Development Of Coronary Heart Disease Research Articles

Plasma proteome association with coronary heart disease and carotid intima media thickness: results from the KORA F4 study

Background and aimsAtherosclerosis is the main cause of stroke and coronary heart disease (CHD), both leading mortality causes worldwide. Proteomics, as a high-throughput method, could provide helpful insights into the pathological mechanisms underlying atherosclerosis. In this study, we characterized the associations of plasma protein levels with CHD and with carotid intima-media thickness (CIMT), as a surrogate measure of atherosclerosis.MethodsThe discovery phase included 1000 participants from the KORA F4 study, whose plasma protein levels were quantified using the aptamer-based SOMAscan proteomics platform. We evaluated the associations of plasma protein levels with CHD using logistic regression, and with CIMT using linear regression. For both outcomes we applied two models: an age-sex adjusted model, and a model additionally adjusted for body mass index, smoking status, physical activity, diabetes status, hypertension status, low density lipoprotein, high density lipoprotein, and triglyceride levels (fully-adjusted model). The replication phase included a matched case-control sample from the independent KORA F3 study, using ELISA-based measurements of galectin-4. Pathway analysis was performed with nominally associated proteins (p-value < 0.05) from the fully-adjusted model.ResultsIn the KORA F4 sample, after Bonferroni correction, we found CHD to be associated with five proteins using the age-sex adjusted model: galectin-4 (LGALS4), renin (REN), cathepsin H (CTSH), and coagulation factors X and Xa (F10). The fully-adjusted model yielded only the positive association of galectin-4 (OR = 1.58, 95% CI = 1.30–1.93), which was successfully replicated in the KORA F3 sample (OR = 1.40, 95% CI = 1.09–1.88). For CIMT, we found four proteins to be associated using the age-sex adjusted model namely: cytoplasmic protein NCK1 (NCK1), insulin-like growth factor-binding protein 2 (IGFBP2), growth hormone receptor (GHR), and GDNF family receptor alpha-1 (GFRA1). After assessing the fully-adjusted model, only NCK1 remained significant (β = 0.017, p-value = 1.39e-06). Upstream regulators of galectin-4 and NCK1 identified from pathway analysis were predicted to be involved in inflammation pathways.ConclusionsOur proteome-wide association study identified galectin-4 to be associated with CHD and NCK1 to be associated with CIMT. Inflammatory pathways underlying the identified associations highlight the importance of inflammation in the development and progression of CHD.

Interplay Between Plasma Glycine and Branched-Chain Amino Acids Contributes to the Development of Hypertension and Coronary Heart Disease.

Higher levels of plasma glycine are linked to a reduced risk, while increased levels of total branched-chain amino acids (tBCAAs) are associated with a higher risk of essential hypertension and coronary heart disease (CHD). As these metabolic components are interconnected, analyzing the tBCAAs/glycine ratio may help to understand their interplay in the pathogenesis of cardiovascular disease. The Cox regression approach was combined with the development of novel genetic tools for assessments of associations between plasma metabolomic data (glycine, tBCAAs, and tBCAAs/glycine ratio) from the UK Biobank and the development of hypertension and CHD. Genome-wide association study was performed on 186 523 White UK Biobank participants to identify new independent genetic instruments for the 2-sample Mendelian randomization analyses. P-gain statistic >10 identified instruments associated with tBCAAs/glycine ratio significantly stronger compared with individual amino acids. Outcomes of genome-wide association study on hypertension and CHD were derived from the UK Biobank (nonoverlapping sample), FinnGen, and CARDIoGRAMplusC4D. The tBCAAs/glycine ratio was prospectively associated with a higher risk of developing hypertension and CHD (hazard ratio quintile Q5 versus Q1, 1.196 [95% CI, 1.109-1.289] and 1.226 [95% CI, 1.160-1.296], respectively). Mendelian randomization analysis demonstrated that tBCAAs/glycine ratio (P-gain >10) was a risk factor for hypertension (meta-analyzed inverse-variance weighted causal estimate 0.45 log odds ratio/SD (95% CI, 0.26-0.64) and CHD (0.48 [95% CI, 0.29-0.67]) with an absolute effect significantly larger compared with the effect of glycine (-0.06 [95% CI, -0.1 to -0.03] and -0.08 [95% CI, -0.11 to -0.05], respectively) or tBCAAs (0.22 [95% CI, 0.09-0.34] and 0.12 [95% CI, 0.01-0.24], respectively). The total BCAAs/glycine ratio is a key element of the metabolic signature contributing to hypertension and CHD, which may reflect biological pathways shared by glycine and tBCAAs.

