Coronary Heart Disease In Type Research Articles

Labilization of the DNA structure in peripheral blood lymphocytes of COVID-19 patients

Introduction. Available data indicate the SARS-CoV-2 coronavirus to be potent of impairing DNA repair processes and cause oxidative stress, which can lead to the accumulation of DNA damage in human cells. However, the DNA-damaging effect of the virus has not yet been sufficiently studied. The purpose of the research was to study the ability of SARS-CoV-2 to cause DNA damage in human peripheral blood lymphocytes. Materials and methods. One hundred forty COVID-19 patients and 24 donors of the control group are included in the study. The level of DNA fragmentation in lymphocytes was determined by alkaline DNA-comet assay. Statistical differences between the mean medians of the «%DNA in the comet tail» (tail DNA%) were assessed using Student’s t-test. The Jeffers test was used to compare the proportions of cells with different levels of DNA-damage. Statistical differences between groups were assessed using the Mann-Whitney test. Results. In the COVID-19 patients, an increase in the level of breaks and alkali-labile sites in DNA was revealed when compared to controls (p = 0.025). In the group of patients infected with SARS-CoV-2, the proportion of comets with DNA damage of up to 5% decreased (p = 0.009), while the proportion of comets containing more than 10% DNA tail increased (p = 0.000). The number of atypical comets compared to the control increased by 3.7 and 5.9 times with mild and moderate severity of the disease, respectively (r = 0.993; p = 0.001). In the association with diseases – coronary heart disease (CHD) and diabetes mellitus type II (DM type 2), the level of DNA fragmentation in lymphocytes statistically significantly increased compared to the group of patients without these diseases. Limitations. A limitation is the lack of data on DNA-structure damage in severe COVID-19 disease. Conclusion. SARS-CoV-2 infection leads to labilization of the DNA structure in human peripheral blood lymphocytes. The level of DNA damage depends on the severity of COVID-19 and the presence of comorbid diseases: CHD and DM type 2. The results of the study are important for understanding the mechanisms of action of the virus on human immunocompetent cells.

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

BackgroundInsulin 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.MethodsA 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).OutcomesThe 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).ConclusionsThe 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.

Supramolecular self‐assembled nanoparticles for targeted therapy of myocardial infarction by enhancing cardiomyocyte mitophagy

AbstractMyocardial infarction accompanied by diabetes mellitus is accepted as the most serious type of coronary heart disease, and among the current treatment strategies, the precise delivery of protective drugs for inhibiting cardiomyocyte apoptosis is still a challenge. In this study, we developed a biodegradable nanoparticles‐based delivery system with excellent macrophage escape, cardiac targeting, and drug release properties to achieve targeted therapy of myocardial infarction. Specifically, a copolymer of p(DMA–MPC–CD) combining self‐adhesion, hydration lubrication, and targeting peptide binding site was successfully prepared by free radical copolymerization, and it was self‐assembled on the surface of melatonin‐loaded dendritic mesoporous silica nanoparticles (bMSNs) following the integration of adamantane‐modified cardiac homing peptide (CHP) based on supramolecular host–guest interaction. Importantly, a hydration layer formed around the zwitterionic phosphorylcholine groups of the multifunctional nanoparticles, which was confirmed by the enhancement in hydration lubrication and reduction in coefficient of friction, prevented the nanoparticles from phagocytosis by the macrophages. The in vivo bioluminescence imaging test indicated that the nanoparticles were endowed with satisfied cardiac targeting capability, and the in vivo mice study demonstrated that the intravenous injection of drug‐loaded nanoparticles (namely bMSNs–Mel@PDMC–CHP) effectively reduced cardiomyocyte apoptosis, alleviated myocardial interstitial fibrosis, and enhanced cardiac function.

