The association between the triglyceride-glucose index and in-stent restenosis in patients undergoing percutaneous coronary intervention: a systematic review and meta-analysis.

BACKGROUND: Insulin resistance (IR) can lead to cellular metabolic disorders, activation of oxidative stress, and endothelial dysfunction, contributing to in-stent restenosis (ISR). The triglyceride-glucose index (TyG index), a new indicator reflecting IR, is extensively researched in the cardiovascular field. This study, through a meta-analysis, aimed to utilize a larger combined sample size and thereby enhance the overall test efficacy to explore the TyG index-ISR relationship. METHODS: A thorough search was conducted in the PubMed, EMBASE, Web of Science, and Cochrane Library databases to find original papers and their references published between 1990 and January 2024. This search included both prospective and retrospective studies detailing the correlation between the TyG index and ISR in individuals with coronary heart disease (CHD). OUTCOMES: The five included articles comprised 3,912 participants, and the odds ratio (OR) extracted from each study was combined using the Inverse Variance method. Results showed that, in the context of CHD patients, each incremental unit in the TyG index, when treated as a continuous variable, corresponded to a 42% elevation in ISR risk (95% CI 1.26-1.59, I²=13%, p < 0.005). When analyzing the TyG index categorically, the results revealed a higher ISR risk in the highest TyG index group compared to the lowest group (OR: 1.69, 95% CI 1.32-2.17, I²=0). Additionally, in patients with chronic coronary syndrome (CCS), each unit increase in the TyG index, the risk of ISR in patients increased by 37% (95% CI 1.19-1.57, I²=0%, p < 0.005). This correlation was also observable in acute coronary syndrome (ACS) patients (OR:1.48, 95% CI 1.19-1.85, I²=0, p < 0.005). CONCLUSIONS: The TyG index, an economical and precise surrogate for IR, is significantly linked with ISR. Furthermore, this correlation is unaffected by the type of coronary heart disease.

Is lysosomal acid lipase activity associated with the presence and severity of coronary artery disease?

BACKGROUND: Lipid metabolism is considerably complex and there can be many critical steps in atherogenesis. The association between lysosomal acid lipase (LAL) activity and coronary artery disease (CAD) has not been elucidated in detail. We aimed to evaluate the association between LAL activity with the presence and severity of CAD in patients who are seen in daily clinical practice. METHODS: Patients who underwent coronary angiography were divided into groups according to the angiography results. Syntax scores and Gensini scores were calculated. The LAL activity was measured from dried blood spots. RESULTS: Median LAL activity values were similar in all study groups (normal coronary arteries: 0.40 nmol/punch/h; non-obstructive CAD: 0.44 nmol/punch/h; obstructive chronic CAD: 0.40 nmol/punch/h; obstructive acute coronary syndrome: 0.48 nmol/punch/h) and there was no correlation between coronary atherosclerotic burden and LAL activity (correlation coefficients Syntax score and LAL: -0.032; Gensini score and LAL: -0.030). In addition, no relationship between serum lipid levels and LAL activity was detected. CONCLUSION: The presence of CAD and its severity is not associated with the LAL activity in patients encountered in daily clinical practice.

Association between estimated pulse wave velocity and in-hospital and one-year mortality of patients with chronic kidney disease and atherosclerotic heart disease: a retrospective cohort analysis of the MIMIC-IV database.

