Intervention effects of low-molecular-weight chondroitin sulfate from the nasal cartilage of yellow cattle on lipopolysaccharide-induced behavioral disorders: regulation of the microbiome-gut-brain axis.

Chondroitin sulfate (CS) is a sulfated linear polysaccharide with different functional activities, including antioxidant, anti-inflammatory, lipid-lowering, and immune regulation. As natural sulfated polysaccharides have high molecular weight, high apparent viscosity, low water solubility, complex structure, and high negative charge, they have difficulty binding to receptors within cells across tissue barriers, resulting in low bioavailability and unclear structure-activity relationships. In this study, an H2O2-Vc oxidative degradation system was employed to perform environmentally friendly and controllable degradation of CS extracted from the nasal cartilage of Shaanxi Yellow cattle. Two low-molecular-weight chondroitin sulfates (LMWCSs), CS-1 (14.8 kDa) and CS-2 (50.9 kDa), that exhibit strong in vitro free radical scavenging ability were obtained, and their structures were characterized. Mice intraperitoneally administered lipopolysaccharide (LPS) were used to explore the cognitive intervention effects of LMWCS. Supplementing CS-1 and CS-2 significantly downregulated the levels of the serum inflammatory factors, TNF-α and IL-1ß, promoted the expression of GSH in the brain, and inhibited the production of the lipid peroxidation product, malondialdehyde (MDA), ultimately inhibiting LPS-induced cognitive impairment in mice. Surprisingly, compared to the LPS model group, the abundances of Streptococcus, Eisenbergiella, Vampirovibrio, Coprococcus, Enterococcus and Lachnoanaerobaculum were significantly increased in the intestines of mice in the CS-1 and CS-2 group, whereas those of Parabacteroides and Mycoplasma were significantly decreased. Altogether, this study provides a theoretical basis for the comprehensive utilization of agricultural and animal resources and the application of brain nutrition, anti-inflammatory, and LMWCS health products.

Rosuvastatin Enhances Lymphangiogenesis after Myocardial Infarction by Regulating the miRNAs/Vascular Endothelial Growth Factor Receptor 3 (miRNAs/VEGFR3) Pathway.

BACKGROUND: Several clinical studies have suggested that the early administration of statins could reduce the risk of in-hospital mortality in acute myocardial infarction (AMI) patients. Recently, some studies have identified that stimulating lymphangiogenesis after AMI could improve cardiac function by reducing myocardial edema and inflammation. This study aimed to identify the effect of rosuvastatin on postinfarct lymphangiogenesis and to identify the underlying mechanism of this effect. METHOD: Myocardial infarction (MI) was induced by ligation of the left anterior descending coronary artery in mice orally administered rosuvastatin for 7 days. The changes in cardiac function, pathology, and lymphangiogenesis following MI were measured by echocardiography and immunostaining. EdU, Matrigel tube formation, and scratch wound assays were used to evaluate the effect of rosuvastatin on the proliferation, tube formation, and migration of the lymphatic endothelial cell line SVEC4-10. The expression of miR-107-3p, miR-491-5p, and VEGFR3 was measured by polymerase chain reaction (PCR) and Western blotting. A gain-of-function study was performed using miR-107-3p and miR-491-5p mimics. RESULTS: The rosuvastatin-treated mice had a significantly improved ejection fraction and increased lymphatic plexus density 7 days after MI. Rosuvastatin also reduced myocardial edema and inflammatory response after MI. We used a VEGFR3 inhibitor to partially reverse these effects. Rosuvastatin promoted the proliferation, migration, and tube formation of SVEC4-10 cells. PCR and Western blot analyses revealed that rosuvastatin intervention downregulated miR-107-3p and miR-491-5p and promoted VEGFR3 expression. The gain-of-function study showed that miR-107-3p and miR-491-5p could inhibit the proliferation, migration, and tube formation of SVEC4-10 cells. CONCLUSION: Rosuvastatin could improve heart function by promoting lymphangiogenesis after MI by regulating the miRNAs/VEGFR3 pathway.

