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Diabetes Mellitus (DM) and Coronary Heart Disease (CHD) are among top causes of patient health issues and fatalities in many countries. At present, terahertz biosensors have been widely used to detect chronic diseases because of their accurate detection, fast operation, flexible design and easy fabrication. In this paper, a Zeonex-based microstructured fiber (MSF) biosensor is proposed for detecting DM and CHD markers by adopting a terahertz time-domain spectroscopy system. A suspended hollow-core structure with a square core and a hexagonal cladding is used, which enhances the interaction of terahertz waves with targeted markers and reduces the loss. This work focuses on simulating the transmission performance of the proposed MSF sensor by using a finite element method and incorporating a perfectly matched layer as the absorption boundary. The simulation results show that this MSF biosensor exhibits an ultra-high relative sensitivity, especially up to 100.35% at 2.2THz, when detecting DM and CHD markers. Furthermore, for different concentrations of disease markers, the MSF exhibits significant differences in effective material loss, which can effectively improve clinical diagnostic accuracy and clearly distinguish the extent of the disease. This MSF biosensor is simple to fabricate by 3D printing and extrusion technologies, and is expected to provide a convenient and capable tool for rapid biomedical diagnosis.

Background and Aims: Studies have shown that elevated serum uric acid (SUA) may increase the risk of coronary heart disease (CHD). However, it is still disputable how mediate effects between metabolic diseases and hyperuricemia affect the incidence of CHD. This study aimed to explore whether metabolic diseases may mediate the connection from hyperuricemia at baseline to the elevated incidence risk of CHD during follow-ups., Methods and Results: Based on the Jinchang cohort, 48 001 subjects were followed for 9 years between June 2011 and December 2019. Multivariate-adjusted Cox regression models were applied to estimate hazard ratios (HRs) of CHD with 95% confidence intervals (CIs). Significantly increased risks of CHD were observed in hyperuricemia (HR:1.46, 95%CI:1.28, 1.67) when compared with normouricemia population. The mediating effect model further demonstrated that metabolic diseases could mediate the association between hyperuricemia and CHD pathogenesis, partially for the combined metabolic diseases with mediation effects of 45.12%, 25.24% for hypertension, 28.58% for overweight or obese status, 29.05% for hypertriglyceridemia, 6.70% for hypercholesterolemia, 3.52% for low high density lipoprotein cholesterol (HDL-C), and 6.51% for high low density lipoprotein cholesterol (LDL-C), respectively., Conclusions: Hyperuricemia significantly increased the risk of incident CHD, and this association was partly mediated by metabolic diseases., Competing Interests: Declaration of competing interest All authors declare no interests of competing., (Copyright © 2022 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.)

Objectives: The aim of this study was to describe and interpret differences in major cardiovascular disease (CVD) mortality during 60 years between Northern European and Southern European cohorts of the Seven Countries Study of Cardiovascular Diseases., Material and Methods: Northern Europe included two cohorts from Finland and one from the Netherlands, and Southern Europe included two cohorts from Italy and two from Greece, for a total of 2360 and 2792 CVD-free men, respectively, at entry examination. Coronary heart disease (CHD), STROKE and other Heart Diseases of Uncertain Etiology (HDUE) deaths were the outcomes and Cox models were solved separately based on 12 risk factors., Results: In 60 years, overall death rates were 99.8% in both Northern and Southern Europe and the pooled CVD rates were 46.9% (significantly higher) and 42.2%, respectively: CHD mortality was higher in Northern Europe, whereas STROKE and HDUE mortality were higher in Southern Europe. Significant Cox coefficients for both areas (but not significantly different between areas) were age, smoking habits, SBP and serum cholesterol for CHD, and only age and SBP did so for STROKE and HDUE. Age at death was lower for CHD, intermediate for STROKE and higher for HDUE in both areas., Conclusion: The advantage for Southern Europe was small in terms of overall CVD death rates, but definitely larger in terms of expectancy of life due to the differences in age at death in the three types of CVD mortality. Mean entry levels of serum cholesterol, 50 mg/dl higher in Northern Europe than in Southern Europe are a major culprit of these outcomes., (Copyright © 2022 Italian Federation of Cardiology - I.F.C. All rights reserved.)

Background: Patients who experience an acute coronary syndrome (ACS) are at high risk of further cardiovascular events. Long-term treatment of cardiovascular risk factors, such as hyperlipidemia, is critical to prevent progression of coronary heart disease. However, many patients do not reach recommended target levels for low-density lipoprotein (LDL) cholesterol, despite receiving lipid-lowering therapy., Objective: To obtain an insight into the current treatment situation for very high-risk patients after an initial ACS in Germany., Methods: The multicenter HYDRA-ACS registry study was initiated to document the clinical characteristics of very high-risk patients with ACS and hyperlipidemia in clinical practice. In addition, lipid profiles, lipid-lowering therapy, and lipid target achievement during treatment were documented over 1 year., Results: 353 patients who were documented had a mean age of 57.3 years, mean body mass index was 28.6 kg/m 2 , and 73.4% were male; 52.4% had a family history of myocardial infarction (MI) and 32.6% a family history of coronary heart disease (CHD). Patients' medical histories commonly included CHD (32.9%), percutaneous coronary intervention (PCI; 25.5%), and previous ACS (23.0%). Common comorbidities included hypertension (68.6%), diabetes (17.3%), heart failure (16.7%), and stable angina pectoris (15.9%). The proportion of patients receiving lipid-lowering therapy increased from 65.7% at baseline to 100% at the 12-month follow-up (p < 0.0001). Substantial increases in use were seen for statins (85.0% vs. 36.5%, p = 0.0002) and cholesterol resorption inhibitors (32.9% vs. 8.6%, p = 0.0003). Use of combination therapy increased. The proportion of patients undertaking physical exercise increased (p < 0.0001), as did consumption of fruit and vegetables (p = 0.0222) and fish (p = 0.0162), while alcohol consumption decreased (p = 0.0019). Median LDL cholesterol level decreased significantly from baseline (87 vs. 166 mg/dL, p < 0.0001), and the proportion of patients with a level < 70 mg/dL increased (50.0% vs. 5.7%, p < 0.0001). Median HDL cholesterol increased (47 vs. 45 mg/dL, p = 0.0235) and median triglyceride level decreased (119 vs. 148 mg/dL, p = 0.0080). The proportion of patients receiving antihypertensive drugs and platelet aggregation inhibitors increased. The most frequent cardiovascular events during the 12-month follow-up were PCI (25.9%) and cardiac catheterization without PCI (12.9%); MI occurred in 2.4% of patients; no deaths were reported., Conclusions: This study provides a contemporary picture of the treatment of hyperlipidemia after ACS in patients in Germany. Despite treatment with lipid-lowering therapy, many patients did not achieve recommended lipid targets by 12 months after an ACS event., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.)

Objective: Coronary heart disease (CHD) is a notable contributor to the burden of human health. Dysregulated long non-coding RNAs (lncRNAs) are implicated in the pathogenesis of CHD. This study investigated the expression pattern of lncRNA LOXL1-AS1 in CHD and its regulatory mechanism in oxidized low-density lipoprotein (ox-LDL)-induced human coronary artery endothelial cell (HCAEC) pyroptosis., Methods: Serum was collected from 62 CHD patients and 62 healthy volunteers for the detection of LOXL1-AS1 expression. The value of LOXL1-AS1 in CHD diagnosis and major cardiovascular adverse event (MACE) prediction was analyzed using the ROC curve. LOXL1-AS1, miR-16-5p, and SNX16 expressions in ox-LDL-treated HCAECs were determined using RT-qPCR. NLPR3, cleaved-caspase-1, and GSDMD-N protein levels were measured using Western blot. IL-1β and IL-18 concentrations were measured using ELISA. The binding relationships between LOXL1-AS1 and miR-16-5p and miR-16-5p and SNX16 were verified. Functional rescue experiment was performed to verify the role of miR-16-5p in HCAEC pyroptosis., Results: LOXL1-AS1 was highly expressed in CHD patients. LOXL1-AS1 had diagnostic value for CHD and predictive value for MACE occurrence. ox-LDL-treated HCAECs showed reduced viability, increased IL-1β and IL-18 concentrations, and elevated NLPR3, cleaved-caspase-1, and GSDMD-N levels. LOXL1-AS1 silencing promoted cell viability and reduced pyroptosis. LOXL1-AS1 bound to miR-16-5p and miR-16-5p targeted SNX16. Inhibition of miR-16-5p reversed the inhibitory effect of LOXL1-AS1 silencing on HCAEC pyroptosis., Conclusion: LOXL1-AS1 was elevated in CHD patients with a good diagnostic value for CHD and predictive value for MACE. LOXL1-AS1 downregulated miR-16-5p expression by binding to miR-16-5p to enhance ox-LDL-induced HCAEC pyroptosis, which may be associated with upregulation of SNX16 transcription., (© 2021. Springer Science+Business Media, LLC, part of Springer Nature.)

