Artificial intelligence (AI) serves as a key technology in global industrial transformation and technological restructuring and as the core driver of the fourth industrial revolution. Currently, deep learning techniques, such as convolutional neural networks, enable intelligent information collection in fields such as tongue and pulse diagnosis owing to their robust feature-processing capabilities. Natural language processing models, including long short-term memory and transformers, have been applied to traditional Chinese medicine (TCM) for diagnosis, syndrome differentiation, and prescription generation. Traditional machine learning algorithms, such as neural networks, support vector machines, and random forests, are also widely used in TCM diagnosis and treatment because of their strong regression and classification performance on small structured datasets. Future research on AI in TCM diagnosis and treatment may emphasize building large-scale, high-quality TCM datasets with unified criteria based on syndrome elements; identifying algorithms suited to TCM theoretical data distributions; and leveraging AI multimodal fusion and ensemble learning techniques for diverse raw features, such as images, text, and manually processed structured data, to increase the clinical efficacy of TCM diagnosis and treatment.
Panvascular disease is a complex systemic disorder. Research by our team has established "kidney deficiency-vascular impairment" as its core pathogenesis. Consequently, we developed a three-tiered progressive prevention and treatment strategy: early prevention phase: focuses on tonifying the kidney and reducing turbidity; mid-term control phase: focuses on tonifying the kidney and stabilizing plaque; late recovery phase: focuses on tonifying the kidney and unblocking collaterals. This targeted therapeutic protocol effectively alleviates clinical symptoms, improves biochemical markers, enhances treatment efficacy, and achieves comprehensive management throughout the disease course. This article systematically elaborates on the concept of "kidney deficiency-vascular impairment" in panvascular disease, summarizes the mechanisms of kidney-tonifying Chinese herbal medicines, aiming to provide a beneficial reference for the whole-course management of panvascular diseases.
Heart Failure (HF) epitomizes a formidable global health quandary characterized by marked morbidity and mortality. It has been established that severe derangements in energy metabolism are central to the pathogenesis of HF, culminating in an inadequate cardiac energy milieu, which, in turn, precipitates cardiac pump dysfunction and systemic energy metabolic failure, thereby steering the trajectory and potential recuperation of HF. The conventional therapeutic paradigms for HF predominantly target amelioration of heart rate, and cardiac preload and afterload, proffering symptomatic palliation or decelerating the disease progression. However, the realm of therapeutics targeting the cardiac energy metabolism remains largely uncharted. This review delineates the quintessential characteristics of cardiac energy metabolism in healthy hearts, and the metabolic aberrations observed during HF, alongside the associated metabolic pathways and targets. Furthermore, we delve into the potential of phytochemicals in rectifying the redox disequilibrium and the perturbations in energy metabolism observed in HF. Through an exhaustive analysis of recent advancements, we underscore the promise of phytochemicals in modulating these pathways, thereby unfurling a novel vista on HF therapeutics. Given their potential in orchestrating cardiac energy metabolism, phytochemicals are emerging as a burgeoning frontier for HF treatment. The review accentuates the imperative for deeper exploration into how these phytochemicals specifically intervene in cardiac energy metabolism, and the subsequent translation of these findings into clinical applications, thereby broadening the horizon for HF treatment modalities.
Background Cardiac fibrosis plays a crucial role in the development of heart failure (HF) following myocardial infarction (MI). Endothelial-mesenchymal transition (EndMT) is one of the key drivers of cardiac fibrosis and subsequent cardiac dysfunction. The traditional Chinese medicine formula Bushen Huoxue Yiqi Formula (BHYF) is an effective prescription for treating HF, significantly improving cardiac function in patients. However, the underlying mechanisms of BHYF's efficacy remain inadequately understood. Objective This study aims to determine whether BHYF ameliorates HF by inhibiting cardiac fibrosis and to elucidate the intrinsic mechanisms involved. Methods A post-MI HF model was established by ligating the left anterior descending coronary artery in rats, and human umbilical vein endothelial cells (HUVEC) were stimulated with hypoxia/reoxygenation (H/R) in vitro. Active compounds in BHYF were identified using HPLC. Cardiac function and morphology were assessed using echocardiography, TTC staining, HE staining, Masson's trichrome, and Sirius Red staining. The mechanism of action of BHYF was evaluated using Western blotting, immunohistochemistry, and immunofluorescence. Results A total of 98 compounds, including glycosides, phenolic compounds, carboxylic acids, and others, were identified or preliminarily identified. BHYF improved cardiac function and myocardial damage in rats with MI-induced HF and mitigated cardiac fibrosis by inhibiting EndMT. Mechanistically, BHYF treatment inhibited EndMT by modulating the SIRT1/Notch1 pathway, thereby exerting anti-fibrotic effects in the heart. Conclusion Targeting EndMT based on the SIRT1/Notch1 pathway, BHYF may represent a novel antifibrotic therapeutic strategy, providing a scientific basis for the development of new cardiovascular drugs.
