-fiber and acetate diet improved. Following 16s rDNA sequencing and integrative bioinformatics, analyses indicated that both high-fiber and acetate diet caused alterations in mice gut microbiota compared with the ISO group, including OTU composition and abundance. In conclusion, high-fiber and acetate diet improve the physiological status, cardiac functions, and fibrotic alterations in ISO-induced hypertrophic mice. Besides, considering the alterations in mice gut microbiota in response to single ISO, both high-fiber and acetate diet treatment, gut microbiota might mediate the favorable benefits of both high-fiber and acetate diet on cardiac hypertrophy.

Clinical effectiveness and efficiency of a new steerable sheath technology for radiofrequency ablation in Chinese patients with atrial fibrillation: a retrospective comparative cohort study.

Background: The clinical effectiveness and efficiency of a steerable sheath for radiofrequency catheter ablation (RFCA) in Chinese patients with atrial fibrillation (AF) needs to be compared with a fixed curve sheath to optimize RFCA procedure. Methods: This retrospective study included adult AF patients with their first RFCA that was conducted by the same electrophysiologist using a steerable sheath (VIZIGO, Biosense Webster, Inc.) or a fixed curve sheath (NaviEase, Synaptic Medical) in a Chinese tertiary care hospital from January to November 2021. The medical records kept at the hospital were the source of study data that included patient baseline characteristics and outcome measures for the clinical effectiveness and efficiency of RFCA procedure. Multivariate generalized linear regression analyses were performed to explore the impact of sheath type on clinical effectiveness and efficiency after adjustment. Results: Fourteen patients using steerable sheath and 34 patients using fixed curve sheath for RFCA were included in the data analysis. Most of patient baseline characteristics associated with the two study groups were comparable except that the steerable sheath group had significantly higher left atrium diameter (41.9±6.5 vs. 38.1±3.9 mm, P=0.017) and larger left atrium volume (150.4±29.5 vs. 126.8±27.5 mL, P=0.017) than the fixed curve sheath group. Using steerable sheath was associated with significantly shorter total pulmonary vein isolation (PVI) fluoroscopy time and post-surgery hospital length of stay (LOS) than using fixed curve sheath in both unadjusted comparisons (PVI fluoroscopy time: 1.3±1.5 vs. 4.0±3.9 min, P=0.004; post-surgery LOS: 2.1±0.7 vs. 2.9±1.5 days, P=0.034) and multivariate generalized regression analyses (PVI fluoroscopy time: coefficient =-0.859, P=0.014; post-surgery LOS: coefficient =-0.303, P=0.018). Conclusions: Compared to fixed curve sheath, steerable sheath used for RFAC could have the potential to shorten the PVI fluoroscopy time and reduce post-surgery LOS in a Chinese real-world hospital setting. Future real-world studies with large sample size are needed to confirm our study findings.

Role of profilin-1 in vasculopathy induced by advanced glycation end products (AGEs).

AIMS: To construct a simple and feasible rat model to mimic diabetic vasculopathy by chronic injection of advanced glycation end products (AGEs) and further determine the role of profilin-1 in vasculopathy in AGE-injection rats. METHODS: Sprague-Dawley rats were injected with AGEs-BSA (25 mg/kg/day) for 0, 20, 30, 40, and 60 days by caudal vein. Then, the morphological changes in the aorta, heart, and kidney and the expression of profilin-1 were assessed. In cultured endothelial cells, shRNA profilin-1 was used to clarify the role of profilin-1 in AGEs-induced vascular endothelial lesions and inflammatory reactions. RESULTS: The aorta, heart, and kidney of the AGE-injection rats had obvious morphological changes. Also, the indicators of vascular remodeling in the aorta significantly increased, accompanied by the increased expression of profilin-1 in the aorta, heart, and kidney and polysaccharide content on the kidney basement membrane. In addition, the protein level of profilin-1 was markedly upregulated in the aorta of AGEs-injected rats and endothelial cells incubated with AGEs. shRNA profilin-1 markedly attenuated the upregulated expression of profilin-1, receptor for AGEs (RAGE), and NF-κB in endothelial cells incubated with AGEs, as well as reduced the high levels of ICAM-1, IL-8, TNF-α, ROS, and apoptosis induced by AGEs. CONCLUSIONS: Exogenous AGEs can mimic diabetic vasculopathy in vivo to some extent and increase profilin-1 expression in the target organs of diabetic complications. Blockade of profilin-1 attenuates vascular lesions and inflammatory reactions, suggesting its critical role in the metabolic memory mediated by AGEs.