BACKGROUND: Carotid-femoral pulse wave velocity has been identified as an autonomous predictor of cardiovascular mortality and kidney injury. This important clinical parameter can be non-invasively estimated using the calculated pulse wave velocity (ePWV). The objective of this study was to examine the correlation between ePWV and in-hospital as well as one-year mortality among critically ill patients with chronic kidney disease (CKD) and atherosclerotic heart disease (ASHD). METHODS: This study included a cohort of 1173 patients diagnosed with both CKD and ASHD, sourced from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. The four groups divided into quartiles according to ePWV were compared using a Kaplan-Meier survival curve to assess variations in survival rates. Cox proportional hazards models were employed to analyze the correlation between ePWV and in-hospital as well as one-year mortality among critically ill patients with both CKD and ASHD. To further investigate the dose-response relationship, a restricted cubic splines (RCS) model was utilized. Additionally, stratification analyses were performed to examine the impact of ePWV on hospital and one-year mortality across different subgroups. RESULTS: The survival analysis results revealed a negative correlation between higher ePWV and survival rate. After adjusting for confounding factors, higher ePWV level (ePWV > 11.90 m/s) exhibited a statistically significant association with an increased risk of both in-hospital and one-year mortality among patients diagnosed with both CKD and ASHD (HR = 4.72, 95% CI = 3.01-7.39, p < 0.001; HR = 2.04, 95% CI = 1.31-3.19, p = 0.002). The analysis incorporating an RCS model confirmed a linear escalation in the risk of both in-hospital and one-year mortality with rising ePWV values (P for nonlinearity = 0.619; P for nonlinearity = 0.267). CONCLUSIONS: The ePWV may be a potential marker for the in-hospital and one-year mortality assessment of CKD with ASHD, and elevated ePWV was strongly correlated with an elevated mortality risk in patients diagnosed with both CKD and ASHD.

Pathological Characteristics and Classification of Unstable Coronary Atherosclerotic Plaques.

Important forensic diagnostic indicators of sudden death in coronary atherosclerotic heart disease, such as acute or chronic myocardial ischemic changes, sometimes make it difficult to locate the ischemic site due to the short death process, the lack of tissue reaction time. In some cases, the deceased died of sudden death on the first-episode, resulting in difficulty for medical examiners to make an accurate diagnosis. However, clinical studies on coronary instability plaque revealed the key role of coronary spasm and thrombosis caused by their lesions in sudden coronary death process. This paper mainly summarizes the pathological characteristics of unstable coronary plaque based on clinical medical research, including plaque rupture, plaque erosion and calcified nodules, as well as the influencing factors leading to plaque instability, and briefly describes the research progress and technique of the atherosclerotic plaques, in order to improve the study on the mechanism of sudden coronary death and improve the accuracy of the forensic diagnosis of sudden coronary death by diagnosing different pathologic states of coronary atherosclerotic plaques.

Correlation between serum Dickkopf-1 (DKK1) levels and coronary artery stenosis.

BACKGROUND AND AIMS: To study the correlation between the level of serum Dickkopf-1 (DKK1) and the degree of coronary artery stenosis in patients with coronary atherosclerotic heart disease. METHODS AND RESULTS: In 2018, general data and biochemical indexes of 311 patients who underwent coronary angiography were recorded. Before procedure, arterial blood was drawn and the concentrations of DKK1, retinol binding protein 4 (RBP4), plasminogen activator inhibitor (PAI-1) were measured. Based on coronary angiography results, subjects were divided into a coronary heart disease (CHD) group; and a non-coronary heart disease (non-CHD)group. The CHD group was divided into three subgroups: the low Gensini score; the middle Gensini score; and the high Gensini score subgroups. Compared with those of the non-CHD group, DKK1, RBP4 and PAI-1 of the CHD group were significantly higher, while the OC was lower. DKK1,RBP4 and PAI-1 levels of the middle and high Gensini subgroups were significantly higher, compared with that of the low Gensini subgroup. Differences between osteocalcin (OC), beta-isomerized C-terminal telopeptidase (ß-CTX), and 25(OH)2D3 of the three subgroups were not significant. Correlation between DKK1 and the inflammatory factors, RBP4 and PAI-1, was positive. Correlation between DKK1 and ß - CTX, 25(OH)2D3 and OC was not significant. DKK1 was a risk factor for CHD. The degree of coronary artery stenosis was related to DKK1 concentration. CONCLUSIONS: Serum DKK1 levels in coronary heart disease patients were significantly higher, and positively correlated with the degree of coronary artery stenosis. DKK1 level is an independent risk factor for coronary heart disease.

Predictive value of coronary artery computed tomography-derived fractional flow reserve for cardiovascular events in patients with coronary artery disease.