BackgroundCoronary heart disease (CHD) is representative of cardiovascular disease and the leading cause of death in humans. Previous studies have shown that kidney disease is associated with CHD, and current treatment options that can improve both cardiac and renal functions still have some limitations. The traditional Chinese medicine Bu-Shen-Huo-Xue granule (BSHXG) can promote blood rheology, inhibit platelet agglutination, and improve heart and kidney functions.MethodsThis is a multicenter, randomized, double-blind, placebo-controlled clinical trial. A total of 210 participants will be randomized to the intervention group and the placebo group. The Guang’anmen Hospital of China Academy of Chinese Medical Sciences is the leading center, and the Affiliated Hospital of Shandong University of Chinese Medicine and the First Affiliated Hospital of Guangzhou University of Chinese Medicine are the participating units. In addition to conventional pharmacotherapy for angina, the intervention group will receive BSHXG while the placebo group will receive BSHXG placebo. All participants will receive 2 months of treatment with 6 months of follow-up. The primary outcome is the efficacy of angina pectoris symptoms in CHD. Secondary outcomes are nitroglycerin arrest, ECG efficacy, Seattle Angina Questionnaire score, serology indicators, assessment of safety, and cardiovascular endpoint events. The transcriptome and metabolome will be used to screen biomarkers for diagnosis and efficacy evaluation.DiscussionThis study aimed to evaluate the efficacy and safety of Bu-Shen-Huo-Xue granule in the treatment of coronary heart disease, and to evaluate the benefits to patients with coronary heart disease from both cardiac and renal indicators.Trial registrationThis trial is approved by the Ethical Review Committee of the Guang’anmen Hospital China Academy of Chinese Medical Sciences with the number 2022-224-KY-01, and has been registered on the Chinese Clinical Trials Registry with the number ChiCTR2300070977 on 27 April 2023.
Hepatitis B virus (HBV)-related liver disease poses a major threat to human health worldwide. Although interferon and nucleoside analogues are commonly administered for treating chronic HBV infection, their use is limited by considerable side effects, drug resistance and incapacity for HBV elimination. Hence, novel HBV therapeutics are urgently required. For numerous years, traditional Chinese botanical drugs have been widely used to treat HBV-related diseases. The natural metabolites derived from these traditional drugs exhibit significant anti-HBV effects and serve as potential novel drugs for treating HBV. For overall understanding the therapeutic potential of these metabolites, the anti-HBV effects and mechanisms of action of 107 natural metabolites are summarized in this article. Mechanistically, these natural metabolites exert their anti-HBV effects by influencing the expression and function of host and/or viral genes, which differs from the mechanism of action of nucleoside analogues. Indeed, combining natural metabolites with nucleoside analogues can exert synergistic effects. Accordingly, natural metabolites or their chemically modified derivatives represent potential novel drugs and adjuvants for anti-HBV treatment.