Importance: Testing for coronary heart disease (CHD) in asymptomatic kidney transplant candidates before transplant is widespread and endorsed by various professional societies, but its association with perioperative outcomes is unclear., Objective: To estimate the association of pretransplant CHD testing with rates of death and myocardial infarction (MI)., Design, Setting, and Participants: This retrospective cohort study included all adult, first-time kidney transplant recipients from January 2000 through December 2014 in the US Renal Data System with at least 1 year of Medicare enrollment before and after transplant. An instrumental variable (IV) analysis was used, with the program-level CHD testing rate in the year of the transplant as the IV. Analyses were stratified by study period, as the rate of CHD testing varied over time. A combination of US Renal Data System variables and Medicare claims was used to ascertain exposure, IV, covariates, and outcomes., Exposures: Receipt of nonurgent invasive or noninvasive CHD testing during the 12 months preceding kidney transplant., Main Outcomes and Measures: The primary outcome was a composite of death or acute MI within 30 days of after kidney transplant., Results: The cohort comprised 79 334 adult, first-time kidney transplant recipients (30 147 women [38%]; 25 387 [21%] Black and 48 394 [61%] White individuals; mean [SD] age of 56 [14] years during 2012 to 2014). The primary outcome occurred in 4604 patients (244 [5.3%]; 120 [2.6%] death, 134 [2.9%] acute MI). During the most recent study period (2012-2014), the CHD testing rate was 56% in patients in the most test-intensive transplant programs (fifth IV quintile) and 24% in patients at the least test-intensive transplant program (first IV quintile, P < .001); this pattern was similar across other study periods. In the main IV analysis, compared with no testing, CHD testing was not associated with a change in the rate of primary outcome (rate difference, 1.9%; 95% CI, 0%-3.5%). The results were similar across study periods, except for 2000 to 2003, during which CHD testing was associated with a higher event rate (rate difference, 6.8%; 95% CI, 1.8%-12.0%)., Conclusions and Relevance: The results of this cohort study suggest that pretransplant CHD testing was not associated with a reduction in early posttransplant death or acute MI. The study findings potentially challenge the ubiquity of CHD testing before kidney transplant and should be confirmed in interventional studies.

Background: The triglyceride-glucose (TyG) index is a reliable alternative biomarker of insulin resistance (IR). However, whether the TyG index has prognostic value in critically ill patients with coronary heart disease (CHD) remains unclear., Methods: Participants from the Medical Information Mart for Intensive Care III (MIMIC-III) were grouped into quartiles according to the TyG index. The primary outcome was in-hospital all-cause mortality. Cox proportional hazards models were constructed to examine the association between TyG index and all-cause mortality in critically ill patients with CHD. A restricted cubic splines model was used to examine the associations between the TyG index and outcomes., Results: A total of 1,618 patients (65.14% men) were included. The hospital mortality and intensive care unit (ICU) mortality rate were 9.64% and 7.60%, respectively. Multivariable Cox proportional hazards analyses indicated that the TyG index was independently associated with an elevated risk of hospital mortality (HR, 1.71 [95% CI 1.25-2.33] P = 0.001) and ICU mortality (HR, 1.50 [95% CI 1.07-2.10] P = 0.019). The restricted cubic splines regression model revealed that the risk of hospital mortality and ICU mortality increased linearly with increasing TyG index (P for non-linearity = 0.467 and P for non-linearity = 0.764)., Conclusions: The TyG index was a strong independent predictor of greater mortality in critically ill patients with CHD. Larger prospective studies are required to confirm these findings., (© 2023. The Author(s).)

Cardiovascular disease (CVD) remains the major cause of morbidity and mortality globally. Accumulating evidence indicates that coronary heart disease (CHD) contributes to the majority of cardiovascular deaths. With the development of precision medicine, the diagnosis and treatment of coronary heart disease are becoming more refined and individualized. Molecular diagnosis technology and individualized treatment are gradually applied to the clinical diagnosis and treatment of CHD. It is great significance to seek sensitive biological indicators to help early diagnosis and improve prognosis of CHD. Liquid biopsy is a minimally invasive technique, which is widely used to detect molecular biomarkers of tumors without invasive biopsy. Compared with the field of oncology, it is not easy to get the diseased tissue in CVD, especially CHD. Therefore, the idea of "fluid biopsy" is very attractive, and its progress may provide new and useful noninvasive indicators for CHD. By analyzing circulating cells or their products in blood, saliva, and urine samples, we can investigate the molecular changes that occur in each patient at a specific point in time, thus continuously monitoring the evolution of CHD. For example, the assessment of cell-free DNA (cfDNA) levels may help predict the severity of acute myocardial infarction and diagnose heart transplant rejection. Moreover, the unmethylated FAM101A gene may specifically track the cfDNA derived from cardiomyocyte death, which provides a powerful diagnostic biomarker for apoptosis during ischemia. In addition, the changes of plasma circulating miR-92 levels may predict the occurrence of acute coronary syndrome (ACS) onset in patients with diabetes. Liquid biopsy can reflect the disease state through patients' body fluids and may noninvasively provide dynamic and rich molecular information related to CHD. It has great application potential in early warning and auxiliary diagnosis, real-time monitoring of curative effect, medication guidance and exploration of drug resistance mechanism, prognosis judgment, and risk classification of CHD. This chapter will review the latest progress of liquid biopsy in accurate diagnosis and treatment of CHD, meanwhile explore the application status and clinical prospect of liquid biopsy in CHD, in order to improve the importance of precision medicine and personalized treatment in this field., (© 2023. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: Hyperlipidemia is one of the independent risk factors for the onset of coronary heart disease (CHD), and our aim is to construct a coronary risk prediction model for patients with hyperlipidemia based on carotid ultrasound in combination with other risk factors., Methods: The nomogram risk prediction model is based on a retrospective study on 820 patients with hyperlipidemia. The predictive accuracy and discriminative ability of the nomogram were determined by receiver operating characteristic (ROC) curves and calibration curves. The results were validated using bootstrap resampling and a prospective study on 39 patients with hyperlipidemia accepted at consenting institutions from 2021 to 2022., Result: In the modeling cohort, 820 patients were included. A total of 33 variables were included in univariate logistic regression. On multivariate analysis of the modeling cohort, independent factors for survival were sex, age, hypertension, plaque score, LVEF, PLT, and HbAlc, which were all selected into the nomogram. The calibration curve for probability of survival showed good agreement between prediction by nomogram and actual observation. The area under the curve (AUC) of the nomogram model was 0.881 (95% CI 0.858∼0.905), with a sensitivity of 79% and a specificity of 81.7%. In the validation cohort, the AUC was 0.75, 95% CI (0.602∼0.906). The sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and accuracy of this model were 54.16%, 80%, 81.25%, 52.17% and 64.1%. This model showed a good fitting and calibration and positive net benefits in decision curve analysis., Conclusion: A nomogram model for CHD risk in patients with hyperlipidemia was developed and validated using 7 predictors, which may have potential application value in clinical risk assessment, decision-making, and individualized treatment associated with CHD.

Background: Coronary heart disease (CHD) and type 2 diabetes (T2D) are two complex diseases with complex interrelationships. However, the genetic architecture of the two diseases is often studied independently by the individual single-nucleotide polymorphism (SNP) approach. Here, we presented a genotypic-phenotypic framework for deciphering the genetic architecture underlying the disease patterns of CHD and T2D., Method: A data-driven SNP-set approach was performed in a genome-wide association study consisting of subpopulations with different disease patterns of CHD and T2D (comorbidity, CHD without T2D, T2D without CHD and all none). We applied nonsmooth nonnegative matrix factorization (nsNMF) clustering to generate SNP sets interacting the information of SNP and subject. Relationships between SNP sets and phenotype sets harboring different disease patterns were then assessed, and we further co-clustered the SNP sets into a genetic network to topologically elucidate the genetic architecture composed of SNP sets., Results: We identified 23 non-identical SNP sets with significant association with CHD or T2D (SNP-set based association test, P < 3.70 × [Formula: see text]). Among them, disease patterns involving CHD and T2D were related to distinct SNP sets (Hypergeometric test, P < 2.17 × [Formula: see text]). Accordingly, numerous genes (e.g., KLKs, GRM8, SHANK2) and pathways (e.g., fatty acid metabolism) were diversely implicated in different subtypes and related pathophysiological processes. Finally, we showed that the genetic architecture for disease patterns of CHD and T2D was composed of disjoint genetic networks (heterogeneity), with common genes contributing to it (pleiotropy)., Conclusion: The SNP-set approach deciphered the complexity of both genotype and phenotype as well as their complex relationships. Different disease patterns of CHD and T2D share distinct genetic architectures, for which lipid metabolism related to fibrosis may be an atherogenic pathway that is specifically activated by diabetes. Our findings provide new insights for exploring new biological pathways., (© 2022. The Author(s).)

Purpose: To investigate incidence of end-stage renal disease (ESRD), and the association of education and coronary heart disease (CHD) with ESRD, in subjects throughout Norway followed from the diagnosis of childhood-onset type 1 diabetes., Methods: All new onset cases of type 1 diabetes 1973-2016 were followed for CHD and ESRD in nation-wide registries through 2017. Ten matched controls per case were selected from the National Population Register. Cox regression was used to estimate hazard ratios, and probabilities were estimated by the cumulative incidence function accounting for competing risk., Results: Among 9311 patients with type 1 diabetes, 130 developed ESRD with a probability of ESRD after 40 years of 5.5%. The rate was 35-fold higher than in controls (aHR = 35.5, 95% CI 23.1 - 54.6). Higher education was associated with lower risk of ESRD compared to low education (aHR = 0.14, 95% CI 0.07 - 0.27). Diagnosed CHD was associated with 14-fold increased rate of ESRD (aHR = 14.3, 95% CI 9.2 - 22.2)., Conclusions: The hazard rate of ESRD was 35-fold higher in cases compared to controls. CHD was associated with a 14-fold increased rate of subsequent ESRD, while higher education was associated with substantially lower rate of ESRD., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Aim: This study aimed to investigate the correlation of ITIH4 with inflammatory cytokines, stenosis degrees and prognosis in coronary heart disease (CHD) patients. Methods: Serum ITIH4 levels of 300 CHD patients and 30 controls, together with levels of TNF-α, IL-6, IL-8 and IL-17A of CHD patients, were determined using ELISA. Results: Serum ITIH4 was reduced in CHD patients versus controls (p < 0.001). ITIH4 was negatively linked with TNF-α, IL-6, IL-8, IL-17A, C-reactive protein, serum creatinine and Gensini score in CHD patients (all p < 0.050). ITIH4 quartile level negatively correlated with the cumulative major adverse cardiovascular event rate (p = 0.041). Conclusion: Serum ITIH4 may serve as an anti-inflammatory biomarker that negatively associates with stenosis degree and major adverse cardiovascular event risk in CHD patients.