Evaluation of the Needs and Experiences of Patients with Hypertriglyceridemia: Social Media Listening Infosurveillance Study.

BACKGROUND: Hypertriglyceridemia is a risk factor for cardiovascular diseases. Internet usage in China is increasing, giving rise to large-scale data sources, especially to access, disseminate, and discuss medical information. Social media listening (SML) is a new approach to analyze and monitor online discussions related to various health-related topics in diverse diseases, which can generate insights into users' experiences and expectations. However, to date, no studies have evaluated the utility of SML to understand patients' cognizance and expectations pertaining to the management of hypertriglyceridemia. OBJECTIVE: The aim of this study was to utilize SML to explore the disease cognition level of patients with hypertriglyceridemia, choice of intervention measures, and the status quo of online consultations and question-and-answer (Q&A) search platforms. METHODS: An infosurveillance study was conducted wherein a disease-specific comprehensive search was performed between 2004 and 2020 in Q&A search and online consultation platforms. Predefined single and combined keywords related to hypertriglyceridemia were used in the search, including disease, symptoms, diagnosis, and treatment indicators; lifestyle interventions; and therapeutic agents. The search output was aggregated using an aggregator tool and evaluated. RESULTS: Disease-specific consultation data (n=69,845) and corresponding response data (n=111,763) were analyzed from 20 data sources (6 Q&A search platforms and 14 online consultation platforms). Doctors from inland areas had relatively high voice volumes and appear to exert a substantial influence on these platforms. Patients with hypertriglyceridemia engaging on the internet have an average level of cognition about the disease and its intervention measures. However, a strong demand for the concept of the disease and "how to treat it" was observed. More emphasis on the persistence of the disease and the safety of medications was observed. Young patients have a lower willingness for drug interventions, whereas patients with severe hypertriglyceridemia have a clearer intention to use drug intervention and few patients have a strong willingness for the use of traditional Chinese medicine. CONCLUSIONS: Findings from this disease-specific SML study revealed that patients with hypertriglyceridemia in China actively seek information from both online Q&A search and consultation platforms. However, the integrity of internet doctors' suggestions on lifestyle interventions and the accuracy of drug intervention recommendations still need to be improved. Further, a combined prospective qualitative study with SML is required for added rigor and confirmation of the relevance of the findings.

Gender disparities in the mediating role of symptom knowledge level in reducing acute coronary syndrome (ACS) decision delay: Findings from a community-based study in China.

BACKGROUND: Implementing training programs to educate patients on the prodromal symptoms of acute coronary syndrome (ACS) may assist patients in accurately recognizing these symptoms, and ultimately decrease their time delay in seeking emergency medical services (EMS). However, the effectiveness of this approach remains uncertain, particularly among the Chinese population. METHODS: A cross-sectional study was conducted within 22 communities in Beijing, China between 2015 and 2018, with a total of 1099 participants recruited. The study utilized a standardized questionnaire to evaluate the presence of intentional decision delay in turning to EMS under a hypothetical chest pain, the participants' knowledge of ACS prodromal symptoms, and whether they had ever received any training programs aimed at increasing their symptom knowledge. Mediation analysis was performed with regression models and bootstrapping methods, and gender difference was further analyzed through moderated mediation analysis. RESULTS: A total of 1099 participants (58.2% female, median [IQR] age 34 [20]) were included in the study. The results of the mediation analysis indicated that training programs were associated with a decrease risk in decision delay, with increased knowledge playing a mediating role (mediation effect/total effect = 36.59%, P < 0.0001). Gender modified this mediation effect, with it being observed only in the male group. Specifically, training programs were not found to significantly decrease decision delay among females (P > 0.05), even though they did improve women's knowledge of ACS prodromal symptoms (ß = 0.57, P = 0.012). CONCLUSION: The results suggested a relationship between prior training programs and reduced decision delay, with increased knowledge of prodromal symptoms of ACS serving as a mediator. However, the effect was only observed in male participants and not in female participants. This highlights the notion that mere transfer of knowledge regarding ACS prodromal symptoms may not be sufficient to mitigate decision delay in the female population. Further research is needed to corroborate these results and to gain deeper insights into the gender-specific barriers encountered in this study.