Objective Inflammation and nutritional status are closely associated with the mortality risk of survivors of cardio-cerebrovascular events. This study aims to evaluate the relationship between inflammation and nutritional indices and mortality among, identifying the most predictive indices.Methods This study included cohort data of the survivors of major adverse cardiovascular and cerebrovascular events (MACCE) from the National Health and Nutrition Examination Survey (NHANES) in 1999-2010. MACCE is defined as a composite of myocardial infarction, heart failure and stroke, and at least one of the three events occurs. The main outcomes were all-cause mortality and cardiovascular mortality. Kaplan-Meier analysis and receiver operating characteristic curves were used to compare the correlation between seven inflammatory nutritional indices (such as Advanced Lung Cancer Inflammation Index, ALI) and mortality among the survivors. A multivariable-adjusted Cox regression and restricted cubic splines analysis identified the most predictive index, with the optimal number of nodes determined by the Akaike information criterion. Subgroup and sensitivity analyses were conducted to assess model stability.Results A total of 2,045 MACCE survivors were included. The higher levels of ALI and serum albumin were significantly associated with lower risks of all-cause and cardiovascular mortality among these individuals. Increases in C-reactive protein to Lymphocyte Ratio, Neutrophil to Serum Albumin Ratio, Neutrophil-to-Lymphocyte Ratio, Systemic Immune-Inflammation Index (SII), and C-reactive protein were similarly correlated with higher mortality risk. ALI outperformed other indices, displaying a distinct L-shaped nonlinear relationship with both all-cause and cardiovascular mortality among MACCE survivors, with an inflection point at 90 indicating the lowest risk. To the left of this inflection, each unit increase in ALI was associated with a 1.3% decrease in all-cause and cardiovascular mortality risk among MACCE patients. To the right, the risk might increase by 0.2%, although the change was not statistically significant. Subgroup analyses and sensitivity analyses showed that the association between ALI and risk of mortality remained stable in most MACCE survivor populations.Conclusion Routine and dynamic monitoring of ALI is helpful for clinicians to assess the mortality risk among MACCE survivors. Anti-inflammatory therapies and appropriate nutritional support are crucial for reducing mortality in these individuals.
Cell death constitutes a critical component of the pathophysiology of cardiovascular diseases. A growing array of non-apoptotic forms of regulated cell death (RCD)—such as necroptosis, ferroptosis, pyroptosis, and cuproptosis—has been identified and is intimately linked to various cardiovascular conditions. These forms of RCD are governed by genetically programmed mechanisms within the cell, with epigenetic modifications being a common and crucial regulatory method. Such modifications include DNA methylation, RNA methylation, histone methylation, histone acetylation, and non-coding RNAs. This review recaps the roles of DNA methylation, RNA methylation, histone modifications, and non-coding RNAs in cardiovascular diseases, as well as the mechanisms by which epigenetic modifications regulate key proteins involved in cell death. Furthermore, we systematically catalog the existing epigenetic pharmacological agents targeting novel forms of RCD and their mechanisms of action in cardiovascular diseases. This article aims to underscore the pivotal role of epigenetic modifications in precisely regulating specific pathways of novel RCD in cardiovascular diseases, thus offering potential new therapeutic avenues that may prove more effective and safer than traditional treatments.
Abstract Objective: Post-myocardial infarction heart failure (post-MI HF) is a prevalent cardiovascular disease. The study aims to preliminarily explore the current research status and development trends in the field of post-MI HF, providing reference ideas and methods for clinical and scientific research. Methods: Publications related to post-MI HF from 2012-2022 in the Web of Science Core Collection's SCI-expanded dataset were extracted. Bibliometric analysis was executed using VOSviewer and R-bibliometrix, encompassing the number of publications, countries, institutions, authors, journals, cited references, and keywords. Results: Within the last decade, 10,929 publications in the domain were published, involving 58,357 authors from 10,437 research institutions across 120 different countries and regions. These findings appeared in 1,446 distinct journals. The United States led in the number of publications, with Harvard Medical School being the most active institution and Kober, Lars from the University of Copenhagen, Denmark, as the leading author. Plos One was the most prolific journal, while Circulationhad the highest citation count. Over the past decade, research hotspots mainly centered on mortality, cardiac remodeling, and prognosis. In the recent two years, emphasis shifted to topics such as mendelian randomization, dapagliflozin, sacubitril/valsartan, COVID-19, and machine learning. Conclusion: The study reveals the overall performance of publications in the post-MI HF research field. The clinical prognosis of patients and cardiac remodeling have been research hotspots over the past decade, yet mortality and readmission remain urgent clinical challenges. Future research trends in this field may revolve around the mechanisms of cardiac remodeling, apoptosis, and inflammation, as well as clinical prognosis studies on patient mortality rates. Additionally, echocardiography and cardiac magnetic resonance technology are gradually becoming important methods for evaluating drug efficacy and elucidating related mechanisms.
