Angina pectoris (AP), a clinical syndrome characterized by paroxysmal chest pain, is caused by insufficient blood supply to the coronary arteries and sudden temporary myocardial ischemia and hypoxia. Long-term AP typically induces other cardiovascular events, including myocardial infarction and heart failure, posing a serious threat to patient safety. However, AP's complex pathological mechanisms and developmental processes introduce significant challenges in the rapid diagnosis and accurate treatment of its different subtypes, including stable angina pectoris (SAP), unstable angina pectoris (UAP), and variant angina pectoris (VAP). Omics research has contributed significantly to revealing the pathological mechanisms of various diseases with the rapid development of high-throughput sequencing approaches. The application of multi-omics approaches effectively interprets systematic information on diseases from the perspective of genes, RNAs, proteins, and metabolites. Integrating multi-omics research introduces novel avenues for identifying biomarkers to distinguish different AP subtypes. This study reviewed articles related to multi-omics and AP to elaborate on the research progress in multi-omics approaches (including genomics, transcriptomics, proteomics, and metabolomics), summarized their applications in screening biomarkers employed to discriminate multiple AP subtypes, and delineated integration methods for multi-omics approaches. Finally, we discussed the advantages and disadvantages of applying a single-omics approach in distinguishing diverse AP subtypes. Our review demonstrated that the integration of multi-omics technologies is preferable for quick and precise diagnosis of the three AP types, namely SAP, UAP, and VAP.

The complement system, a coordinator and facilitator of the innate immune response, plays an essential role in maintaining host homeostasis. It promotes clearance of pathogen- and danger-associated molecular patterns, regulates adaptive immunity, and can modify various metabolic processes such as energy expenditure, lipid metabolism, and glucose homeostasis. In this review, we will focus on the intricate interplay between complement components and lipid metabolism. More precisely, we will display how alterations in the activation and regulation of the complement system affect pathological outcome in lipid-associated diseases, such as atherosclerosis, obesity, metabolic syndrome, age-related macular degeneration, and metabolic dysfunction-associated steatotic liver disease. In addition to that, we will present and evaluate underlying complement-mediated physiological mechanisms, observed both in vitro and in vivo. Our manuscript will demonstrate the clinical significance of the complement system as a bridging figure between innate immunity and lipid homeostasis.

Cardiovascular diseases are the leading cause of death globally, and atherosclerosis is the major contributor to the development and progression of cardiovascular diseases. Immune responses have a central role in the pathogenesis of atherosclerosis, with the complement system being an acknowledged contributor. Chronic activation of liver-derived and serum-circulating canonical complement sustains endothelial inflammation and innate immune cell activation, and deposition of complement activation fragments on inflamed endothelial cells is a hallmark of atherosclerotic plaques. However, increasing evidence indicates that liver-independent, cell-autonomous and non-canonical complement activities are underappreciated contributors to atherosclerosis. Furthermore, complement activation can also have atheroprotective properties. These specific detrimental or beneficial contributions of the complement system to the pathogenesis of atherosclerosis are dictated by the location of complement activation and engagement of its canonical versus non-canonical functions in a temporal fashion during atherosclerosis progression. In this Review, we summarize the classical and the emerging non-classical roles of the complement system in the pathogenesis of atherosclerosis and discuss potential strategies for therapeutic modulation of complement for the prevention and treatment of atherosclerotic cardiovascular disease.

Coronary stent implantation is usually used to treat unstable angina to alleviate stenosis or occlusion, promoting blood flow restoration and alleviating symptoms such as myocardial ischemia. And postoperative cardiac rehabilitation is essential for enhancing recovery and prognosis. Nevertheless, conventional rehabilitation lacks specificity, particularly for elderly patients with multiple comorbidities and poor compliance, rendering it less effective.

To investigate the effects of systematic cardiac rehabilitation training in elderly patients with unstable angina following coronary stenting intervention.

A retrospective enrollment was conducted comprising fifty-four elderly patients with unstable angina pectoris who underwent systematic cardiac rehabilitation training after receiving coronary intervention as the rehabilitation group, while fifty-three elderly patients who received basic nursing and rehabilitation guidance measures after coronary intervention were assigned to the control group. Differences in Seattle Angina Questionnaire scores, survival quality (SF-36) scores, cardiopulmonary exercise function assessment index, echocardiographic cardiac function index, and adverse cardiovascular events were compared between the two groups.