Background and Aims: This study aimed to explore the profile of multimorbidity phenotype clusters and their discrepancy in mortality and the efficiency of combined interventions on blood pressure, glucose and lipid in each cluster., Methods: Fine and Gray competing risk regression models and Kaplan-Meier curves were used to assess the association between multimorbidity and mortality and rehospitalization. Fine and Gray competing risk regression models and subgroup analyses were used to estimate the relations between combined interventions and mortality., Results: Three distinct multimorbidity clusters were observed: Class 1 named severe class, Class 2 termed moderate class, and Class 3 named mild class. Competing risk regression models revealed that patients in Class 1 have the greatest burden of mortality and rehospitalization compared to Class 3 after confounder adjustment, with HRs 1.43 (95% CI 1.30-1.56, P &lt; 0.001) and 2.97 (95% CI 2.74-3.21, P &lt; 0.001), respectively. The patients in Class 2 have moderate risk of mortality and rehospitalization compared to Class 3 after confounder adjustment, with HRs 1.41 (95% CI 1.30-1.52, P &lt; 0.001) and 2.39 (95% CI 2.23-2.56, P &lt; 0.001), respectively. Furthermore, we found that combined interventions on blood pressure, glucose and lipid simultaneously could further benefit on survival compared to each individual intervention or two in combine., Conclusions: This study found that multimorbidity among patients with CHD was common and increased the risks of death and rehospitalization. Three multimorbidity clusters that were significantly associated with death and rehospitalization were identified. Simultaneous intervention on blood pressure, glucose and lipid level may further benefit CHD patient in survival., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Background and Aims: Plasma low-density lipoprotein cholesterol (LDL-C) and lipoprotein(a) (Lp(a)) are both associated with coronary heart disease (CHD). This study investigated whether elevated plasma Lp(a) concentration was associated with increased CHD risk when LDL-C was low (≤100 mg/dL) in individuals not on statin therapy., Methods: Participants from the Multi-Ethnic Study of Atherosclerosis (MESA) (n = 4,585) were categorized into four groups: Group 1: LDL-C ≤ 100 mg/dL, Lp(a) < 50 mg/dL; Group 2: LDL-C > 100 mg/dL, Lp(a) < 50 mg/dL; Group 3: LDL-C ≤ 100 mg/dL, Lp(a) ≥ 50 mg/dL; and Group 4: LDL-C > 100 mg/dL, Lp(a) ≥ 50 mg/dL. The relationship of Lp(a) and LDL-C with time to CHD events was assessed with Kaplan Meier curves and multivariable Cox proportional hazard models., Results: Participants were followed for a mean of 13.4 years and a total of 315 CHD events occurred. Compared to participants with LDL-C ≤ 100 mg/dL and Lp(a) < 50 mg/dL, those with LDL-C > 100 mg/dL and Lp(a) < 50 mg/dL (Group 2) demonstrated no increased risk for CHD events (HR: 0.92; 95% CI: 0.69, 1.21). However, participants with LDL-C ≤ 100 mg/dL and Lp(a) ≥ 50 mg/dL (Group 3) and those with LDL-C > 100 mg/dL and Lp(a) ≥ 50 mg/dL (Group 4) exhibited significantly increased risk of CHD events compared to Group 1 (HR: 1.83; 95% CI: 1.02, 3.27) and Group 2 (HR: 1.61; 95% CI: 1.15, 2.26), respectively., Conclusions: When Lp(a) was elevated, risk of CHD events increased, regardless of baseline LDL-C., Competing Interests: Declaration of competing interests The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Dr. Shapiro has participated in scientific advisory boards with the following entities: Amgen; Novartis; Novo Nordisk; and has served as a consultant for Regeneron. Dr. Rikhi and Dr. Ashburn are supported by the National Heart, Lung, And Blood Institute of the National Institutes of Health under Award Number T32HL076132. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. The remaining authors have nothing to disclose., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Aims: This study explored the associations of genetic susceptibility and adherence to a healthy lifestyle with incident coronary heart disease (CHD) and stroke in individuals with hypertension., Methods and Results: This study included 258 531 European descendants with hypertension at baseline from UK Biobank. Genetic risk of CHD and stroke was estimated using polygenic risk scores derived from 300 and 87 single-nucleotide polymorphisms, respectively. Lifestyle scores were calculated based on 4 lifestyle components (no obesity, no current smoking, regular physical activity and healthy diet). Cox regression with age as the underlying timescale was fit for incident CHD (n = 7470) and stroke (n = 5015), separately. A favourable lifestyle (3-4 lifestyle components) was associated with 37% and 30% lower hazards of CHD (95% confidence intervals, 32-42%) and stroke (23-37%), compared with an unfavourable lifestyle (0-1 lifestyle component), at all levels of genetic risk. Evidence of interaction between genetic susceptibility and lifestyle adherence was found for stroke (P = 0.036): no evidence of interaction for CHD (P = 0.524). A favourable lifestyle at high genetic risk had lower 12-year absolute risk of CHD and stroke, compared with an unfavourable lifestyle at low-to-intermediate genetic (exception: an unfavourable lifestyle at low CHD genetic risk)., Conclusion: Adhering to a healthy lifestyle is associated with lower CHD and stroke risk regardless of genetic risk among individuals with hypertension. Risk of CHD and stroke for those at high genetic risk but adhering to a healthy lifestyle was generally lower than for those at low-to-intermediate genetic risk but adhering to an unhealthy lifestyle., Competing Interests: Conflict of interest: None declared., (© The Author(s) 2022. Published by Oxford University Press on behalf of European Society of Cardiology.)

Background: Hispanics are a heterogeneous population with differences in the prevalence of cardiovascular disease (CVD) and its related risk factors among ethnic sub-groups. This study evaluated the association of genetic admixture and CVD in self-identified Hispanic women from the Women's Health Initiative (WHI)., Methods: Data came from the WHI Observational Study and the Clinical Trial Components conducted among postmenopausal women. The CVD outcomes included coronary heart disease (CHD) and stroke. The proportions of European (EUR), sub-Saharan African (AFR), and Amerindian (AMI) admixture were estimated using 92 ancestry-informative markers. Cox regression models were used to assess the relationship between genetic admixture and CVD adjusting for age, lifestyle risk factors, known risk factors, and neighborhood socioeconomic status., Results: Among 5195 participants EUR ancestry was associated with a lower CHD risk after adjusting for age (HR 0.41, p = 0.02), and in the fully adjusted model (HR 0.40, p = 0.03). AFR ancestry was associated with a higher CHD risk after adjusting for age (HR 2.91, p = 0.03), but it only showed a trend in in the fully adjusted model (HR 2.46, p = 0.10). AMI ancestry was not statistically significantly associated with CHD and none of the genetic admixture proportions were statistically significantly associated with stroke (p > 0.05)., Conclusion: EUR ancestry was associated with a lower risk of CHD in Hispanic women. This highlights the need to account for genetic admixture in future CVD studies to consider different heritage groups to understand the role that genetic, neighborhood socioeconomic status, and environmental factors contribute to CVD health disparities in Hispanic women., (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: End-stage renal disease is associated with a high risk of cardiovascular events. It is unknown, however, whether mild-to-moderate kidney dysfunction is causally related to coronary heart disease (CHD) and stroke., Methods: Observational analyses were conducted using individual-level data from 4 population data sources (Emerging Risk Factors Collaboration, EPIC-CVD [European Prospective Investigation into Cancer and Nutrition-Cardiovascular Disease Study], Million Veteran Program, and UK Biobank), comprising 648 135 participants with no history of cardiovascular disease or diabetes at baseline, yielding 42 858 and 15 693 incident CHD and stroke events, respectively, during 6.8 million person-years of follow-up. Using a genetic risk score of 218 variants for estimated glomerular filtration rate (eGFR), we conducted Mendelian randomization analyses involving 413 718 participants (25 917 CHD and 8622 strokes) in EPIC-CVD, Million Veteran Program, and UK Biobank., Results: There were U-shaped observational associations of creatinine-based eGFR with CHD and stroke, with higher risk in participants with eGFR values <60 or >105 mL·min -1 ·1.73 m -2 , compared with those with eGFR between 60 and 105 mL·min -1 ·1.73 m -2 . Mendelian randomization analyses for CHD showed an association among participants with eGFR <60 mL·min -1 ·1.73 m -2 , with a 14% (95% CI, 3%-27%) higher CHD risk per 5 mL·min -1 ·1.73 m -2 lower genetically predicted eGFR, but not for those with eGFR >105 mL·min -1 ·1.73 m -2 . Results were not materially different after adjustment for factors associated with the eGFR genetic risk score, such as lipoprotein(a), triglycerides, hemoglobin A1c, and blood pressure. Mendelian randomization results for stroke were nonsignificant but broadly similar to those for CHD., Conclusions: In people without manifest cardiovascular disease or diabetes, mild-to-moderate kidney dysfunction is causally related to risk of CHD, highlighting the potential value of preventive approaches that preserve and modulate kidney function.