Isolated right ventricular Takotsubo cardiomyopathy in Guillain-Barré syndrome.

BACKGROUND: Takotsubo cardiomyopathy can present itself in the most varied clinical forms, with extremely variable electrocardiogram anomalies and presence of comorbidities with a significant systemic commitment. Guillain-Barré Syndrome concomitant with isolated right ventricular Takotsubo cardiomyopathy is a rare entity. Here we present a patient with Guillain-Barré syndrome who had electrocardiogram abnormalities consistent with isolated right ventricular Takotsubo cardiomyopathy which have not been described in literature. This case report may prompt early identification of right ventricular involvement in neurological comorbidities, especially if the electrocardiogram is not frankly suggestive of an acute ischemic condition linked to coronary artery disease. CASE PRESENTATION: A 37-year-old woman was misdiagnosed as acute coronary syndrome because of abnormally elevated troponin T level and electrocardiogram findings in the Emergency Department. Due to absence of any significant stenosis in the main coronary artery, the primary diagnosis was ruled out. Based on reanalysis of the ECG abnormalities, the patient was diagnosed as a case of isolated right ventricular Takotsubo cardiomyopathy in Guillain-Barré Syndrome. This case demonstrates the importance of electrocardiogram as a critical tool to identify isolated right ventricular Takotsubo cardiomyopathy in Guillain-Barré Syndrome. Indeed, in this case, the electrocardiogram abnormalities were distributed beyond the territory of a single coronary artery distribution. CONCLUSIONS: The described electrocardiogram findings of isolated right ventricular Takotsubo cardiomyopathy in Guillain-Barré Syndrome may facilitate identification of right ventricular involvement in neurological diseases.

Unusual course of congenital complete heart block in an adult: A case report.

BACKGROUND: Congenital complete heart block (CCHB) with normal cardiac structure and negativity for anti-Ro/La antibody is rare. Additionally, CCHB is much less frequently diagnosed in adults, and its natural history in adults is less well known. CASE SUMMARY: A 23-year-old woman was admitted to our hospital for frequent syncopal episodes. She had bradycardia at the age of 1 year but had never had impaired exercise capacity or a syncopal episode before admission. The possible diagnosis of acquired complete atrioventricular block was carefully ruled out, and then the diagnosis of CCHB was made. According to existing guidelines, permanent pacemaker implantation was recommended, but the patient declined. With regular follow-up for 28 years, the patient had an unusually good outcome without any invasive intervention or medicine. She had an uneventful pregnancy and led a normally active life without any symptoms of low cardiac output or syncopal recurrence. CONCLUSION: This case implies that CCHB in adulthood may have good clinical outcomes and does not always require permanent pacemaker implantation.

Genome-wide analysis of methylation in rat fetal heart under hyperglycemia by methylation-dependent restriction site-associated DNA sequencing.

Diabetes mellitus causes an increased incidence of congenital heart malformations. However, the pathogenesis and potential epigenetic mechanism involved in this process are unclear. In this study, we used MethylRAD sequencing to compare changes in methylation levels in the genomic landscapes in the fetal heart in a rat model of hyperglycemia. Our results showed that methylation of CCGG/CCNGG sites were mostly enriched in intergenic regions, followed by intron, exon, upstream and the 5' and 3' untranslated regions. qRT-PCR results confirmed the MethylRAD sequencing findings, suggesting that abnormal CCGG/CCNGG methylation in the upstream region regulated gene expression. The differential methylation genes (DMGs) based on the CCGG and CCNGG sites in the upstream region were examined by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis. Gene Ontology indicated that the CCGG-based DMGs involved in biological process and function were mainly related to transcription and co-SMAD binding. The CCNGG-based DMGs were mainly related to transcription and cytokine-mediated signaling pathways. Kyoto Encyclopedia of Genes and Genomes analysis indicated that CCGG-based DMGs were mainly involved in the Wnt signaling and TGF-ß signaling pathways. CCNGG-based DMGs were involved in the TNF signaling and apoptosis pathways. These genes may play dominant roles in cardiomyocyte apoptosis and heart disease and require further study. These genes may also serve as potential molecular targets or diagnostic biomarkers for heart malformations under hyperglycemia.