Taking appreciation to heart: appreciation at work and cardiovascular risk in male employees.

While perceived appreciation at work has been associated with self-reported health and wellbeing, studies considering biological health markers are lacking. In this study, we investigated whether appreciation at work would relate to coronary heart disease (CHD) risk as well as the specificity of this proposed association. Our study comprised a total of 103 male participants, including apparently healthy, medication-free, non-smoking men in the normotensive to hypertensive range (n = 70) as well as medicated hypertensive and CHD patients (n = 33). CHD risk was assessed by blood pressure [mean arterial pressure (MAP)], the diabetes marker glycated hemoglobin A1c (HbA1c), blood lipids [total cholesterol (TC)/high-density lipoprotein-cholesterol (HDL-C) ratio], coagulation activity (D-dimer and fibrinogen), and inflammation [interleukin (IL)-6, tumor necrosis factor-alpha (TNF-α), and C-reactive protein (CRP)]. Perceived appreciation at work, as well as potentially confounding psychological factors (social support, self-esteem, and work strain due to a lack of appreciation), were measured by self-report questionnaires. We found higher appreciation at work to relate to lower overall composite CHD risk (p's ≤ 0.011) and, in particular, to lower MAP (p's ≤ 0.007) and lower blood lipids (p's ≤ 0.031) in medication-free participants as well as all participants. This overall association was independent of confounding factors, including related psychological factors (p's ≤ 0.049). Our findings indicate that appreciation at work might be an independent health-promoting resource in terms of CHD risk. Implications include that encouraging appreciation at work may help reduce the development and progression of CHD.

The identification of metabolites from gut microbiota in coronary heart disease via network pharmacology

Although the gut microbial metabolites exhibit potential effects on coronary heart disease (CHD), the underlying mechanism remains unclear. In this study, the active gut microbial metabolites acting on CHD and their potential mechanisms of action were explored through a network pharmacological approach. We collected a total of 208 metabolites from the gutMgene database and 726 overlapping targets from the similarity ensemble approach (SEA) and SwissTargetPrediction (STP) database, and ultimately identified 610 targets relevant to CHD. In conjunction with the gutMGene database, we identified 12 key targets. The targets of exogenous substances were removed, and 10 core targets involved in CHD were eventually retained. The microbiota–metabolites–targets–signalling pathways network analysis revealed that C-type lectin receptor signalling pathway, Lachnospiraceae, Escherichia, mitogen-activated protein kinase 1, prostaglandin-endoperoxidase synthase 2, phenylacetylglutamine and alcoholic acid are notable components of CHD and play important roles in the development of CHD. The results of molecular docking experiments demonstrated that AKT1-glycocholic acid and PTGS2-phenylacetylglutamine complexes may act on C-type lectin receptor signalling pathways. In this study, the key substances and potential mechanisms of gut microbial metabolites were analysed via network pharmacological methods, and a scientific basis and comprehensive idea were provided for the effects of gut microbial metabolites on CHD.

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.

Depression and coronary heart disease: mechanisms, interventions, and treatments.

Coronary heart disease (CHD), a cardiovascular condition that poses a significant threat to human health and life, has imposed a substantial economic burden on the world. However, in contrast to conventional risk factors, depression emerges as a novel and independent risk factor for CHD. This condition impacts the onset and progression of CHD and elevates the risk of adverse cardiovascular prognostic events in those already affected by CHD. As a result, depression has garnered increasing global attention. Despite this growing awareness, the specific mechanisms through which depression contributes to the development of CHD remain unclear. Existing research suggests that depression primarily influences the inflammatory response, Hypothalamic-pituitary-adrenocortical axis (HPA) and Autonomic Nervous System (ANS) dysfunction, platelet activation, endothelial dysfunction, lipid metabolism disorders, and genetics, all of which play pivotal roles in CHD development. Furthermore, the effectiveness and safety of antidepressant treatment in CHD patients with comorbid depression and its potential impact on the prognosis of CHD patients have become subjects of controversy. Further investigation is warranted to address these unresolved questions.

Association of plasma proteomics with incident coronary heart disease in individuals with and without type 2 diabetes: results from the population-based KORA study.

