miR-27a-3p is a multifunctional miRNA that plays a critical role in the process of angiogenesis. However, its specific effect on coronary heart disease (CHD), particularly on the regulation of downstream molecules and the resulting impact on endothelial cell injury, has not yet been fully elucidated. This study aimed to explore the relationship between miR-27a-3p and CHD and its underlying mechanical molecular pathways in CHD patients and modeled endothelial cells with techniques such as RT-qPCR, RNA sequencing and bioinformatics. Consequently, the expression of miR-27a-3p was significantly decreased in CHD patients. In endothelial cells, overexpression of miR-27a-3p was observed to decrease malonaldehyde, gamma H2A histone family member X and interleukin 6 while increased superoxide dismutase, thus reduced endothelial injury and senescence. RNA sequencing and bioinformatics revealed glutamate ionotropic receptor NMDA type subunit 2D (GRIN2D) as a target gene of miR-27a-3p, and dual luciferase assays confirmed the direct binding of miR-27a-3p to the 3'UTR of GRIN2D. Subsequent validation experiments demonstrated that miR-27a-3p inhibited the protein expression of GRIN2D and PKC and suppressed the activation of the MAPK/ERK signaling pathway by reduced downstream MEK and ERK phosphorylation, leading to enhanced endothelial apoptosis. In conclusion, miR-27a-3p played a crucial role in regulating endothelial cell dysfunction which may trigger coronary atherosclerosis and CHD by targeting GRIN2D in the PKC/MEK/ERK signaling pathway.

Inflammation plays a pivotal role in Cardiovascular disease (CVD) which are a major global health burden. The oil-supplemented Mediterranean diet (MED) is associated with anti-inflammatory effects. The current study evaluates the impact of an olive oils-supplemented MED on pro-inflammatory biomarkers and soluble adhesion molecules.

Regarding PRISMA guideline, this study was conducted and PubMed, Scopus, Web of Science (ISI), Embase, CINAHL databases as well as Google Scholar and Cochrane Library were systematically searched till June 2024.

15 clinical trials (20 arms) comprising 2477 adults aged 23-80 years were included in the systematic review and 9 of them were entered in the meta-analysis. We revealed that following an enriched MED with olive oils can reduce Interleukin-6 (IL-6) (SMD: - 1.85; 95% CI: -3.69 to -0.01, I2: 99.29%) and c-reactive protein (CRP) or high-sensitivity CRP (hs-CRP) (SMD: - 0.96; 95% CI: -1.49 to -0.44, I2: 91.85%); however, tumor necrosis factor α (TNFα), monocyte chemoattractant protein-1 (MCP-1) and interferon gamma (IFN-γ) did not improved. Moreover, a positive impact on the levels of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1) and P-selectin [(SMD: -2.37; 95% CI: -4.34 to -0.40, I2: 99.38%), (SMD: -1.10; 95% CI: -2.10 to -0.10, I2: 94.96%) and (SMD: -0.65; 95% CI: -1.18 to -0.12, I2: 59.33%), respectively] were observed; however, E-selectin was unchanged.

The olive oils-supplemented MED demonstrates significant anti-inflammatory benefits and improvements in soluble adhesion molecules, supporting its role in reducing CVD risk. However, further studies are required to address the high heterogeneity and confirm these findings in diverse populations.

PROSPERO (CRD42023425225).

Myocardial infarction (MI) is an important risk factor of cardiovascular disease (CVD) and its incidence has been on the rise globally. Myocardial ischemia/reperfusion (I/R) injury is frequently detected in the ischemic myocardium. Recent studies have shown that ubiquitination plays an important role in the cardiac pathophysiological processes. Herein, we investigated the role and molecular mechanism of Ovarian tumor deubiquitinase 1 (OTUD1) in I/R induced myocardial injury. It was observed that the myocardial OTUD1 was upregulated in I/R-induced heart tissues and global deletion of OTUD1 significantly ameliorated I/R induced myocardial injury and dysfunction. Similarly, silencing or overexpression OTUD1 affected the hypoxia/reoxygenation (H/R) induced cell apoptosis in cultured cardiomyocytes. Mechanistically, immunoprecipitation-mass spectrometry revealed that OTUD1 directly bound to receptor for activated C-kinase 1 (RACK1) which has been identified as a scaffold protein for multiple kinases including mitogen-activated protein kinase (MAPKs) and Inhibitor of nuclear factor kappa B kinase (IKK). OTUD1 could cleave K63-linked polyubiquitin chains to enhance RACK1 phosphorylation, thus modulating MAPKs and nuclear factor kappa B (NF-κB) signaling. Finally, silencing of RACK1 reverses OTUD1-promoted H/R induced myocardial apoptosis. In conclusion, our findings suggest that OTUD1 promotes I/R-induced heart injury by deubiquitinating RACK1, suggesting that OTUD1 is a potential therapeutic target for myocardial I/R.

Cerebrovascular and cardiovascular diseases are pathophysiologically interconnected. In the past, researchers have mainly focused on developing one herbal medicine treatment. Single herb often fails to address the multifactorial pathology of these diseases. The pathogenesis and progression of the disease are complex, making the therapeutic effect of a single herb potentially limiting. Traditional Chinese medicine emphasizes herb pairs, which enhance therapeutic efficacy through synergistic interactions.

This review focused on the mechanisms and potential clinical applications of Chinese herb pairs such as Astragali Radix-Carthami Flos, Salviae Miltiorrhizae Radix-Puerariae Lobatae Radix, Salviae Miltiorrhizae Radix-Chuanxiong Rhizoma, Salviae Miltiorrhizae Radix-Notoginseng Radix, Salviae Miltiorrhizae Radix-Carthami Flos, Astragali Radix-Angelicae Sinensis Radix, Notoginseng Radix-Carthami Flos, and Astragali Radix-Salviae Miltiorrhizae Radix, as well as provided a scientific basis for clinical applications of Chinese herb pairs.

A systematic search and collection of studies on Chinese herb pairs in cardiovascular and cerebrovascular diseases was carried out using electronic databases such as PubMed, CNKI, Wan Fang Database, Baidu Scholar, and Web of Science. The keywords searched included Chinese herb pairs, cardiovascular disease, cerebrovascular disease, Astragali Radix, Salviae Miltiorrhizae Radix, Angelicae Sinensis Radix, Carthami Flos, Notoginseng Radix, and so on.

Studies revealed that the Chinese herb pairs had more beneficial effects than single herb and demonstrated a variety of roles in cardiovascular and cerebrovascular diseases. Preclinical studies indicated that Chinese herb pairs are more effective than single herb in treating cardiovascular and cerebrovascular diseases by modulating disease-related pathways and molecular targets. Further research is needed to fully explore their potential. The review also outlined the potential clinical applications of these Chinese herb pairs, highlighting their safety and efficacy.