Endothelial Microparticle-Mediated Transfer of microRNA-19b Inhibits the Function and Distribution of Lymphatic Vessels in Atherosclerotic Mice.

In recent years, the function of the lymphatic system in atherosclerosis has attracted attention due to its role in immune cell trafficking, cholesterol removal from the periphery, and regulation of the inflammatory response. However, knowledge of the mechanisms regulating lymphangiogenesis and lymphatic function in the pathogenesis of atherosclerosis is limited. Endothelial microparticles carrying circulating microRNA (miRNA)s are known to mediate cell-cell communication, and our previous research showed that miRNA-19b in EMPs (EMPmiR-19b) was significantly increased in circulation and atherosclerotic vessels, and this increase in EMPmiR-19b promoted atherosclerosis. The present study investigated whether atherogenic EMPmiR-19b influences pathological changes of the lymphatic system in atherosclerosis. We first verified increased miR-19b levels and loss of lymphatic system function in atherosclerotic mice. Atherogenic western diet-fed ApoE-/- mice were injected with phosphate-buffered saline, EMPs carrying control miRNA (EMPcontrol), or EMPmiR-19b intravenously. The function and distribution of the lymphatic system was assessed via confocal microscopy, Evans blue staining, and pathological analysis. The results showed that lymphatic system dysfunction existed in the early stage of atherosclerosis, and the observed pathological changes persisted at the later stage, companied by an increased microRNA-19b level. In ApoE-/- mice systemically treated with EMPmiR-19b, the distribution, transport function, and permeability of the lymphatic system were significantly inhibited. In vitro experiments showed that miRNA-19b may damage the lymphatic system by inhibiting lymphatic endothelial cell migration and tube formation, and a possible mechanism is the inhibition of transforming growth factor beta receptor type II (TGF-ßRII) expression in lymphatic endothelial cells by miRNA-19b. Together, our findings demonstrate that atherogenic EMPmiR-19b may destroy lymphatic system function in atherosclerotic mice by downregulating TGF-ßRII expression.

Case Report: Familial Pseudohyperkalemia Due to Red Blood Cell Membrane Leak in a Chinese Patient.

Hyperkalemia is a critical condition requiring careful evaluation and timely intervention. Many conditions could manifest as pseudohyperkalemia and it's important to differentiate them as inappropriate potassium-lowering therapy might lead to detrimental outcomes. A 56-year-old female was admitted for hyperkalemia (5.62-8.55 mmol/L). She had no symptoms or signs of hyperkalemia. A comprehensive work-up of hyperkalemia retrieved no valuable findings. Her blood samples underwent incubation tests at different temperatures and revealed temperature-dependent potassium leaks from red blood cells. Based on all test results, a diagnosis of hyperkalemia caused by red blood cell membrane defects was suspected. Whole-genome sequencing revealed a heterozygous c.1123C>T (p. R375W) mutation in the ABCB6 gene and confirmed the diagnosis of familial pseudohyperkalemia (FP). FP is an inherited benign condition in which red blood cells have increased cold-induced permeability to potassium. The patient was discharged with no additional treatment and she was suggested avoiding blood donation.

Potentially Inappropriate Medication and Associated Factors Among Older Patients with Chronic Coronary Syndrome at Hospital Discharge in Beijing, China.

