Abstract:With the significant improvement of cancer survival rate, coronary heart disease has become the main non-cancer cause of death in long-term cancer survivors. Cancer patients have specific risk challenges compared with ordinary patients, including cardiovascular toxicity caused by anti-tumor therapy, atypical clinical manifestations, and limitations in the applicability of traditional risk assessment tools. This makes the diagnosis and treatment of coronary heart disease in cancer patients challenging. In recent years, machine learning (ML) has developed rapidly in the medical field.In order to optimize the diagnosis and treatment process of coronary heart disease in cancer patients, researchers have developed a large number of ML models that integrate multimodal information such as clinical features, imaging information and laboratory examination. The application of ML improves the predictive ability of coronary heart disease risk and the sensitivity of early screening in cancer patients, and avoids subjective errors in traditional diagnostic models. It can also guide doctors to implement personalized treatment for patients and improve their prognosis. This review summarizes the typical application of ML in the diagnosis and treatment of coronary heart disease, discusses the research status and challenges of ML in the diagnosis and treatment of coronary heart disease, and looks forward to its future clinical application trend.

Abstract:Aim To investigate whether maternal exercise can reduce the susceptibility of adult offspring from obese dams to cerebral ischemia-reperfusion injury. Methods Female C57BL/6J mice were fed either normal chow diet (NCD, 10% kCal from fat) or high-fat diet (HFD, 60% kCal from fat) starting at 5 weeks of age. After 8 weeks, the female mice were randomly assigned to four groups:normal chow diet and sedentary (NCD-SED), normal chow diet and exercise (NCD-EX), high-fat diet and sedentary (HFD-SED), and high-fat diet and exercise (HFD-EX). The female mice in the exercise groups underwent unloaded swimming (32～34 ℃, 20 cm deep, for 60 min/day, 6 days/week). After the 4-week exercise intervention, female mice were paired with males fed a normal diet for mating at a 2∶1 ratio. The day when a vaginal plug was detected and sperm were verified by vaginal cytology was defined as gestational day 1 (GD1). During gestation, exercise was continued for dams in the exercise groups (45 min/day, 5 days/week). Maternal pre-pregnancy body weight, body composition and glucose tolerance were assessed, and fetal growth parameters and placental efficiency were evaluated at term. Subsequently, 3-month-old offspring were selected as research subjects to establish the transient middle cerebral artery occlusion/reperfusion (tMCAO/R) model, and the cerebral infarct area was measured. Results (1) Pre-pregnancy body weight, body fat percentage, and the area under the curve for the glucose tolerance test were significantly higher in HFD-SED dams than those in NCD-SED dams (P＜0.01), whereas these metrics were significantly lower in HFD-EX dams than those in HFD-SED dams (P＜0.05). (2) Body weight during gestational was consistently higher in the HFD-SED group than that in the NCD-SED group (P＜0.05). From GD15 to GD18, the body weight of HFD-EX dams was significantly lower than that of HFD-SED dams (P＜0.05). There was no significant difference in litter size among the groups. (3) No significant difference was observed in the body length of fetuses among all groups (P＞0.05). The HFD-SED group exhibited significantly higher fetal weight and placental weight (P＜0.01), but significantly lower placental efficiency (P＜0.01) than those in the NCD-SED group. Conversely, fetal weight and placental weight were significantly decreased, while placental efficiency was significantly increased in the HFD-EX group compared with the HFD-SED group (P＜0.01). (4) At 3 months of age, the body weight and body fat of both male and female offspring were significantly higher in the HFD-SED group than in the NCD-SED group, whereas they were significantly decreased in the HFD-EX group compared with the HFD-SED group (P＜0.05). (5) Compared with the NCD-SED group, offspring of the HFD-SED group showed a significantly larger cerebral infarct area induced by tMCAO/R injury (P＜0.05). However, maternal exercise significantly reduced the infarct area in the offspring of the HFD-EX group (P＜0.05). Conclusion Maternal aerobic exercise mitigates high-fat diet-induced fetal overgrowth and excessive adiposity in adult offspring, and reduces their susceptibility to cerebral ischemia-reperfusion injury.