Coronary heart disease (CHD) is a major global health concern, especially among individuals with type 2 diabetes (T2D). Given the crucial role of proteins in various biological processes, this study aimed to elucidate the aetiological role and predictive performance of protein biomarkers on incident CHD in individuals with and without T2D. The discovery cohort included 1492 participants from the Cooperative Health Research in the Region of Augsburg (KORA) S4 study with 147 incident CHD cases (45 vs. 102 cases in the group with T2D and without T2D, respectively) during 15.6 years of follow-up. The validation cohort included 888 participants from the KORA-Age1 study with 70 incident CHD cases (19 vs. 51 cases in the group with T2D and without T2D, respectively) during 6.9 years of follow-up. We measured 233 plasma proteins related to cardiovascular disease and inflammation using proximity extension assay technology. Associations of proteins with incident CHD were assessed using Cox regression and Mendelian randomization (MR) analysis. Predictive models were developed using priority-Lasso and were evaluated on top of Framingham risk score variables using the C-index, category-free net reclassification index (cfNRI), and relative integrated discrimination improvement (IDI). We identified two proteins associated with incident CHD in individuals with and 29 in those without baseline T2D, respectively. Six of these proteins are novel candidates for incident CHD. MR suggested a potential causal role for hepatocyte growth factor in CHD development. The developed four-protein-enriched model for individuals with baseline T2D (ΔC-index: 0.017; cfNRI: 0.253; IDI: 0.051) and the 12-protein-enriched model for individuals without baseline T2D (ΔC-index: 0.054; cfNRI: 0.462; IDI: 0.024) consistently improved CHD prediction in the discovery cohort, while in the validation cohort, significant improvements were only observed for selected performance measures (with T2D: cfNRI: 0.633; without T2D: ΔC-index: 0.038; cfNRI: 0.465). This study identified novel protein biomarkers associated with incident CHD in individuals with and without T2D and reaffirmed previously reported protein candidates. These findings enhance our understanding of CHD pathophysiology and provide potential targets for prevention and treatment.

Plasma lipidomic markers of diet quality are associated with incident coronary heart disease in American Indian adults: the Strong Heart Family Study

BackgroundIdentifying lipidomic markers of diet quality is needed to inform the development of biomarkers of diet, and to understand the mechanisms driving the diet- coronary heart disease (CHD) association. ObjectivesThis study aimed to identify lipidomic markers of diet quality and examine whether these lipids are associated with incident CHD. MethodsUsing liquid chromatography–mass spectrometry, we measured 1542 lipid species from 1694 American Indian adults (aged 18–75 years, 62% female) in the Strong Heart Family Study. Participants were followed up for development of CHD through 2020. Information on the past year diet was collected using the Block Food Frequency Questionnaire, and diet quality was assessed using the Alternative Healthy Eating Index-2010 (AHEI). Mixed-effects linear regression was used to identify individual lipids cross-sectionally associated with AHEI. In prospective analysis, Cox frailty model was used to estimate the hazard ratio (HR) of each AHEI-related lipid for incident CHD. All models were adjusted for age, sex, center, education, body mass index, smoking, alcohol drinking, level of physical activity, energy intake, diabetes, hypertension, and use of lipid-lowering drugs. Multiple testing was controlled at a false discovery rate of <0.05. ResultsAmong 1542 lipid species measured, 71 lipid species (23 known), including acylcarnitine, cholesterol esters, glycerophospholipids, sphingomyelins and triacylglycerols, were associated with AHEI. Most of the identified lipids were associated with consumption of ω-3 (n–3) fatty acids. In total, 147 participants developed CHD during a mean follow-up of 17.8 years. Among the diet-related lipids, 10 lipids [5 known: cholesterol ester (CE)(22:5)B, phosphatidylcholine (PC)(p-14:0/22:1)/PC(o-14:0/22:1), PC(p-38:3)/PC(o-38:4)B, phosphatidylethanolamine (PE)(p-18:0/20:4)/PE(o-18:0/20:4), and sphingomyelin (d36:2)A] were associated with incident CHD. On average, each standard deviation increase in the baseline level of these 5 lipids was associated with 17%–23% increased risk of CHD (from HR: 1.17; 95% CI: 1, 1.36; to HR: 1.23; 95% CI: 1.05, 1.43). ConclusionsIn this study, lipidomic markers of diet quality in American Indian adults are found. Some diet-related lipids are associated with risk of CHD beyond established risk factors.