SignificanceSince the advent of Optical Coherence Tomography (OCT) two decades ago, there has been substantial advancement in our understanding of intravascular biology. Identifying culprit lesion pathology through OCT could precipitate a paradigm shift in the treatment of patients with Acute Coronary Syndrome. Given the technical prowess of OCT in the realm of cardiology, bibliometric analysis can reveal trends and research focal points in the application of OCT for cardiovascular diseases. Concurrently, meta-analyses provide a more comprehensive evidentiary base, supporting the clinical efficacy of OCT-guided Percutaneous Coronary Intervention (PCI).DesignThis study employs a dual approach of Bibliometric and Meta-analysis.MethodsRelevant literature from 2003 to 2023 was extracted from the Web of Science Core Collection (WoSCC) and analyzed using VOSviewer, CiteSpace, and R for publication patterns, countries, institutions, authors, and research hotspots. The study compares OCT-guided and coronary angiography-guided PCI in treating adult coronary artery disease through randomized controlled trials (RCTs) and observational studies. The study has been reported in the line with PRISMA and AMSTAR Guidelines.ResultsAdhering to inclusion and exclusion criteria, 310 publications were incorporated, demonstrating a continual rise in annual output. Chinese researchers contributed the most studies, while American research wielded greater influence. Analysis of trends indicated that research on OCT and angiography-guided PCI has become a focal topic in recent cohort studies and RCTs. In 11 RCTs (n = 5,277), OCT-guided PCI was not significantly associated with a reduction in the risk of Major Adverse Cardiac Events (MACE) (Odds ratio 0.84, 95% CI 0.65–1.10), cardiac death (0.61, 0.36–1.02), all-cause death (0.7, 0.49–1.02), myocardial infarction (MI) (0.88, 0.69–1.13), target lesion revascularization (TLR) (0.94, 0.7–1.27), target vessel revascularization (TVR) (1.04, 0.76–1.43), or stent thrombosis (0.72, 0.38–1.38). However, in 7 observational studies (n = 4,514), OCT-guided PCI was associated with a reduced risk of MACE (0.66, 0.48–0.91) and TLR (0.39, 0.22–0.68).ConclusionOur comprehensive review of OCT in cardiovascular disease literature from 2004 to 2023, encompassing country and institutional origins, authors, and publishing journals, suggests that OCT-guided PCI does not demonstrate significant clinical benefits in RCTs. Nevertheless, pooled results from observational studies indicate a reduction in MACE and TLR.
Acute myocardial infarction (MI), despite significant progress in its treatment, remains a leading cause of chronic heart failure and cardiovascular events such as cardiac arrest. Promoting angiogenesis in the myocardial tissue after MI to restore blood flow in the ischemic and hypoxic tissue is considered an effective treatment strategy. The repair of the myocardial tissue post-MI involves a robust angiogenic response, with mechanisms involved including endothelial cell proliferation and migration, capillary growth, changes in the extracellular matrix, and stabilization of pericytes for neovascularization. In this review, we provide a detailed overview of six key pathways in angiogenesis post-MI: the PI3K/Akt/mTOR signaling pathway, the Notch signaling pathway, the Wnt/β-catenin signaling pathway, the Hippo signaling pathway, the Sonic Hedgehog signaling pathway, and the JAK/STAT signaling pathway. We also discuss novel therapeutic approaches targeting these pathways, including drug therapy, gene therapy, protein therapy, cell therapy, and extracellular vesicle therapy. A comprehensive understanding of these key pathways and their targeted therapies will aid in our understanding of the pathological and physiological mechanisms of angiogenesis after MI and the development and application of new treatment strategies.
Coronary artery disease(CAD) caused by atherosclerosis(AS) is a major contributor to the global burden of disease. The pathogenesis of CAD is complex, and the subset and function of cardiac macrophages are important factors affecting the occurrence and development of AS and the prognosis of CAD. Recent studies have shown that some traditional Chinese medicine(TCM) formulas and active ingredients can regulate macrophage subsets involved in the inflammation, injury, and repair process of CAD. This paper summarized the significant role of macrophages in AS and myocardial infarction. Based on the plasticity of macrophages, this paper elaborated that traditional Chinese medicine prevented and attenuated AS by regulating macrophage subsets, reducing the level of inflammatory factors, and promoting macrophage autophagy.Traditional Chinese medicine participated in the cardiac repair process after myocardial infarction by accelerating the recruitment of M2 macrophages, inhibiting the polarization of M1 macrophages mediated by glycolysis, inhibiting M1 macrophage-mediated cardiac nerve remodeling, and promoting M2 macrophage-mediated angiogenesis. In addition, in vitro studies on the regulation of macrophage subsets by the active ingredients of traditional Chinese medicine were also reviewed. It was pointed out that nuclear factor kappa B(NF-κB), adenosine 5'-monophosphate(AMP)-activated protein kinase(AMPK), phosphoinositide 3-kinase/protein kinase B(PI3K/Akt), chemokine(C-C motif) ligand 2/C-C chemokine receptor type 2(CCL2/CCR2) were the key targets and pathways for the regulation of macrophages by TCM.