Chinese herb pairs showed good promise as an alternative therapy for cardiovascular and cerebrovascular diseases due to their multi-component and multi-target characteristics. Consequently, further research was necessary to fully explore the potential of Chinese herb pairs in treating cardiovascular and cerebrovascular diseases, based on the current data.

Ischaemic heart diseases (IHD) are among the major causes of mortality in the elderly population. Although timely reperfusion is a common treatment for IHD, it causes additional damage to the ischaemic myocardium known as ischaemia-reperfusion (IR) injury. Considering the importance of preventing reperfusion injuries, we aimed to examine the combination effect of mitochondrial transplantation (MT) and coenzyme Q10 (CoQ10) in myocardial IR injury of aged male rats. Seventy-two aged male Wistar rats were randomly divided into six groups: Sham, IR, CoQ10, MT, combination therapy (MT + CoQ10) and vehicle. Myocardial IR injury was established by occlusion of the left anterior descending coronary artery followed by reopening. Young male Wistar rats were used as mitochondria donors. Isolated mitochondria were injected intraventricularly (500 µL of a respiration buffer containing 6 × 106 ± 5 × 105 mitochondria/mL) in MT-receiving groups at the onset of reperfusion. CoQ10 (10 mg/kg/day) was injected intraperitoneally for 2 weeks before IR induction. Twenty-four hours after reperfusion, haemodynamic parameters, myocardial infarct size (IS), lactate dehydrogenase (LDH) release and cardiac mitochondrial function (mitochondrial reactive oxygen species (ROS) generation and membrane potential) were measured. The combination of MT and CoQ10 improved haemodynamic index changes and reduced IS and LDH release (P < 0.05). It also decreased mitochondrial ROS generation and increased membrane potential (P < 0.05). CoQ10 also showed a significant cardioprotective effect. Combination therapy displayed greater cardioprotective effects than single treatments. This study revealed that MT and CoQ10 combination treatment can be considered as a promising cardioprotective strategy to reduce myocardial IR injury in ageing, in part by restoring mitochondrial function.

This study investigated the metabolic mechanisms underlying the association between malnutrition and poor prognosis in coronary artery disease (CAD). We hypothesized that specific metabolites associated with nutritional status impact all-cause mortality and Major Adverse Cardiovascular Events in CAD patients. To test this hypothesis, we evaluated the nutritional status of 5182 CAD patients from multiple centers using three nutritional risk screening tools and analyzed the impact on CAD outcomes with restricted cubic splines and Cox regression. Poor nutritional status was found to be linked to increased adverse outcomes. Further analysis using multiple linear regression and mediation analysis identified elevated concentrations of β-pseudouridine and dulcitol, and decreased concentrations of l-tryptophan and LPC (18:2/0:0), among other metabolites, as mediators of this association. Employing Least Absolute Shrinkage and Selection Operator for variable selection, we integrated these metabolites with clinical variables, which significantly improved the predictive accuracy for adverse outcomes. Our results highlight significant metabolic disparities in CAD patients based on nutritional status and provide novel insights into the role of nutrition-associated metabolites in CAD prognosis. These findings suggest that customized nutritional interventions targeting these metabolites could positively influence the progression of CAD.

Acute myocardial infarction is a leading cause of morbidity and mortality worldwide1. Clinical studies have shown that the severity of cardiac injury after myocardial infarction exhibits a circadian pattern, with larger infarcts and poorer outcomes in patients experiencing morning-onset events2-7. However, the molecular mechanisms underlying these diurnal variations remain unclear. Here we show that the core circadian transcription factor BMAL17-11 regulates circadian-dependent myocardial injury by forming a transcriptionally active heterodimer with a non-canonical partner-hypoxia-inducible factor 2 alpha (HIF2A)12-16-in a diurnal manner. To substantiate this finding, we determined the cryo-EM structure of the BMAL1-HIF2A-DNA complex, revealing structural rearrangements within BMAL1 that enable cross-talk between circadian rhythms and hypoxia signalling. BMAL1 modulates the circadian hypoxic response by enhancing the transcriptional activity of HIF2A and stabilizing the HIF2A protein. We further identified amphiregulin (AREG)16,17 as a rhythmic target of the BMAL1-HIF2A complex, critical for regulating daytime variations of myocardial injury. Pharmacologically targeting the BMAL1-HIF2A-AREG pathway provides cardioprotection, with maximum efficacy when aligned with the pathway's circadian phase. These findings identify a mechanism governing circadian variations of myocardial injury and highlight the therapeutic potential of clock-based pharmacological interventions for treating ischaemic heart disease.

Coronary artery disease (CAD), clinically manifested as coronary syndrome (CS), is the leading cause of death and a significant contributor to morbidity worldwide. Elevated serum homocysteine levels have been associated with an increased risk of cardiovascular diseases, including CAD. Despite extensive research, the relationship between serum homocysteine and coronary syndromes with related short-term mortality is still under-studied. The main objective of this study is to evaluate the correlation between serum homocysteine levels and various types of CS, as well as in-hospital mortality in these patients.

This multicenter study included 381 CS patients from Afghanistan, Egypt, and Pakistan tertiary care hospitals. The relation of serum homocysteine levels with different types of CS as well as with in-hospital mortality was measured and analyzed using inferential statistics (ANOVA, Kruskal-Wallis test, Tukey's post-hoc, Pearson correlation, etc.) and regression analysis (Binary regression).

Among 381 patients from both genders, 160 were from Pakistan, 130 from Egypt, and 91 from Afghanistan. There was no significant difference in baseline characteristics, like age, gender, homocysteine level, CS type, and mortality, among the three countries (p > 0.05). The one-way ANOVA, the Kruskal Wallis Test, and Tukey's post hoc test showed a significant difference among different CS groups based on serum homocysteine levels, and Pearson correlation showed a strong correlation between serum homocysteine and CS (r = 0.4). Binary regression analysis showed a 10.5% increase in in-hospital mortality for each 1 µmol/L increase in homocysteine levels.

Serum homocysteine could serve as a valuable biomarker and mortality predictor in CS patients.

Unexpected cardiovascular events are likely to occur within a short period following an acute myocardial infarction (AMI). The sodium-glucose co-transporter 2 inhibitor (SGLT2-I) is a recently recommended drug for the treatment of AMI. However, its role in the risk of the outcomes following an AMI, including all-cause death and heart failure readmission, remains controversial. Therefore, in this study, we explored the effect of SGLT2-Is on cardiovascular outcomes after an AMI.