Role of angiotensin II and neuroendocrine factors in immunological regulation in patients with coronary heart disease: prospective cross-sectional study

BACKGROUND: Among chronic noncommunicable diseases, cardiovascular diseases, particularly coronary heart disease (CHD), are the leading cause of death. The rennin-angiotensin-aldosterone system plays an important role in CHD development and progression; however, its role in the regulation of immunoneuroendocrine interactions requires further analysis.&#x0D; OBJECTIVE: To study the relationship between angiotensin II (AT II) and molecular regulators of the activity of whole blood mononuclear cells (MNCs) in patients with angina pectoris.&#x0D; MATERIALS AND METHODS: This cross-sectional study enrolled 65 patients with exertional angina aged 45–67 years, including 19 apparently healthy individuals. The levels of interleukins (ILs), transforming growth factor-β1 (TGF-β1), prostaglandin E2 (PG E2), serotonin, thyroid-stimulating hormone (TSH), and AT II in the blood serum were determined. In MNCs, the concentrations of protein kinases FAK, JNK, p38, and ERK, signal transducers, and activators of transcription (STAT 3, 5A, and 6) were determined.&#x0D; RESULTS: In patients with coronary artery disease, the production of TGF-β1 increased by 7.2% (p=0.00001), AT II by 136.9% (p=0.0001), serotonin by 129.0% (p=0.00001), IL-18 by 92.5% (p=0.00001), TSH by 51.7% (p=0.0012), ERK protein kinase content by 86.4% (p=0.0001), JNK by 56.8% (p=0.0001), and FAK by 55.3% (p=0.00002). The levels of IL-15 also decreased by 38.1% (p=0.0001), PG E2 by 39.5% (p=0.0001), and STAT3 by 52.5% (p=0.0001).&#x0D; CONCLUSION: The nature of the identified relationships among the analyzed factors allows us to consider AT II as a factor that ensures adaptive coupling of immune and neuroendocrine regulatory mechanisms in patients with coronary artery disease, contributing to a change in the balance between macrophages and T-helper types 1 and 2.

Abstract 13367: Plasma Lipidomic Markers of Diet Quality Are Associated With Risk of Coronary Heart Disease in American Indians

Background: Diet quality can affect lipid profiles and subsequent risk of coronary heart disease (CHD). Identifying lipidomic markers of diet quality is needed to inform the development of biomarkers of diet, and to understand the mechanisms driving the diet-CHD relation. Objective: To identify lipidomic markers of diet quality and examine whether these lipids are associated with incident CHD. Methods: We studied 1,694 American Indians (aged 18-75, 62% women) who were free of CHD and had lipidomic and dietary data at baseline (2001-2003). Participants were followed for development of CHD through 2020 (mean follow-up: 17.8 years; total incident cases of CHD: 147). Information on past year diet was collected using the Block Food Frequency Questionnaire, and diet quality was assessed using the Alternative Healthy Eating Index-2010 (AHEI). Mixed effects linear regression was used to identify individual lipid species associated with AHEI at baseline. Cox frailty model was used to estimate the hazard ratio of each AHEI-related lipid for CHD risk. All models adjusted for age, sex, center, education, BMI, smoking, alcohol drinking, level of physical activity, energy intake, diabetes, hypertension, and use of lipid-lowering drugs. Results: Among 1,542 lipid species measured, 71 lipid species (23 known) were associated with AHEI at FDR&lt;0.05. Of these, 10 lipids (5 known) were associated with incident CHD (Figure 1 ). The 5 known lipids associated with incident CHD were CE(22:5) B, PC(p-14:0/22:1)/PC(o-14:0/22:1), PC(p-38:3)/PC(o-38:4) B, PE(p-18:0/20:4)/PE(o-18:0/20:4), and SM(d36:2) A. On average, per standard deviation increase in the baseline level of these lipids was associated with 17%-23% increased risk of CHD. These AHEI-related lipids are enriched in glycerophospholipid metabolism. Conclusion: We identified lipidomic markers of diet quality in American Indians. Some diet-related lipids are associated with risk of CHD beyond established risk factors.

Genetic polymorphisms in VEGFA and VEGFR2 genes associated with coronary heart disease susceptibility and severity.