Multiple coronary heart diseases are risk factors for mental health disorders: A mendelian randomization study

BackgroundPrevious observational studies have suggested associations between Coronary Heart Disease (CHD) and Mental Health Disorders (MHD). However, the causal nature of these relationships has remained elusive. ObjectiveThe purpose of this study is to elucidate the causal relationships between eight distinct types of CHD and six types of MHD using Mendelian randomization (MR) analysis. MethodsThe MR analysis employed a suite of methods including inverse variance-weighted (IVW), MR-Egger, weighted mode, weighted median, and simple mode techniques. To assess heterogeneity, IVW and MR-Egger tests were utilized. MR-Egger regression also served to investigate potential pleiotropy. The stability of IVW results was verified by leave-one-out sensitivity analysis. ResultsWe analyzed data from over 2,473,005 CHD and 803,801 MHD patients, informed by instrumental variables from large-scale genomic studies on European populations. The analysis revealed a causal increase in the risk of Major Depressive Disorder and Mania associated with Coronary Artery Disease and Myocardial Infarction. Heart Failure was found to causally increase the risk for Bipolar Disorder and Schizophrenia. Atrial Fibrillation and Ischemic Heart Diseases were positively linked to Generalized Anxiety Disorder and Mania, respectively. There was no significant evidence of an association between Hypertensive Heart Disease, Hypertrophic Cardiomyopathy, Pulmonary Heart Disease, and MHD. Reverse MR analysis indicated that MHD do not serve as risk factors for CHD. ConclusionsThe findings suggest that specific types of CHD may act as risk factors for certain MHDs. Consequently, incorporating psychological assessments into the management of patients with CHD could be advantageous.

Microvascular Disease, Cardiovascular Health, and Risk of Coronary Heart Disease in Type 2 Diabetes: A UK Biobank Study.

The interplay between cardiovascular health metrics (CVHMs) and microvascular disease (MVD) in relation to the risk of incident coronary heart disease (CHD) among individuals with type 2 diabetes mellitus (T2DM) remains to be evaluated. To investigate the role of MVD and CVHMs in the development of CHD among T2DM. We included 19,664 participants with T2DM from the UK Biobank who had data on CVH metrics (CVHMs) and were free of CHD during recruitment. CVHMs were defined based on five behavioral (body mass index, diet, sleep duration, smoking, and regular exercise) and three biological factors (glycemic control, hyperlipidemia, and hypertension). MVD was defined as the presence of retinopathy, peripheral neuropathy, and chronic kidney disease. HR and 95% CI of CHD were estimated by multivariable Cox regression models. There were 3,252 incident cases of CHD recorded after a median follow-up of 12.3 years. After multivariable adjustment, each MVD was separately associated with risk of CHD, and those who had 1 or ≥2 MVD had a 27% and an 87% increased risk of developing CHD, respectively. Each of the unfavorable CVHMs was associated with a higher risk of CHD. As compared with MVD-free participants who had ideal CVHMs, those who had ≥2 MVD and had poor CVHMs were at particularly high risk of incident CHD (HR=4.58; 95% CI: 3.58, 5.86), similarly when considering behavioral CVH or biological CVH separately. On an additive scale, there was a positive statistically significant interaction between number of MVD and CVHMs. Coexistence of multiple MVDs was associated with a substantially higher risk of CHD among individuals with T2DM. Such an association may be amplified by unfavorable CVHMs.

Polymorphism of IL-12/IL-23 axis is associated with coronary heart disease.