Objective: To identify coronary heart disease risk factors in young and middle-aged persons and develop a tailored risk prediction model., Methods: A retrospective cohort study was used in this research. From January 2017 to January 2020, 553 patients in the Department of Cardiology at a tertiary hospital in Anhui Province were chosen as research subjects. The research subjects were separated into two groups based on the results of coronary angiography performed during hospitalization ( n = 201) and non-coronary heart disease ( n = 352). R software (R 3.6.1) was used to analyze the clinical data of the two groups. A logistic regression prediction model and three machine learning models, including BP neural network, Extreme gradient boosting (XGBoost), and random forest, were built, and the best prediction model was chosen based on the relevant parameters of the different machine learning models., Results: Univariate analysis identified a total of 24 indexes with statistically significant differences between coronary heart disease and non-coronary heart disease groups, which were incorporated in the logistic regression model and three machine learning models. The AUCs of the test set in the logistic regression prediction model, BP neural network model, random forest model, and XGBoost model were 0.829, 0.795, 0.928, and 0.940, respectively, and the F1 scores were 0.634, 0.606, 0.846, and 0.887, indicating that the XGBoost model's prediction value was the best., Conclusion: The XGBoost model, which is based on coronary heart disease risk factors in young and middle-aged people, has a high risk prediction efficiency for coronary heart disease in young and middle-aged people and can help clinical medical staff screen young and middle-aged people at high risk of coronary heart disease in clinical practice., Competing Interests: The authors declare that they have no competing interests., (© 2022 Cao et al.)

Background: We aimed to investigate the gender difference in the association between changes in metabolic syndrome (MetS) and its components with the risk of cardiovascular disease (CVD) and coronary heart disease (CHD) among adult participants in the Tehran lipid and glucose study cohort., Methods: A total of 4624 adults (aged ≥ 30 years) who participated in two Phases 2 (2002-2005) and 3 (2005-2008) were included and followed up until 2018. Based on the status of MetS and its components in two phases, we divided participants into four groups: MetS-free, MetS-developed, MetS-recovery and MetS-stable groups, and similar categories were defined for MetS components. Multiple Cox regression models were used to estimate the adjusted hazard ratios (HRs) and 95% confidence intervals (95% CIs), and women-to-men ratios of HRs (RHRs)., Results: During a median follow-up of 11.6 years, 619 CVD events (292 women) and 512 CHD events (230 women) occurred. In both genders, the MetS-stable group had the highest risk of CVD and CHD, compared with the MetS-free group, but the associations were stronger in women than men: the HR (95% CI) were (2.76, 2.00-3.82) and (3.08, 2.15-4.40) for CVD and CHD, respectively, in women, and (1.60, 1.23-2.09) and (1.74, 1.30-2.31) for men. The multivariate adjusted women-to-men RHRs were (1.72, 1.16-2.56) for CVD and (1.77, 1.14-2.73) for CHD. Only among women, the risks for CVD in MetS-recovery group (1.67, 1.06-2.63) and MetS-developed group (1.89, 1.16-3.06|) were higher than MetS-free group. For CHD, women in MetS-developed group (1.86, 1.07-3.22) had higher risk than MetS-free group. However, no evidence of gender difference was observed in these associations. Among MetS components, persistent high blood pressure (BP) conferred greater risk for CVD and CHD in women than men; the women-to-men RHRs of CVD and CHD for high BP-stable groups were 1.54 (1.05-2.26) and 1.62 (1.07-2.47), respectively. For CHD events, persistent high fasting plasma glucose was associated with greater risk in women than men with women-to-men RHRs of 1.62 (1.09-2.40)., Conclusion: Change in MetS and its key components were associated with different risks for CVD events in both genders, with generally stronger associations in women than men., (© 2022. The Author(s).)

Background: Type 1 diabetes is associated with accelerated vascular aging and advanced atherosclerosis resulting in increased rates of cardiovascular disease and premature death. We evaluated associations between Leukocyte telomere length (LTL), allelic variations (SNPs) in LTL-related genes and the incidence of coronary heart disease (CHD) in adults with long-standing type 1 diabetes., Methods: We assessed associations of LTL, measured at baseline by RT-PCR, and of SNPs in 11 LTL-related genes with the risk of coronary heart disease (CHD: myocardial infarction or coronary revascularization) and all-cause death during follow-up in two multicenter French-Belgian prospective cohorts of people with long-standing type 1 diabetes., Results: In logistic and Cox analyses, the lowest tertile of LTL distribution (short telomeres) at baseline was associated with the prevalence of myocardial infarction at baseline and with increased risk of CHD (Hazard ratio 3.14 (1.39-7.70), p = 0.005, for shorter vs longer tertile of LTL) and all-cause death (Hazard ratio 1.63 (95% CI 1.04-2.55), p = 0.03, for shorter vs combined intermediate and longer tertiles of LTL) during follow-up. Allelic variations in six genes related to telomere biology (TERC, NAF1, TERT, TNKS, MEN1 and BICD1) were also associated with the incidence of CHD during follow-up. The associations were independent of sex, age, duration of diabetes, and a range of relevant confounding factors at baseline., Conclusions: Our results suggest that short LTL is an independent risk factor for CHD in people with type 1 diabetes., (© 2022. The Author(s).)

Introduction: Coronary heart disease (CHD) is a dynamic process in which there are interactions between endothelial dysfunction, oxidative stress, and inflammatory responses. The aim of the present study was to investigate the function and mechanism of HSCARG in the treatment of CHD., Methods: Male apolipoprotein E/low-density lipoprotein receptor-deficient mice were given a high-fat diet with 21% fat and 0.15% cholesterol for the in vivo model. Human umbilical vein endothelial cells were incubated with angiotensin II for the in vitro model. HSCARG expression was inhibited in patients or mice with CHD., Results: HSCARG reduced oxidative stress in mice with CHD. HSCARG also reduced reactive oxygen species (ROS)-oxidative stress in the in vitro model. HSCARG induced p47phox expression in the in vitro model by NF-κB activity. The regulation of nuclear factor kappa B (NF-κB) activity or p47phox expression participates in the effects of HSCARG in CHD., Conclusion: Altogether, our data indicate that HSCARG reduced ROS-oxidative stress in in vivo and in vitro models of CHD via p47phox by NF-κB activity and may be a clinical target for CHD.

Background: DNA methylation-regulated genes have been demonstrated as the crucial participants in the occurrence of coronary heart disease (CHD). The machine learning based on DNA methylation-regulated genes has tremendous potential for mining non-invasive predictive biomarkers and exploring underlying new mechanisms of CHD., Results: First, the 2085 age-gender-matched individuals in Framingham Heart Study (FHS) were randomly divided into training set and validation set. We then integrated methylome and transcriptome data of peripheral blood leukocytes (PBLs) from the training set to probe into the methylation and expression patterns of CHD-related genes. A total of five hub DNA methylation-regulated genes were identified in CHD through dimensionality reduction, including ATG7, BACH2, CDKN1B, DHCR24 and MPO. Subsequently, methylation and expression features of the hub DNA methylation-regulated genes were used to construct machine learning models for CHD prediction by LightGBM, XGBoost and Random Forest. The optimal model established by LightGBM exhibited favorable predictive capacity, whose AUC, sensitivity, and specificity were 0.834, 0.672, 0.864 in the validation set, respectively. Furthermore, the methylation and expression statuses of the hub genes were verified in monocytes using methylation microarray and transcriptome sequencing. The methylation statuses of ATG7, DHCR24 and MPO and the expression statuses of ATG7, BACH2 and DHCR24 in monocytes of our study population were consistent with those in PBLs from FHS., Conclusions: We identified five DNA methylation-regulated genes based on a predictive model for CHD using machine learning, which may clue the new epigenetic mechanism for CHD., (© 2022. The Author(s).)

Coronary heart disease is one of the major causes of deaths around the globe. Predicating a heart disease is one of the most challenging tasks in the field of clinical data analysis. Machine learning (ML) is useful in diagnostic assistance in terms of decision making and prediction on the basis of the data produced by healthcare sector globally. We have also perceived ML techniques employed in the medical field of disease prediction. In this regard, numerous research studies have been shown on heart disease prediction using an ML classifier. In this paper, we used eleven ML classifiers to identify key features, which improved the predictability of heart disease. To introduce the prediction model, various feature combinations and well-known classification algorithms were used. We achieved 95% accuracy with gradient boosted trees and multilayer perceptron in the heart disease prediction model. The Random Forest gives a better performance level in heart disease prediction, with an accuracy level of 96%.

Objective: Fear of recurrence is a common psychosocial sequela among patients with heart disease. Analyses of coronary heart disease, particularly in elderly patients, are relatively rare. This study aimed to investigate the current situation in this context, as well as the influencing fear factors concerning recurrence in elderly patients with coronary heart disease., Methods: A total of 200 elderly outpatients with coronary heart disease were recruited to participate in this survey from a tertiary hospital in Baoding (China). The questionnaires included items from the Disease Progression Simplified Scale, the Simplified Coping Style Questionnaire, and the Social Support Rating Scale (SSRS). Univariate and multivariate regression analyses were adopted to investigate the influencing factors on the fear of recurrence., Results: The fear of recurrence score in elderly patients with coronary heart disease was (38.46 ± 8.13), among which 119 cases (59.5%) scored higher than 34 points. The SSRS total average score was (34.89 ± 9.83) points. Positive coping style and social support were negatively correlated with the total score of recurrence fear (r =  - 0.621, - 0.413, both P < 0.001). There was a positive correlation between negative coping style and the total score of recurrence fear (r = 0.232, P < 0.001). Multiple linear regression analysis showed that the course of the disease, the number of disease recurrence cases, active coping, and social support were relevant factors in fear of recurrence (all P < 0.05)., Conclusion: The detection rate of fear of recurrence in elderly patients with coronary heart disease was relatively high but could be reduced by active interventions and enhancing social support., (© 2022. The Author(s).)