Abstract Objective: Coronary heart disease, a prevalent cardiovascular disorder, has a well-established pathogenesis. However, uncertainty exists regarding the cellular response's chemical process. miRNAs are essential in silencing target genes and reducing the synthesis of corresponding proteins, thereby influencing cell functions. This study aims to explore potential miRNA biomarkers in coronary heart disease and their correlation with clinical manifestations. Methods: Based on prior research by our team, 16 miRNAs were selected for qPCR detection. The differentially expressed independent sample t-tests identified miRNAs in patients with coronary heart disease. To assess diagnostic performance, ROC curve analysis was carried out, and the diagnostic model for coronary heart disease was established using logistic regression. Quantitative correlation analysis between miRNAs and clinical manifestations was conducted, and miRNAs associated with clinical manifestations were subjected to enrichment analysis. Additionally, linear regression was used to analyze the correlation between miRNAs and the blood stasis syndrome questionnaire score of coronary heart disease. Results: 12 miRNAs, including the miR-144-5p, miR-15b-5p, miR-3591-3p, miR-4459, miR-190a-5p, miR-3158-5p, miR-1268b, miR-499a-5p, miR-146a-5p, miR-4448, miR-146b-5p, and miR-223-3p, were found to exhibit differential expression in patients with coronary heart disease. The diagnostic model established in this study could classify 86.5% of the study subjects correctly. Although several miRNAs were found to have associations with clinical manifestations, the degree of correlation was weak. However, both miR-15b-5p and miR-3158-5p showed linear correlations with the blood stasis syndrome questionnaire score in patients who have coronary heart disease. Conclusion: The 12 miRNAs identified in this study have great potential as biomarkers for the diagnosis of coronary heart disease, and the diagnostic model developed in this research could assist in diagnosing this cardiovascular disorder. Several miRNAs were found to regulate vascular endothelial function, vascular smooth muscle transformation, neuronal apoptosis, inflammation, and other pathways, with implications for various clinical manifestations of coronary heart disease. Furthermore, there is a positive correlation between the expression of miR-15b-5p and miR-3158-5p and the blood stasis syndrome score, which exhibits an ascending trend.
Traditional Chinese medicine(TCM)with a long history in China has demonstrated unique advantages in treating a variety of cardiovas-cular diseases,with promising prospects.We exemplify the TCM advantages with 3 major cardiovascular diseases:coronary heart dis-ease,hypertension,and chronic heart failure.With both national and international guidelines,consensus,systematic reviews,and ran-domized controlled trials as evidence,we used the modified Jadad and AMSTAR-1 scales to evaluate the evidence quality and then sys-tematically evaluated the clinical effects and benefits of TCM on cardiovascular diseases,aiming to provide fresh insights into the research methodologies and future development directions for TCM-dominant diseases.