IL12B encodes the shared p40 subunit (IL-12p40) of IL-12 and IL-23, which have diverse immune functions and are closely related to the occurrence and development of atherosclerosis (AS). However, the exact role of IL12B in coronary heart disease (CHD) was still unknown. A case-control association analysis was performed between five single nucleotide polymorphisms (SNPs) of IL12B (rs1003199, rs3212219, rs2569254, rs2853694 and rs3212227) and CHD in Chinese Han population (1824 patients with CHD vs. 2784 controls). Logistic regression analyses were used to study the relationships between SNPs and CHD, while multiple linear regression analyses were used to test the association between the SNP and the severity of CHD. In addition, the plasma IL12B concentration of CHD patients were detected by ELISA. We detected a significant association between one of the SNPs, rs2853694-G and CHD (padj = 2.075 × 10-5 , OR, 0.773 [95% CI, 0.686-0.870]). Stratified analysis showed that rs2853694 was associated with CHD in both male and female populations and was significantly associated with both early- and late-onset CHD. In addition, rs2853694 is also related to the different types of CHD including clinical-CHD and anatomical-CHD. Moreover, there are significant differences in serum IL12B concentrations between rs2853694-TT carriers and rs2853694-GT carriers in CHD patients (p = 0.010). A common variant of IL12B was found significantly associated with CHD and its subgroups. As a shared subunit of IL-12 and IL-23, IL-12p40 may play a key role in IL-12/IL-23 axis mediated AS, which is expected to be an effective therapeutic target for CHD.

Genetic relationship between ageing and coronary heart disease: a Mendelian randomization study.

Genetic relationship between ageing and coronary heart disease has not been well investigated. The aim of the study was to explore the association of several ageing biomarkers with the risk of several types of coronary heart disease using the Mendelian randomization approach. Summary data for telomere length, four epigenetic clocks (such as intrinsic epigenetic age acceleration), four types of coronary heart disease (such as myocardial infarction) were collected from the most updated and available genome-wide association studies. Instrumental variables were extracted from the exposure-related summary data according to correlation, independence and exclusivity assumptions. Three Mendelian randomization methods (such as inverse variance weighted) were used for causal inference. Four sensitivity analyses (such as MR-Egger intercept) were performed to prevent horizontal pleiotropy. Inverse variance weighted reported that longer telomere length was related to the lower risk of myocardial infarction, angina pectoris, unstable angina pectoris and coronary atherosclerosis (P = 8.840e-11, P = 9.830e-04, P = 1.539e-05, P = 2.607e-09). Inverse variance weighted also reported that four epigenetic clocks might be not implicated in the risk of these coronary heart diseases. Furthermore, there was not enough evidence to confirm the effect of coronary heart disease on these ageing biomarkers. Longer telomere length, but not the epigenetic clock changes, genetically decreased the risk of coronary heart disease. Considering that telomere length and epigenetic clocks were two independent ageing biomarkers, the correlation between ageing and coronary heart disease might be redefined at the genetic level.

Effective fraction of Gualou-Xiebai-Banxia decoction inhibits the apoptosis of myocardial cells induced by ox-LDL via FGF21/FGFR1/βKlotho-FRS2α signal pathway

Ethnopharmacological relevanceThe Gualou-Xiebai-Banxia decoction (GXBD), a classical traditional Chinese medicine (TCM) formula, has beneficial effects in turbid phlegm obstruction syndrome, a type of coronary heart disease (CHD). However, the underlying mechanism and effective constituents of GXBD remain elusive. Our previous studies have shown that the effective constituents of GXBD may be enriched in the n-butanol fraction (GXB-N) and water fraction (GXB-W), the targets of which remain unknown. Aim of the studyTo investigate whether GXB-N and GXB-W protect myocardial cells (MCs) via fibroblast growth factor 21 (FGF21) signaling and, if so, to elucidate the underlying mechanisms. Furthermore, to investigate the targets of GXB-N and GXB-W as potential therapeutic targets for cardiovascular disease (CVD). Materials and methodsCell viability and apoptosis were assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays, respectively. The content of FGF21 in the medium was measured using enzyme-linked immunosorbent assay (ELISA). Protein expression was detected using immunofluorescence and western blotting. ResultsApoptosis increased markedly in MCs exposed to oxidized low density lipoprotein (ox-LDL) 100 μg/mL, with increased expression of FGF21, FGFR1 and βKlotho, phosphorylation of fibroblast receptor substrate 2α (FRS2α) was suppressed. Following incubation with GXB-N and GXB-W 200 μg/mL, the expression of FGF21, FGFR1, and βKlotho and the phosphorylation of FRS2α were increased. ConclusionOx-LDL may inhibit the phosphorylation of FRS2α, inducing considerable FGF21 resistance and resulting in MC apoptosis. GXB-N and GXB-W restored and enhanced FGF21 sensitivity in MCs, consequently rescuing cells from ox-LDL-induced apoptosis. The FGF21-FRS2α signal pathway may be part action targets of these two effective fractions of GXBD.

