Light physical activity predicts long-term mortality in individuals with a different cardiovascular health status: a cohort study.

Studies have showed that LIPA seems to be favorably associated with mortality in the general population and illness individuals, but the association between different cardiovascular health status and mortality is not clear. After adjustment , the HRs of LIPA in individuals with CVRF and CVD from quartiles 2-4 were less than 1, which were 0.78 (95%CI, 0.61 ~ 0.99; P = 0.042), 0.63 (95%CI, 0.47 ~ 0.83; P = 0.001), 0.55（95%CI, 0.40 ~ 0.76; P < 0.001）, and 0.52 (95%CI, 0.37 ~ 0.74; P < 0.001)，0.39 (95%CI, 0.27 ~ 0.58; P < 0.001), 0.33 (95%CI, 0.22 ~ 0.51; P < 0.001) LIPA is beneficial for reducing mortality, but the shape of the association depends on cardiovascular health status.

Effect of omega-3 fatty acids supplementation on the prognosis of coronary artery disease: A meta-analysis of randomized controlled trials.

AIMS: To evaluate whether omega-3 fatty acids (É·-3 FAs) supplementation can improve cardiovascular outcomes in patients with established coronary artery disease (CAD). DATA SYNTHESIS: Five electronic databases were searched for randomized controlled trials that evaluated the effect of É·-3 FAs on cardiovascular outcomes in patients with CAD. The language was restricted to English. The risk ratio was pooled. Subgroup analyses were conducted to evaluate whether study-level variables might act as effect modifiers. A total of 12 studies involving 29913 patients were included. É·-3 FAs had no effects on major adverse cardiovascular events (MACEs) (RR, 0.93; 95 % CI: 0.85 to 1.01, P = 0.09). While É·-3 FAs reduced the incidences of all-cause death (RR, 0.90; 95 % CI: 0.83 to 0.97, P = 0.005), cardiovascular death (RR, 0.82; 95 % CI: 0.75 to 0.90, P < 0.0001), myocardial infarction (RR, 0.77; 95 % CI: 0.68 to 0.86, P < 0.0001), revascularization (RR, 0.80; 95 % CI: 0.69 to 0.93, P = 0.003), sudden cardiac death (RR, 0.67; 95 % CI: 0.52 to 0.86, P = 0.002) and hospitalization for heart failure or unstable angina pectoris (RR, 0.75; 95 % CI: 0.58 to 0.97, P = 0.03) in CAD. It did not statistically reduce the risk of stroke (RR, 0.96; 95 % CI: 0.77 to 1.21, P = 0.76). The favorable effects of É·-3 FAs on MACEs were significant in subgroups of intervention with EPA and baseline triglyceride ≥1.7 mmol/L. CONCLUSION: É·-3 FAs supplementation, especially EPA, appears to be an effective adjunct therapy for improving the prognosis of CAD. REGISTRATION NUMBER: PROSPERO CRD42022311237.

Refractory angina pectoris: a 20-year (2003-2022) bibliometric analysis.

Background: The increasing number of patients with refractory angina pectoris, combined with the aging population and improved survival rates among coronary heart disease patients, presents a significant challenge in contemporary cardiovascular medicine. The treatment of refractory angina has been an ongoing area of exploration, yet a comprehensive analysis of the existing literature on this topic is currently lacking. Therefore, this study aims to provide the first bibliometric analysis of publications related to refractory angina. Methods: A systematic search was conducted in the Web of Science database to identify articles related to refractory angina published between 2003 and 2022. The inclusion criteria were limited to articles and reviews written in English. CiteSpace software was utilized to conduct a collaborative network analysis of countries/regions, institutions and authors, co-occurrence analysis of keywords, and co-citation analysis of authors and references. Results: A total of 1,386 publications were identified, with an annual publication volume exhibiting fluctuation over time. American and European countries and institutions demonstrated a leading position in terms of research output. Henry TD emerged as the most prolific researcher in the field, while Mannheimer C received the highest number of citations. The primary research hotspot within this field focused on the treatment of refractory angina, with recent emphasis on emerging treatments such as stem cell therapy and the coronary sinus reducer. A significant number of clinical trials have been conducted, with a continuous focus on patient benefits, quality of life, and survival prognosis. Conclusion: Significant progress has been made in the field of refractory angina pectoris in recent years. Novel treatment methods, including spinal cord stimulation, enhanced external counterpulsation, stem cell therapy, and the coronary sinus reducer, hold promising therapeutic prospects. However, further high-quality evidence-based research is essential to support these emerging interventions. Additionally, the development of comprehensive evidence-based guidelines for refractory angina treatment is crucial. Such guidelines would provide clinicians with a framework to navigate the complexities of treatment choices and optimize patient care in this challenging condition.

Efficacy and safety of Qixue Tongzhi Granule in improving the exercise capacity of stable coronary artery disease: study protocol for a multicenter, randomized, double-blind, placebo-controlled trial.