Abstract:Aim To explore the effects of pyruvate dehydrogenase kinase isoenzyme 1 (PDK1) on endothelial cell injury and dysfunction. Methods siRNA-PDK1 was used to knock down PDK1 expression, and human umbilical vein endothelial cells (HUVEC) were treated with phosphate-buffered saline (PBS) or oxidized low density lipoprotein (ox-LDL) to investigate the role of PDK1 in ox-LDL-induced vascular endothelial cell injury and its biological dysfunction.Reactive oxygen species (ROS) production and mitochondrial damage in HUVEC were detected using ROS and mitochondrial activity staining kits. The apoptosis levels of HUVEC were detected via flow cytometry apoptosis assay kit, and the damage of HUVEC and its changes in recruitment and adhesion ability to THP-1 cells were detected through crystal violet staining and Dil staining. The mRNA and protein expression of CD86, CD206, NOD-like receptor protein 3 (NLRP3), interleukin-1β (IL-1β) and monocyte chemoattractant protein-1 (MCP-1) were detected by Western blot and RT-qPCR.The expression levels of CD86 and CD206 were evaluated by immunofluorescence staining. Superoxide dismutase (SOD) and malondialdehyde (MDA) concentrations were measured with corresponding kits, while the secretions of cytokines including MCP-1, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were detected with ELISA kits. Results Compared with HUVEC treated with ox-LDL, knocking down PDK1 expression resulted in reduced ROS production, reduced mitochondrial damage, restored SOD activity, decreased MDA concentrations, decreased apoptosis levels, inhibited activation of nuclear factor-κB (NF-κB) and NLRP3 inflammasomes, decreased release of inflammatory factors (IL-1β and IL-18) and chemokines (MCP-1, ICAM-1 and VCAM-1), decreased number of THP-1 cells, increased expression of CD206 and arginine-1 (Arg-1) in THP-1 cells, and inhibited expression of CD86 and inducible nitric oxide synthase (iNOS) in THP-1 cells (all P＜0.05). Conclusion Knocking down the expression of PDK1 in endothelial cells can reduce oxidative stress and inflammatory response caused by ox-LDL, thereby improving the biological function of endothelial cells.

Abstract:Aim To investigate the correlation between atherogenic index of plasma (AIP) and the occurrence of coronary in-stent neoatheroma (ISNAM) after coronary stent implantation. Methods A total of 164 consecutive patients with coronary in-stent restenosis (ISR) who were admitted to the Department of Cadiology, Beijing Anzhen hospital and underwent coronary intravascular optical coherence tomography from January 2019 to December 2021 were enrolled. Patients were divided into ISNAM group (75 cases) and non-ISNAM (89 cases) based on the presence of ISNAM. AIP and other clinical features were compared between the two groups. Logistic regression analysis was used to evaluate the risk of ISNAM occurrence. The receiver operating characteristic (ROC) curve was used to analyze the predictive efficacy of AIP.Results The proportions of patients admitted for acute coronary syndrome (ACS) and patients with hypertension in the ISNAM group were significantly higher than those in the non-ISNAM group (P＜0.05). The glycated hemoglobin level in the ISNAM group was 1.1 times that of the non-ISNAM group (P＜0.05), and the AIP was 2.4 times that of the non-ISNAM group (P＜0.01). Logistic regressions analysis showed that longer duration since coronary stent implantation, hypertension, and elevated AIP were independent risk factors for coronary ISNAM. The area under the curve (AUC) of AIP for predicting neoatheroma was 0.664 (95%CI:0.561～0.767, P＝0.003). Conclusion Elevated AIP was an independent risk factor for ISNAM after coronary stent implantation. Beyond strict control of low density lipoprotein cholesterol, clinicians should also improve the overall lipid profile to correct metabolic abnormalities and enhance patient prognosis.