Significance: Findings from this study hold considerable significance, offering invaluable data on the correlation between specific physical health conditions and suicide risk in primary or general healthcare settings-an understudied yet critical area that has implications for the efficiency, cost, and burden of widespread suicide prevention strategies.Objective: To evaluate the suicide risks of patients with cardiovascular disorders compared to the general population, and to construct a disease-suicide risk predictive model, emphasizing the contribution of various diseases to the risk of suicideData sources: For this study, we retrieved human research studies published up until June 2023 from PubMed, Cochrane Library, Embase, Web of Science, CINAHL, and PsycINFO, employing the search term "(((suicide) OR (self-harm) OR (suicidality)) AND ((cardiovascular diseases) OR (heart diseases)))." We also conducted searches on databases from countries referenced in the selected articles. We extracted data from existing works by Junting Chi and Dante Duarte to facilitate comparisons and ensure the compatibility of our methodology.Data extraction and synthesis: The preregistered systematic review and meta-analysis followed Cochrane and PRISMA guidelines. Data were extracted into standardized tables per a prespecified structured checklist, and quality scores were added. Heterogeneity was tested via I2. For pooled effect estimates, we used random-effects models. The Begg and Egger tests, sensitivity analyses were performed.Main outcomes and measures: Suicidal tendencies among cardiovascular disease patients from inception to the present: an examination of suicide ideation, planning, and attempts.Results: Of 17427 search results, 13 articles were included in the systematic review and meta-analysis. Metaanalysis showed a significantly higher suicidality in patients with cardiovascular disorders: general CVD (OR = 1.44, 95% CI 1.08-1.93; P < 0.01, I-2 =91.7%), CHF (OR = 1.68, 95% CI 1.56-1.81; P < 0.05, I-2 =60.2%), Ischemic HD (OR = 1.50, 95% CI 1.22-1.85; P < 0.01, I-2 =91.4%), hypertension (OR = 1.15, 95% CI 1.08-1.23, P < 0.01, I-2 =87.3%), dyslipidemia (OR = 0.83, 95% CI 0.75-0.92, P < 0.01, I2 =82.2%), cerebrovascular disease (OR=1.84, 95% CI 1.78-1.90, P = 0.617, I-2 =0%). Cardiovascular disorders also showed a significantly elevated suicide mortality rate with a pooled SMR of 2.74 (95% CI: 2.19-3.43, P < 0.01, I-2 =98.1%). In our further meta-analysis investigating suicide risk in 16 diseases including cardiovascular ones, a model was developed assigning each disease a score. Results indicated that, despite cardiovascular diseases' risk impact, mood disorders, substance abuse disorders, and depression were more significant contributors. Conclusions and relevance: This study, through a meta-analysis, reveals a link between cardiovascular disorders and increased suicide rates, making these patients primary targets for suicide prevention. And we've developed a model highlighting the contribution of multiple diseases, not just cardiovascular, to suicide risk.
Acute myocardial infarction (MI) is a prevalent and highly fatal global disease. Despite significant reduction in mortality rates with standard treatment regimens, the risk of heart failure (HF) remains high, necessitating innovative approaches to protect cardiac function and prevent HF progression. Cardiac resident macrophages (cMacs) have emerged as key regulators of the pathophysiology following MI. cMacs are a heterogeneous population composed of subsets with different lineage origins and gene expression profiles. Several critical aspects of post-MI pathophysiology have been shown to be regulated by cMacs, including recruitment of peripheral immune cells, clearance and replacement of damaged myocardial cells. Furthermore, cMacs play a crucial role in regulating cardiac fibrosis, risk of arrhythmia, energy metabolism, as well as vascular and lymphatic remodeling. Given the multifaceted roles of cMacs in post-MI pathophysiology, targeting cMacs represents a promising therapeutic strategy. Finally, we discuss novel treatment strategies, including using nanocarriers to deliver drugs to cMacs or using cell therapies to introduce exogenous protective cMacs into the heart.