Synthesis of benzo[b][1,5]diazocin-6(5H)-one derivatives via the Cu-catalysed oxidative cyclization of 2-aryl-1H-indoles with 1,1-enediamines.

A novel protocol for the synthesis of highly functionalized benzo[b][1,5]diazocin-6(5H)-one derivatives (BDCOs, 4 and 5) from 2-aryl-1H-indoles and 1,1-enediamines was developed via a complex cascade of reactions including regioselective free radical oxidation, the 1,2-addition of imine, imine-enamine tautomerization, intramolecular cyclization, and ring expansion. The cascade reaction was enabled by refluxing a mixture of two substrates in the presence of di-tert-butyl peroxide (DTBP) as an oxidant and anhydrous CuI as a catalyst in toluene under argon protection. Consequently, a series of BDCOs (4 and 5) were synthesized with high regioselectivity in good yield. This protocol can be used for the synthesis of functionalized BDCOs via a one-pot oxidative annulation reaction rather than a multi-step reaction, which is suitable for both combinatorial and parallel syntheses of BDCOs.

Berberine up-regulates miR-340-5p to protect myocardial ischaemia/reperfusion from HMGB1-mediated inflammatory injury.

AIMS: Myocardial ischaemia/reperfusion injury (MIRI) is a major cause of heart failure after myocardial infarction. Berberine (BBR) presents anti-inflammatory and immunosuppressive properties in many diseases. Our research looked into the therapeutic effects and mechanism of BBR in MIRI. METHODS AND RESULTS: MIRI animal and cell models were established. The mRNA and protein expressions were assessed using reverse transcription and quantitative real-time polymerase chain reaction and western blot. The haemodynamic parameters (left ventricular ejection fraction and left ventricular ejection fraction) were detected by echocardiography. The myocardial infarct size and myocardium lesion were assessed by triphenyltetrazolium chloride and haematoxylin-eosin staining. The levels of injury factors were determined by ELISA. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling staining was performed to analyse cell apoptosis. Dual luciferase reporter gene and RNA immunoprecipitation assays were carried out to verify the interaction between miR-340-5p and HMGB1. BBR administration could improve the haemodynamic parameters and infarct size in MIRI rats (all P < 0.05). In MIRI rat model, BBR reduced cardiomyocyte apoptosis and inflammation (all P < 0.05). BBR could promote miR-340-5p expression (0.64 ± 0.21, P < 0.05), which is lowly expressed in MIRI group (0.24 ± 0.10, P < 0.01) in compare with the sham group (0.99 ± 0.01). MiR-340-5p knockdown abolished the protective effects of BBR on H/R-treated cardiomyocytes (all P < 0.05). BBR suppressed the HMGB1/TLR4/NF-κB pathway activation in MIRI. HMGB1 functioned as the target of miR-340-5p, and its silencing reversed the effect of miR-340-5p inhibitor on BBR-treated MIRI. CONCLUSIONS: In MIRI, BBR repressed HMGB1-mediated TLR4/NF-κB signalling pathway through miR-340-5p to suppress cardiomyocyte apoptosis and inflammation.

Ectopic Acsl6 Overexpression Partially Improves Isoproterenol-Induced Cardiac Hypertrophy In Vivo and Cardiomyocyte Hypertrophy In Vitro.