Background: Racial differences in metabolomic profiles may reflect underlying differences in social determinants of health by self-reported race and may be related to racial disparities in coronary heart disease (CHD) among women in the United States. However, the magnitude of differences in metabolomic profiles between Black and White women in the United States has not been well-described. It also remains unknown whether such differences are related to differences in CHD risk., Methods: Plasma metabolomic profiles were analyzed using liquid chromatography-tandem mass spectrometry in the WHI-OS (Women's Health Initiative-Observational Study; 138 Black and 696 White women), WHI-HT trials (WHI-Hormone Therapy; 156 Black and 1138 White women), MESA (Multi-Ethnic Study of Atherosclerosis; 114 Black and 219 White women), JHS (Jackson Heart Study; 1465 Black women with 107 incident CHD cases), and NHS (Nurses' Health Study; 2506 White women with 136 incident CHD cases). First, linear regression models were used to estimate associations between self-reported race and 472 metabolites in WHI-OS (discovery); findings were replicated in WHI-HT and validated in MESA. Second, we used elastic net regression to construct a racial difference metabolomic pattern (RDMP) representing differences in the metabolomic patterns between Black and White women in the WHI-OS; the RDMP was validated in the WHI-HT and MESA. Third, using conditional logistic regressions in the WHI (717 CHD cases and 719 matched controls), we examined associations of metabolites with large differences in levels by race and the RDMP with risk of CHD, and the results were replicated in Black women from the JHS and White women from the NHS., Results: Of the 472 tested metabolites, levels of 259 (54.9%) metabolites, mostly lipid metabolites and amino acids, significantly differed between Black and White women in both WHI-OS and WHI-HT after adjusting for baseline characteristics, socioeconomic status, lifestyle factors, baseline health conditions, and medication use (false discovery rate <0.05); similar trends were observed in MESA. The RDMP, composed of 152 metabolites, was identified in the WHI-OS and showed significantly different distributions between Black and White women in the WHI-HT and MESA. Higher RDMP quartiles were associated with an increased risk of incident CHD (odds ratio=1.51 [0.97-2.37] for the highest quartile comparing to the lowest; P trend =0.02), independent of self-reported race and known CHD risk factors. In race-stratified analyses, the RDMP-CHD associations were more pronounced in White women. Similar patterns were observed in Black women from the JHS and White women from the NHS., Conclusions: Metabolomic profiles significantly and substantially differ between Black and White women and may be associated with CHD risk and racial disparities in US women.

Glucosamine is widely used around the world and as a popular dietary supplement and treatment in patients with osteoarthritis in China; however, the real-world cardiovascular risk of glucosamine in long-term use is still unclear. A retrospective, population-based cohort study was performed, based on the Beijing Medical Claim Data for Employees from 1 January 2010 to 31 December 2017. Patients newly diagnosed with osteoarthritis were selected and divided into glucosamine users and non- glucosamine users. The glucosamine users group was further divided into adherent, partially adherent, and non-adherent groups according to the medication adherence. New-onset cardiovascular diseases (CVD) events, coronary heart diseases (CHD), and stroke, were identified during the observational period. COX proportional regression models were used to estimate the risks. Of the 685,778 patients newly diagnosed with osteoarthritis including 240,419 glucosamine users and 445,359 non-users, the mean age was 56.49 (SD: 14.45) years and 59.35% were females. During a median follow-up of 6.13 years, 64,600 new-onset CVD, 26,530 CHD, and 17,832 stroke events occurred. Glucosamine usage was significantly associated with CVD (HR: 1.10; 95% CI: 1.08−1.11) and CHD (HR: 1.12; 95% CI: 1.09−1.15), but not with stroke (HR: 1.03; 95% CI: 0.99−1.06). The highest CVD risk was shown in the adherent group (HR: 1.68; 95% CI: 1.59−1.78), followed by the partially adherent group (HR: 1.26, 95% CI: 1.22−1.30), and the non-adherent group (HR: 1.03; 95% CI: 1.02−1.05), with a significant dose−response relationship (p-trend < 0.001). In this longitudinal study, adherent usage of glucosamine was significantly associated with a higher risk for cardiovascular diseases in patients with osteoarthritis.

Aims: This study aimed to evaluate the association between physical activity and the incidence of coronary heart disease (CHD) in individuals with and without CHD risk factors., Methods and Results: EPIC-CVD is a case-cohort study of 29 333 participants that included 13 582 incident CHD cases and a randomly selected sub-cohort nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Self-reported physical activity was summarized using the Cambridge physical activity index (inactive, moderately inactive, moderately active, and active). Participants were categorized into sub-groups based on the presence or the absence of the following risk factors: obesity (body mass index ≥30 kg/m2), hypercholesterolaemia (total cholesterol ≥6.2 mmol/L), history of diabetes, hypertension (self-reported or ≥140/90 mmHg), and current smoking. Prentice-weighted Cox regression was used to assess the association between physical activity and incident CHD events (non-fatal and fatal).Compared to inactive participants without the respective CHD risk factor (referent), excess CHD risk was highest in physically inactive and lowest in moderately active participants with CHD risk factors. Corresponding excess CHD risk estimates amongst those with obesity were 47% [95% confidence interval (CI) 32-64%] and 21% (95%CI 2-44%), with hypercholesterolaemia were 80% (95%CI 55-108%) and 48% (95%CI 22-81%), with hypertension were 80% (95%CI 65-96%) and 49% (95%CI 28-74%), with diabetes were 142% (95%CI 63-260%), and 100% (95%CI 32-204%), and amongst smokers were 152% (95%CI 122-186%) and 109% (95%CI 74-150%)., Conclusions: In people with CHD risk factors, moderate physical activity, equivalent to 40 mins of walking per day, attenuates but does not completely offset CHD risk., Competing Interests: Conflict of interest: All the authors have nothing relevant to disclose., (© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Background: A key outcome in coronary heart disease (CHD) is Health Related Quality of Life (HRQoL), and family functioning is important in the management of CHD. But few studies have examined both together, and little is known about them among inpatients with CHD in less developed areas of China. Therefore, this study aimed to assess the HRQoL and family functioning status of inpatients with CHD in Lanzhou from Northwest China, and identify the factors that affect their HRQoL., Methods: A cross‑sectional study was conducted in 224 CHD inpatients at one major hospital. Sociodemographic data and disease information of CHD inpatients were collected by face-to-face using a structured questionnaire and data were also obtained from patient medical records. HRQoL was measured using the Sickness Impact Profile (SIP). Family functioning was measured using the family APGAR index. Multiple binary logistic regression analysis (MBLRA) was used to explore potential risk factors associated with HRQoL, and Pearson's correlations were used to assess the relationship between family functioning and HRQoL., Results: The overall, physical and psychosocial SIP scores were 25.03 ± 8.52, 18.61 ± 9.90 and 28.08 ± 9.64, respectively. The total family APGAR score was 6.11 ± 2.45. MBLRA found older age, poorer cardiac function and more severe disease were associated with poorer HRQoL, while better family functioning, higher monthly income, and urban living were associated with better HRQoL. Family functioning was weakly to moderately correlated with total and psychosocial HRQoL., Conclusions: Older and less affluent inpatients with lower educational level, less family support and more severe CHD have poorest quality of life, and health care providers should consider interventions to support them., (© 2022. The Author(s).)

Objective: To investigate the association between subfertility and risk of cardiovascular disease (CVD) outcomes., Design: Prospective study., Setting: Population-based cohort., Patient(s): We studied 31,629 women and 17,630 men participating in the Trøndelag Health Study., Intervention(s): Self-reported subfertility. As men were not directly asked about fertility, male partners of female participants were identified through linkage to the Medical Birth Registry of Norway and assigned the fertility information obtained from their partners., Main Outcome Measure(s): The primary outcomes were stroke and coronary heart disease in women and men with and without a history of subfertility. The secondary outcomes were myocardial infarction and angina (subgroups of coronary heart disease) and any CVD (stroke or coronary heart disease). Information on CVD was available by linkage to hospital records. We used Cox proportional hazards models adjusted for age at participation in the Trøndelag Health Study (linear + squared), birth year, smoking history, cohabitation, and education. Cardiometabolic factors were assessed in separate models., Result(s): A total of 17% of women and 15% of men reported subfertility. In women, subfertility was modestly associated with an increased risk of stroke (age-adjusted hazard ratio [aaHR], 1.19; 95% confidence interval [CI], 1.02-1.39; adjusted hazard ratio [aHR]; 1.18; 95% CI, 1.01-1.37) and coronary heart disease (aaHR, 1.19; 95% CI, 1.06-1.33; aHR, 1.16; 95% CI, 1.03-1.30) compared with fertile women. In men, we observed a weak positive association for stroke (aaHR, 1.11; 95% CI, 0.91-1.34; aHR, 1.10; 95% CI, 0.91-1.33) and a weak inverse association for coronary heart disease (aaHR, 0.92; 95% CI, 0.81-1.05; aHR, 0.93; 95% CI, 0.81-1.06)., Conclusion(s): We observed modestly increased risks of CVD outcomes in women and some weak associations in men, although with no strong statistical evidence on sex differences. We acknowledge that we were only able to include men linked to pregnancies ending at 12 completed gestational weeks or later, potentially resulting in selection bias and misclassification of history of subfertility in analyses of male partners. Despite the large sample size, our results indicate the need for larger studies to obtain precise results in both sexes and determine whether there are true sex differences., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Understanding the predictive utility of previously derived polygenic risk scores (PRSs) for long-term risk of coronary heart disease (CHD) and its additive value beyond traditional risk factors can inform prevention strategies., Methods: Data from adults 20 to 59 years of age who were free of CHD from the FOS (Framingham Offspring Study) and the ARIC (Atherosclerosis Risk in Communities) study were analyzed. Because the PRS was derived from samples of predominantly European ancestry, individuals who self-reported White race were included. The sample was stratified by age and cohort: young (FOS, 20-39 years [median, 30 years] of age), early midlife (FOS, 40-59 years [median, 43] years of age), and late midlife (ARIC, 45-59 years [median, 52 years] of age). Two previously derived and validated prediction tools were applied: (1) a 30-year traditional risk factor score and (2) a genome-wide PRS comprising >6 million genetic variants. Hazard ratios for the association between each risk estimate and incident CHD were calculated. Predicted and observed rates of CHD were compared to assess discrimination for each model individually and together with the optimism-corrected C index (95% CI)., Results: Among 9757 participants, both the traditional risk factor score (hazard ratio per 1 SD, 2.60 [95% CI, 2.08-3.27], 2.09 [95% CI, 1.83-2.40], and 2.11 [95% CI, 1.96-2.28]) and the PRS (hazard ratio, 1.98 [95% CI, 1.70-2.30], 1.64 [95% CI, 1.47-1.84], and 1.22 [95% CI, 1.15-1.30]) were significantly associated with incident CHD in young, early midlife, and late midlife, respectively. Discrimination was similar or better for the traditional risk factor score (C index, 0.74 [95% CI, 0.70-0.78], 0.70 [95% CI, 0.67-0.72], and 0.72 [95% CI, 0.70-0.73]) compared with an age- and sex-adjusted PRS (0.73 [95% CI, 0.69-0.78], 0.66 [95% CI, 0.62-0.69], and 0.66 [95% CI, 0.64-0.67]) in young, early-midlife, and late-midlife participants, respectively. The ΔC index when PRS was added to the traditional risk factor score was 0.03 (95% CI, 0.001-0.05), 0.02 (95% CI, -0.002 to 0.037), and 0.002 (95% CI, -0.002 to 0.006) in young, early-midlife, and late-midlife participants, respectively., Conclusions: Despite a statistically significant association between PRS and 30-year risk of CHD, the C statistic improved only marginally with the addition of PRS to the traditional risk factor model among young adults and did not improve among midlife adults. PRS, an immutable factor that cannot be directly intervened on, has minimal clinical utility for long-term CHD prediction when added to a traditional risk factor model.