BACKGROUND: Coronary computed tomography-derived fractional flow reserve (FFR-CT) assesses whether coronary artery lesions will result in myocardial ischemia. This study aimed to evaluate the predictive value of FFR-CT for cardiovascular events in patients with coronary artery disease (CAD). METHODS: Data were collected retrospectively from patients with CAD who underwent FFR-CT at our hospital from January 2020 to February 2022 (1-year average follow-up). Patients were divided into ischemic (FFR-CT ≤ 0.80) and non-ischemic (FFR-CT > 0.80) groups. The incidence of endpoint events (cardiac death, acute myocardial infarction, unplanned revascularization, unstable angina, and stable angina) was calculated. The FFR-CT value was correlated with endpoint events using Cox regression models and Kaplan-Meier survival curves. RESULTS: We recruited 134 patients (93 [69.4%] and 41 [30.6%] patients in the ischemic and non-ischemic groups, respectively). The ischemic group had a higher proportion of men, patients with type 2 diabetes and hypertension, and patients taking antiplatelet drugs and ß­blockers than did the non-ischemic group (all p < 0.05), whereas other parameters were comparable. Multivariate Cox regression analysis revealed no significant differences in cardiac death, acute myocardial infarction, unplanned revascularization, and unstable angina between the groups. The incidence of stable angina events (hazard ratio: 3.092, 95% confidence interval: 1.362-7.022, p = 0.007) was significantly higher in the ischemic group. Kaplan-Meier survival analysis revealed a significant difference in event-free survival for stable angina between the groups (p = 0.002). CONCLUSION: In patients with CAD, FFR-CT showed an independent predictive value for stable angina within 1 year of examination.

The Value of the Apolipoprotein B/Apolipoprotein A1 Ratio in Predicting the Rapid Progression of Non-Culprit Coronary Lesions in Acute Coronary Syndrome in Patients with Diabetes Mellitus after Percutaneous Coronary Intervention.

This study aims to assess the predictive value of the apolipoprotein B (ApoB) /apolipoprotein A1 (ApoA1) ratio in acute coronary syndrome (ACS) in patients with diabetes mellitus (DM) for the rapid progression (RP) of non-culprit coronary lesions (NCCLs) after percutaneous coronary intervention (PCI) and observe the effect of the ApoB/ApoA1 ratio on major adverse cardiac events (MACE).A total of 175 patients with DM presenting with ACS who received a PCI and an average 13-month follow-up coronary angiography (CAG) were enrolled from January 2015 to December 2020. According to the CAG, the patients were divided into the RP group and the non-RP group. MACE was defined as a composite of death from cardiac causes, cardiac arrest, myocardial infarction, or rehospitalization from unstable or progressive angina at the end of a 24-month follow-up.The low-density lipoprotein cholesterol (LDL-C), ApoB, ApoB/ApoA1 ratio, and LDL-C/high-density lipoprotein cholesterol (HDL-C) ratio levels at baseline were significantly higher in the RP group than in the non-RP group. The ApoA1 level at baseline in the non-RP group was significantly higher than in the RP group. The predictive significance of the ApoB/ApoA1 ratio (area under the curve (AUC) = 0.712) for the RP of NCCLs was significantly higher than those of ApoA1, ApoB, LDL-C/HDL-C ratio (AUC = 0.628, AUC = 0.640, and AUC = 0.620, respectively). A higher ApoB/ApoA1 ratio and the RP of NCCLs were significantly associated with the occurrence of MACE.The ApoB/ApoA1 ratio was an effective clinical indicator for the RP of NCCLs after PCI in patients with DM presenting with ACS. The high ApoB/ApoA1 ratio and the RP of NCCLs were two risks for MACE.

Report on Cardiac Gross Pathologic Measurements of Sudden Cardiac Death in Adults.

OBJECTIVES: To analyze the gross pathological data of sudden cardiac death (SCD) with different causes, to provide data support for the identification of sudden cardiac death with unknown causes. METHODS: A total of 167 adult SCD cases in the archive of the Forensic Expertise Institute of Nanjing Medical University from 2010 to 2020 were collected. The gross pathological data of SCD cases were summarized and the characteristics of different causes of death were statistically analyzed. RESULTS: The ratio of male to female SCD cases was 3.4∶1. Coronary heart disease was the leading cause of SCD, and mainly distributed in people over 40 years old. SCD caused by myocarditis was mainly distributed in young people and the mean age of death was (34.00±9.55) years. By analyzing the differences in cardiac pathological parameters of SCD with different causes, it was found that the aortic valve circumference was significantly dilated in the SCD caused by aortic aneurysm or dissection (P<0.05). The heart weight of SCD caused by aortic aneurysm or dissection and combined factors was greater, and both pulmonary and tricuspid valvular rings were dilated in the SCD caused by combined factors in adult males (P<0.05). CONCLUSIONS: Various gross pathological measures of SCD with different causes are different, which has reference value in the cause of death identification of SCD.