Abstract:Aim To explore the relationship between monocyte-to-high density lipoprotein ratio (MHR), triglyceride-glucose index (TyG) and restenosis after drug-coated balloon therapy for coronary artery in-situ stenosis lesions. Methods From January 2022 to December 4,5 patients who underwent drug-coated balloon dilatation and subsequent coronary angiography re-examination were included. According to the results of re-examination, they were divided into non-stenosis group (59 cases) and restenosis group (56 cases). Univariate/multivariate regression analysis, correlation analysis and ROC curve analysis were used to evaluate the effect and predictive value of MHR and TyG on the occurrence of restenosis. Results Compared with the non-stenosis group, the proportion of diabetic patients, monocyte count, fasting blood glucose, triglyceride, low density lipoprotein cholesterol, lipoprotein (a), MHR and TyG were significantly increased in the restenosis group (P＜0.05). Logistic regression analysis showed that elevated levels of MHR and TyG were independent risk factors for restenosis after drug-coated balloon dilatation. Moreover, MHR and TyG were positively correlated with the occurrence of restenosis after drug-coated balloon therapy. ROC curve analysis showed that MHR and TyG had good predictive value for restenosis after drug-coated balloon therapy, and the predictive value of their combined use was further enhanced. Conclusion The elevated levels of MHR and TyG are significantly correlated with the risk of restenosis after drug-coated balloon therapy for in-situ coronary stenosis, and they serve as potential indicators for effectively predicting the occurrence of restenosis.

Abstract:Aim To investigate the correlation between inter-arm systolic blood pressure difference (sIAD), inter-ankle systolic blood pressure difference (sIAND) and subclinical target organ damage (including left ventricular hypertrophy, arteriosclerosis, proteinuria, and composite target organ damage). Methods This study enrolled 2 069 participants from the 2023 follow-up of the Hanzhong Pediatric Hypertension Research cohort. sIAD and sIAND were measured using a non-invasive automatic waveform analyzer. Participants were divided into normal and abnormal sIAND groups based on sIAND values of ＜10 mmHg or ≥10 mmHg. Logistic regression analysis was used to assess the relationships between sIAD, sIAND and subclinical target organ damage. Restricted cubic spline models were employed to evaluate the dose-response relationship between sIAD, sIAND and composite target organ damage. The area under the receiver operating characteristic curve (AUC) was used to compare the diagnostic performance of different criteria for sIAD and sIAND in identifying subclinical target organ damage. Results The participants had an average age of 48.28 years, with 46.7% being female. There were 1 466 individuals with normal sIAND and 603 with abnormal sIAND. After adjusting for multiple confounding factors, sIAD was significantly associated with an increased risk of arterial stiffness (OR＝1.2,5%CI:1.00～1.04). However, sIAD was not significantly associated with left ventricular hypertrophy (LVH), proteinuria, or composite target organ damage. Compared with the normal sIAND group, the abnormal sIAND group had significantly higher risks of LVH (OR＝1.2,5%CI:1.18～2.50), arterial stiffness (OR＝1.5,5%CI:1.33～2.06), proteinuria (OR＝1.8,5%CI:1.36～2.33), and composite target organ damage (OR＝1.6,5%CI:1.43～2.15). Restricted cubic spline models indicated a significant linear association between sIAND and subclinical target organ damage (P for linearity ＜0.001), whereas no significant linear or nonlinear relationships were observed for sIAD. Furthermore, in terms of diagnostic efficacy for composite target organ damage, the combined use of sIAD and sIAND showed comparable efficacy to using sIAND alone, whereas using sIAD alone was significantly less effective. Conclusion sIAND, but not sIAD, is significantly associated with subclinical target organ damage, suggesting that sIAND may serve as a predictive indicator for subclinical target organ damage.