ABSTRACT: The increase in cardiac myocyte size is a critical issue in cardiac hypertrophy development. In this study, 61 differentially expressed genes between hypertrophic rats and normal controls were enriched in the positive modulation of fatty acid uptake, fatty acid metabolism and degradation, cardiac conduction, and the oxidation of carbohydrates and other processes. Acsl6 was significantly downregulated in hypertrophic rat and mouse hearts according to online data. Based on the experimental data, Acsl6 was underexpressed in ISO-induced cardiac hypertrophy mouse model and isoproterenol (ISO)-induced cardiomyocyte hypertrophy cell model. In vivo, Acsl6 overexpression partially attenuated ISO-induced increases in the cross-sectional area and cardiac hypertrophy, elevated hypertrophic markers, and caused impairment of cardiac function. In vitro, Acsl6 overexpression partially attenuated ISO-induced cardiomyocyte hypertrophy and increased hypertrophic markers. Conclusively, Ascl6 is downregulated in ISO-induced cardiac hypertrophy mouse model and ISO-induced cardiomyocyte hypertrophy cell model. Acsl6 overexpression could partially improve cardiac hypertrophy in vivo and cardiomyocyte hypertrophy in vitro, possibly through the regulation of HIF-1α/Hippo pathway.

Emerging role of m6 A modification in cardiovascular diseases.

Cardiovascular diseases (CVDs) contribute to the leading cause of death worldwide. Despite significant improvements in CVDs diagnosis and treatment, a continued effort to explore novel therapeutic strategies is urgently need. N6-methyladenosine (m6 A) RNA methylation, well known as the most prevalent type of RNA modifications, involved in RNA stability, nuclear exports, translation, and decoy, plays a crucial role in the pathogenesis of a variety of diseases, including CVDs, cancer, and drug resistance. Here, our article summarizes cellular functions of m6 A modulators and recent research progress concerning the functions and mechanisms of m6 A methylation in CVDs, in hope of providing references for exploring novel therapeutic approaches and potential biomarkers in the treatment of CVDs.

Effect of profilin-1 on the asymmetric dimethylarginine-induced vascular lesion-associated hypertension.

Previous studies have demonstrated that the levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthesis, are strongly associated with hypertension, diabetes, and cardiovascular diseases. Profilin-1, an actin-binding protein, has been documented to be involved in endothelial injury and in the proliferation of vascular smooth muscle cells resulting from hypertension. However, the role of profilin-1 in ADMA-induced vascular injury in hypertension remains largely unknown. Forty healthy subjects and forty-two matched patients with essential hypertension were enrolled, and the related indexes of vascular injury in plasma were detected. Rat aortic smooth muscle cells (RASMCs) were treated with different concentrations of ADMA for different periods of time and transfected with profilin-1 small hairpin RNA to interrupt the expression of profilin-1. To determine the role of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway, RASMCs were pretreated with AG490 or rapamycin. The expression of profilin-1 was tested using real-time polymerase chain reaction (PCR) and western blot analysis. Cell proliferation was measured by flow cytometry and 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazoliumbromide assays. Compared with healthy subjects, the levels of ADMA and profilin-1 were markedly elevated in hypertensive individuals, while the levels of NO were significantly decreased (p < 0.05). In vitro, studies showed ADMA-induced profilin-1 expression in a concentration- and time-dependent manner in RASMCs (p < 0.05), concomitantly with promoting the proliferation of RASMCs. Furthermore, ADMA-mediated proliferation of RASMCs and upregulation expression of profilin-1 were inhibited by blockade of the JAK2/STAT3 pathway or knockdown of profilin-1. Profilin-1 implicated in the ADMA-mediated vascular lesions in hypertension.

Nomogram Prediction Model for Diabetic Retinopathy Development in Type 2 Diabetes Mellitus Patients: A Retrospective Cohort Study.