PubMed, Web of Science, and Embase were searched without language restrictions to retrieve case-control studies published before April 2024. Citations were independently screened by two authors, and the studies meeting the predefined inclusion criteria were retained. Data on author names, year of publication, location of the study group, gender and age of participants, outcome assessment, adjusted odds ratios (ORs) and 95% confidence intervals (CIs), and the follow-up period were extracted.

Eight studies were eligible for inclusion, and these studies showed that the use of SGLT2-Is after an AMI was significantly associated with a lower risk of hospitalization for heart failure (OR: 0.66, 95% CI 0.57-0.76, p < 0.01) and a lower incidence of major cardiovascular adverse events (OR: 0.79, 95% CI 0.70-0.89, p < 0.01), but was unrelated to a lower incidence of all-cause mortality (OR: 0.84, 95% CI 0.69-1.02, p = 0.07).

Compared with placebo, SGLT2-I therapy following an AMI can reduce the risk of heart failure hospitalization and the incidence of major cardiovascular adverse events, but has no effect on all-cause mortality.

CRD42024542335, https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42024542335.

Dietary inflammatory potential and genetic factors are reported as being linked to coronary heart disease (CHD). We aimed to investigate their joint association with CHD incidence.

We included 51 889 British participants from the UK Biobank who completed the 24-h dietary assessment at baseline. We used reduced rank regression and stepwise linear regression analyses to generate an empirical dietary inflammatory pattern (EDIP) score to assess dietary inflammatory potential. A polygenic risk score (PRS) for CHD was constructed based on 1.7 million genetic variants. During a median follow-up of 11 years, 1346 incident cases of CHD were observed. High EDIP scores significantly increased the risk of CHD with the hazard ratio (HR) [95% confidence interval (CI)] of 1.26 (1.10-1.45) for high EDIP scores (T3) compared with low EDIP scores (T1). Interestingly, we observed a gradient in the risk of CHD across PRS categories, with the HRs of 1.12 (95% CI: 0.73-1.71), 1.20 (95% CI: 1.01-1.43), and 1.42 (95% CI: 1.10-1.83) in low (Q1), intermediate (Q2-4), and high (Q5) PRS categories, respectively. When the joint effect was examined, individuals with high PRS (Q5) and high EDIP scores (T3) would have the highest risk of CHD with a HR of 3.87 (95% CI: 2.74-5.46) compared with individuals with both low PRS (Q1) and low EDIP scores.

High dietary inflammatory potential was associated with a higher CHD risk, especially in those with high PRS, suggesting that a comprehensive assessment of inflammatory diet and genetic factors may be beneficial in the prevention of CHD.

The coexistence of anxiety or depression with coronary heart disease (CHD) is a significant clinical challenge in cardiovascular medicine. Recent studies have indicated that hypothalamic-pituitary-adrenal (HPA) axis activity could be a promising focus in understanding and addressing the development of treatments for comorbid CHD and anxiety or depression. The HPA axis helps to regulate the levels of inflammatory factors, thereby reducing oxidative stress damage, promoting platelet activation, and stabilizing gut microbiota, which enhance the survival and regeneration of neurons, endothelial cells, and other cell types, leading to neuroprotective and cardioprotective benefits. This review addresses the relevance of the HPA axis to the cardiovascular and nervous systems, as well as the latest research advancements regarding its mechanisms of action. The discussion includes a detailed function of the HPA axis in regulating the processes mentioned. Above all, it summarizes the therapeutic potential of HPA axis function as a biomarker for coronary atherosclerotic heart disease combined with anxiety or depression.

The effectiveness of statin use in preventing adverse cardiovascular events in individuals with atrial fibrillation (AF) has remained uncertain. This study aimed to assess whether statin use could lead to better outcomes among individuals with AF.

We enrolled 397 787 patients with AF from January 1, 2012 to December 31, 2020. Patients with AF were divided into 2 groups (statin user and statin nonuser), and the risks of composite outcomes (including ischemic stroke, hemorrhagic stroke, and transient ischemic attack), all-cause death, and major adverse cardiovascular events (which encompassed cardiovascular death, myocardial infarction, stroke, and heart failure hospitalization) were analyzed. We analyzed 288 958 patients with newly diagnosed AF (mean age, 73 years; 44% women; mean CHA2DS2-VASc score, 3.5). Compared with patients without statin use, statin users had lower risks of composite end points (adjusted hazard ratio [HR], 0.91 [95% CI, 0.87-0.94]; P<0.01). In regard to all-cause death, statin users exhibited a 67% risk reduction compared with statin nonusers (adjusted HR, 0.33 [95% CI, 0.32-0.33]; P<0.01). Statin use was also associated with reduced incidence of major adverse cardiovascular events (adjusted HR, 0.64 [95% CI, 0.63-0.66]; P<0.01). In the subgroups stratified by CHA2DS2-VASc score, statin therapy was particularly effective for patients with CHA2DS2-VASc scores 0 to 3 for composite end points but consistently reduced all-cause mortality and major adverse cardiovascular events across all score categories.

Among patients with newly diagnosed AF, statin use was associated with lower risk of ischemic stroke, hemorrhagic stroke, transient ischemic attack, all-cause mortality, and major adverse cardiovascular events.

Wnt (wingless-type MMTV integration site family) signaling is an evolutionary conserved system highly active during embryogenesis, but in adult hearts has low activities under normal conditions. It is essential for a variety of physiological processes including stem cell regeneration, proliferation, migration, cell polarity, and morphogenesis, thereby ensuring homeostasis and regeneration of cardiac tissue. Its dysregulation and excessive activation during pathological conditions leads to morphological and functional changes in the heart resulting in impaired myocardial regeneration under pathological conditions such as myocardial infarction, heart failure, and coronary artery disease. Several groups of Wnt inhibitors have demonstrated the ability to modulate the Wnt pathway and thereby significantly reduce fibrosis and improve cardiac function after myocardial ischemia. Their inhibitory effect can be realized at multiple levels, which include the inhibition of Wnt ligands, the inhibition of Frizzled receptors, the stabilization of the β-catenin destruction complex, and the disruption of nuclear β-catenin interactions. In this review, we overview the function of Wnt signaling in responses of cardiac cells to pathological conditions, especially ischemic heart disease, with an emphasis on the use of inhibitors of this signaling as a therapeutic approach. Finally, we summarize the current knowledge about the potential of the targeting of Wnt signaling in therapeutic applications.

There is lack of predictive models for the risk of severe complications during hospitalization in patients with acute myocardial infarction (AMI). In this study, we aimed to create a nomogram to forecast the likelihood of in-hospital severe complications in AMI.