​Vascular endothelial growth factor A (VEGFA) is well acknowledged as a powerful angiogenesis-promoting agent mainly through its receptor VEGFR2. Ischemia stimulates VEGFA/VEGFR2 signaling pathway and elevated serum levels of VEGFA were detected in coronary heart disease (CHD) patients. The goal of the current study is to determine how four SNPs in the genes for VEGFA (rs3025039 and rs699947) and VEGFR2 (rs2305948 and rs1870377) contribute to the development of CHD. We also wanted to use the Gensini score to confirm if these four SNPs have an effect on the severity of coronary lesions. In this case-control research, we used the restriction fragment length polymorphism of the polymerase chain reaction to genotype 239 CHD patients and 200 controls. Age, sex, smoking behavior, and obesity were taken into account in the statistical analysis. Two VEGFA/VEFGR2 signaling pathway SNPs (rs699947 and rs1870377) were found to be associated with CHD (C vs. A, P = 0.002; OR = 1.47 (1.12-1.93); A vs. T, P = 0.001; OR = 1.58 (1.17-2.13) respectively). The rs2305948 showed no allelic associations with CHD susceptibility, although we noticed a slight association under the recessive model of rs3025039 TT genotype (p = 0.023; OR = 6.41 (1.14-36.12)) only under adjusted analyses. In addition, both VEGFA SNPs (rs699947and rs3025039) were found to be associated with high Gensini score (p < 0.001). Our research helps to shed further light on the pathophysiology of CHD. The VEGFA/VEGFR2 signaling pathway may have been downregulated, increasing CHD susceptibility and risk.

The prevalence and factors associated with coronary heart disease in patients with gout

Background. Gout is associated with increased risk of cardiovascular disease (CVD) morbidity and mortality. Therefore, an association between coronary heart disease (CHD) and gout deserves careful examination. The aim of this study was to determine the prevalence of CHD and factors associated with CHD in patients (pts) with gout. Methods. 286 male patients with gout were included; age – 51.2 [42.8; 59.4] years (ys), disease duration – 6.2 [3.8; 12.1] ys. All patients underwent standard clinical examination, screening traditional risk factors (TRF) of CVD. We estimated the adjusted odds ratio (OR) and 95% confidence interval (95% CI). Results. CHD was found in 111 out of the 286 pts (38.8%), MI had a history in 29.7%. Compared to individuals with CHD, participants without CHD were older (56.7 [52.1; 61.1] vs 46.2 [40.6; 53.4] ys), had longer duration of gout (9.3 [4.7; 15.1] vs 5.6 [3.3; 9.7] ys) (for all p&lt;0.05). Abdominal obesity (OR=3.6; 95% CI: 1.2–10.9), family history of CHD (OR=2.2; 95% CI: 1.3–5.4), disease duration of gout more 10 ys (OR=2.8; 95% CI: 1.6–4.7), age of gout onset &lt;35 ys (OR=5.5; 95% CI: 2.6–11.7), intraosseous tophi (OR=3.03; 95% CI: 1.8–5.01), nephrolithiasis (OR=1.7; 95% CI: 1.04–3.04), renal failure (OR=5.6; 95% CI: 2.7–11.4), serum total cholesterol (TC) (OR=1.6; 95% CI: 1.0–2.8), serum creatinine (OR=2.5; 95% CI: 1.2–5.1), increased the risk for CHD in patients with a gout. Conclusions. The prevalence of CHD was 38.8% among individuals with gout (third of patients had a history of MI 29.7%). Our study showed that both TRFs of CVD and the severity of gout and a history of renal failure contribute to the development of CHD in patients with gout.

Significance of RNA N6-methyladenosine regulators in the diagnosis and subtype classification of coronary heart disease using the Gene Expression Omnibus database.

Many investigations have revealed that alterations in m6A modification levels may be linked to coronary heart disease (CHD). However, the specific link between m6A alteration and CHD warrants further investigation. Gene expression profiles from the Gene Expression Omnibus (GEO) databases. We began by constructing a Random Forest model followed by a Nomogram model, both aimed at enhancing our predictive capabilities on specific m6A markers. We then shifted our focus to identify distinct molecular subtypes based on the key m6A regulators and to discern differentially expressed genes between the unique m6A clusters. Following this molecular exploration, we embarked on an in-depth analysis of the biological characteristics associated with each m6A cluster, revealing profound differences between them. Finally, we delved into the identification and correlation analysis of immune cell infiltration across these clusters, emphasizing the potential interplay between m6A modification and the immune system. In this research, 37 important m6Aregulators were identified by comparing non-CHD and CHD patients from the GSE20680, GSE20681, and GSE71226 datasets. To predict the risk of CHD, seven candidate m6A regulators (CBLL1, HNRNPC, YTHDC2, YTHDF1, YTHDF2, YTHDF3, ZC3H13) were screened using the logistic regression model. Based on the seven possible m6A regulators, a nomogram model was constructed. An examination of decision curves revealed that CHD patients could benefit from the nomogram model. On the basis of the selected relevant m6A regulators, patients with CHD were separated into two m6A clusters (cluster1 and cluster2) using the consensus clustering approach. The Single Sample Gene Set Enrichment Analysis (ssGSEA) and CIBERSORT methods were used to estimate the immunological characteristics of two separate m6A Gene Clusters; the results indicated a close association between seven candidate genes and immune cell composition. The drug sensitivity of seven candidate regulators was predicted, and these seven regulators appeared in numerous diseases as pharmacological targets while displaying strong drug sensitivity. m6A regulators play crucial roles in the development of CHD. Our research of m6A clusters may facilitate the development of novel molecular therapies and inform future immunotherapeutic methods for CHD.