PURPOSE: Medication therapy is crucial in the management of chronic coronary syndrome (CCS). The use of potentially inappropriate medications (PIMs) contributes to poor outcomes in older patients, making it a major public health concern. However, few studies are available on PIMs use in older Chinese CCS patients. To investigate the frequency of prescribed PIMs at discharge and explore risk factors in older adults with CCS. PATIENTS AND METHODS: The cross-sectional study was conducted in a tertiary hospital in China over three months, from 1st October to 31st December, 2019. CCS patients aged over 60 years who were discharged alive were recruited. Information on demographics and medications at discharge was collected. Clinical data including diagnoses, frailty status, New York Heart Association (NYHA) class and age-adjusted Charlson Comorbidity Index (ACCI) were evaluated in each patient. PIMs were identified using the 2019 Beers criteria. Binary logistic regression was performed to recognize variables related to PIMs. RESULTS: A total of 447 eligible patients with 2947 medications were included. The prevalence of PIMs use was 38%. Medications to be avoided, to be used with caution, and with drug-drug interactions were 38.4%, 48.9% and 12.7% of the PIMs, respectively. Medications with drug-disease/syndrome interactions and those adjusted for kidney function were not identified. The common PIMs were diuretics (37.1%), benzodiazepines and benzodiazepine receptor agonist hypnotics (15.2%), glimepiride (13.1%), and co-prescription of potassium-sparing diuretics and renin-angiotensin system (RAS) inhibitors (9.7%). Individuals with frailty syndrome, polypharmacy, multiple comorbidities, atrial fibrillation, psychiatric disorders and greater NYHA class severity were more likely to receive PIMs. CONCLUSION: Prescription of PIMs was a common burden in older adults. A CCS multidisciplinary team is needed to control PIMs, especially in vulnerable older patients.

Identification of monocyte-associated genes as predictive biomarkers of heart failure after acute myocardial infarction.

BACKGROUND: Acute myocardial infarction (AMI) is a major contributor of heart failure (HF). Peripheral blood mononuclear cells (PBMCs), mainly monocytes, are the essential initiators of AMI-induced HF. The powerful biomarkers for early identification of AMI patients at risk of HF remain elusive. We aimed to identify monocyte-related critical genes as predictive biomarkers for post-AMI HF. METHODS: We performed weighted gene co-expression network analysis (WGCNA) on transcriptomics of PBMCs from AMI patients who developed HF or did not. Functional enrichment analysis of genes in significant modules was performed via Metascape. Then we obtained the single-cell RNA-sequencing data of recruited monocytes/macrophages from AMI and control mice using the Scanpy and screened 381 differentially expressed genes (DEGs) between the two groups. We validated the expression changes of the 25 genes in cardiac macrophages from AMI mice based on bulk RNA-sequencing data and PBMCs data mentioned above. RESULTS: In our study, the results of WGCNA showed that two modules containing 827 hub genes were most significantly associated with post-AMI HF, which mainly participated in cell migration, inflammation, immunity, and apoptosis. There were 25 common genes between DEGs and hub genes, showing close relationship with inflammation and collagen metabolism. CUX1, CTSD and ADD3 exhibited consistent changes in three independent studies. Receiver operating characteristic curve analysis showed that each of the three genes had excellent performance in recognizing post-AMI HF patients. CONCLUSION: Our findings provided a set of three monocyte-related biomarkers for the early prediction of HF development after AMI as well as potential therapeutic targets of post-AMI HF.

An Hypothesis: Disproportion Between Cardiac Troponin and B-Type Natriuretic Peptide Levels-A High Risk and Poor Prognostic Biomarker in Patients With Fulminant Myocarditis?

In our clinical practice, we recently found some patients with severe fulminant myocarditis (FM) who showed persistently elevated cardiac troponin (cTn) levels and "seemingly normal" B-type natriuretic peptide (BNP) level, and who subsequently progressed to poor outcomes. Indeed, this sounds contrary to conventional wisdom, but it is not an accidental phenomenon. Fulminant myocarditis is a rapidly progressive disease associated with high mortality. Recent studies have shown that patients with FM are significantly more likely to require heart transplantation than those without FM. Prompt diagnosis of FM and the institution of advanced cardiac life support will save more lives. Cardiac troponin and BNP are widely used diagnostic markers. Cardiac troponin is a specific marker of cardiac injury and its level correlates with the severity of cardiac injury. However, plasma BNP has a dual identity; it is not only a marker of cardiac pressure/volume overload, but it is also a cardioprotective factor that provides effective neurohormonal compensation to maintain homeostasis. Similar to fulminant hepatitis (characterised by diffuse inflammation and massive parenchymal cell necrosis) sometimes showing disproportion between transaminase level and bilirubin level, the disproportion between cTn and BNP levels in FM seems to be consistent with its severe histopathological changes, including diffuse infiltration of the myocardium by inflammatory cells, as well as severe cardiomyocyte injury and necrosis. Moreover, in previous studies, a lower BNP level was found to be an adverse prognostic marker in end-stage heart failure. All these findings indicate that in patients with FM with a persistently high cTn level and ominous clinical presentation, a "seemingly normal" BNP level is not a friendly signal. We hypothesise that the combination of a persistently elevated cTn level and low BNP level in patients with FM indicates worse myocardial injury and poor prognosis.