Abstract:Aim To investigate the optimal dual antiplatelet therapy (DAPT) regimen within 12 months after percutaneous coronary intervention (PCI) for improving the prognosis of acute coronary syndrome (ACS) patients with high ischemic risk. Methods A total of 3 053 ACS patients who underwent PCI in our hospital from March 2017 to September 2023 and were identified as having high ischemic risk according to the OPT-BIRISK study criteria were retrospectively enrolled. According to the different DAPT within 12 months after PCI, they were divided into three groups:①There were 1 729 cases in the conventional treatment group, who were treated with aspirin 100 mg＋clopidogrel 75 mg; ②There were 270 cases in the de-escalation treatment group, who were treated with aspirin 100 mg＋ticagrelor 180 mg (ticagrelor 90 mg, Bid) within 3 months after surgery, and then downgraded to aspirin 100 mg＋clopidogrel 75 mg or aspirin 100 mg＋ticagrelor 120 mg (ticagrelor 60 mg, Bid) after 3 months;③There were 1 054 cases in the intensive treatment group, who were treated with aspirin 100 mg＋ticagrelor 180 mg (ticagrelor 90 mg, Bid). The average follow-up time was (11.138±2.094) months. The primary endpoint was the major adverse cardiovascular and cerebrovascular events (MACCE) that occurred during the follow-up period, including cardiac death, myocardial infarction, revascularization, and stroke. The safety endpoint was bleeding events, including TIMI major bleeding and minor bleeding. Results The incidence of MACCE in the intensive treatment group was lower than that in the conventional treatment group (2.372% vs. 4.743%, P＝0.002) and the de-escalation treatment group (2.372% vs. 5.185%, P＝0.015), and the incidence of bleeding events was higher than that in the conventional treatment group (22.676% vs. 13.939%, P＜0.001) and the de-escalation treatment group (22.676% vs. 13.333%, P＝0.001). There was no statistically significant difference in the incidence of MACCE and bleeding events between the conventional treatment group and the de-escalation treatment group, and there was also no statistically significant difference in the incidence of major bleeding among the three groups (P＞0.05). Cox regression results showed that intensive antiplatelet therapy was associated with a lower risk of MACCE (HR＝0.5,5%CI:0.265～0.816, P＝0.008) and a higher risk of bleeding events (HR＝1.5,5%CI:1.369～2.098, P＜0.001). Conclusion For ACS patients with high ischemic risk after PCI, intensive antiplatelet therapy (aspirin combined with ticagrelor) was associated with a reduced incidence of ischemic events without increasing the risk of major bleeding compared with treatment with clopidogrel and de-escalation therapy.

Abstract:Aim To investigate the predictive value of monocyte to high density lipoprotein cholesterol ratio (MHR) for acute myocardial infarction (AMI) and the severity of coronary stenosis in patients with type 2 diabetes mellitus (T2DM). Methods A retrospective case-control study was conducted. 137 T2DM patients with AMI (myocardial infarction group) who were hospitalized in the Second Hospital of Shanxi Medical University due to chest pain from January 2022 to March 2023 were included, and 137 T2DM patients without AMI (non-myocardial infarction group) were selected by propensity score matching method. Coronary angiography was performed in both groups. The correlation between MHR and the risk of AMI occurrence and the severity of coronary stenosis was analyzed. Results The monocyte count and MHR in the myocardial infarction group were significantly higher than those in the non-myocardial infarction group (P＜0.001), while the level of high density lipoprotein cholesterol (HDLC) was significantly lower than that in the non-myocardial infarction group (P＝0.005). Multivariate Logistic regression showed that MHR was an independent risk factor for AMI in T2DM patients (OR＝62.0,5%CI:12.21～317.78, P＜0.001). ROC curve analysis showed that the area under the curve of MHR for predicting AMI in T2DM patients was 0.704 (sensitivity was 0.796, specificity was 0.540). Further analysis of multivariate Logistic regression based on binary division of MHR showed that after adjusting for confounding factors, the risk of AMI in T2DM patients with high MHR group (MHR≥0.38) was 1.978 times higher than that in T2DM patients with low MHR group (MHR＜0.38) (OR＝2.8,5%CI:1.744～5.086, P＜0.001). Multivariate linear regression analysis showed that the Gensini score of T2DM patients increased by 47.177 points for every 1.0 increase in MHR (β＝47.7,5%CI:25.165～69.188, P＜0.001). Conclusions MHR is positively correlated with the risk of AMI in T2DM patients, and positively correlated with the severity of coronary stenosis in T2DM patients. By monitoring MHR levels, early prediction of AMI and the severity of coronary stenosis in T2DM patients can be achieved.