Association between the LRP5 rs556442 gene polymorphism and the risks of NAFLD and CHD in a Chinese Han population.

BACKGROUND: Multiple studies have demonstrated the involvement of low-density lipoprotein receptor-related protein 5 (LRP5) in metabolism-related diseases. This study explored the relationship between the LRP5 rs556442 gene polymorphism and the risks of non-alcoholic fatty liver disease (NAFLD) and coronary heart disease (CHD) in a Chinese Han population. METHODS: This retrospective case-control study included 247 patients with NAFLD, 200 patients with CHD, 118 patients with both NAFLD and CHD, and 339 healthy controls from June 2018 to June 2019 at Qingdao Municipal Hospital. Basic information and clinical characteristics were collected for all subjects. The genotype and allele frequency of LRP5 rs556442 were determined. RESULTS: The genotype distributions of LRP5 rs556442 differed significantly between the CHD and NAFLD + CHD groups (P < 0.05). The LRP5 rs556442 GG genotype markedly promoted the risk of NAFLD in CHD patients [odds ratio (OR) = 2.857, 95% confidence interval (CI): 1.196-6.824, P = 0.018). After adjustment for sex, age, and body mass index (BMI), this association remained significant (OR = 3.252, 95% CI: 1.306-8.102, P = 0.011). In addition, the LRP5 rs556442 AA + AG genotype was associated with an increased BMI in obese NAFLD patients (OR = 1.526, 95% CI: 1.004-2.319, P = 0.048). However, after adjustment for sex and age, this association was no longer significant (OR = 1.504, 95% CI: 0.991-2.282, P = 0.055). CONCLUSIONS: This study found that the LRP5 rs556442 GG genotype increased the risk of NAFLD in CHD patients and AA + AG genotype may be associated with an increased BMI in obese NAFLD patients among a Chinese Han population. Trial registration ChiCTR, ChiCTR1800015426. Registered 28 March 2018-Retrospectively registered, http://www.chictr.org.cn/showproj.aspx?proj=26239 .

Predictive value of LDL/HDL ratio in coronary atherosclerotic heart disease.

BACKGROUND: Dyslipidemia is one of independent risk factors for coronary atherosclerotic heart disease (CAHD). We determined whether the LDL/HDL ratio is better than LDL-C or HDL-C alone in predicting the severity of CAHD. METHODS: We performed a retrospective study of 1351 patients with myocardial ischemia who underwent coronary angiography between January 2018 and December 2019 in Shanghai Ninth People's Hospital. Spearman correlation analysis, logistic regression model, Cox proportional hazards model and multicollinearity were used to evaluate LDL/HDL ratio for predicting CAHD severity compared to LDL-C or HDL-C alone. RESULTS: Higher LDL/HDL ratio was seen in CAHD patients than controls (2.94 ± 1.06 vs 2.36 ± 0.78, P < 0.05). LDL/HDL ratio was significantly associated with the severity of coronary vascular stenosis. The area under the ROC curve of LDL-C, HDL-C, LDL/HDL ratio used to predict CAHD are 0.574 (95% CI 0.547-0.600, P < 0.001), 0.625 (95% CI 0.598-0.651, P < 0.001), 0.668 (95% CI 0.639-0.697, P = 0.000), respectively. The cut-off value of LDL/HDL ratio is 2.517, and the sensitivity and specificity are 65% and 61%, respectively. LDL/HDL ratio was related to the prevalence of CAHD and the odds ratio (OR) was 2.39 [95% confidence interval (CI) 1.698-2.593, P = 0.00] in multicollinearity regression model. CONCLUSION: LDL/HDL ratio may become a better predictor of CAHD severity, compared to LDL-C or HDL-C.