BACKGROUND: This study is aimed at investigating the systemic risk factors of diabetic retinopathy and further establishing a risk prediction model for DR development in T2DM patients. METHODS: This is a retrospective cohort study including 330 type 2 diabetes mellitus (T2DM) patients who were followed up from December 2012 to November 2020. Multivariable cox regression analysis identifying factors associated with the hazard of developing diabetic retinopathy (DR) was used to construct the DR risk prediction model in the form of nomogram. RESULTS: 50.6% of participants (mean age: 58.60 ± 10.55) were female, and mean duration of diabetes was 7.09 ± 5.36 years. After multivariate cox regression, the risk factors for developing DR were age (HR 1.068, 95%Cl 1.021-1.118, P = 0.005), diabetes duration (HR 1.094, 95%Cl 1.018-1.177, P = 0.015), HbA1c (HR 1.411, 95%Cl 1.113-1.788, P = 0.004), albuminuria (HR 6.908, 95%Cl 1.794-26.599, P = 0.005), and triglyceride (HR 1.554, 95%Cl 1.037-2.330, P = 0.033). The AUC values of the nomogram for predicting developing DR at 3-, 4-, and 5-year were 0.854, 0.845, and 0.798. CONCLUSION: Combining age, diabetes duration, HbA1c, albuminuria, and triglyceride, the nomogram model is effective for early recognition and intervention of individuals at high risk of DR development.

Cerebral infarction as the first symptom in acute promyelocytic leukemia: A case report and literature review. / ä»¥è„‘æ¢—æ­»ä¸ºé¦–å‘ç—‡çŠ¶çš„æ€¥æ€§æ—©å¹¼ç²’ç»†èƒžç™½è¡€ç— 1例及文献回顾.

In the clinical settings, disseminated intravascular coagulation (DIC) and complications such as hemorrhage are commonly seen in acute promyelocytic leukemia patients, whereas thrombosis is rarely reported. We reported a case here that the patient presented with cerebral infarction as the first manifestation. During the admission, the patient encountered differentiation syndrome, pulmonary embolism, pulmonary hemorrhage, and myocardial ischemia, as well as bleeding and thrombosis complications. Hence the patient was diagnosed as DIC. After the treatment of blood transfusion instead of anticoagulation, his condition was stable and the remission was completely achieved. The treatment experience provides guides for other patients with similar complications of simultaneous bleeding and thrombosis.

Beta 2-Microglobulin and the Severity of Coronary Stenosis in Patients With Acute Coronary Syndrome.

BACKGROUND: Previous studies have shown that beta 2-microglobulin (B2M) could predict all-cause mortality and cardiovascular mortality in various groups of people. However, the relationship between B2M and severity of coronary stenosis in patients with acute coronary syndrome has not been established. METHODS: We enrolled 872 consecutive patients admitted with acute coronary syndrome in our study. All participants underwent coronary angiography examination or stent implantation after admission. The severity of coronary stenosis was assessed by Gensini score and the presentation of triple-vessel disease. B2M and other biochemical parameters were measured. All subjects were divided into quartiles of B2M. Multivariate linear regression and logistic regression were applied in the analysis. RESULTS: Gensini score and the prevalence of triple-vessel disease were elevated in accordance with increasing B2M quartiles (p=0.002 and p<0.001, respectively). Multivariate regression showed diabetes (p=0.031), high-sensitivity C-reactive protein (hs-CRP, p=0.043) and B2M (p=0.006) were positively correlated with Gensini score. Logistic regression analysis revealed that the crude and fully adjusted odds ratios of triple-vessel disease were 2.34 (95% CI: 1.58-3.46) and 1.97 (95% CI: 1.14-3.40) in the fourth quartile of B2M compared with the first quartile, respectively. However, no interactive relationships were found in subgroup analysis by estimated glomerular filtration rate or hs-CRP in the above associations, neither in the distribution of Gensini score (p for interaction>0.05 for both). CONCLUSION: Our data indicated that B2M was an independent risk factor of coronary stenosis in patients with acute coronary syndrome.

Correlations of DAPT score and PRECISE-DAPT score with the extent of coronary stenosis in acute coronary syndrome.