From August 2020 to January 2023, 1024 patients with AMI including the modeling group (n=717) and the validation group (n=307) admitted in Changsha Central Hospital's emergency department. Conduct logistic regression analysis, both univariate and multivariate, on the pertinent patient data from the modeling cohort at admission, identify independent risk factors, create a nomogram to forecast the likelihood of severe complications in patients with AMI, and assess the accuracy of the graph's predictions in the validation cohort.

Age, heart rate, mean arterial pressure, diabetes, hypertension, triglycerides and white blood cells were seven independent risk factors for serious complications in AMI patients. Based on these seven variables, the nomogram model was constructed. The nomogram has high predictive accuracy (AUC=0.793 for the modeling group and AUC=0.732 for the validation group). The calibration curve demonstrates strong consistency between the anticipated and observed values of the nomogram in the modeling and validation cohorts. Moreover, the DCA curve results show that the model has a wide threshold range (0.01-0.73) and has good practicality in clinical practice.

This study developed and validated an intuitive nomogram to assist clinicians in evaluating the probability of severe complications in AMI patients using readily available clinical data and laboratory parameters.

To describe the prevalence of self-reported coronary heart disease (CHD) and assess the influence of varied risk factors on it in Tianjin.

This study included a total of 102,576 individuals aged 35 to 75 from 13 community health centers and grassroots hospitals in Tianjin. Basic information, questionnaire responses, physical examinations, and laboratory tests of each participant were researched, and documented. Participants were categorized into CHD group and non-CHD group. Multivariate logistic regression was utilized to evaluated the relationships between associated factors and CHD.

The prevalence of self-reported CHD was 2.56%, 3.97% among men and 1.69% among women. In multivariate logistic regression analysis, older age (41-65 years: OR: 7.37, 95% CI: 4.56-11.94; >65 years: OR:17.88, 95% CI: 11.02-29.01), female sex (OR: 0.40, 95% CI: 0.36-0.44), education (sedentary level: OR: 0.88, 95% CI: 0.79-0.97; high level: OR: 0.74, 95% CI: 0.63-0.87), family annual income (10,000-50,000 yuan: OR: 0.68, 95% CI: 0.60-0.77; >50,000 yuan: OR: 0.71, 95% CI: 0.62-0.82), recently drinking habits (2-4 times /month: OR: 0.75, 95% CI: 0.63-0.90; 2-3 times/week: OR: 0.69, 95% CI: 0.56-0.86; >4 times/week: OR: 0.72, 95% CI: 0.63-0.83), obesity (OR: 1.17, 95% CI: 1.07-1.28), central obesity (OR: 1.51, 95% CI: 1.33-1.71), hypertension (OR: 1.60, 95% CI: 1.43-1.80), dyslipidemia (OR: 0.90, 95% CI: 0.83-0.98), diabetes mellitus (OR: 2.02, 95% CI: 1.85-2.19), stroke (OR: 1.42, 95% CI: 1.24-1.63), family history (CVD: OR: 4.48, 95% CI: 4.00-5.01; stroke: OR: 1.83, 95% CI: 1.58-2.12) were associated with CHD (P < 0.05).

These findings highlight growing concerns regarding the escalating rates of CHD. Implementing multifaceted, population-based interventions is crucial to mitigate the burden of cardiovascular conditions.

The study received approval from the Ethics Committee of Tianjin Chest Hospital (approval number: 2018KY-003-01). Written informed consent was obtained from all survey participants.

The role of the complement inhibitory proteins CD46 and CD59 in the immune response to an acute coronary syndrome (ACS) is unknown. We investigated the relationships between the shedding of CD46 and CD59 into the circulation, reflected by plasma levels of soluble CD46 and CD59, and the risk for post-ACS complications.

We measured plasma sCD46 and sCD59 in a cohort of 546 ACS patients within 24 h after hospital admission, and after 6-weeks in a subgroup of 114 patients. Study outcomes were incident heart failure (HF), major adverse cardiovascular events (MACE) and mortality during a median follow-up period of up to 3.3 years. Echocardiography at 1-year was performed in the follow-up subgroup.

Elevated sCD46 and sCD59 were correlated with increased levels of inflammatory mediators and metalloproteinases in plasma, and were associated with increased risk for MACE in Cox proportional hazard models adjusted for cardiovascular risk factors and revascularization [HR 95% CI 1.24 (1.02-1.52), p = 0.034 for sCD46 and 1.18 (1.00-1.38), p = 0.049 for sCD59]. Elevated sCD59 was also associated with higher incidence of HF [HR 95% CI 1.41 (1.15-1.74), p = 0.001], and with lower left ventricular ejection fraction at 1-year post-ACS (Spearman r = - 0.234, p = 0.020). We found no associations between plasma levels of the proteins at 6 weeks and outcomes.

Shedding of the complement regulators CD46 and CD59 in plasma in the acute phase of ACS is associated with a negative prognosis. Plasma sCD46 and sCD59 could reflect the degree of local immune activation and serve as prognostic biomarkers in ACS patients.

Myocardial infarction (MI), one of the leading causes of death worldwide, urgently needs further understanding of the pathological process and effective therapies. SO2 in endoplasmic reticulum in several cardiovascular diseases has been reported to be particularly important. However, the role of endogenous SO2 in endoplasmic reticulum in treating myocardial infarction is still ambiguous and needs to be elucidated. Herein, we developed TPA-HI-SO2 as the first endoplasmic reticulum-targeting fluorescent agent for specific imaging and detection of sulfur dioxide derivatives both in vitro and in vivo. TPA-HI-SO2 shows a highly sensitive and selective response to SO2 derivatives over other anions in aqueous solution with a satisfactory response time and detection limit. Furthermore, TPA-HI-SO2 decreased the SO2 concentration in H9C2 cells treated with H2O2 and in an MI mouse model. Most importantly, TPA-HI-SO2 protects H9C2 cells from H2O2-induced apoptosis and obviously protects against myocardial infarction in vivo through neutralization of endogenous SO2. Taken together, we developed the first ER-targeting ratiometric fluorescent probe for endogenous SO2 with excellent biocompatibility, high selectivity and sensitivity in this paper. More importantly, we demonstrated an obvious increase of the endogenous SO2 concentration in a myocardial infarction mouse model for the first time, which suggests that neutralization of endogenous SO2 in endoplasmic reticulum could be a promising therapeutic strategy for myocardial infarction.

Previous lipidomics studies have identified various lipid predictors for cardiovascular risk, however, with limited predictive increment, sometimes using too many predictor variables at the expense of practical efficiency.