Abstract:Atherosclerosis (As) is a chronic inflammatory disease, in which persistent inflammation serves as a key mechanism driving plaque formation and progression. Heat shock protein family B member 1 (HSPB1), a member of the small heat shock protein family, functions as a molecular chaperone and is widely expressed in various cells and tissues. The expression of HSPB1 is regulated by heat shock factor 1 (HSF1), which directly activates its transcription by binding to the heat shock element (HSE). Recent studies have revealed that HSPB1 plays an important role in the progression of atherosclerosis, primarily by modulating the expression of inflammatory factors, influencing lipid metabolism, and regulating programmed cell death, thereby attenuating plaque inflammation and exerting anti-atherosclerotic effects. This review systematically elaborates on the mechanisms by which HSPB1 suppresses inflammatory responses to modulate the progression of As, and further summarizes HSPB1-targeted therapeutic strategies for atherosclerosis, including the development of specific agonists and innovative applications of nano-drug delivery system (NDDS), aiming to provide new theoretical foundations and therapeutic directions for the prevention and treatment of As.

Abstract:Cardiovascular disease has become the leading cause of death in both urban and rural populations in China.Recent studies have found mitochondrial dysfunction, such as mitochondrial dynamics imbalance, dysregulation of autophagy, mitochondrial membrane depolarization and mPTP opening, apoptosis, excessive production of reactive oxygen species, reduction of ATP synthesis and calcium ion disorder, affect the normal physiological function of cardiovascular cells, and promote the occurrence and development of atherosclerosis, hypertension, ischemia-reperfusion injury, hypertrophic cardiomyopathy, arrhythmia, heart failure, etc., thus leading to various cardiovascular diseases. This paper reviews the role of mitochondrial dysfunction in cardiovascular diseases and aims to provide new ideas for the research and treatment of cardiovascular diseases.

Abstract:Vascular calcification is the pathological basis of multiple diseases, and its main mechanism is the abnormal deposition of calcium and phosphorus. MicroRNAs (miRNA) are a class of short non-coding RNA molecules that participate in the processes of gene transcription and translation. Studies have shown that miRNA expression is altered under pathological conditions such as hyperphosphatemia, hyperglycemia, or chronic kidney disease. These alterations, via different signaling pathways, affect the osteogenic transdifferentiation of vascular smooth muscle cells and the expression of osteogenic markers, and thus promote or inhibit the progression of vascular calcification. miRNA hold promise as therapeutic targets for vascular calcification or biomarkers reflecting the level of vascular calcification. This paper aims to summarize the mechanism pathways and relevant achievements of miRNA in regulating vascular calcification, providing a reference for the research on miRNA and vascular calcification.

Abstract:Post-myocardial infarction ventricular remodeling can lead to heart failure and poor outcomes, and its mechanisms mainly involve dynamic regulation of immune cells and their interactions with the microenvironment. However, the dynamic evolutionary process and functional diversity of immune cell subpopulations still require further investigation. The development of Single-cell sequencing technology has revealed the functional diversity exhibited by immune cell subpopulations at different stages of injury. These subpopulations crucially determine the final outcomes of inflammation resolution and tissue repair through core mechanisms such as cell-cell interactions, metabolic reprogramming, and signaling pathways regulation. In the future, it is still necessary to integrate advanced technologies such as spatial multiomics and nanodelivery to overcome translational bottlenecks. This article comprehensively summarizes the roles of key immune cell subpopulations and their molecular mechanisms in ventricular remodeling after myocardial infarction, and discusses therapeutic strategies for targeted immune regulation. 〖JP