Dual antiplatelet therapy (DAPT) score and PRECISE-DAPT score were recommended for decision making of optimal DAPT in discriminating the risk of thrombosis and bleeding. But the relationships between 2 scoring tools with the extent of coronary stenosis have not been established.We retrospectively enrolled 359 patients of acute coronary syndrome (ACS) who received percutaneous coronary intervention. Both DAPT score and PRECISE-DAPT score were calculated, and patients were divided by their recommended cut-offs. Gensini score and triple-vessel disease (3-VD) were chosen to evaluate the severity of coronary stenosis.Overall, 54.9% and 10.0% of the patients had higher DAPT score (≥2) or PRECISE-DAPT score (≥25). Patients with higher DAPT score had increased stent counts, total length of stents, Gensini score, and proportion of 3-VD, but decreased minimum diameter of stent. But these differences were not found in PRECISE-DAPT subgroups. When divided into quartiles of both scoring systems, the highest Gensini score and proportions of 3-VD were found in the fourth quartile of both DAPT score and PRECISE-DAPT score. Moreover, both DAPT score and PRECISE-DAPT score were independent risk factors of Gensini score after adjustment (P < .001 and P = .047). Furthermore, an increase of 1 point of DAPT score and 5 points of PRECISE-DAPT score resulted by 51% (odds ratios [OR]: 1.51, 95% confidence interval [CI]:1.19-1.91, P = .001) and 34% (OR: 1.34, 95% CI: 1.11-1.62, P = .003) increase in risk of 3-VD after adjustment.Both DAPT score and PRECISE-DAPT score were independently associated with the degree of coronary stenosis in patients with ACS.

Association of Serum Prealbumin with Angiographic Severity in Patients with Acute Coronary Syndrome.

BACKGROUND Serum prealbumin (PA), which is a nutritional index, has been found to be associated with severities and prognoses of various diseases. However, there are no reports about the relationship between PA and angiographic severity of coronary artery disease. MATERIAL AND METHODS This cross-sectional study included 867 patients with acute coronary syndrome (ACS) who underwent coronary angiography. Patients were divided into quartiles of PA and coronary artery stenosis was determined by angiographic Gensini score, the presence of high Gensini score (Gensini score ≥120), and triple-vessel disease. Multivariate linear and logistic regression analyses were performed to explore the relationship between PA and disease severity in a coronary angiogram. RESULTS There was a significant and independent negative correlation between PA and Gensini score in multivariate linear regression (p=0.015). Logistic regression analysis revealed that crude odds ratios of triple-vessel disease and high Gensini score were 2.47 (95% CI: 1.66-3.67) and 1.83 (95% CI: 1.50-3.49), respectively, in the first quartile of PA compared with the fourth quartile and the results remained significant for high Gensini score after adjustment for confounding factors. In addition, estimated glomerular filtration rate, liver function, and high-sensitivity C-reactive protein (hs-CRP) had no interactive relationships in the above associations. Patients with lower levels of albumin or higher levels of hs-CRP or the ratio of hs-CRP to PA (hs-CRP/PA) also had more severe coronary atherosclerosis. CONCLUSIONS PA is negatively and independently associated with angiographic severity in patients with ACS, indicating for potential use in estimating the burden of coronary atherosclerosis.

Effective Adsorption and Removal of Phosphate from Aqueous Solutions and Eutrophic Water by Fe-based MOFs of MIL-101.

Although many efforts have been devoted to the adsorptive removal of phosphate from aqueous solutions and eutrophic water, it is still highly desirable to develop novel adsorbents with high adsorption capacities. In this study, Fe-based metal-organic frameworks (MOFs), MIL-101 and NH2-MIL-101, are fabricated through a general facile strategy. Their performance as an adsorbent for phosphate removal is investigated. Experiments are performed to study the effects of various factors on the phosphate adsorption, including adsorbent dosage, contact time and co-existing ions. Both MIL-101(Fe) and NH2-MIL-101(Fe) show highly effective removal of phosphates from aqueous solutions, and the concentration of phosphates decrease sharply from the initial 0.60 mg·L-1 to 0.045 and 0.032 mg·L-1, respectively, within just 30 min of exposure. The adsorption kinetics and adsorption isotherms reveal that NH2-MIL-101(Fe) has higher adsorption capacity than MIL-101(Fe) possibly due to the amine group. Furthermore, the Fe-based MOFs also exhibit a high selectivity towards phosphate over other anions such as chloride, bromide, nitrate and sulfate. Particularly, the prepared Fe-based MIL-101 materials are also capable of adsorbing phosphate in an actual eutrophic water sample and display better removal effect.