To search for lipid predictors of future coronary heart disease (CHD) with stronger predictive power and efficiency to guide primary intervention.

We conducted a prospective nested case-control study involving 1,621 incident CHD cases and 1:1 matched controls. Lipid profiling of 161 lipid species for baseline fasting plasma was performed by liquid chromatography-mass spectrometry.

In search of CHD predictors, seven lipids were selected by elastic-net regression during over 90% of 1000 cross-validation repetitions, and the derived composite lipid score showed an adjusted odds ratio of 3.75 (95% confidence interval: 3.15, 4.46) per standard deviation increase. Addition of the lipid score into traditional risk model increased c-statistic to 0.736 by an increment of 0.077 (0.063, 0.092). From the seven lipids, we found mediation of CHD risk from baseline diabetes through sphingomyelin (SM) 41:1b with a considerable mediation proportion of 36.97% (P < 0.05). We further found that the positive associations of phosphatidylcholine (PC) 36:0a, SM 41:1b, lysophosphatidylcholine (LPC) 18:0 and LPC 20:3 were more pronounced among participants with higher exposure to fine particulate matter or its certain components, also to ozone for LPC 18:0 and LPC 20:3, while the negative association of cholesteryl ester (CE) 18:2 was attenuated with higher black carbon exposure (P < 0.05).

We identified seven lipid species with greatest predictive increment so-far achieved for incident CHD, and also found novel biomarkers for CHD risk stratification among individuals with diabetes or heavy air pollution exposure.

Epidemiologic associations estimated from observational data are often confounded by genetics due to pervasive pleiotropy among complex traits. Many studies either neglect genetic confounding altogether or rely on adjusting for polygenic scores (PGS) in regression analysis. In this study, we unveil that the commonly employed PGS approach is inadequate for removing genetic confounding due to measurement error and model misspecification. To tackle this challenge, we introduce PENGUIN, a principled framework for polygenic genetic confounding control based on variance component estimation. In addition, we present extensions of this approach that can estimate genetically unconfounded associations using GWAS summary statistics alone as input and between multiple generations of study samples. Through simulations, we demonstrate superior statistical properties of PENGUIN compared to the existing approaches. Applying our method to multiple population cohorts, we reveal and remove substantial genetic confounding in the associations of educational attainment with various complex traits and between parental and offspring education. Our results show that PENGUIN is an effective solution for genetic confounding control in observational data analysis with broad applications in future epidemiologic association studies.

Cardiovascular diseases are characterized by chronic inflammation, leading to increased inflammatory markers that can cause cell damage and death. Phase angle has emerged as a marker of cellular health. It is considered a prognostic factor in various acute and chronic conditions. However, few studies have examined its association with cardiovascular disease risk measures. This study aims to investigate the relationship between phase angle, the general Framingham risk score, and the HEARTS cardiovascular risk score.

This cross-sectional study included a convenience sample of adult patients of 2 primary health care services. Phase angle was measured using multifrequency bioimpedance analysis at 50 kHz. The risk of cardiovascular events was calculated using the Framingham and HEARTS risk scores. Statistical analysis included generalized linear regression models, unadjusted and adjusted according to sex and age, to determine the association between scores, risk factors, and phase angle.

The study included 164 individuals with a mean age 52.2 (SD 17.9). According to the HEARTS score, low-risk patients had higher phase angle values than those with high or very high risk [ß = -0.57 (95% CI -0.95; -0.19), P = 0.003]. Framingham scores showed a trend toward significance for higher mean phase angle values in low-risk than high-risk patients [ß = -0.43 (95% CI -0.88 to 0.02), P = 0.06].

Phase angle values were lower in high and very high-risk patients than in low-risk patients, which shows that phase angle is a promising risk predictor for patients with cardiovascular diseases.

Coronary artery bypass graft (CABG) is one of the preferred treatments for patients with heart problems, especially in individuals with other comorbidities and when multiple arteries are narrowed. This study aimed to assess the effects of administrating curcumin-piperine on patients who underwent CABG surgery.

This was a randomized, double-blind, placebo-controlled clinical trial, in which 80 eligible adults who underwent CABG surgery, were randomized into 4 groups. Patients received 3 tablets daily for 5 days after the surgery, which contained curcumin-piperine (each tablet contained 500 mg curcumin +5 mg piperine) or a placebo (each tablet contained 505 mg maltodextrin). Group A received 3 placebo tablets, group B received 2 placebos and one curcumin-piperine tablet, group C received 1 placebo and 2 curcumin-piperine tablets, and group D received 3 curcumin-piperine tablets. Before and after the intervention, C-reactive protein (CRP), total antioxidant capacity (TAC), cardiometabolic factors, clinical outcomes, and 28-day mortality were evaluated.

Between-group analysis showed that CRP significantly decreased (P = 0.028), and TAC significantly increased (P = 0.033) after the intervention (Post hoc analysis showed that for CRP, the difference was between group B and D, and for TAC was between group C and D). Between-group analysis also showed that creatine kinase mono-phosphate (CK-MB) marginally reduced (P = 0.077); however, changes for troponin I (P = 0.692), lactate dehydrogenase (LDH) (P = 0.668), ejection fraction (P = 0.340), and arterial fibrillation (P = 0.99) were not significant. Blood urea nitrogen (P = 0.820) and serum creatinine (P = 0.244) did not show notable changes between groups.

Supplementation with curcumin-piperine had a promising effect on serum CRP and TAC. It also had a favorable impact on CK-MB among patients who underwent CABG surgery.

IRCT20201129049534N4, available on https://en.irct.ir/trial/56930.

It has been previously demonstrated that the maintenance of ischemic acidic pH or the delay of intracellular pH recovery at the onset of reperfusion decreases ischemic-induced cardiomyocyte death.

To examine the role played by nitric oxide synthase (NOS)/NO-dependent pathways in the effects of acidic reperfusion in a regional ischemia model.

Isolated rat hearts perfused by Langendorff technique were submitted to 40 min of left coronary artery occlusion followed by 60 min of reperfusion (IC). A group of hearts received an acid solution (pH = 6.4) during the first 2 min of reperfusion (AR) in absence or in presence of l-NAME (NOS inhibitor). Infarct size (IS) and myocardial function were determined. In cardiac homogenates, the expression of P-Akt, P-endothelial and inducible isoforms of NOS (P-eNOS and iNOS) and the level of 3-nitrotyrosine were measured. In isolated cardiomyocytes, the intracellular NO production was assessed by confocal microscopy, under control and acidic conditions. Mitochondrial swelling after Ca2+ addition and mitochondrial membrane potential (Δψ) were also determined under control and acidosis.