Aims: To evaluate the sex-specific predictive value of N-terminal pro B-type natriuretic peptide (NT-proBNP), high sensitivity cardiac troponin T (hs-cTnT) and creatine kinase myocardial band (CK-MB) for 10-year risk prediction of coronary heart disease (CHD), stroke, heart failure (HF) and composite outcomes., Methods: Five-thousand four-hundred thirty individuals (mean age 68.6 years, 59.9% women) from the Rotterdam Study, with biomarker measurements between 1997 and 2001, were included. Participants were followed until 2015. We fitted 'basic' models using traditional cardiovascular risk factors. Improvements in c-statistics and net reclassification improvement (NRI) for events and non-events were calculated., Results: During a median follow-up of 14 years, 747 (13.8%), 563 (10.4%), and 664 (12.2%) participants were diagnosed with CHD, stroke, and HF, respectively. NT-proBNP improved the discriminative performance of the 'basic' model for all endpoints (c-statistic improvements ranging from 0.007 to 0.050) and provided significant event-NRI for HF (14.3% in women; 10.7% in men) and for stroke in men (9.3%). The addition of hs-cTnT increased c-statistic for CHD in women by 0.029 (95% CI, 0.011-0.047) and for HF in men by 0.034 (95% CI, 0.014-0.053), and provided significant event-NRI for CHD (10.3%) and HF (7.8%) in women, and for stroke (8.4%) in men. The added predictive value of CK-MB was limited., Conclusion: NT-proBNP and hs-cTnT provided added predictive value for various cardiovascular outcomes above traditional risk factors. Sex differences were observed in the predictive performance of these biomarkers., Competing Interests: Conflict of interest: None declared., (© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.)

The aim was to analyze the infection, influencing factors, and clinical manifestations of Helicobacter pylori infection, coronary heart disease, and cytotoxin-associated protein A infection, so as to provide reference for the improvement of clinical diagnosis and treatment level of in-depth treatment. This paper presents a clinical observation method based on Helicobacter pylori infection, risk factors, and cytotoxin-associated protein A in patients with coronary heart disease. Methods. 237 patients with CHD diagnosed and tested by 14C breath test were selected from inpatients of cardiovascular diseases in a hospital for retrospective analysis. The clinical data, serum deepening indicators, Hcy, and other factors were analyzed through general condition investigation, previous history investigation, and physical examination. The patients were observed by the SPSS22.0 statistical data processing method. The results showed that among the respondents, 175 cases were HP-positive, the infection rate was 73.8%, 77 patients with stable angina pectoris were 64.9%, and 160 patients with acute coronary heart disease were 78.1%. The difference between the groups was statistically significant ( P < 0.05). Conclusion . Helicobacter pylori cytotoxic-associated protein A can increase the risk of gastric cancer, and Helicobacter pylori eradication treatment is more conducive to reduce the incidence of gastric cancer and ensure the safety of patients., Competing Interests: The authors declare no conflicts of interest with respect to the research, authorship, and/or publication of this article., (Copyright © 2022 Xiaoyuan Wang et al.)

Background: Early detection could significantly improve the prognosis of coronary heart disease (CHD). In-invitro diagnostic technique may provide a solution when sufficient biomarkers could be identified. Pertinent associations between blood-based aberrant DNA methylation and smoking, the pathogenesis of atherosclerosis, and CHD have been robustly demonstrated and replicated, but that studies in Chinese populations are rare. The blood-based methylation of aryl-hydrocarbon receptor repressor (AHRR) cg05575921 and 6p21.33 cg06126421 has been associated with cardiovascular mortality in Caucasians. Here, we aim to investigate whether the AHRR and 6p21.33 methylation in the blood is associated with CHD in the Chinese population., Methods: In this case-control study, 180 CHD patients recruited at their first registration in our study center, and 184 controls randomly selected from the people who participated in the annual health examination were enrolled. Methylation intensities of 19 CpG sites, including AHRR cg05575921, 6p21.33 cg06126421, and their flanking CpG sites, were quantified by mass spectrometry. The association between methylation intensities and CHD was estimated by logistic regression analyses adjusted for covariant., Results: Compared to the controls, lower methylation of 6p21.33&#95;CpG&#95;4.5/cg06126421 was independently associated with increased odds of being a CHD patient (OR per - 10% methylation = 1.42 after adjustment for age, gender, and batch effect; p = 0.032 by multiple testing corrections). No association between blood-based AHRR methylation and CHD was found., Conclusions: 6p21.33 methylation exhibits a significant association with CHD. The combination of 6p21.33 methylation and conventional risk factors might be an intermediate step towards the early detection of CHD., (© 2022. The Author(s).)

Aims: In patients with coronary heart disease (CHD), we investigated whether it is possible to accurately assess the probability of short-term control of risk factors (blood pressure, cholesterol, smoking) based on individual and large-area residential characteristics., Methods and Results: We merged individual data of participants from EUROASPIRE V who were hospitalized for CHD (2014-2017) and interviewed and examined for risk factor control (2016-2017), with large-area residential data provided by Eurostat for Nomenclature of Territorial Units for Statistics (NUTS) regions using postal codes. Data from 2562 CHD patients in 16 countries were linked to data from 60 NUTS 2 and 121 NUTS 3 regions. The median time between hospitalization and interview was 14 months. We developed prediction models to assess the probability of risk factor control at interview using data from the time of hospitalization: (i) baseline models including 35 variables on patients' demographic, clinical, and socio-economic characteristics and (ii) extended models additionally considering nine variables on large-area residential characteristics. We calculated and internally validated c-indices to assess the discriminative ability of prediction models. Baseline models showed good discrimination with c-indices of 0.69, 0.70, and 0.76 for blood pressure control, cholesterol control, and smoking cessation, respectively. Extended models for blood pressure, cholesterol, and smoking yielded improved c-indices of 0.72, 0.71, and 0.78, respectively., Conclusion: Our results indicate that the probability of risk factor control in CHD patients can be accurately assessed using individual and large-area residential characteristics, allowing for an identification of patients who are less likely to achieve risk factor targets., Competing Interests: Conflict of interest: K.K. had research grant support from the European Society of Cardiology (paid to the Imperial College London). K.S.M. had a doctoral fellowship from the German Heart Foundation. All other authors declare that there is no conflict of interest., (© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Background and Aims: Oxidized phospholipids carried on the apolipoprotein B-100 (OxPL-apoB) component of Lp(a) are predictive of coronary heart disease (CHD), but the role of oxidized phospholipids carried on plasminogen (OxPL-PLG) is unknown. We examined the independent effects of OxPL-apoB and OxPL-PLG for risk of CHD before and after adjustment for Lp(a)., Methods: Plasma levels of OxPL-apoB, OxPL-PLG, plasminogen and Lp(a) were measured in the PROCARDIS study of early-onset CHD (906 cases/858 controls). Multivariable logistic regression was used to estimate the odds ratios (OR) for each biomarker with CHD after adjustment for established risk factors., Results: Mean levels of OxPL-apoB were higher in cases than controls, but levels of OxPL-PLG and plasminogen were similar. For OxPL-apoB, individuals in the top vs bottom fifth had 2-fold higher age and sex-adjusted OR of CHD (OR = 2.61 [95%CI: 1.91, 3.55]), which were partially attenuated after adjustment for established risk factors. The findings for OxPL-apoB and CHD in PROCARDIS were comparable with those of a meta-analysis of all such studies. However, the associations of OxPL-apoB with CHD were fully attenuated by additional adjustment for Lp(a) (OR = 0.93 [0.54,1.60]). Neither OxPL-PLG nor plasminogen were associated with CHD. Overall, there were no differences in the predictive value for CHD of high vs normal levels (<20th or >80th percentile) of OxPL-apoB, OxPL-PLG, plasminogen or Lp(a) after stratifying for each other., Conclusions: These results highlight the context-dependency of OxPL in plasma and suggest that their associated risk of CHD is chiefly mediated by their carriage on Lp(a)., (Crown Copyright © 2022. Published by Elsevier B.V. All rights reserved.)