Constructing a prognostic tool for predicting the risk of non-adherence to antiplatelet therapy in discharged patients with coronary heart disease: a retrospective cohort study.

To investigate the incidence and influencing factors affecting the non-adherence behavior of patients with coronary heart disease (CHD) to antiplatelet therapy after discharge and to construct a personalized predictive tool. In this retrospective cohort study, 289 patients with CHD who were admitted to the Department of Cardiology of The First Affiliated Hospital of the University of Science and Technology of China between June 2021 and September 2021 were enrolled. The clinical data of all patients were retrospectively collected from the hospital information system, and patients were followed up for 1 year after discharge to evaluate their adherence level to antiplatelet therapy, analyze their present situation and influencing factors for post-discharge adherence to antiplatelet therapy, and construct a nomogram model to predict the risk of non-adherence. Based on the adherence level to antiplatelet therapy within 1 year after discharge, the patients were divided into the adherence (n=216) and non-adherence (n=73) groups. Univariate analysis revealed statistically significant differences between the two groups in terms of variable distribution, including age, education level, medical payment method, number of combined risk factors, percutaneous coronary intervention, duration of antiplatelet medication, types of drugs taken at discharge, and CHD type (P<0.05). Furthermore, multivariate logistic regression analysis revealed that, except for the medical payment method, all the seven abovementioned variables were independent risk factors for non-adherence to antiplatelet therapy (P<0.05). The areas under the receiver operating characteristic curve before and after the internal validation of the predictive tool based on the seven independent risk factors and the nomogram were 0.899 (95% confidence interval [CI]: 0.858-0.941) and 0.89 (95% CI: 0.847-0.933), respectively; this indicates that the tool has good discrimination ability. The calibration curve and Hosmer-Lemeshow goodness of fit test revealed that the tool exhibited good calibration and prediction consistency (χ2=5.17, P=0.739). In this retrospective cohort study, we investigated the incidence and influencing factors affecting the non-adherence behavior of patients with CHD after discharge to antiplatelet therapy. For this, we constructed a personalized predictive tool based on seven independent risk factors affecting non-adherence behavior. The predictive tool exhibited good discrimination ability, calibration, and clinical applicability. Overall, our constructed tool is useful for predicting the risk of non-adherence behavior to antiplatelet therapy in discharged patients with CHD and can be used in personalized intervention strategies to improve patient outcomes.

Effect Sacubitril/Valsartan in patients with Acute Myocardial Infarction (AMI): a systematic review and meta-analysis

Background: Acute Myocardial Infarction (AMI) is a type of coronary heart disease with high morbidity and mortality. The renin-angiotensin-aldosterone system (RAAS) is an important endocrine system in controlling blood pressure and cardiovascular homeostasis and is responsible for AMI. In patients with AMI or a heart attack, sacubitril/valsartan has been shown to reduce the risk of heart failure and death. This study aims to evaluate the effect of sacubitril/valsartan in AMI patients. Methods: In order to evaluate the effects of sacubitril/valsartan in patients with AMI, three databases, including PubMed, Cochrane Library, and the ClinicalTrials website, were searched. The final search was performed in January 2023. The meta‑analysis was subsequently performed with Revman 5.4 software and a total of three studies were included. Results: The results of the main outcomes showed that sacubitril/valsartan has no significant reduction in major adverse cardiovascular and cerebrovascular events (MACCEs) odds ratio (OR), 0.70; 95% confidence interval (CI), 0.38‑1.30; P=0.26] and incidence of acute heart failure (AHF) (OR, 0.52; 95% CI, 0.24‑1.15; P=0.11). The secondary outcomes showed no effect of sacubitril/valsartan to increase left ventricular remodeling. Conclusion: In conclusion, the present meta‑analysis revealed that sacubitril/valsartan could not effectively reduce the incidence of MACCEs and AHF in patients with AMI. In the future, a meta‑analysis study will be designed with many studies to reduce the incidence of MACCEs and AHF effectively.