AR decreased IS, improved postischemic myocardial function recovery, increased P-Akt and P-eNOS, and decreased iNOS and 3-nitrotyrosine. NO production increased while mitochondrial swelling and Δψ decreased in acidic conditions. l-NAME prevented the beneficial effects of AR.

Our data strongly supports that a brief acidic reperfusion protects the myocardium against the ischemia-reperfusion injury through eNOS/NO-dependent pathways.

Introduction The risk of sudden death in patients with chronic coronary syndrome (CCS) is increased by unbalanced cardiovascular autonomic function. Since myocardial ischemia appears to be the cause of this condition of autonomic dysregulation, treating this condition should improve and correct the autonomic functions. Improving myocardial perfusion by PCI might have beneficial effects on the recovery of autonomic balance in ischemia-triggered autonomic dysregulation. Objective In the present study, autonomic modulation in patients with CCS was evaluated before and after percutaneous coronary intervention (PCI) using cardiovascular reflex tests. Methods A total of 30 CCS patients were recruited from the cardiology outpatient department. The patients were tested with cardiovascular reflex tests (lying to standing, 30:15 ratio, Valsalva ratio, isometric handgrip test, and deep breathing test) before and after PCI. The licensed statistical software SPSS version 21.0 was used to compile and analyse the data. Results Out of 30 patients, parasympathetic reactivity tests conducted post-PCI were significantly higher as compared to pre-PCI patients: (1) lying to standing - 30:15 ratio (1.17± 0.102 versus 1.03± 0.064, p=0.000); (2) Valsalva ratio (1.42±0.276 versus 1.02±0.133, p=0.000), (3) delta heart rate in deep breathing test (17.23± 3.004 bpm versus 7.85± 4.076 bpm, p=0.000), and (4) expiration to inspiration (E:I) ratio (1.25± 0.050 versus 1.11± 0.064, p=0.000. Among sympathetic reactivity tests, lying to standing test for fall in systolic blood pressure was significantly higher in the pre-PCI state than post-PCI (-20.73± 10.29 versus -2.33± 7.67, p=0.000). The rise in DBP of the isometric handgrip test was significantly higher in post-PCI compared to pre-PCI patients (36.73±8.39 mm Hg versus 16.63±8.47 mm Hg, p=0.000). Conclusion Resting autonomic tone as determined by cardiovascular reflex testing reveals an increase in both parasympathetic and sympathetic reactivity following PCI in CCS, according to the findings of this preliminary study. As a result, we propose that noninvasive procedures like cardiovascular reflex tests be used to stratify the likelihood of illness development in the future.

Cardiovascular diseases are the leading cause of morbidity and mortality in the United States. Despite the complexity of cardiovascular disease etiology, we do not fully comprehend the interactions between non-modifiable factors (e.g., age, sex, and race) and modifiable risk factors (e.g., health behaviors and occupational exposures).

We examined proximal and distal drivers of cardiovascular disease and elucidated the interactions between modifiable and non-modifiable risk factors.

We used a machine learning approach on four cohorts (2005-2012) of the National Health and Nutrition Examination Survey data to examine the effects of risk factors on cardiovascular risk quantified by the Framingham Risk Score (FRS) and the Pooled Cohort Equations (PCE). We estimated a network of risk factors, computed their strength centrality, closeness, and betweenness centrality, and computed a Bayesian network embodied in a directed acyclic graph.

In addition to traditional factors such as body mass index and physical activity, race and ethnicity and exposure to heavy metals are the most adjacent drivers of PCE. In addition to the factors directly affecting PCE, sleep complaints had an immediate adverse effect on FRS. Exposure to heavy metals is the link between race and ethnicity and FRS.

Heavy metal exposures and race/ethnicity have similar proximal effects on cardiovascular disease risk as traditional clinical and lifestyle risk factors, such as physical activity and body mass. Our findings support the inclusion of diverse racial and ethnic groups in all cardiovascular research and the consideration of the social environment in clinical decision-making.

There is limited research on the relationship between Systemic Oxidative Stress (SOS) status and inflammatory indices. Adding onto existing literature, this study aimed to examine the association between dietary Oxidative Balance Score (OBS) and lifestyle OBS (which make up the overall OBS), and Cardiovascular Disease (CVD) prevalence at different Systemic Immune Inflammation Index (SII) and Systemic Inflammatory Response Index (SIRI) levels.

This study involved 9,451 subjects selected from the National Health and Nutrition Examination Survey (NHANES) 2007-2018. The OBS comprised 20 dietary and lifestyle factors. Statistical methods included Weighted Linear Regression Analysis (WLRA), Logistic Regression Analysis (LRA), Sensitivity Analysis (SA), and Restricted Cubic Spline (RCS) analysis.

The multivariate WLRA revealed that OBS was significantly negatively correlated with both SII (β = -5.36, p < 0.001) and SIRI (β = -0.013, p < 0.001) levels. In SA, removing any single OBS component had no significant effect on the WLRA results of SII and SIRI. Further subgroup analyses revealed that OBS was more impactful in lowering SII in women than in men. Additionally, OBS was more significantly negatively correlated with SII and SIRI in the low-age group than in the high-age group. Moreover, RCS analysis confirmed this linear relationship. Compared to dietary OBS, lifestyle OBS exerted a more significant effect on Coronary Artery Disease (CAD) (OR: 0.794, p = 0.002), hypertension (OR: 0.738, p < 0.001), Congestive Heart Failure (CHF) (OR: 0.736, p = 0.005), Myocardial Infarction (MI) (OR: 0.785, p = 0.002), and stroke (OR: 0.807, p = 0.029) prevalence. Furthermore, SIRI exhibited a significant interaction in the relationship between overall OBS, dietary OBS, and CHF (P for interaction < 0.001). On the other hand, SII had a significant interaction in the relationship between overall OBS, dietary OBS, and MI (P for interaction < 0.05).

OBS, including lifestyle and dietary OBS, were significantly negatively associated with SII and SIRI. Higher lifestyle OBS was associated with reduced risks of CAD, hypertension, CHF, MI, and stroke.

Radix Salviae miltiorrhizae, also known as Danshen in Chinese, effectively activates the blood and resolves stasis. Total salvianolic acids (SA) is the main active ingredient of Danshen, and related preparations, such as salvianolate injection are commonly used clinically to treat myocardial ischemia-reperfusion injury (MIRI). However, the potential targets and key active ingredients of SA have not been sufficiently investigated.

This study aimed to investigate the mechanism of action of SA in treating MIRI.

Network pharmacology and molecular docking techniques were used to predict SA targets against MIRI. The key acting pathway of SA were validated by performing experiments in a rat MIRI model.