Therapeutic targets of rosuvastatin on heart failure and associated biological mechanisms: A study of network pharmacology and experimental validation.

To explore the potential targets underlying the effect of rosuvastatin on heart failure (HF) by utilizing a network pharmacology approach and experiments to identify the results. PharmMapper and other databases were mined for information relevant to the prediction of rosuvastatin targets and HF-related targets. Then, the rosuvastatin-HF target gene networks were created in Cytoscape software. Eventually, the targets and enriched pathways were examined by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Furthermore, we constructed an HF animal model and used rosuvastatin to treat them, identifying the changes in heart function and related protein expression. We further used different cells to explore the mechanisms of rosuvastatin. Thirty-five intersection targets indicated the therapeutic targets linked to HF. GO analysis showed that 481 biological processes, 4 cellular components and 23 molecular functions were identified. KEGG analysis showed 13 significant treatment pathways. In animal experiments, rosuvastatin significantly improved the cardiac function of post-myocardial infarction mice and prevented the development of HF after myocardial infarction by inhibiting IL-1Β expression. Cell experiments showed that rosuvastatin could reduce the expression of IL-1B in HUVEC and THP-1 cells. The therapeutic mechanism of rosuvastatin against HF may be closely related to the inhibition of the expression of apoptosis-related proteins, inflammatory factors, and fibrosis-related genes. However, IL-1Β is one of the most important target genes.

Efficacy and safety of catheter-based renal denervation for heart failure with reduced ejection fraction: a systematic review and meta-analysis.

PURPOSE: To perform a comprehensive meta-analysis of all available evidence on the efficacy and safety of catheter-based renal denervation for heart failure with reduced ejection fraction. METHODS: We searched English and Chinese databases and calculated the weighted mean difference or standardized mean difference and 95% confidence intervals to estimate the efficacy and safety of renal denervation for heart failure. All relevant studies were screened and a meta-analysis was conducted using Review Manager 5.4. RESULTS: A total of 11 studies were identified for the meta-analysis. For the primary outcomes, the results showed that renal denervation significantly improved ejection fraction (weighted mean difference 6.42), left ventricular end-systolic diameter (weighted mean difference -3.95), left ventricular end-diastolic diameter (weighted mean difference -4.17) and left atrial diameter (weighted mean difference -4.09). For the secondary outcomes, renal denervation reduced the B-type natriuretic peptide level, heart rate, systolic blood pressure and diastolic blood pressure. However, further analysis revealed that renal denervation improved heart function but did not further reduce the heart rate and blood pressure compared with the control group. CONCLUSION: Treatment with renal denervation can significantly improve heart function and structure in patients with heart failure. In addition, the level of B-type natriuretic peptide can be reduced after renal denervation treatment. Renal denervation did not further reduce heart rate and blood pressure compared with the control group. Therefore, the treatment of heart failure with renal denervation is effective and safe.

Anxiety and clinical outcomes of patients with acute coronary syndrome: a meta-analysis.