Healthy lifestyle, DNA methylation age acceleration, and incident risk of coronary heart disease

BackgroundDNA methylation clocks emerged as a tool to determine biological aging and have been related to mortality and age-related diseases. Little is known about the association of DNA methylation age (DNAm age) with coronary heart disease (CHD), especially in the Asian population.ResultsMethylation level of baseline blood leukocyte DNA was measured by Infinium Methylation EPIC BeadChip for 491 incident CHD cases and 489 controls in the prospective China Kadoorie Biobank. We calculated the methylation age using a prediction model developed among Chinese. The correlation between chronological age and DNAm age was 0.90. DNA methylation age acceleration (Δage) was defined as the residual of regressing DNA methylation age on the chronological age. After adjustment for multiple risk factors of CHD and cell type proportion, compared with participants in the bottom quartile of Δage, the OR (95% CI) for CHD was 1.84 (1.17, 2.89) for participants in the top quartile. One SD increment in Δage was associated with 30% increased risk of CHD (OR = 1.30; 95% CI 1.09, 1.56; Ptrend = 0.003). The average number of cigarette equivalents consumed per day and waist-to-hip ratio were positively associated with Δage; red meat consumption was negatively associated with Δage, characterized by accelerated aging in those who never or rarely consumed red meat (all P < 0.05). Further mediation analysis revealed that 10%, 5% and 18% of the CHD risk related to smoking, waist-to-hip ratio and never or rarely red meat consumption was mediated through methylation aging, respectively (all P for mediation effect < 0.05).ConclusionsWe first identified the association between DNAm age acceleration and incident CHD in the Asian population, and provided evidence that unfavorable lifestyle-induced epigenetic aging may play an important part in the underlying pathway to CHD.

Association of High sensitivity C-reactive protein (Hs-CRP) with poor Glycaemic control and Coronary Heart Disease in Type 2 Diabetes Mellitus

High sensitivity C-reactive protein (Hs-CRP) is a sensitive marker of subclinical inflammation associated with atherosclerosis. Uncontrolled diabetes mellitus (DM) is one of the important risk factors of coronary heart disease (CHD). The aim of this study was to evaluate the association between Hs-CRP levels and both glycaemic control and CHD in Syrian type 2 diabetes mellitus (T2DM) patients. A random sample of 108 subjects was selected from T2DM and/or CHD patients seen in the National Centre for Diabetes, and the outpatient clinic of cardiology department at Tishreen University Hospital in Latakia. Four groups were formed: Group 1 [T2DM (+) CHD (-), N=29], Group 2 [T2DM (-) CHD (+), N=25], Group 3 [T2DM (+) CHD (+), N=29], and Group 4 (T2DM (-) CHD (-), N=25). Serum Hs-CRP and glycated haemoglobin (HBA1C) were determined. The SPSS 25.0 program was used for the statistical analysis. Probability (P) value less than 0.05 was considered statistically significant. Mean Hs-CRP level was higher in T2DM subjects with (5.23±1.56mg/l) or without (2.29±0.78mg/l) CHD compared to T2DM (-) CHD (-) patients (0.16±0.04mg/l), (p&lt;0.0001 for both). Mean Hs-CRP level in T2DM with CHD was not only higher than T2DM patients without CHD (p&lt;0.0001), but also than non-diabetic subjects with CHD (2.56±0.45mg/l) (p&lt;0.0001). There was a positive correlation between serum Hs-CRP and HBA1C in T2DM patients with CHD (r=0.781, P&lt;0.0001), Similarly, Hs-CRP levels were positively and significantly correlated with HBA1C in T2DM patients without CHD (r=0.800, p&lt;0.0001). We also noticed that for every 1.0% increase in HbA1c there was an 77% increase in the likelihood of having an elevated Hs-CRP. We concluded that Hs-CRP was strongly correlated with glycaemic control in T2DM patients. The highest Hs-CRP level was observed in T2DM with CHD patients. Hs-CRP could predict the incidence of coronary heart disease in T2DM patients.