Twenty potential ingredients and 54 targets of SA in treating MIRI were identified. Ingredient-target-pathway network analysis revealed that salvianolic acid B and rosmarinic acid had the highest degree value. Pathway enrichment analysis showed that SA may regulate MIRI through the IL-17 signaling pathway, and this result was confirmed in the rat MIRI experiment.

The results of this study indicate that SA may protect MIRI by regulating the IL-17 pathway.

Acute myocardial infarction (AMI) represents the leading cause of cardiovascular death worldwide, and it is thus pivotal to develop effective approaches for the timely detection of AMI markers, especially possessing the characteristics of antibody-free, signal amplification, and manipulation convenience. We herein construct a MoS2 nanosheet-powered CRISPR/Cas12a sensing strategy for sensitive determination of miR-499, a superior AMI biomarker to protein markers. The presence of miR-499 at a trace level is able to induce a significantly enhanced fluorescence signal in a DNA-based molecular engineering platform, which consists of CRISPR/Cas12a enzymatic reactions and MoS2 nanosheet-controllable signal reporting components. The MoS2 nanosheets were characterized by using atomic force microscopy (AFM) and transmission electron microscope (TEM). The detection feasibility was verified by using polyacrylamide gel electrophoresis (PAGE) analysis and fluorescence measurements. The detection limit is determined as 381.78 pM with the linear range from 0.1 ⅹ 10-9 to 13.33 ⅹ 10-9 M in a fast manner (about 30 min). Furthermore, miRNA detection in real human serum is also conducted with desirable recovery rates (89.5 %-97.6 %), which may find potential application for the clinic diagnosis. We describe herein the first example of MoS2 nanosheet-based signal amplified fluorescence sensor for effective detection of AMI-related miRNA.

Metabolic disorders (MDs), including dyslipidemia, non-alcoholic fatty liver disease, diabetes mellitus, obesity and cardiovascular diseases are a significant threat to human health, despite the many therapies developed for their treatment. Different classes of bioactive compounds, such as polyphenols, flavonoids, alkaloids, and triterpenes have shown therapeutic potential in ameliorating various disorders. Most of these compounds present low bioavailability when administered orally, being rapidly metabolized in the digestive tract and liver which makes their metabolites less effective. Moreover, some of the bioactive compounds cannot fully exert their beneficial properties due to the low solubility and complex chemical structure which impede the passive diffusion through the intestinal cell membranes. To overcome these limitations, an innovative delivery system of phytosomes was developed. This review aims to highlight the scientific evidence proving the enhanced therapeutic benefits of the bioactive compounds formulated in phytosomes compared to the free compounds. The existing knowledge concerning the phytosomes' preparation, their characterization and bioavailability as well as the commercially available phytosomes with therapeutic potential to alleviate MDs are concisely depicted. This review brings arguments to encourage the use of phytosome formulation to diminish risk factors inducing MDs, or to treat the already installed diseases as complementary therapy to allopathic medication.

The associations of changes in sleep patterns with incident cardiovascular disease (CVD) are not fully elucidated, and whether these associations are modified by genetic susceptibility remains unknown.

To investigate the associations of 5-year changes in sleep patterns with incident CVD and whether genetic susceptibility modifies these associations.

This prospective cohort study of the Dongfeng-Tongji cohort was conducted from 2008 to 2018 in China. Eligible participants included those with complete sleep information at baseline survey (2008-2010) and the first follow-up survey (2013); participants who had no CVD or cancer in 2013 were prospectively assessed until 2018. Statistical analysis was performed in November 2023.

Five-year changes in sleep patterns (determined by bedtime, sleep duration, sleep quality, and midday napping) between 2008 and 2013, and polygenic risk scores (PRS) for coronary heart disease (CHD) and stroke.

Incident CVD, CHD, and stroke were identified from 2013 to 2018. Cox proportional hazards regression models were applied to estimate hazard ratios (HRs) and 95% CIs.

Among 15 306 individuals (mean [SD] age, 65.8 [7.4] years; 8858 [57.9%] female and 6448 male [42.1%]), 5474 (35.78%) had persistent unfavorable sleep patterns and 3946 (25.8%) had persistent favorable sleep patterns. A total of 3669 incident CVD cases were documented, including 2986 CHD cases and 683 stroke cases, over a mean (SD) follow-up of 4.9 (1.5) years. Compared with those with persistent unfavorable sleep patterns, individuals with persistent favorable sleep patterns over 5 years had lower risks of incident CVD (HR, 0.80; 95% CI, 0.73-0.87), CHD (HR, 0.84; 95% CI, 0.76-0.92), and stroke (HR, 0.66; 95% CI, 0.54-0.82) in the subsequent 5-year period. No significant effect modification by PRS was observed for sleep pattern change and CHD or stroke risk. However, sleep pattern changes and PRS were jointly associated with the CHD and stroke risk in a dose-dependent manner, with the lowest risk being among those with persistent favorable sleep patterns combined with low PRS (HR for CHD, 0.65; 95% CI, 0.52-0.82 and HR for stroke, 0.48; 95% CI, 0.29-0.79).

In this cohort study of middle-aged and older Chinese adults, individuals with persistent favorable sleep patterns had a lower CVD risk, even among those with higher genetic risk. These findings highlight the importance of maintaining favorable sleep patterns for CVD prevention.

Myosteatosis, rather than low muscle mass, is the primary etiologic factor of sarcopenia in patients with type 2 diabetes mellitus (T2DM). Myosteatosis may lead to a series of metabolic dysfunctions, such as insulin resistance, systematic inflammation, and oxidative stress, and all these dysfunctions are closely associated with the acceleration of T2DM and atherosclerosis.

To investigate the association between myosteatosis and coronary artery calcification (CAC) in patients with T2DM.

Patients with T2DM, who had not experienced major cardiovascular events and had undergone both abdominal and thoracic computed tomography (CT) scans, were included. The mean skeletal muscle attenuation was assessed using abdominal CT images at the L3 level. The CAC score was determined from thoracic CT images using the Agatston scoring method. Myosteatosis was diagnosed according to Martin's criteria. Severe CAC (SCAC) was defined when the CAC score exceeded 300. Logistic regression and decision tree analyses were performed.

A total of 652 patients with T2DM were enrolled. Among them, 167 (25.6%) patients had SCAC. Logistic regression analysis demonstrated that myosteatosis, age, duration of diabetes, cigarette smoking, and alcohol consumption were independent risk factors of SCAC. Myosteatosis was significantly associated with an increased risk of SCAC (OR = 2.381, P = 0.003). The association between myosteatosis and SCAC was significant in the younger patients (OR = 2.672, 95%CI: 1.477-4.834, P = 0.002), but not the older patients (OR = 1.456, 95%CI: 0.863-2.455, P = 0.188), and was more prominent in the population with lower risks of atherosclerosis. The decision tree analyses prioritized older age as the primary variable for SCAC. In older patients, cigarette smoking was the main contributing factor for SCAC, while in younger patients, it was myosteatosis.