Apolipoprotein E containing high-density lipoprotein (apoE-HDL) and apoE-HDL cholesterol (apoE-HDL-C) are recently recognized as potential biomarkers for coronary heart disease (CHD). We herein developed a two-stage, enzyme-assisted, dual-signal aptasensor that enables a useful electrochemical sensing platform for simultaneous determination of apoE-HDL, apoE-HDL-C, and total HDL-C presented in the sample. The detection scheme consists of two subsystems. In subsystem (I), the level of apoE-HDL is evaluated upon the binding of apoE-specific aptamer and subsequently methylene blue (MB)-labeled DNA displacement occurs on the electrode surface, resulting in electrochemical reduction of methylene blue. In subsystem (II), two kinds of cholesterol levels (apoE-HDL-C and total HDL-C) can be measured. For apoE-HDL-C, the amount of cholesterol in apoE-HDL captured by the aptamer in the first step can be further determined with the aid of surfactant, cholesterol esterase, cholesterol oxidase, and p-aminophenol-mediated electrochemical signal amplification. As for total HDL-C, the amount of cholesterol is determined by the same approach as that used for apoE-HDL-C determination, but without washing (separation). The linear dynamic range for apoE-HDL determination is from 1 to 100 mg/dL (R 2  = 1.00). For cholesterol standards, the linear dynamic range is determined to be 0-250 mg/dL (R 2  = 0.98). Finally, serial dilutions of purified human HDL preparations were examined using the newly developed aptasensor; the percentage of apoE-HDL-C to HDL-C was found to be ~10%, which correlated well with previously reported values. In conclusion, we successfully developed an electrochemical aptasensor that allows concurrent quantification of apoE-HDL, apoE-HDL-C, and HDL-C on the same platform, offering an efficient, convenient, and purification-free sensing strategy for predictive CHD biomarkers., (© 2022. Springer-Verlag GmbH Germany, part of Springer Nature.)

Background and Aims: Familial hypercholesterolemia (FH) is a genetic disorder characterized by lifelong elevated low-density lipoprotein cholesterol (LDL-C) and increased risk of premature coronary heart disease (CHD). Cholesterol-lowering therapy (statins) reduces CHD risk, but have been available only in the last 25 years, thus, elderly FH patients have been exposed to elevated LDL-C levels most of their life. Surprisingly, some of these have never experienced any CHD event, raising the question whether they present CHD resistant characteristics. Identifying possible cardioprotective biomarkers could contribute to future CHD preventive treatment, therefore, we aimed to identify metabolic markers in event-free elderly FH subjects., Methods and Results: We used a high-throughput nuclear magnetic resonance (NMR) spectroscopy platform to quantify a large number of metabolites in serum samples from 83 FH patients ≥65 years, and analyze differences between subjects with (n = 39) and without (n = 44) CHD. Mean age was 70 years in both groups (57% and 38% female in the event-free group and CHD group, respectively). The event-free group had significantly higher levels of large and extra-large high-density lipoprotein (HDL) particles, and higher concentration of Apolipoprotein A1 (ApoA1) and cholesterol in HDL and HDL2 particles, compared to the CHD group (p ≤ 0.05 for all)., Conclusion: CHD resistant elderly FH patients have higher levels of large HDL particles. The mechanisms behind the event-free survival among these patients remain unclear; hence, a deeper understanding of the metabolic profile in event-free elderly FH subjects may lead to development of novel preventive therapies., Competing Interests: Declaration of competing interest Dr. Bogsrud has received research grants and/or personal fees from Amgen and Sanofi, none of which are related to the content of this manuscript. Dr. Christensen has received research grants and/or personal fees from Mills DA and Amgen, none of which are related to the content of this manuscript. Dr. Retterstøl has received research grants and/or personal fees from Akcea, Amgen, Mills, Sanofi and Sunnovion, none of which are related to the content of this manuscript. MD. Dr. Ulven has received research grants from Mills DA, TINE BA and Olympic Seafood, none of which are related to the content of this manuscript. Dr. Holven has received research grants and/or personal fees from TINE, Mills, Amgen, Sanofi and Olympic Seafood, none of which are related to the content of this manuscript. Msc. Melnes, Msc. Thorsen, Msc. Fossum, PhD Narverud have nothing to disclose., (Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.)

Background: Cardiovascular disease is the world major cause of death. There is sufficient evidence that patients with coronary heart disease (CHD) experience poor quality of life. Health literacy and self efficacy are modifiable psychosocial factors that could affect quality of life, and these factors should be considered as targets for intervention. As the relationships among health literacy, self efficacy, and quality of life in the CHD population have not been well understood. Thus, we constructed the structure equation model in these valuables., Methods: A cross-sectional study of a convenience sample among 200 patients with CHD were participated from outpatient clinics in three tertiary general hospitals in Baoding City in mainland China, from December 2018 to June 2019. Data regarding demographic features, health literacy, self efficacy and quality of life were assessed. A structure equation model was used to construct and validate the pathways., Results: The mean age of the study sampled patients was 65.37 years old. The average level of health literacy, self efficacy and quality of life were 9.6 ± 3.5, 28.8 ± 13.9 and 381.8 ± 130.1 respectively. Significant associations were observed from health literacy to quality of life, and self efficacy played a partial mediating role between health literacy and quality of life in the CHD population. Health literacy and self efficacy explained for 59.6% of the variance in quality of life., Conclusions: Health literacy had a direct influence on quality of life, and an indirect influence on quality of life via self efficacy in the patients with CHD., (© 2022. The Author(s).)

Background: Coronary heart disease (CHD) is one of the most common causes of morbidity and mortality in type 2 diabetes mellitus (T2DM). Oxidative stress is one of the important contributors to the pathogenesis of CHD. Sestrin2 is a stress-induced antioxidant protein that plays a important role in T2DM and CHD. However, the relationship between serum Sestrin2 levels and T2DM with CHD remains unclear., Aim: This study aimed to investigate the relationship between serum Sestrin2 levels and CHD in patients with type 2 diabetes., Methods: A total of 70 T2DM patients with CHD and 69 T2DM patients were enrolled in this study. Clinical features and metabolic indices were identified. Serum Sestrin2 was measured by ELISA., Results: Serum Sestrin2 levels in T2DM-CHD groups were significantly lower compared with the T2DM group (11.17 (9.79, 13.14) ng/mL vs 9.46 (8.34, 10.91) ng/mL). Bivariate correlation analysis revealed that serum Sestrin2 levels were negatively correlated with age (r = - 0.256, P = 0.002), BMI (r = - 0.206, P = 0.015), FBG (r = - 0.261, P = 0.002) and Tyg index (r = - 0.207, P < 0.014). Binary logistic regression suggested that low serum Sestrin2 levels were related to the increased risk of T2DM-CHD (P < 0.05). In addition, the receiver operating characteristic analysis revealed that the area under the curve of Sestrin2 was 0.724 (95% CI 0.641-0.808, P < 0.001) to predict T2DM-CHD patients (P < 0.001)., Conclusion: The Sestrin2 levels were highly associated with CHD in diabetes patients. Serum Sestrin2 may be involved in the occurrence and development of diabetic with CHD., (© 2022. The Author(s).)

Objective: To investigate the correlation between CML, sRAGE, and esRAGE and the measure of atherosclerosis of coronary heart disease., Methods: From June 2019 to December 2021, there were 100 patients in all suffering from coronary heart disease (CHD) selected as the observation group. On the basis of Gensini score, they were divided into mild group (Gensini score < 12 points), moderate group (12 points ≤ Gensini score ≤60 points), and severe group (Gensini score > 60). Apart from that, 50 normal people staying in our hospital for physical examination were chosen as the control group in the meantime. N in each group was detected and compared ε -Carboxymethyl lysine (CML), soluble advanced glycation end product receptor (sRAGE), and endogenous secretory advanced glycation end product receptor (esRAGE). Pearson correlation coefficient was adapted to assay the relevance between CML, sRAGE, and esRAGE, as well as the degree of atherosclerosis in CHD. Receiver operator characteristic (ROC) curve was applied to during the evaluation of the diagnosis of CML, sRAGE, and esRAGE, as well as their combined detection of severe atherosclerosis in CHD., Results: In contrast with the control group, the level of serum CML together with sRAGE in the observation group was considerably elevated, while the level of esRAGE appeared in a downward trend ( P  < 0.05). The level of serum CML and sRAGE was directly proportional to the measure of atherosclerosis in CHD, while the level of esRAGE was inversely proportional to the measure of atherosclerosis in CHD ( P  < 0.05). That is to say that serum CML and sRAGE were positive in matter of the measure of atherosclerosis in CHD, while esRAGE negatively appertains to the measure of atherosclerosis in CHD ( P  < 0.05). Serum CML, sRAGE, and esRAGE could effectively diagnose severe atherosclerosis in CHD, and the combined detection sensitivity (89.79%), specificity (77.16%), accuracy (86.12%), positive predictive value (86.63%), negative predictive value (88.59%), and area under ROC curve (AUC) (0.924) were higher ( P  < 0.05)., Conclusion: CML and sRAGE, as well as esRAGE, are bound up with the degree of atherosclerosis in CHD, which is conducive to clinical diagnosis and treatment., Competing Interests: The authors declare that they have no conflicts of interest or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Wenjun Liu et al.)