Efficacy and safety of new oral anticoagulants combined with antiplatelet drugs in the treatment of coronary heart disease: Systematic evaluation and meta-analysis.

OBJECTIVE: To analyze the efficacy and safety of antiplatelet drugs combined with new oral anticoagulants (noac) in the treatment of coronary atherosclerotic heart disease (CAD). METHODS: The randomized controlled trials of noac combined with antiplatelet therapy in Cochrane, CNKI, PubMed, EMBASE, Wanfang, Google Scholar, and Baidu library were searched using the literature database. Two researchers independently searched and screened to ensure the consistency of the results, and the literature was summarized and analyzed by Revman 5.3 software. RESULTS: Five research results were included. The results showed that the incidence of mace [95% CI 0.75-0.95, or = 0.84,p = .04], the incidence of major and minor bleeding [95% CI 1.25-5.16, or = 2.54,p = .01], the mortality of cardiovascular disease [95% CI 0.78-0.96, or = 0.86, p = .05], the total mortality [95% CI 0.79-0.95, or = 0.87, p = .003], and the incidence of myocardial infarction in patients with CAD treated with noac and antiplatelet drugs [95% CI 0.77-0.95, or = 0.85, p = .004] was lower than that treated with antiplatelet drugs alone, and the difference was statistically significant (p < .05); the incidence of fatal bleeding [95% CI 0.81-2.08, or = 1.30, p = .28], the incidence of stroke [95% CI 0.50-1.03, or = 0.71, p = .07], and the incidence of intracranial hemorrhage [95% CI 1.02-2.56, or = 1.61, p = .06]. There was no significant difference with antiplatelet drugs alone (p > .05). CONCLUSION: Noac combined with antiplatelet drugs can reduce mace, total mortality, the incidence of myocardial infarction, and cardiovascular mortality in patients with CAD, but may increase the risk of bleeding.

Surgical treatment of coronary atherosclerotic heart disease with right coronary artery aneurysm: a case report.

INTRODUCTION: The etiology of coronary artery aneurysms is unknown. Coronary atherosclerosis is considered to be the main etiology. This case reports a patient with a large coronary aneurysm of the right coronary artery. CASE REPORT: A 65-year-old woman was hospitalized with intermittent chest pain and underwent coronary angiography and echocardiography which showed a large coronary aneurysm of the right coronary artery. The patient recovered well after ligation of coronary artery aneurysms with additional coronary artery bypass grafting. DISCUSSION: The etiology of coronary aneurysms is unknown, which is relatively rare and mostly secondary. Majority of coronary artery aneurysms are located in the right coronary artery. There is currently no standard treatment. Surgical treatment of coronary artery aneurysms may be considered as a safe treatment option. CONCLUSION: The standard surgical treatment for coronary artery aneurysms is unclear. For symptomatic large coronary aneurysms, ligation of coronary artery aneurysms with additional coronary artery bypass grafting can achieve good results.

A review of the association between oral bacterial flora and obstructive sleep apnea-hypopnea syndrome comorbid with cardiovascular disease.

PURPOSE: Obstructive sleep apnea-hypopnea syndrome (OSAHS), a common sleep disorder, has been shown to be an independent risk factor for cardiovascular disease (CVD). Recent studies have focused on the important roles of microorganisms in human health; for example, microorganisms are reportedly associated with obesity, metabolic disorders, and CVD. The number of oral bacteria in patients with OSAHS is considerably higher than that in healthy individuals, and infection with oral bacterial pathogens is associated with the development of CVD. However, whether changes in the oral microbiota mediate the development of OSAHS and CVD remains unknown. METHODS: Therefore, we attempted to review the association between changes in oral microbiota in patients with OSAHS and the development of CVD. RESULTS: Oral microbiota possibly acts via multiple pathways including direct invasion, platelet aggregation, immune response, inflammatory response, and oxidative stress response, leading to the development of CVD in patients with OSAHS. In particular, the strains Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia have demonstrated profound effects. OSAHS leads to changes in the oral bacterial flora and thus may facilitate the occurrence and development of CVD. CONCLUSION: We propose that the underlying mechanism of CVDs resulting from oral microbiota in patients with OSAHS should be elucidated in further studies.

