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Objective To identify the risk factors of women with premature coronary artery disease (PCAD) in the Kashgar area, mainly Uyghur residents, providing evidence for effective prevention and treatment of PCAD in this region. Methods Two hundred and forty-four Uighur females in Kashgar area who were hospitalized for coronary angiography (CAG) were enrolled. According to the results of CAG and ages, they were divided into three groups： 69 cases in the control group, 104 cases in the PCAD group, and 71 cases in the late-onset coronary artery disease group. Clinical data were compared among three groups. Univariate and multivariable logistic regression analyses were used to identify the risk factors of PCAD. Results The mean age of onset in the PCAD group was (54.25±6.97) years, and 42.3% of them were admitted due to AMI, accounting for 59.4% in patients with coronary heart disease. Compared with the control group, patients with PCAD had higher prevalence of hypertension and diabetes mellitus, and higher levels of CHOL, TG, APO-B, Hcy and GLU, whereas lower levels of ALB and HGB (all P < 0.05), while compared with the late-onset coronary artery disease group, PCAD group had a lower level of Cys-C, but higher levels of ALB and APO-B, and there was no significant difference in other indicators between two groups (all P > 0.05). Multivariate logistic regression analysis showed that diabetes mellitus [OR = 4.349, 95%CI(1.411, 13.402)], hypertension [OR = 3.121, 95%CI(1.467, 6.639)], APO-B/APO-A1 ratio [OR = 5.603, 95%CI(1.128, 27.838)], Hcy [OR =1.188, 95%CI(1.070, 1.318)] were the independent risk factors of PCAD. Conclusions The onset of coronary heart disease is relatively common in female patients aged < 65 years. Diabetes mellitus, hypertension, high APO-B/APO-A1 ratio and high Hcy level are the independent risk factors for women with PCAD in Kashgar area. Early screening and intervention are needed to prevent PCAD in Kashgar area.

Enhanced external counterpulsation （EECP） is a non-invasive auxiliary circulatory technology and device, which plays a therapeutic role by synchronizing cardiac systolic and diastolic movement, improving hemodynamics, enhancing vascular endothelial function, and exerting anti-atherosclerosis effect, etc. Currently, EECP is widely applied in the clinical prevention and treatment of cardiovascular diseases, such as chronic heart insufficiency, ischemic cardiomyopathy and refractory angina pectoris. With the gradual attention and continuous promotion of cardiac rehabilitation in China, EECP has played a critical role in the treatment and rehabilitation of cardiovascular diseases. In the future, EECP will serve as an important cardiac adjuvant therapy and benefit patients in primary medical treatment. In this article, the application and research progress on EECP in cardiovascular rehabilitation were reviewed, aiming to provide evidences for the clinical application and development of EECP in cardiovascular rehabilitation.

Ginsenoside Rb1 (Rb1) exerts many beneficial effects and protects against cardiovascular disease. To investigate whether Rb1 could attenuate age-related vascular impairment and identify the mechanism. Female C57BL/6J mice aged 2 and 18 months, randomly assigned to Young, Young + 20 mg/kg Rb1, Old + vehicle, Old + 10 mg/kg Rb1 and Old + 20 mg/kg Rb1 groups, were daily intraperitoneal injected with vehicle or Rb1 for 3 months. The thoracic aorta segments were used to inspect the endothelium-dependent vasorelaxation. Left thoracic aorta tissues were collected for histological or molecular expression analyses, including ageing-related proteins, markers relevant to calcification and fibrosis, and expression of Gas6/Axl. We found that in Old + vehicle group, the expression of senescence proteins and cellular adhesion molecules were significantly increased, with worse endothelium-dependent thoracic aorta relaxation (58.35% ± 2.50%) than in Young group (88.84% ± 1.20%). However, Rb1 treatment significantly decreased the expression levels of these proteins and preserved endothelium-dependent relaxation in aged mice. Moreover, Rb1 treatment also reduced calcium deposition, collagen deposition, and the protein expression levels of collagen I and collagen III in aged mice. Furthermore, we found that the downregulation of Gas6 protein expression by 41.72% and mRNA expression by 52.73% in aged mice compared with young mice was abrogated by Rb1 treatment. But there was no significant difference on Axl expression among the groups. Our study confirms that Rb1 could ameliorate vascular injury, suggesting that Rb1 might be a potential anti-ageing related vascular impairment agent. [ABSTRACT FROM AUTHOR]

Introduction: Percutaneous coronary intervention (PCI)-related myocardial infarction (type 4a MI) and major periprocedural myocardial injury have been demonstrated leading to poor prognosis of patients with coronary heart disease (CHD) undergoing elective PCI and still remain high occurrence even after the therapy of dual antiplatelet agents and statins. Proprotein convertase subtilisin/kexin type 9 inhibitor alirocumab has been shown to be effectively in reducing the risk of acute MI (AMI). However, the effect of alirocumab on preventing PCI-related MI or major periprocedural myocardial injury in patients with CHD undergoing elective PCI remains uncertain., Methods and Analysis: Alirocumab effect on Preventing Periprocedural ischaemic Events in coronary heart diseAse patients undergoing coronary StEnting trial is a multicentre, open-label, randomised controlled trial aiming to determine whether alirocumab could reduce the incidence of type 4a MI or major periprocedural myocardial injury in patients with CHD undergoing elective PCI. In total, 422 non-AMI CHD patients planned to undergo elective PCI will be randomly assigned to receive standard pharmacotherapy of CHD (control group) or additional use of subcutaneous alirocumab 75 mg 1 day before procedure (alirocumab group). The primary outcome is type 4a MI or major periprocedural myocardial injury defined as high-sensitivity cardiac troponin elevating above 5×99 th percentile upper reference limit in 48 hours after PCI. Patients will continue receiving standard pharmacotherapy or additional biweekly subcutaneous alirocumab 75 mg for 3 months according to the initial randomisation group. We will follow up for 3 months and record all the major adverse cardiovascular events (MACEs). Incidence of PCI-related MI or major periprocedural myocardial injury, and MACE in 3 months after PCI will be compared between control group and alirocumab group., Ethics and Dissemination: Ethics approval has been obtained from the Medical Ethics Committee of the Third Affiliated Hospital of Sun Yat-sen University with approval number: (2022)02-140-01. The results of this study will be reported through peer-reviewed journals and conference presentations., Trial Registration Number: ChiCTR2200063191., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Cardiovascular and cerebrovascular diseases are leading causes of death worldwide, accounting for more than 40% of all deaths in China. Acute myocardial infarction (AMI) is a common cardiovascular disease and traditionally divided into ST-segment (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI), which are known with different prognoses and treatment strategies. However, key regulatory genes and pathways involved in AMI that may be used as potential biomarker for prognosis are unknown. In this study, we employed both bulk and single-cell RNA-seq to construct gene regulatory networks and cell-cell communication networks. We first constructed weighted gene co-expression networks for differential expressed genes between STEMI and NSTEMI patients based on whole-blood RNA-seq transcriptomics. Network topological attributes (e.g., node degree, betweenness) were analyzed to identify key genes involved in different functional network modules. Furthermore, we used single-cell RNA-seq data to construct multilayer signaling network to infer regulatory mechanisms of the above key genes. PLAUR (receptor for urokinase plasminogen activator) was found to play a vital role in transducing inter-cellular signals from endothelial cells and fibroblast cells to intra-cellular pathways of myocardial cells, leading to gene expression involved in cellular response to hypoxia. Our study sheds lights on identifying molecular biomarkers for diagnosis and prognosis of AMI, and provides candidate key regulatory genes for further experimental validation.