Background: Despite optimal medical therapy, patients with stable coronary artery disease (SCAD) still have a high risk of recurrent cardiovascular events. Exercise capacity measured by cardiopulmonary exercise testing (CPET) is a good surrogate marker for the long-term prognosis of SCAD. Qixue Tongzhi Granule (QTG) is created by academician Chen Keji and has the function of tonifying qi, promoting blood circulation, and regulating qi-flowing. This trial aims to investigate the efficacy and safety of QTG in improving exercise tolerance, alleviating angina pectoris and anxiety/depression symptoms, promoting health-related quality of life, and reducing the risk of adverse cardiovascular events in subjects with SCAD. Methods: This is a randomized, double-blind, placebo-controlled trial. 150 SCAD patients with qi deficiency, blood stasis, and liver qi stagnation syndrome are enrolled. Patients will be randomly allocated to the QTG or placebo groups at a 1:1 ratio. QTG and placebo will be added to the modern guideline-directed medical therapy for 12 weeks and patients will be followed up for another 24 weeks. The primary outcome is the improvement of metabolic equivalents measured by CPET. The secondary outcomes are cumulative incidence of composite endpoint events, other indicators in CPET, changes in the Seattle Angina Questionnaire, traditional Chinese medicine syndrome scale, 12 items of Short Form Health Survey Questionnaire, Patient Health Questionnaire-9, and Generalized Anxiety Disorder-7, changes of ST-T segment in the electrocardiogram, improvement of left ventricular ejection fraction and left ventricular end-diastolic diameter in echocardiography. In addition, metabolomics analysis will be performed based on blood samples. Adverse events and safety evaluations will also be documented. A full analysis set, per protocol set, and safety analysis set will be conducted. Discussion: This clinical trial can enrich treatment options for CHD patients with low cardiorespiratory fitness and psychological imbalance, and it may also create a new situation for promoting the application of traditional Chinese medicine in cardiac rehabilitation.Clinical Trial Registration: [http://www.chictr.org.cn], identifier: [ChiCTR2200058988].

Ginsenoside Re inhibits myocardial fibrosis by regulating miR-489/myd88/NF-κB pathway.

Background: Myocardial fibrosis (MF) is an advanced pathological manifestation of many cardiovascular diseases, which can induce heart failure and malignant arrhythmias. However, the current treatment of MF lacks specific drugs. Ginsenoside Re has anti-MF effect in rat, but its mechanism is still not clear. Therefore, we investigated the anti-MF effect of ginsenoside Re by constructing mouse acute myocardial infarction (AMI) model and AngⅡ induced cardiac fibroblasts (CFs) model. Methods: The anti-MF effect of miR-489 was investigated by transfection of miR-489 mimic and inhibitor in CFs. Effect of ginsenoside Re on MF and its related mechanisms were investigated by ultrasonographic, ELISA, histopathologic staining, transwell test, immunofluorescence, Western blot and qPCR in the mouse model of AMI and the AngⅡ-induced CFs model. Results: MiR-489 decreased the expression of α-SMA, collagenⅠ, collagen Ⅲ and myd88, and inhibited the phosphorylation of NF-κB p65 in normal CFs and CFs treated with AngⅡ. Ginsenoside Re could improve cardiac function, inhibit collagen deposition and CFs migration, promote the transcription of miR-489, and reduce the expression of myd88 and the phosphorylation of NF-κB p65. Conclusion: MiR-489 can effectively inhibit the pathological process of MF, and the mechanism is at least partly related to the regulation of myd88/NF-κB pathway. Ginsenoside Re can ameliorate AMI and AngⅡ induced MF, and the mechanism is at least partially related to the regulation of miR-489/myd88/NF-κB signaling pathway. Therefore, miR-489 may be a potential target of anti-MF and ginsenoside Re may be an effective drug for the treatment of MF.

The Role of miRNA in the Regulation of Angiogenesis in Ischemic Heart Disease.

Despite continued improvements in primary prevention and treatment, ischemic heart disease (IHD) is the most common cause of mortality in both developing and developed countries. Promoting angiogenesis and reconstructing vascular network in ischemic myocardium are critical process of postischemic tissue repair. Effective strategies to promote survival and avoid apoptosis of endothelial cells in the ischemic myocardium can help to achieve long-term cardiac angiogenesis. Therefore, it is of great importance to investigate the molecular pathophysiology of angiogenesis in-depth and to find the key targets that promote angiogenesis. Recently years, many studies have found that microRNAs play important regulatory roles in almost all process of angiogenesis, including vascular sprouting, proliferation, survival and migration of vascular endothelial cells, recruitment of vascular progenitor cells, and control of angiopoietin expression. This review presents detailed information about the regulatory role of miRNAs in the angiogenesis of IHD in recent years, and provides new therapeutic ideas for the treatment of IHD.

Frontiers and Hotspots Evolution in Psycho-cardiology: A Bibliometric Analysis From 2004 to 2022.

In the last 20 years, research on the topic of psycho-cardiology has gradually entered the public eye, with more innovations and applications of evidence-based medical research, biological mechanism research, and guideline consensus in the field of psycho-cardiology. This study uses a bibliometric approach to visualize and analyze the literature within the field of psycho-cardiology over the last 20 years to visualize the development process, research hotspots, and cutting-edge trends in clinical practice, mechanisms, and management strategies related to psycho-cardiology. Quantitative description and evaluation of 409 articles published in the field from 2004-2022 were conducted using CiteSpace and VOSviewer, to provide a theoretical reference for the development of psycho-cardiology.

Long Noncoding RNAs Involved in Cardiomyocyte Apoptosis Triggered by Different Stressors.

Cardiomyocytes are essential to maintain the normal cardiac function. Ischemia, hypoxia, and drug stimulation can induce pathological apoptosis of cardiomyocytes which eventually leads to heart failure, arrhythmia, and other cardiovascular diseases. Understanding the molecular mechanisms that regulate cardiomyocyte apoptosis is of great significance for the prevention and treatment of cardiovascular diseases. In recent years, more and more evidences reveal that long noncoding RNAs (lncRNAs) play important regulatory roles in myocardial cell apoptosis. They can modulate the expression of apoptosis-related genes at post-transcriptional level by altering the translation efficacy of target mRNAs or functioning as a precursor for miRNAs or competing for miRNA-mediated inhibition. Moreover, reversing the abnormal expression of lncRNAs can attenuate and even reverse the pathological apoptosis of cardiomyocytes. Therefore, apoptosis-related lncRNAs may become a potential new field for studying cardiomyocyte apoptosis and provide new ideas for the treatment of cardiovascular diseases.