NEAT1/miR-140-3p/MAPK1 mediates the viability and survival of coronary endothelial cells and affects coronary atherosclerotic heart disease.

Studies have shown that long non-coding RNAs (lncRNA) play critical roles in coronary atherosclerotic heart disease (CAD). However, the function of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in CAD is unclear. In this study, we aimed to investigate the functions of lncRNA NEAT1 in CAD. RT-PCR and western blot analysis were carried out to examine the expressions of related RNAs. Colony formation assay, cell proliferation assay, apoptosis assay, and dual-luciferase reporter assay were conducted to investigate the abilities of colony migration, cell proliferation, apoptosis, and targeting. The results showed that NEAT1 was up-regulated in CAD blood samples and in human coronary endothelial cells (HCAECs). Transfection of pcNEAT1 significantly inhibited the survival rate of HCAECs and induced apoptosis of HCAECs. MiR-140-3p was down-regulated in HCAECs. NEAT1 directly targeted miR-140-3p, and the expression of miR-140-3p was inversely correlated with the expression of NEAT1 in CAD patients. In addition, co-transfection of NEAT1 with miR-140-3p mimic reversed the effect of pcNEAT1 on cell viability and apoptosis. mitogen-activated protein kinase 1 (MAPK1) was proved to be a target gene of miR-140-3p, and the miR-140-3p mimic was shown to reduce the expression of MAPK1 in HCAECs. pcNEAT1 significantly increased the expression level of MAPK1, while shNEAT1 significantly reduced the expression level of MAPK1. Our results revealed that lncRNA NEAT1 increased cell viability and inhibited CAD cell apoptosis possibly by activating the miR-140-3p/MAPK1 pathway, and lncRNA NEAT1 might serve as a potential therapeutic target for CAD.

Changes in plasma levels of RIPK1, RIPK3, and MLKL in patients with coronary atherosclerotic heart disease and its clinical predictive value. / å† çŠ¶åŠ¨è„‰ç²¥æ ·ç¡¬åŒ–æ€§å¿ƒè„ç— æ‚£è€ è¡€æµ†RIPK1，RIPK3及MLKLæ°´å¹³å˜åŒ–åŠå ¶ä¸´åºŠé¢„æµ‹ä»·å€¼.

OBJECTIVES: Coronary atherosclerotic heart disease (CHD) is caused by coronary atherosclerosis, which leads to stenosis and even occlusion of the lumen, resulting in myocardial ischemia, and necrosis subsequently. Its prevalence has been high for a long time. The prevention and treatment of CHD are important. The study aimed to investigate the role of plasma levels of receptor-interacting protein kinase 1 (RIPK1), receptor-interacting protein kinase 3 (RIPK3), and mixed-lineage kinase domain-like protein (MLKL) in patients with CHD and its clinical predictive value. METHODS: A total of 190 patients with CHD who were diagnosed by coronary angiography and 70 healthy subjects in cardiovascular department from September 2015 to May 2017 were enrolled in this study. Patients with CHD were assigned into 4 groups: Patients with stable angina pectoris (SAP, n=46), patients with unstable angina pectoris (UAP, n=56), patients with non-ST-segment elevation myocardial infarction (NSTEMI, n=42), and patients with ST-segment elevation myocardial infarction (STEMI, n=46). Patients with CHD were assigned into a single-vessel lesion group, a double-vessel lesion group, and a multi-vessel lesion group according to the results of coronary angiography, and the severity of coronary artery stenosis was determined by Gensini score. Plasma levels of RIPK1, RIPK3, and MLKL were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: The plasma levels of RIPK1, RIPK3, and MLKL in patients with CHD were significantly higher than those in the controls (P<0.05). The plasma levels of RIPK1, RIPK3, and MLKL in the UAP group were significantly higher than those in the SAP group (P<0.05). The plasma levels of RIPK1, RIPK3, and MLKL in NSTEMI and STEMI group were significantly higher than those in the UAP group (P<0.05). There was no significant difference between the NSTEMI group and STEMI group (P>0.05). The plasma levels of RIPK1, RIPK3 and MLKL were significantly increased with numbers of coronary artery lesions (P<0.05), which were positively correlated with Gensini scores. The multivariate logistic regression analysis showed that plasma levels of RIPK1, RIPK3, and MLKL were independent risk factors for severe coronary artery stenosis.The average period of follow-up was 24 months after hospital discharge. The patients were divided into 2 groups according to whether they had major adverse cardiovascular events (MACE). Compared with patient without MACE, patient with MACE had higher levels of RIPK1, RIPK3, and MLKL (P<0.05). Receiver operator characteristic (ROC) curve analysis showed that the area under curve of RIPK1 was 0.72 (P<0.001), the area under curve of RIPK3 was 0.83 (P<0.001), and the area under curve of MLKL was 0.75 (P<0.001). CONCLUSIONS: Plasma levels of RIPK1, RIPK3, and MLKL are closely related to CHD, and they have predictive value for the prognosis evaluation for patients with CHD.