Molecular Mechanisms of Mitochondrial Quality Control in Ischemic Cardiomyopathy.

Ischemic cardiomyopathy (ICM) is a special type of coronary heart disease or an advanced stage of the disease, which is related to the pathological mechanism of primary dilated cardiomyopathy. Ischemic cardiomyopathy mainly occurs in the long-term myocardial ischemia, resulting in diffuse myocardial fibrosis. This in turn affects the cardiac ejection function, resulting in a significant impact on myocardial systolic and diastolic function, resulting in a decrease in the cardiac ejection fraction. The pathogenesis of ICM is closely related to coronary heart disease. Mainly due to coronary atherosclerosis caused by coronary stenosis or vascular occlusion, causing vascular inflammatory lesions and thrombosis. As the disease progresses, it leads to long-term myocardial ischemia and eventually ICM. The pathological mechanism is mainly related to the mechanisms of inflammation, myocardial hypertrophy, fibrosis and vascular remodeling. Mitochondria are organelles with a double-membrane structure, so the composition of the mitochondrial outer compartment is basically similar to that of the cytoplasm. When ischemia-reperfusion induces a large influx of calcium into the cell, the concentration of calcium ions in the mitochondrial outer compartment also increases. The subsequent opening of the membrane permeability transition pore in the inner mitochondrial membrane and the resulting calcium overload induces the homeostasis of cardiomyocytes and activates the mitochondrial pathway of apoptosis. Mitochondrial Quality Control (MQC), as an important mechanism for regulating mitochondrial function in cardiomyocytes, affects the morphological structure/function and lifespan of mitochondria. In this review, we discuss the role of MQC (including mitophagy, mitochondrial dynamics, and mitochondrial biosynthesis) in the pathogenesis of ICM and provide important evidence for targeting MQC for ICM.

Complications after One-Year Observation of Patients with Type 2 Diabetes Mellitus and Various Types of Coronary Heart Disease

Aim: Evaluation of complications after one-year observation in patients with acute and chronic coronary heart disease (CHD) depending on the presence of type 2 diabetes mellitus (T2DM). Material and methods: This comparative clinical study included 202 men and women with acute and chronic CHD. Patients were divided into four groups, depending on the presence of type 2 diabetes mellitus: acute CHD and T2DM; acute CHD without T2DM (control group); chronic CHD and T2DM; chronic CHD without T2DM (control group). Depending on the results of clinical status and coronary angiography data, patients underwent myocardial revascularization (balloon angioplasty without stenting, stenting, coronary bypass grafting, stenting + coronary bypass grafting) followed by pharmacological treatment. One-year composite endpoints included: recurrent myocardial infarction, acute cerebrovascular accident, readmission, and death. Results: After admission, up to 80% of patients, regardless of CHD type and glycemic status, underwent revascularization. Patients without T2DM underwent stenting significantly more often compared with patients with T2DM. Coronary artery bypass grafting, including in combination with stenting, was more frequent in patients with T2DM with acute and chronic CHD. One year after discharge, readmissions and reoperations were more prevalent among patients with acute and chronic CHD and T2DM. The groups did not differ by the number of nonfatal and fatal complications. The total number of endpoints in patients with T2DM, regardless of the CHD type, were 2 times higher compared with the control group (p<0.001). Conclusion: Patients with acute and chronic CHD without T2DM, underwent stenting of one coronary artery more often, while patients with T2DM underwent coronary bypass surgery, including in combination with stenting. After one year of observation, the number of complications in patients with various CHD types and T2DM was higher than those without T2DM. This once again indicates the need for comprehensive secondary prevention.