Evolution of the search for a common mechanism of congenital risk of coronary heart disease and type 2 diabetes mellitus in the chromosomal locus 9p21.3.

9.21.3 chromosomal locus predisposes to coronary heart disease (CHD) and type 2 diabetes mellitus (DM2), but their overall pathological mechanism and clinical applicability remain unclear. The review uses publications of the study results of 9.21.3 chromosomal locus in association with CHD and DM2, which are important for changing the focus of clinical practice. The eligibility criteria are full-text articles published in the PubMed database (MEDLINE) up to December 31, 2022. A total of 56 publications were found that met the inclusion criteria. Using the examples of the progressive stages in understanding the role of the chromosomal locus 9p.21.3, scientific ideas were grouped, from a fragmentary study of independent pathological processes to a systematic study of the overall development of CHD and DM2. The presented review can become a source of new scientific hypotheses for further studies, the results of which can determine the general mechanism of the congenital risk of CHD and DM2 and change the focus of clinical practice.

Analysis of Cardiovascular Risk Factors in Patients with Coronary Heart Disease Qualified for Off-Pump Coronary Bypass

The aim. To analyze the prevalence of cardiovascular risk factors for circulatory diseases in patients with coronary heart disease (CHD) after coronary bypass surgery (off-pump coronary artery bypass grafting).&#x0D; Material and methods. The study included 991 subjects (786 men, 205 women), mean age 64.3 ± 1.4 years. All the study participants underwent off-pump coronary bypass surgery.&#x0D; Results. Based on modern ideas about risk factors for circulatory diseases and CHD, it is impossible to ignore the influence of cardiovascular factors, both modifiable and non-modifiable. The analysis of medical and social risk factors for CHD, which include age, body weight, eating habits and smoking, showed that these medical and social factors are common among patients with CHD. It was found that the prevalence of excess body weight among men with CHD was significantly higher in patients with multivessel lesions than in those with 1-vessel lesions (p=0.05, χ2=3.69). Among women with CHD, excess body weight was significantly higher in the clinical group with multivessel lesions compared to 2-vessel lesions (p=0.002, χ2=9.06). It was also found that the prevalence of excess body weight was significantly higher in clinical groups with 1-vessel lesions among men compared to women (p=0.04, χ2=3.95). It was established that the frequency of obesity was significantly more common in women of different clinical groups compared to men: with 1-vascular lesions (p=0.04, χ2=3.95); with 2-vessel lesions (p=0.0001, χ2=24); with multivessel lesions (p=0.0001, χ2=186.57). It was established that men smoke significantly more often than women (p=0.0001, χ2=31.22). The obtained results complement the scientific data of the world epidemiological studies regarding the determination of the role of medical and social factors in the development of CHD. The article analyzes excess body weight, obesity and smoking as the leading etiological factors for CHD. It was established that the risk of developing CHD is reliably associated with excess body weight, obesity and smoking, among different clinical groups of male and female patients, both with single-vessel lesions and with multivessel lesions in CHD.&#x0D; Conclusions. Analysis of cardiovascular risk factors for the development of CHD, which include age, body weight, eating habits, and smoking, showed that their further study is relevant, as these are common among patients with CHD. It was established that frequency of excess body weight in patients with CHD, both in men and women, was significantly higher among individuals with multivessel lesions. The prevalence of obesity among patients with CHD presented for off-pump coronary artery bypass grafting was significantly higher among women in groups with different numbers of affected coronary vessels. As for smoking, it was established that this behaviorally associated habit is significantly more common among men with CHD. The reliable patterns of prevalence of excess body weight, obesity and smoking in patients with CHD established as a result of the study of cardiovascular factors prove that these factors have high etiological contribution to the development, course and number of affected vessels in CHD.