[Research Progress in Fractional Flow Reserve].

Coronary atherosclerotic heart disease is a heart disease caused by coronary artery stenosis or obstruction, resulting in myocardial ischemia, hypoxia or necrosis. Its examination methods include electrocardiogram, hematological examination, coronary CT, coronary angiography and intravascular imaging technology, etc. In recent years, blood Fractional Flow Reserve(FFR) has been widely used to measure the degree of coronary artery stenosis in the treatment of coronary heart disease. Based on the related literature at home and abroad, elaborated the FFR measurements of coronary artery stenosis degree background significance, basic principle and implementation method, on the basis of inductive expounds the FFR examination of clinical research and the advantages and disadvantages, at the same time a preliminary prospect on the development of technology of FFR iFR-the future instantaneous waveform ratio and the functional SYNTAX score has a broad space for development.

[Tongmai Yangxin Pills in treatment for angina pectoris of coronary heart disease: a systematic review of randomized clinical trails].

To systematically review the efficacy and safety of Tongmai Yangxin Pills in treatment for angina pectoris of coronary heart disease. CNKI, WanFang, VIP, SinoMed, PubMed, EMbase and the Cochrane Library databases were retrieved online to collect randomized controlled trials(RCTs) of Tongmai Yangxin Pills for angina pectoris of coronary heart disease since the establishment to November 2018. Two investigators screened out literatures independently, extracted data and assessed the risk of bias of included studies. The risk assessment of included references was made according to criteria recommended by Cochrane Handbook 5.3. Meta-analysis was then performed by RevMan 5.3 software. A total of 9 RCTs were included. The results of Meta-analysis showed that compared with the single application of chemotherapy, the combined administration with Tongmai Yangxin Pills and Western medicine could significantly improve the clinical efficacy of angina(RR=1.22, 95%CI[1.13, 1.31]), the improvement rate of electrocardiogram(RR=1.31, 95%CI[1.21, 1.42]), and the clinical efficacy of traditional Chinese medicine(TCM) syndrome(RR=1.17, 95%CI[1.02, 1.35]). Only one study reported adverse events, while 5 studies reported no adverse event. According to current evidences, in the treatment of angina pectoris of coronary heart disease, Tongmai Yangxin Pills has a better clinical efficacy in the treatment of angina pectoris of coronary heart disease in terms of the improvement rate of electrocardiogram and the clinical efficacy of TCM syndrome. Due to the limited quality and quantity of the included studies, more high-quality studies are required to verify the above conclusions.

Association of polymorphisms in MALAT1 with risk of coronary atherosclerotic heart disease in a Chinese population.