Objective: Type 2 diabetes mellitus (T2DM) is often accompanied by undiagnosed dyslipidemia. Research on the association of unconventional lipid markers with prediabetes (pre-DM) and T2DM simultaneously is limited in coronary heart disease (CHD) patients., Methods: This study included 28,476 patients diagnosed with CHD. Their lipid levels, including triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C), were measured, and non-traditional lipid parameters were calculated. The patients were divided into three groups based on the diabetic status including normoglycemic (NG), pre-DM, and T2DM. Multiple logistic regression was used to compare the association of TG/HDL-C and other non-traditional lipid parameters with pre-DM and T2DM. The tertiles of TG/HDL-C included T1 (TG/HDL-C < 1.10), T2 (1.10 ≤ TG/HDL-C ≤ 1.89) and T3 (TG/HDL-C > 1.89). Low and high TG/HDL-C was defined with sex-specific cutoff points., Results: Multiple logistic regression results showed that the non-traditional lipid parameters, including non-HDL-C, LDL-C/HDL-C, TC/HDL-C, non-HDL-C/HDL-C and TG/HDL-C, were all correlated with the risk of pre-DM and T2DM. Meanwhile TG/HDL-C showed the strongest correlation (odds ratio [OR]: 1.19; 95% confidence interval [CI] 1.16-1.23), (OR: 1.36; 95% CI 1.33-1.39). When dividing TG/HDL-C into tertiles, using T1 as a reference, T3 was observed to have the highest association with both pre-DM and T2DM (OR: 1.60; 95% CI 1.48-1.74), (OR: 2.79; 95% CI 2.60-3.00). High TG/HDL-C was significantly associated with pre-DM and T2DM (OR: 1.69; 95% CI 1.52-1.88), (OR: 2.85; 95% CI 2.60-3.12). The association of TG/HDL-C with T2DM and pre-DM existed across different sex, age, smoking, and drinking statuses., Conclusion: Elevated non-traditional lipid parameters were significantly associated with pre-DM and T2DM in CHD patients, especially TG/HDL-C. High TG/HDL-C was the risk factor with a strong correlation with the risk of pre-DM and T2DM., (© 2022. The Author(s).)

As genetic inheritance is an inevitable risk factor in the development of coronary heart disease (CHD), it is critical to identify the polymorphisms of CHD risk. This study explored whether the NPAS4 polymorphisms are related to the CHD risk in the Chinese Han population. Five SNPs in NPAS4 were genotyped using Agena Mass ARRAY from 499 CHD and 500 controls. RT-PCR detected the NPAS4 expression levels in peripheral blood mononuclear cells from 50 CHD and 50 controls. χ 2 test compared the distributions of gender, allele and genotypes frequencies between cases and controls. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (95% CIs). MDR analyzed the SNP-SNP interactions on risk of CHD. U test compared the differences in gene expression between different groups. The results showed that rs4466842 was correlated with an increased CHD risk in overall, males and age ≤ 60; rs117186164 and rs12785321 were significantly related to an increased CHD risk in male and age ≤ 60, respectively; haplotype A rs117186164 C rs4466842 was significantly correlated with an increased CHD risk. SNP-SNP interactions results showed that the best model was the four-locus model was the combination of rs117770654, rs117957381, rs12785321, and rs4466842 (CVC = 10/10, Testing Sensitivity = 0.647). The expression levels of NPAS4 in the case group (0.365 ± 0.139) were significantly lower than that in the control group (0.782 ± 0.224) (P < 0.001). The results revealed that SNPs in NPAS4 may play an important role in the occurrence and development of CHD., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Aims: The onset of the COVID-19 pandemic saw the suspension of centre-based cardiac rehabilitation (CBCR) and has underscored the need for home-based cardiac telerehabilitation (HBCTR) as a feasible alternative rehabilitation delivery model. Yet, the effectiveness of HBCTR as an alternative to Phase 2 CBCR is unknown. We aimed to conduct a meta-analysis to quantitatively appraise the effectiveness of HBCTR., Methods and Results: PubMed, EMBASE, CENTRAL, CINAHL, Scopus, and PsycINFO were searched from inception to January 2021. We included randomized controlled trials (RCTs) comparing HBCTR to Phase 2 CBCR or usual care in patients with coronary heart disease (CHD). Out of 1588 studies, 14 RCTs involving 2869 CHD patients were included in this review. When compared with usual care, participation in HBCTR showed significant improvement in functional capacity {6-min walking test distance [mean difference (MD) 25.58 m, 95% confidence interval (CI) 14.74-36.42]}; daily step count (MD 1.05 K, 95% CI 0.36-1.75) and exercise habits [odds ratio (OR) 2.28, 95% CI 1.30-4.00)]; depression scores (standardized MD -0.16, 95% CI -0.32 to 0.01) and quality of life [Short-Form mental component summary (MD 2.63, 95% CI 0.06-5.20) and physical component summary (MD 1.99, 95% CI 0.83-3.16)]. Effects on medication adherence were synthesized narratively. HBCTR and CBCR were comparably effective., Conclusion: In patients with CHD, HBCTR was associated with an increase in functional capacity, physical activity (PA) behaviour, and depression when compared with UC. When HBCTR was compared to CBCR, an equivalent effect on functional capacity, PA behaviour, QoL, medication adherence, smoking behaviour, physiological risk factors, depression, and cardiac-related hospitalization was observed., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.)

Coronary heart disease (CHD) is one of the primary causes of death globally. There are several diagnostic techniques for CHD at present, but they are invasive and with limited accuracy. In the work, measurement of human urine based on surface-enhanced Raman spectroscopy (SERS) was proposed to diagnose CHD. Urine samples of 157 CHD patients and 63 healthy controls (HC) were investigated by SERS. Statistical analysis of the measured data was then performed. It was found that there were intensity differences in nine Raman peaks (1223/1243/1272/1463/1481/1516/1536/1541/1550 cm -1 ) between CHD and HC in their average SERS spectrum. Furthermore, principal component analysis (PCA)-linear discriminant analysis (LDA) was then utilized to establish a prediction model to classify CHD and HC. It revealed that the accuracy, specificity and sensitivity of the prediction model validated by leave-one-patient-out cross validation (LOPOCV) were 84.09%, 92.06% and 80.89%, respectively. Therefore, the proposed method can be employed as a non-invasive, rapid and accurate tool for CHD diagnosis in clinical application., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Background: Due to the lack of research, this study aimed to assess the association between the specific range of heart rate and cardiovascular (CV) death in coronary heart disease (CHD) patients., Hypothesis: Heart rate of 70-79 bpm may be associated with reduced risk of CV death in CHD patients., Methods: This retrospective cohort study collected the data of CHD patients from the eight cycles of the Health and Nutrition Examination Survey (NHANES). The included patients were divided into four groups: <60, 60-69, 70-79, and ≥80 bpm. The start of follow-up date was the mobile examination center date, the last follow-up date was December 31, 2015. The average follow-up time was 81.70 months, and the longest follow-up time was 200 months. Competing risk models were developed to evaluate the association between heart rate and CV death, with hazard ratios (HRs) and 95% confidence intervals (CIs) calculated., Results: A total of 1648 patients with CHD were included in this study. CHD patients at heart rate of <60 (HR, 1.35; 95% CI, 1.34-1.36), 60-69 (HR, 1.05; 95% CI, 1.04-1.06) or ≥80 (HR, 1.39; 95% CI, 1.38-1.41) bpm had a higher risk of CV death than those at heart rate of 70-79 bpm., Conclusions: Heart rate of <70 or ≥80 bpm was associated with an elevated risk of CV death among CHD patients. Continuous monitoring of heart rate may help to screen for health risks and offer early interventions to corresponding patients., (© 2022 The Authors. Clinical Cardiology published by Wiley Periodicals LLC.)

Background and Aims: Observational studies have examined serum urate levels in relation to coronary heart disease (CHD) and myocardial infarction (MI). Whether these associations are causal remains controversial, due to confounding factors and reverse causality. We aim to investigate the causality of these associations using Mendelian randomization method., Methods and Results: Instrumental variables were obtained from the largest genome-wide association studies of serum urate (457,690 individuals) to date. Summary statistics were from CARDIoGRAMplusC4D consortium (60,801 CHD cases; 43,676 MI cases), FinnGen (21,012 CHD cases; 12,801 MI cases), UK Biobank (10,157 CHD cases; 7018 MI cases), and Biobank Japan (29,319 CHD cases). Inverse-variance weighted method was applied as the main results. Other statistical methods and reverse MR analysis were conducted in the supplementary analyses. Elevated genetically determined serum urate levels were associated with increased risks of CHD and MI. The association pattern remained for the datasets in FinnGen, the combined results of three independent data sources (CHD: odds ratio (OR), 1.10; 95%CI, 1.06-1.15; p = 4.2 × 10 -6 ; MI: OR, 1.12; 95%CI, 1.07-1.18; p = 2.7 × 10 -6 ), and East Asian population. Interestingly, sex-specific subgroup analyses revealed that these associations kept in men only, but not among women in individuals of European ancestry. No consistent evidence was found for the causal effect of CHD or MI on serum urate levels., Conclusion: We provide consistent evidence for the causal effect of genetically predicted serum urate levels on CHD and MI, but not the reverse effect. Urate-lowering therapy may be of cardiovascular benefit in the prevention of CHD and MI, especially for men., Competing Interests: Declaration of competing interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.)

Coronary heart disease (CHD) is the leading cause of morbidity and mortality world-wide and has been characterized as a chronic immunoinflammatory, fibroproliferative disease fueled by lipids. Great advances have been made in elucidating the complex mechanistic interactions among risk factors associated with CHD, yielding abundant success towards preventive measures and the development of pharmaceuticals to prevent and treat CHD via attenuation of lipoprotein-mediated risk. However, significant residual risk remains. Several potentially modifiable CHD risk factors ostensibly contributing to this residual risk have since come to the fore, including systemic inflammation, diabetes mellitus, high-density lipoprotein, plasma triglycerides (TG) and remnant lipoproteins (RLP), lipoprotein(a) (Lp[a]), and vascular endothelial dysfunction (ED). Herein, we summarize the body of evidence implicating each of these risk factors in residual CHD risk., (Copyright © 2021 Elsevier Inc. All rights reserved.)