Myosteatosis is a novel risk factor for atherosclerosis in patients with T2DM, especially in the population with younger ages and fewer traditional risk factors.

Opium abuse and exposure to heavy metals elevate the risk of coronary artery disease (CAD). Therefore, we aimed to determine the association between opium abuse and blood lead levels (BLLs) and the CAD complexity. We evaluated patients with acute coronary symptoms who underwent coronary angiography, and those with >50% stenosis in at least one of the coronary arteries were included. Furthermore, Synergy between PCI with Taxus and Cardiac Surgery I (SYNTAX I) score and BLLs were measured. Based on the opium abuse, 95 patients were subdivided into opium (45) and control (50) groups. Differences in demographics and CAD risk factors were insignificant between the two groups. The median BLLs were remarkably higher in the opium group than in controls (36 (35.7) and 20.5 μg/dL (11.45), respectively, p = 0.003). We also revealed no significant differences in SYNTAX score between the two groups (15.0 (9.0) and 17.5 (14.0), respectively, p = 0.28). Additionally, we found no significant correlation between BLLs and the SYNTAX scores (p = 0.277 and r = -0.113). Opium abuse was associated with high BLLs. Neither opium abuse nor high BLLs were correlated with the complexity of CAD. Further studies are warranted to establish better the relationship between opium abuse, BLLs, and CAD.

Mediation analysis aims to determine how intermediate variables affect exposure to disease. In this study, 25-hydroxyvitamin D (25(OH)D) was evaluated to assess its role in mediating heavy metal exposure and cardiovascular disease (CVD).

A total of 9,377 participants from the National Health and Nutrition Examination Survey (NHANES) for the years 2011-2018 were included. Firstly, restricted cubic spline (RCS), and multivariable logistic regression model were performed to estimate the association between heavy metal exposure (Cadmium, Lead, Mercury, Manganese, and Selenium), as well as serum 25(OH)D and CVD. Secondly, using generalized linear regression model and generalized additive models with smooth functions, we investigated the correlation between heavy metal exposure and serum 25(OH)D. Finally, the mediation effect of serum 25(OH)D in the associations between heavy metal exposure and CVD was explored.

The RCS plots revealed that Cadmium, and Lead were positively and linearly associated with CVD, while Mercury, and Manganese were inversely and linearly associated with CVD. Additionally, a roughly L- and U-shaped relationship existed between Selenium, as well as 25(OH)D and CVD. When potential confounding factors were adjusted for, serum 25(OH)D had negative associations with Cadmium, Lead, and Manganese, while serum 25(OH)D had positive relationship with Selenium. There was a mediation effect between Manganese exposure and CVD, which was mediated by 25(OH)D.

According to the mediation analysis, the negative association between Manganese exposure and incident CVD was increased by 25(OH)D. The increasing dietary intake of Vitamin D could increase the protective effect of manganese intake on CVD.

Epidemiologic associations estimated from observational data are often confounded by genetics due to pervasive pleiotropy among complex traits. Many studies either neglect genetic confounding altogether or rely on adjusting for polygenic scores (PGS) in regression analysis. In this study, we unveil that the commonly employed PGS approach is inadequate for removing genetic confounding due to measurement error and model misspecification. To tackle this challenge, we introduce PENGUIN, a principled framework for polygenic genetic confounding control based on variance component estimation. In addition, we present extensions of this approach that can estimate genetically-unconfounded associations using GWAS summary statistics alone as input and between multiple generations of study samples. Through simulations, we demonstrate superior statistical properties of PENGUIN compared to the existing approaches. Applying our method to multiple population cohorts, we reveal and remove substantial genetic confounding in the associations of educational attainment with various complex traits and between parental and offspring education. Our results show that PENGUIN is an effective solution for genetic confounding control in observational data analysis with broad applications in future epidemiologic association studies.

The existing literature has explored carpal tunnel syndrome (CTS) and determined that it could be a risk for coronary artery disease (CAD), but there has been little research comparing the relevance of CAD with other neuromuscular disorders (NMDs) to CTS. This case-control study explored the association between CTS, stenosing tenosynovitis (ST), and ulnar side NMDs and CAD. The study utilized data from Taiwan's National Health Insurance Research Database, focusing on health insurance claims. Between January 2000 and December 2011, we employed the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) diagnostic codes to identify 64,025 CAD patients as the case group. The control group consisted of an equal number of individuals without CAD, matched for age, sex, and index year of CAD. Logistic regression analysis was employed to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) for each variable. Multivariate analysis, after adjusting for sociodemographic factors and comorbidities, revealed a significantly higher likelihood of a previous diagnosis of CTS in the CAD group compared to the comparison control group. However, neither ST nor the ulnar side NMDs had any statistical significance. These results indicated that median nerve injury, rather than other NMDs, may uniquely serve as a predisposing factor of CAD.

Strategies targeting standard modifiable cardiovascular risk factors (SMuRFs), including hypertension, diabetes, hypercholesterolemia, and smoking, have been well established to prevent coronary heart disease. However, few studies have evaluated the management and outcomes of older patients without SMuRFs after myocardial infarction.

The authors sought to evaluate the profile of patients with ST-segment elevation myocardial infarction (STEMI) aged ≥75 years without SMuRFs.

This study is based on the CCC-ACS (Improving Care for Cardiovascular Disease in China-Acute Coronary Syndrome) project. Patients aged ≥75 years with a first presentation of STEMI were enrolled in this study between November 2014 and December 2019. Modified Poisson regression was used to evaluate the association between SMuRF-less and in-hospital outcomes.

Among 10,775 patients with STEMI aged ≥75 years, 1,633 (15.16%) had no SMuRFs. Compared with those with SMuRF, SMuRF-less patients received less evidence-based treatment. In-hospital mortality was similar among patients with and without SMuRFs (5.44% vs 5.14%; P = 0.630). However, after adjustment for patient characteristics and treatment, being SMuRF-less was significantly associated with a reduced risk of mortality (RR: 0.80; 95% CI: 0.65-0.99; P = 0.043). SMuRF-less patients also had a significantly reduced risk of in-hospital death when only adjusting for in-hospital treatment (RR: 0.78; 95% CI: 0.63-0.98; P = 0.030), regardless of patient characteristics.