Development and validation of a clinical prediction model for detecting coronary heart disease in middle-aged and elderly people: a diagnostic study

ObjectiveTo develop and validate a multivariate prediction model to estimate the risk of coronary heart disease (CHD) in middle-aged and elderly people and to provide a feasible method for early screening and diagnosis in middle-aged and elderly CHD patients.MethodsThis study was a single-center, retrospective, case–control study. Admission data of 932 consecutive patients with suspected CHD were retrospectively assessed from September 1, 2020 to December 31, 2021 in the Department of Integrative Cardiology at China-Japan Friendship Hospital. A total of 839 eligible patients were included in this study, and 588 patients were assigned to the derivation set and 251 as the validation set at a 7:3 ratio. Clinical characteristics of included patients were compared between derivation set and validation set by univariate analysis. The least absolute shrinkage and selection operator (Lasso) regression analysis method was performed to avoid collinearity and identify key potential predictors. Multivariate logistic regression analysis was used to construct a clinical prediction model with identified predictors for clinical practice. Bootstrap validation was used to test performance and eventually we obtained the actual model. And the Hosmer–Lemeshow test was carried out to evaluate the goodness-fit of the constructed model. The area under curve (AUC) of receiver operating characteristic (ROC), calibration curve, decision curve analysis (DCA), and clinical impact curve (CIC) were plotted and utilized with validation set to comprehensively evaluate the predictive accuracy and clinical value of the model.ResultsA total of eight indicators were identified as risk factors for the development of CHD in middle-aged and elderly people by univariate analysis. Of these candidate predictors, four key parameters were defined to be significantly related to CHD by Lasso regression analysis, including age (OR 1.034, 95% CI 1.002 ~ 1.067, P = 0.040), hemoglobin A1c (OR 1.380, 95% CI 1.078 ~ 1.768, P = 0.011), ankle-brachial index (OR 0.078, 95% CI 0.012 ~ 0.522, P = 0.009), and brachial artery flow-mediated vasodilatation (OR 0.848, 95% CI 0.726 ~ 0.990, P = 0.037). The Hosmer–Lemeshow test showed a good calibration performance of the clinical prediction model (derivation set, χ2 = 7.865, P = 0.447; validation set, χ2 = 11.132, P = 0.194). The ROCs of the nomogram in the derivation set and validation set were 0.722 and 0.783, respectively, suggesting excellent predictive power and suitable performance. The clinical prediction model presented a greater net benefit and clinical impact based on DCA and CIC analysis.ConclusionOverall, the development and validation of the multivariate model combined the laboratory and clinical parameters of patients with CHD, which could be beneficial to the individualized prediction of middle-aged and elderly people, and helped to facilitate clinical assessments and decisions during treatment and management of CHD.

The COVID-19 Pandemic and Coronary Heart Disease: the Next Surge.

In this narrative review, we highlight different ways in which the COVID-19 pandemic has impacted coronary heart disease (CHD) burden and how a surge in morbidity and mortality may be expected in the near future. We also discuss potential solutions, and the direction subsequent research and corrective actions should take. COVID-19 has been implicated in the development and worsening of CHD via acute and chronic mechanisms in the form of plaque rupture, destabilization, and sustenance of a chronic inflammatory state leading to long COVID syndrome and increased rates of myocardial infarction. However, indirectly the pandemic is likely to further escalate the CHD burden through poor health behaviors such as tobacco consumption, reduced physical activity, economic devastation and its associated sequelae, and regular cardiac care interruptions and delays. COVID-19 has increased the total CHD burden and will require extensive resource allocation and multifaceted strategies to curb future rise.

Association of demographics, cardiovascular indicators and disability characteristics with 7-year coronary heart disease incident in persons with disabilities