BACKGROUND: Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) plays an important role in vascular remodeling. Down-regulation of MALAT1 can inhibit the proliferation of vascular endothelial cells and vascular smooth muscle cells, reduce cardiomyocyte apoptosis and improve left ventricular function, which is closely linked to numerous pathological processes such as coronary atherosclerotic heart disease (CAD). The aim of this study was to investigate whether polymorphisms in MALAT1 were associated with the susceptibility to CAD. METHODS: A total of 508 CAD patients and 562 age-, gender-, and ethnicity-matched controls were enrolled in this study. Four polymorphisms in MALAT1 (i.e., rs11227209, rs619586, rs664589, and rs3200401) were genotyped using a TaqMan allelic discrimination assay. RESULTS: The rs619586 AG/GG genotypes and G allele were associated with a reduced risk of CAD (AG/GG vs. AA: adjusted OR = 0.66, 95% CI: 0.48-0.91; G vs. A: adjusted OR = 0.68, 95% CI: 0.51-0.90). Stratification analyses showed that CAD patients with rs11227209 CG/GG, rs619586 AG/GG, and rs3200401 CT/TT genotypes exhibited lower levels of TCH (P = 0.02, 0.04, and 0.02, respectively). Moreover, CGCC haplotype was associated with a decreased risk of CAD (OR = 0.28, 95% CI: 0.16-0.48). Multivariate logistic regression analysis identified some independent risk factors for CAD, including rs619586 and rs664589. Subsequent combined analysis showed that the combined genotypes of rs619586AG/GG and rs664589CC were associated with a reduced risk of CAD (OR = 0.29; 95%CI, 0.16-0.53). CONCLUSIONS: These findings indicate that rs619586AG/GG genotypes in MALAT1 may protect against the occurrence of CAD.

Low LPA gene kringle IV-2 repeat copy number association with elevated lipoprotein (a) concentration as an independent risk factor of coronary atherosclerotic heart disease in the Chinese Han population.

BACKGROUND: Lipoprotein (a) [Lp(a)], which is genetically determined by the LPA gene kringle IV type 2 (KIV-2) repeat copy number, has previously been reported in different populations. However, it is uncertain if the same occurs in the Chinese Han population. This study explored the correlation of Lp(a) mass or particle concentration with KIV-2 repeat copy number and application for coronary atherosclerotic heart disease (CAHD) risk assessment. METHODS: A cross-sectional study including 884 subjects was conducted. The Lp(a) level and routine risk factors of CAHD were compared. The KIV-2 copy number distribution, relationship with Lp(a), and assessment for CAHD risk were explored. RESULTS: The mean of Lp(a) mass or particle concentration in the CAHD group was higher than that in the non-CAHD group, while the KIV-2 copy number in the CAHD group was lower. Lp(a) had auxiliary values in gauging the type of plaque and was significantly higher in the soft-plaque group than that in the other two groups (200 mg/L [21.5 nmol/L], 166 mg/L [18.6 nmol/L], 149 mg/L [17.1 nmol/L], respectively, P < 0.05). Kappa test indicated divergence for the same individual using two Lp(a) concentrations (kappa value was 0.536 [< 0.75]). Elevated Lp(a) was an independent CAHD risk factor, whatever mass or particle concentration, and large KIV-2 copy number was a protective factor. CONCLUSION: Lp(a) level and small KIV-2 copy number are risk factors for CAHD in the Chinese Han population; furthermore, elevated Lp(a) may gauge the type of coronary plaque.

Prevention of cardiac hypertrophy by the use of a glycosphingolipid synthesis inhibitor in ApoE-/- mice.

ApoE-/- mice fed a high fat and high cholesterol (HFHC) diet (20% fat and 1.25% cholesterol) from 12 weeks of age to 36 weeks revealed an age-dependent increase in the left ventricular mass (LV mass) and decline in fractional shortening (FS%), which worsened with HFHC diet. These traits are indicative of maladaptive pathological cardiac hypertrophy and dysfunction. This was accompanied by loading of glycosphingolipids and increased gene expression of ANP, BNP in myocardial tissue. Masson's trichrome staining revealed a significant increase in cardiomyocyte size and fibrosis. In contrast, treatment with 5 and 10 µM D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of glucosylceramide synthase and lactosylceramide synthase, dose-dependently decreased the load of glycosphingolipids and preserved fractional shortening and maintained left ventricular mass to normal 12-week-old control levels over a 6 month treatment period. Our mechanistic studies showed that D-PDMP inhibited cardiac hypertrophy by inhibiting the phosphorylation of mitogen-activated protein kinase (MAPK). We propose that associating increased glycosphingolipid synthesis with cardiac hypertrophy could serve as a novel approach to prevent this phenotype in experimental animal models of diet -induced atherosclerotic heart disease.