OBJECTIVES: Anxiety has been suggested to be associated with poor outcomes in patients with acute coronary syndrome (ACS). However, results of previous follow-up studies were inconsistent. The aim of this meta-analysis was to evaluate the association between anxiety and clinical outcomes in patients with ACS, and to investigate the potential role of depression underlying the above association. DESIGN: A meta-analysis of prospective follow-up studies. SETTING: Hospitals. PARTICIPANTS: Patients with ACS. INTERVENTIONS: We included related prospective follow-up studies up through 20 July 2019 that were identified by searching PubMed and Embase databases. A random-effect model was used for the meta-analysis. Anxiety was evaluated by validated instruments at baseline. PRIMARY AND SECONDARY OUTCOME MEASURES: We determined the association between anxiety and risks of mortality and adverse cardiovascular events (MACEs) in patients with ACS. RESULTS: Our analysis included 17 studies involving 39 038 patients wqith ACS. Anxiety was independently associated with increased mortality risk (adjusted risk ratio (RR) 1.21, 95% CI 1.07 to 1.37, p=0.002) and MACEs (adjusted RR 1.47, 95% CI 1.24 to 1.74, p<0.001) in patients with ACS. Subgroup analyses showed that depression may at least partly confound the association between anxiety and poor outcomes in patients with ACS. Adjustment of depression significantly attenuated the association between anxiety and MACEs (adjusted RR 1.25, 95% CI 1.04 to 1.52, p=0.02). Moreover, anxiety was not significantly associated with mortality risk after adjusting for depression (adjusted RR 0.88, 95% CI 0.66 to 1.17, p=0.37). CONCLUSIONS: Anxiety is associated with increased risk of mortality and MACEs in patients with ACS. However, at least part of the association may be confounded by concurrent depressive symptoms in these patients.

Depression predicts the risk of adverse events after percutaneous coronary intervention: A meta-analysis.

BACKGROUND: Depression is correlated with poor prognosis in patients with coronary artery disease (CAD). The goal of this meta-analysis was to assess the influence of depression on the risks of major adverse cardiovascular events (MACEs) and all-cause mortality after percutaneous coronary intervention (PCI). METHODS: Cohort studies were obtained by searching PubMed and Embase databases. Cohort studies regarding the association between depression and risks of MACEs and mortality after PCI were included. Heterogeneity was determined using the Cochrane's Q test and calculated using I2. A fixed-effect model was used if no significant heterogeneity was detected; otherwise a random-effect model was applied. The adjusted risk ratio [RR] for the incidences of MACEs and all-cause mortality in patients with depression were compared to those without depression. RESULTS: Nine cohorts including 4,555 CAD patients who underwent PCI were included in this meta-analysis, and 1,108 of these patients were diagnosed with depression. There were no significant differences among studies evaluating MACEs and mortality risks (I2 = 25% and 0%, respectively). Pooled results showed that depression was associated with higher risk of MACEs (RR: 2.10, 95% confidence interval [CI]: 1.59 to 2.77, p <  0.001) and all-cause mortality (RR: 1.76, 95% CI: 1.45 to 2.13, p < 0.001) during follow-up after PCI. LIMITATIONS: Available full text peer reviewed studies were limited and only studies in English were included in this analysis. CONCLUSIONS: Depressive symptoms were independently associated with adverse cardiovascular outcomes in patients who received PCI. Psychological therapy that does not increase cardiac burden or induce pharmacological side effects may be a better strategy to treat depression associated with PCI.

Lymphatic system identification, pathophysiology and therapy in the cardiovascular diseases.

The mammalian circulatory system comprises both the cardiovascular system and the lymphatic system. In contrast to the closed, high-pressure and circular blood vascular circulation, the lymphatic system forms an open, low-pressure and unidirectional transit network from the extracellular space to the venous system. It plays a key role in regulating tissue fluid homeostasis, absorption of gastrointestinal lipids, and immune surveillance throughout the body. Despite the critical physiological functions of the lymphatic system, a complete understanding of the lymphatic vessels lags far behind that of the blood vasculatures due to the challenge of their visualization. During the last 20 years, discoveries of underlying genes responsible for lymphatic vessel biology, combined with state-of-the-art lymphatic function imaging and quantification techniques, have established the importance of the lymphatic vasculature in the pathogenesis of cardiovascular diseases including lymphedema, obesity and metabolic diseases, dyslipidemia, hypertension, inflammation, atherosclerosis and myocardial infraction. In this review, we highlight the most recent advances in the field of lymphatic vessel biology, with an emphasis on the new identification techniques of lymphatic system, pathophysiological mechanisms of atherosclerosis and myocardial infarction, and new therapeutic perspectives of lymphangiogenesis.