Surface modification of hollow magnetic Fe3O4@NH2-MIL-101(Fe) derived from metal-organic frameworks for enhanced selective removal of phosphates from aqueous solution.

Hollow magnetic Fe3O4@NH2-MIL-101(Fe) derived from metal-organic frameworks are fabricated through a general facile strategy. The synthetic parameters are regulated to control the shape of the as-prepared samples. The concentration of phosphates decreased sharply from the initial 0.60 to 0.045 mg.L(-1) with the exposure time in 50 minutes. The correlation between the most significant parameters such as contact time, adsorbent dose, pH, as well as adsorption capacities was optimized, and the effects of these parameters on the removal efficiency of phosphates were investigated. Surface functionalization of magnetic hollow materials is a well-designed way to bridge the gap between high adsorption activity, excellent separation and recovery of phosphates from the water treatment system. Therefore, it exhibits a remarkable selective removal of phosphates from aqueous solution.

Comparison of QT Interval Readings in Normal Sinus Rhythm Between a Smartphone Heart Monitor and a 12-Lead ECG for Healthy Volunteers and Inpatients Receiving Sotalol or Dofetilide.

INTRODUCTION: A variety of medications ranging from antiarrhythmics to psychotropics, as well as conditions such as bradycardia, can prolong the QT interval, increasing the risk for life-threatening arrhythmias. Monitoring the corrected QT interval (QTc) is therefore critical for patient safety. The recent development of smart phone heart monitors (SHM) may allow for easier QTc monitoring. We sought to evaluate the accuracy of an SHM for assessing the QTc, as compared to the standard 12-lead ECG. METHODS AND RESULTS: We compared the QTc interval in lead-I and lead-II between an SHM and 12-lead ECG. Healthy volunteers and hospitalized patients in sinus rhythm being loaded on dofetilide or sotalol were included. Manual and automatic measurements were studied. Across 99 healthy volunteers, the SHM QTc demonstrated good agreement (bias = 4 milliseconds, standard deviation of bias = 11 milliseconds) compared to the 12-lead ECG, using the Bland-Altman method of agreement. Across all hospitalized patients, the SHM was capable of demonstrating QTc prolongation. Between the 12-lead ECG and SHM, lead-I measurements had reasonable agreement (bias = 3 milliseconds, standard deviation of bias = 46 milliseconds). A QTc of > 500 milliseconds was associated with a higher likelihood (OR = 12.0; 95% CI 1.5-111.4; P = 0.02) to not achieve perfect agreement. CONCLUSION: The SHM is accurate in measuring QTc interval in sinus rhythm when compared to 12-lead ECG in healthy volunteers. For patients receiving QT prolonging antiarrhythmics, SHM is capable of detecting QTc prolongation, and lead-I of the SHM is most accurate in measuring the QTc if < 500 milliseconds.

Meta-analysis Identifies Serum C-Reactive Protein as an Indicator of Atrial Fibrillation Risk After Coronary Artery Bypass Graft.

A meta-analysis-based study was conducted to examine the clinical value of serum C-reactive protein (CRP) levels in predicting postoperative atrial fibrillation (POAF) in patients with coronary artery disease (CAD) who underwent coronary artery bypass graft. Computer-based search of scientific literature databases was performed to identify relevant studies in strict accordance with our inclusion and exclusion criteria. Data extracted from the selected studies were used to perform meta-analysis using the STATA 12.0 statistical software. Standardized mean differences (SMDs) with their 95% confidence interval (95% CI) were calculated. The database search strategy initially identified 62 articles (Chinese = 17, English = 45). After multiple levels of screening and validation, 15 case-control studies (Chinese = 1, English = 14), containing of a total of 3110 atrial fibrillation patients (POAF = 925, non-POAF = 2185), were selected for our meta-analysis. The meta-analysis results confirmed that serum CRP level was remarkably higher in patients with POAF compared with non-POAF (SMD = 1.36; 95% CI, 0.44-2.28; P = 0.004). Ethnicity-stratified analysis revealed that elevated serum CRP levels were associated with an increased risk of POAF in white patients with CAD (SMD = 0.85; 95% CI, 0.12-1.58; P = 0.022), but not Asian patients with CAD (SMD = 3.31, 95% CI, -0.04 to 6.66; P = 0.053). Elevated CRP levels, indicating profound inflammation, may be associated with significantly increased risk of POAF in patients with CAD who underwent coronary artery bypass graft. Thus, serum CRP levels are important for early diagnosis and monitoring of POAF in high-risk patients.