Can case-based payment contain healthcare costs? - A curious case from China

We adopted a difference-in-difference (DID) design to evaluate the impact of a case-based payment pilot in Tianjin, China on hospital admission, utilization of varied therapeutic regimes, and the associated costs. We used claim data of all admissions of angina and acute myocardial infarction during July 2015 to June 2018, 18 months before and after the program. Our analyses were supported by convincing common trends tests and a couple of sensitivity analyses. As intended, for patients who received percutaneous coronary stenting (PCS) and were counted in the case-based payment system, we showed that the program decreased length-of-stay, per-admission spending, and out-of-pocket spending by 20.8%, 14.2%, and 95.5%, respectively, but did not increase readmissions. However, when considering all patients who suffered from the two types of coronary heart diseases, we found that the program otherwise increased per-admission spending by nearly 11%. As a result, the program took a perverse effect in increasing monthly spending for the health insurance scheme and the society by 1005.6 thousand USD (47·5%) and 1095·7 thousand USD (34·7%), respectively. Increases in hospital admissions, and proportion of performing PCS accounted for 66·7% and 39·2% of the rise, respectively. In addition, our analysis provided evidence of health providers’ cream-skimming behaviors, including selecting younger patients with lower CCI in the case-based system, up-coding complications, and keeping higher cost patients in the fee-for-service payment system. We draw lessons that case-based payment may make an unintended impact that increases healthcare costs when incentives are not properly designed.

Indicators of regional arterial stiffness in young patients with different types of coronary heart disease

Indicators of regional arterial stiffness in young patients with different types of coronary heart disease

Fibrosis-4 Index Is Closely Associated with Arterial Damage and Future Risk of Coronary Heart Disease in Type 2 Diabetes.

This study evaluated the association between fibrosis-4 (FIB 4) index and arterial damage or future risk of coronary heart disease (CHD) in type 2 diabetes. The study subjects were 253 patients with type 2 diabetes. The FIB4 index, as a marker of hepatic fibrosis based on age, aspartate aminotransferase and alanine aminotransferase levels, and platelet count, was calculated for all subjects. Carotid intima-media thickness (IMT), carotid artery calcification (CAC), and aortic arch calcification (AAC) grade (0–2) were assessed as atherosclerotic variables. The Suita score was calculated as the future risk of coronary heart disease (CHD). We assessed whether the FIB4 index was associated with both atherosclerotic variables and the Suita score. FIB4 index was significantly associated with IMT (r = 0.241, P < 0.001) and Suita score (r = 0.291, P < 0.001). Subjects with CAC showed a significantly higher FIB4 index score compared to subjects without (1.70 ± 0.74 and 1.24 ± 0.69, respectively, P < 0.001), whereas the FIB4 index was significantly elevated with a higher grade of AAC (1.24 ± 0.74, 1.56 ± 0.66, and 1.79 ± 0.71, respectively, P < 0.001). Linear regression analysis adjusted for clinical characteristics indicated that the FIB4 index was positively associated with IMT, Suita score, CAC, and AAC grade (β = 0.241, P=0.004; β = 2.994, P < 0.001; β = 0.139, P=0.001; and β = 0.265, P < 0.001, respectively). FIB4 index is closely associated with arterial damage and future risk of CHD in type 2 diabetes.

Correlation Analysis Between Required Surgical Indexes and Complications in Patients With Coronary Heart Disease.