ObjectivePrevious studies had demonstrated that disability increases mortality in patients with coronary heart disease (CHD). However, for people who had been disabled but do not have baseline cardiovascular disease, there is still limited data on how they might develop CHD. This study aimed to investigate the incidence and predictors of CHD in people with disabilities.MethodsWe conducted a 7-year retrospective study utilizing data from the Shanghai Comprehensive Information Platform for Persons with Disabilities Rehabilitation. Subjects aged over 18 years with at least four annual complete electronic health records were included. The primary outcome was CHD, defined as ischemic heart disease or myocardial infarction. Kaplan–Meier analysis and log-rank tests were used to compare cumulative CHD for sub-populations, stratified by age, gender, and the classification of disabilities. Cox regression was used to identify the potentially important factors.ResultsOut of 6419 persons with disabilities, 688 CHD cases (mean age 52.95 ± 7.17 years, male 52.2%) were identified, with a cumulative incidence of 10.72% and an incidence density of 15.15/1000 person-years. The incidence density of CHD is higher in the male gender, people over 45 years, and those with physical disabilities. Male (HR = 1.294, 95% CI, 1.111–1.506), hypertension (HR = 1.683, 95% CI, 1.405–2.009), diabetes mellitus (HR = 1.488, 95% CI, 1.140–1.934), total cholesterol (HR = 1.110, 95% CI, 1.023–1.204), and physical disabilities (HR = 1.122, 95% CI, 1.019–1.414) were independently associated with CHD.ConclusionThe findings indicate that the incidence of CHD differs across disability categories rather than the severity of disability. People with physical disabilities had significantly higher risks for the development of CHD. The underlying physiological and pathological factors need to be further studied.

Hsa_circRNA_0000284 acts as a ceRNA to participate in coronary heart disease progression by sponging miRNA-338-3p via regulating the expression of ETS1

Coronary heart disease (CHD) is a prevalent global cause of death. Research suggests that circular RNAs (circRNAs) play a role in the development of CHD. In this study, we investigated the expression of hsa_circRNA_0000284 in peripheral blood leukocytes (PBLs) obtained from a cohort of 94 CHD patients aged over 50 years, as well as 126 age-matched healthy controls (HC). An in vitro inflammatory and oxidative injury cell model that simulates CHD was used to evaluate changes in hsa_ circRNA _0000284 under stress. CRISPR/Cas9 technology was used to evaluate changes in hsa_circRNA_0000284 expression. An hsa_ circRNA_0000284 overexpression and silencing cell model was used to analyze the biological functions of hsa_circRNA_0000284. Bioinformatics, qRT-PCR, viral transfection technology, and luciferase assays were used to evaluate the potential hsa_circRNA_0000284/miRNA-338-3p/ETS1 axis. Western blotting analysis was performed to detect protein expression. Herein, PBLs from CHD patients exhibited downregulation of hsa_circRNA_0000284 expression. Exposure to oxidative stress and inflammation can induce damage to human umbilical endothelial cells, resulting in the downregulation of hsa_circRNA_0000284 expression. The expression of hsa_circRNA_0000284 in EA-hy926 cells was significantly reduced after the AluSq2 element of hsa_circRNA_0000284 had been knocked out. The expression of hsa_circRNA_0000284 affected proliferation, cycle distribution, aging, and apoptosis in EA-hy926 cells. Consistent with the results of cell transfection experiments and luciferase assays, Western blotting showed that hsa_circRNA_0000284 plays a role in the regulation of hsa-miRNA-338-3p expression. Subsequently, hsa-miRNA-338-3p was found to be involved in the regulation of ETS1 expression. Communicated by Ramaswamy H. Sarma

Mendelian randomization study reveals a causal relationship between serum iron status and coronary heart disease and related cardiovascular diseases.

Growing observational studies have shown that abnormal systemic iron status is associated with Coronary heart disease (CHD). However, these results from observational studies was not entirely consistent.It remains unclear whether this relationship represents causality.It is necessary to explore the causal relationship between iron status and CHD and related cardiovascular diseases (CVD). We aimed to investigate the potential casual relationship between serum iron status and CHD and related CVD using a two-sample Mendelian randomization (MR) approach. Genetic statistics for single nucleotide polymorphisms (SNPs) between four iron status parameters were identified in a large-scale genome-wide association study (GWAS) conducted by the Iron Status Genetics organization. Three independent single nucleotide polymorphisms (SNPs) (rs1800562, rs1799945, and rs855791) aligned with four iron status biomarkers were used as instrumental variables. CHD and related CVD genetic statistics We used publicly available summary-level GWAS data. Five different MR methods random effects inverse variance weighting (IVW), MR Egger, weighted median, weighted mode, and Wald ratio were used to explore the causal relationship between serum iron status and CHD and related CVD. In the MR analysis, we found that the causal effect of serum iron (OR = 0.995, 95% CI = 0.992-0.998, p = 0.002) was negatively associated with the odds of coronary atherosclerosis (AS). Transferrin saturation (TS) (OR = 0.885, 95% CI = 0.797-0.982, p = 0.02) was negatively associated with the odds of Myocardial infarction (MI). This MR analysis provides evidence for a causal relationship between whole-body iron status and CHD development. Our study suggests that a high iron status may be associated with a reduced risk of developing CHD.