IL-8 up-regulates proliferative angiogenesis in ischemic myocardium in rabbits through phosphorylation of Akt/GSK-3ß(ser9) dependent pathways.

BACKGROUND: Therapeutic myocardial angiogenesis is an important compensatory mechanism in severely coronary stenosis. Previous studies demonstrated that interleukin-8 (IL-8) not only plays an important role in inflammation, but also a potent angiogenic factor through p38 mitogen-activated protein kinase (p38MAPK), nuclear factor-kappaB (NK-κB)-dependent pathway in carcinoma. Our study sought to investigate the effects of IL-8 on the angiogenesis and the underlying mechanism in the ischemic myocardium. METHODS: Acute myocardial infarction animal model was established with male rabbits by directly suturing the left anterior descending branch, then lentivirus-mediated IL-8 was quarterly injected into the borderline of infarction area immediately. We employed CoCl2 induced hypoxic HUVECs for in vitro ischemia study. Left ventricular end-diastolic diameter (LVEDd) and ejection fraction (EF) were measured by echocardiography in pre-operation and at 6(th) week after operation. CD34 was detected with immunohistochemisty to analyse angiogenesis. Western blot was performed with regard to IL-8, protein kinase B (PKB/Akt) and Glycogen synthase kinase-3ß(ser9) (GSK-3ß(ser9)). For the HUVECs' proliferation and apoptosis, multiscan spectrum reader at A570 nm and annexin V-FITC/PI staining method were used respectively. RESULTS: The levels of IL-8, phosphorylated Akt and GSK-3ß(ser9) in focal myocardium significantly increased, and the over expression of IL-8 led to an increasing in angiogenesis in rabbits. Hypoxia inhibited cell proliferation and promoted apoptosis. IL-8 induced cell proliferation, phosphorylation of Akt and GSK-3ß(ser9), inhibited apoptosis and Caspase3 expression in HUVECs, which were attenuated by anti-IL-8 or the Akt inhibitor LY294002. CONCLUSIONS: The present results indicate that IL-8 can increase angiogenesis in myocardial infarction, which maybe through enhancing Akt and GSK-3ß(ser9) expression, and inhibiting myocardial apoptosis.

Correlation between GDF 15 gene polymorphism and the collateral circulation in acute non-ST segment elevated myocardial infarction.

OBJECTIVE: To investigate the correlation between growth differentiation factor 15 (GDF 15) + 157 A/T polymorphism and the formation of collateral circulation in acute non-ST segment elevated myocardial infarction in Han population of Shandong province. METHOD: The medical records of 200 cases of patients undergoing selective coronary angiography were analyzed, and the arterial blood specimens of included patients were collected before coronary angiography. Based on the results of coronary angiography, patients were divided into acute myocardial infarction (AMI) group and normal control group; AMI group was divided into collateral group and non-collateral group by Rentrop's grading method; polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing methods were used to analyze the GDF 15 + 157 A/T polymorphism in the two groups. RESULTS: There were statistically significant differences in GDF 15 + 157 A/T AA and AT distribution between AMI group and the control group (P = 0.002); and there was statistically significant difference in allele frequencies between the two groups (P = 0.006); for AMI group, there were statistically significant differences in GDFAA and AT genotype distribution between patients with and without collateral (P = 0.014), and there was statistically significant difference in allele frequencies between the two (P = 0.025). CONCLUSION: There was correlation between GDF 15 + 157 A/T polymorphism and the formation of collateral circulation in patients with non-ST-segment elevated myocardial infarction.