ObjectiveThis aim of this study is to screen the differential molecules of kidney deficiency and blood stasis (KDBS) syndrome in coronary heart disease by high-throughput sequencing. In addition, the study aims to verify the alterations in the expression levels of miR-4685-3p and its regulated downstream, namely, C1QC, C4, and C5, using quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay (ELISA), and to determine whether the complement and coagulation cascade pathway is the specific pathogenic pathway.MethodsPatients diagnosed with unstable angina pectoris with KDBS syndrome, patients with non-kidney deficiency blood stasis (NKDBS) syndrome, and a Normal group were recruited. The clinical symptoms of each group were further analyzed. Illumina's NextSeq 2000 sequencing platform and FastQC software were used for RNA sequencing and quality control. DESeq software was used for differential gene expression (DGE) analysis. qPCR and ELISA verification were performed on DGE analysis.ResultsThe DGE profiles of 77 miRNA and 331 mRNA were selected. The GO enrichment analysis comprised 43 biological processes, 49 cell components, and 42 molecular functions. The KEGG enrichment results included 40 KEGG pathways. The PCR results showed that, compared with the Normal group, the miR-4685-3p levels decreased in the CHD_KDBS group (P = 0.001), and were found to be lower than those observed in the CHD_NKDBS group. The downstream mRNA C1 regulated by miR-4685-3p showed an increasing trend in the CHD_KDBS group, which was higher than that in the Normal group (P = 0.0019). The mRNA C4 and C5 in the CHD_KDBS group showed an upward trend, but the difference was not statistically significant. ELISA was utilized for the detection of proteins associated with the complement and coagulation cascade pathway. It was found that the expression level of C1 was significantly upregulated in the CHD_KDBS group compared with the Normal group (P < 0.0001), which was seen to be higher than that in the CHD_NKDBS group (P < 0.0001). The expression levels of C4 and C5 in the CHD_KDBS group were significantly lower than the Normal group, and were lower than that in the CHD_NKDBS group (P < 0.0001).ConclusionThe occurrence of CHD_KDBS might be related to the activation of the complement and coagulation cascade pathway, which is demonstrated by the observed decrease in miR-4685-3p and the subsequent upregulation of its downstream C1QC. In addition, the expression levels of complement C4 and C5 were found to be decreased, which provided a research basis for the prevention and treatment of this disease.
Background:The association between isolated diastolic hypertension (IDH) and cardiovascular events has been inconsistently reported. This meta-analysis of cohort studies was designed to investigate the effect of the 2018 European Society of Cardiology (ESC) definition of IDH on the risk of composite cardiovascular events, cardiovascular mortality, all-cause mortality, and all strokes including ischemic stroke (IS) and hemorrhagic stroke (HS).Methods:PubMed, Embase, the Cochrane Library, and Web of Science were searched from inception to July 6, 2021. Cohort studies that investigated the association between IDH and cardiovascular events risk, compared to normotension, were included. Pooled hazard ratios (HRs) and 95% CIs were calculated using a random-effects models and heterogeneity was evaluated usingQ-test andI2statistic. The robustness of the associations was identified using sensitivity analysis. The methodological quality of the studies was assessed using the Newcastle–Ottawa scale. Publication bias was assessed using funnel plot, trim-and-fill method, Begg's test, and Egger's test.Results:A total of 15 cohort studies (13 articles) including 489,814 participants were included in this meta-analysis. The follow-up period ranged from 4.3 to 29 years. IDH was significantly associated with an increased risk of composite cardiovascular events (HR 1.28, 95% CI: 1.07–1.52,p= 0.006), cardiovascular mortality (HR 1.45, 95% CI: 1.07–1.95,p= 0.015), all strokes (HR 1.44, 95% CI: 1.04–2.01,p= 0.03), and HS (HR 1.64, 95% CI: 1.18–2.29,p= 0.164), but not associated with all-cause mortality (HR 1.20, 95% CI: 0.97–1.47,p= 0.087) and IS (HR 1.56, 95% CI: 0.87–2.81,p= 0.137). Subgroup analysis further indicated that IDH in the younger patients (mean age ≤ 55 years) and from Asia were significantly associated with an increased risk of composite cardiovascular events, while the elderly patients (mean age ≥ 55 years), Americans, and Europeans were not significantly associated with an increased risk of composite cardiovascular events.Conclusion:This meta-analysis provides evidence that IDH defined using the 2018 ESC criterion is significantly associated with an increased risk of composite cardiovascular events, cardiovascular mortality, all strokes and HS, but not significantly associated with all-cause death and IS. These findings also emphasize the importance for patients with IDH to have their blood pressure within normal, especially in the young adults and Asians.Trial Registration:PROSPERO, Identifier: CRD42021254108.
Ginseng (Panax ginseng C.A.Mey.) is the dry root and rhizome of the Araliaceae ginseng plant. It has always been used as a tonic in China for strengthening the body. Cardiovascular disease is still the main cause of death in the world. Some studies have shown that the functional components of ginseng can regulate the pathological process of various cardiovascular diseases through different mechanisms, and its formulation also plays an irreplaceable role in the clinical treatment of cardiovascular diseases. Therefore, this paper elaborates the current pharmacological effects of ginseng functional components in treating cardiovascular diseases, summarizes the adverse reactions of ginseng, and sorts out the Chinese patent medicines containing ginseng formula which can treat cardiovascular diseases.