A total of 215 patients with coronary heart disease (CHD) were analyzed with SPSS. Samples of different genders showed significance in the obtuse marginal branch of the left circumflex branch × 1, the diagonal branch D1 × 1, and the ms PV representation. Patients with left circumflex branch occlusion are more male and tend to be younger. Age displayed a positive correlation with left intima-media thickness (IMT) and right IMT. This indicated that as age increases, the values of left IMT and right IMT increase. Samples of different CHD types showed significance in the obtuse marginal branch of the left circumflex branch × 1, the middle part of RCA × 1, and the middle part of the left anterior descending branch × 1.5. For non-ST-segment elevation angina pectoris with acute total vascular occlusion, the left circumflex artery is the most common, followed by the right coronary artery and anterior descending branch. Ultrasound of carotid IMT in patients with CHD can predict changes in left ventricular function, but no specific correlation between left and right common carotid IMT was found. Samples with or without the medical history of ASCVD showed significance in the branch number of coronary vessel lesions. The value of the branch number of coronary vessel lesions in patients with atherosclerotic cardiovascular disease (ASCVD) was higher than in those without ASCVD. The occurrence of complication is significantly relative with the distance of left circumflex branch × 1, the middle segment of left anterior descending branch × 1.5, and the distance of left anterior descending branch × 1. For patients without complications, the values in the distal left circumflex branch × 1, the middle left anterior descending branch × 1.5, and the distal left anterior descending branch × 1 were higher than those for patients with complications. The VTE scores showed a positive correlation with the proximal part of RCA × 1, the branch number of coronary vessel lesions, the posterior descending branch of left circumflex branch × 1, the distal part of left circumflex branch × 1, and the middle part of left anterior descending branch × 1.5.

Integrated Analysis Reveals S100a8/a9 Regulates Autophagy and Apoptosis through the MAPK and PI3K-AKT Signaling Pathway in the Early Stage of Myocardial Infarction.

Myocardial infarction (MI), a type of coronary heart disease, has had a significantly increased incidence in recent years. The balance of cardiomyocyte apoptosis and autophagy after MI is one of the main determinants of patient prognosis. Both affect myocardial fibrosis and ventricular remodeling and regulate cell survival. However, there are few studies on the regulation mechanism of cardiomyocyte autophagy and apoptosis in the early stage after MI. In this study, based on analyzing the scRNA-seq and mRNA-seq data of mice in the early stage of MI, we found that the expression of S100a8 and S100a9 increased first and then decreased in the early stage of MI, and their expression level changed with the number of neutrophils. Further, through the functional enrichment analysis of the differentially expressed genes, we found that S100a8 and S100a9 were simultaneously associated with autophagy and apoptosis and could regulate autophagy and apoptosis of cardiomyocytes through MAPK or PI3K-AKT signaling pathways. This study provides valuable insights for clarifying the pathogenesis of early stage MI and improving its early treatment.

Identification of Serum Metabolomics Characteristics in Patients with Stable Angina Pectoris Using UHPLC-QE-MS.

Background Stable angina pectoris (SAP) is one of the main types of coronary heart disease (CHD). To improve treatment outcomes, more effective biomarkers are needed. Currently, studies on the metabolic characteristics of SAP are lacking. Here, we explored the serum metabolomic profile of SAP and identified potential biomarkers and related pathways to assist the clinical diagnosis and treatment of SAP. Method Thirty patients with SAP patients and 30 healthy controls (CON) without stenosis were selected for this study. All patients underwent coronary angiography. The metabolites of the two groups' serum samples were investigated using UHPLC-QE-MS. Changes in serum metabolic profile were evaluated using multivariate statistical analysis and pathway analysis. Result OPLS-DA analysis identified significant differences in the serum metabolic profiles between patients with SAP and CON. Twenty-five differential metabolites were identified between patients from SAP and CON groups, including choline, creatine, L-arginine, beta-guanidinopropionic acid, isopalmitic acid, xanthine, LysoPC (18 : 1), and LysoPC (20 : 3). Pathway analysis found that these differential metabolites were involved in energy metabolism, oxidative stress, purine metabolism, and other metabolic pathways. Conclusion By comparing the serum metabolic profiles of SAP patients with a control group, we identified 25 potential biomarkers that could improve the clinical diagnosis and treatment of SAP.