Identifying patients with refusal of percutaneous coronary intervention for acute myocardial infarction: a classification and regression tree analysis.

The purpose of the present study is to develop and validate a prediction tool to identify patients who refuse to receive percutaneous coronary intervention (PCI) rapidly. We developed a risk stratification model using the derivation cohort of 288 patients with ST segment elevation myocardial infarction (STEMI) in our hospital and validated it in a prospective cohort of 115 patients. There were 52 (18.1%) patients and 18 (15.7%) patients who refused PCI among derivation and validation cohort, respectively. A classification and regression tree (CART) analysis and multivariate logistic regression were used for statistical analysis. The decision-making factors for refusal of PCI were also investigated. The CART analysis and logistic regression both showed that self-rated mild symptom was the most significant predictor of not choosing PCI. The model generated three risk groups. The high-risk group included: self-rated mild symptoms; self-rated severe symptom, glomerular filtration rate < 60 ml/min/1.73m2. The intermediate-risk group included: self-rated severe symptom, glomerular filtration rate ≥ 60 ml/min/1.73m2 and age ≥ 75 years. The low-risk group included: self-rated severe symptom, glomerular filtration rate ≥ 60 ml/min/1.73m2 and age < 75 years. The prevalence for refusal of PCI of the three groups were 45%-44%, 18% and 4%, respectively. The sensitivity was 88% and the negative predictive value was 96%. And similar results were obtained when this prediction tool was applied prospectively to the validation cohort. Patients at low and high risk can be easily identified for refusal of PCI by the prediction tool using common clinical data. This practical model might provide useful information for rapid recognition and early response for this kind of crowd.

Effects of familial hypercholesterolemia-associated genes on the phenotype of premature myocardial infarction.

BACKGROUND: The incidence of premature myocardial infarction (PMI) has gradually increased in recent years. Genetics plays a central role in the development of PMI. Familial hypercholesterolemia (FH) is one of the most common genetic disorders of cholesterol metabolism leading to PMI. OBJECTIVE: This study investigated the relationship between FH-associated genes and the phenotype of PMI to clarify the genetic spectrum of PMI diseases. METHOD: This study enrolled PMI patients (n = 225) and detected the mutations in their FH-associated genes (LDLR, APOB, PCSK9, LDLRAP1) by Sanger sequencing. At the same time, patients free of PMI (non-FH patients, n = 56) were enrolled as control, and a logistic regression analysis was used to identify risk factors associated with PMI. The diagnosis of FH was confirmed using "2018 Chinese expert consensus of FH screening and diagnosis" before the prevalence and clinical features of FH were analyzed. RESULTS: Pathogenic mutations in LDLR, APOB, PCSK9 and LDLRAP1 genes were found in 17 of 225 subjects (7.6%), and all mutations were loss of function (LOF) and heterozygous. The genotype-phenotype relationship of patients carrying FH-associated mutations showed high heterogeneity. The logistic regression analysis showed that the smoking history, obesity and the family history of premature CHD were independent risk factors of PMI. In this study, a total of 19 patients (8.4%) were diagnosed as FH, and the proportion of smoking subjects in FH patients was higher than that in non-FH patients. CONCLUSIONS: FH-associated gene mutations were present in about 7.6% of Chinese patients with PMI. In addition to genetic factors, smoking history, lifestyle and other environmental factors may play a synergistic role in determining the phenotype of PMI. TRIAL REGISTRATION: Essential gene mutation of cholesterol metabolism in patients with premature myocardial infarction. ChiCTR-OCH-12002349.Registered 26 December 2014, http://www.chictr.org.cn/showproj.aspx?proj=7201 .