After intervention, the rehabilitation group observed greater VO2 Max, maximum metabolic equivalent, eft ventricular ejection fraction, left ventricular end-diastolic diameter and smaller left ventricular end-systolic diameter. And the rehabilitation group observed greater scores of physical activity limitation, stable angina pectoris, treatment satisfaction, and SF-36 score. The incidence of adverse cardiovascular events in the two groups, showed no significant difference.

Systematic cardiac rehabilitation following coronary stenting in elderly patients with unstable angina pectoris can enhance cardiac function recovery, consequently enhancing both quality of life and cardiopulmonary exercise tolerance.

In the past few years, circulating complement C1q involvement in atherosclerosis has garnered growing research interest in addition to the emerging recognition of the novel lipid marker named atherogenic index of plasma (AIP). Nevertheless, among patients experiencing low-density lipoprotein cholesterol (LDL-C) levels less than 1.8mmol/L, the interplay between C1q combined with the AIP for coronary artery disease (CAD) is ambiguous.

Patients were stratified into a non-CAD and CAD group according to their coronary angiography. The association between C1q in conjunction with the AIP and CAD was explored using restricted cubic spline analyses and logistic regression models. To assess how it predicted, a receiver operating characteristic analysis was undertaken.

A total of 7270 patients comprised 1476 non-CAD patients and 5794 patients diagnosed with CAD were analyzed. A comparison of the two groups showed that the C1q levels were notably higher compared to the CAD group, while AIP exhibited an inverse trend. Across quartiles of C1q, the AIP demonstrated a decline with increasing C1q levels, and significant differences were observed between the groups. A correlation analysis underscored a notable negative correlation between the two variables. Univariate and multivariate logistic regression analyses revealed significant associations between CAD and the C1q quartile groups/AIP. Furthermore, compared with the Q4 group, a decrease in the C1q levels corresponded to an escalation in CAD risk, with the odds ratio rising from 1.661 to 2.314.

In conclusion, there appears to be a notable positive correlation between the combination of C1q with the AIP and CAD.

To determine the association between complement C1q and vulnerable plaque morphology among coronary artery disease (CAD) patients. We conducted a retrospective observational study of 221 CAD patients admitted to The Second Affiliated Hospital of Xi'an Jiaotong University. Intravascular optical coherence tomography was utilized to describe the culprit plaques' morphology. Using logistic regression analysis to explore the correlation between C1q and vulnerable plaques, and receiver operator characteristic (ROC) analysis assess the predictive accuracy. As reported, the complement C1q level was lower in ACS patients than CCS patients (18.25 ± 3.88 vs. 19.18 ± 4.25, P = 0.045). The low complement-C1q-level group was more prone to develop vulnerable plaques. In lipid-rich plaques, the complement C1q level was positively correlated with the thickness of fibrous cap (r = 0.480, P = 0.041). Univariate and multivariate logistic regression analyses suggested that complement C1q could be an independent contributor to plaques' vulnerability. For plaque rupture, erosion, thrombus, and cholesterol crystals, the areas under the ROC curve of complement C1q level were 0.873, 0.816, 0.785, and 0.837, respectively (P < 0.05 for all). In CAD patients, the complement C1q could be a valuable indicator of plaque vulnerability.

This study focuses on recent advances in proteomics and provides an up-to-date use of this technology in identifying cardiovascular disease (CVD) biomarkers. A total of eight electronic databases (PubMed, EMBASE, Web of Science, Cochrane Library, Wanfang, Vip, Sinomed, and CNKI) were searched and five were used for integrative analysis of sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic ratio (DOR) and 1 secondary indicator area under the curve (AUC). This systematic review and integrative analysis summarized potential biomarkers previously identified by proteomics. The integrative analysis suggested that proteomics technology had high clinical value in CVD diagnosis. The findings provided new possible directions for the prevention or diagnosis of CVD.

Monocytes are associated with human cardiovascular disease progression. Monocytes are segregated into three major subsets: classical (cMo), intermediate (iMo), and nonclassical (nMo). Recent studies have identified heterogeneity within each of these main monocyte classes, yet the extent to which these subsets contribute to heart disease progression is not known. Peripheral blood mononuclear cells (PBMC) were obtained from 61 human subjects within the Coronary Assessment of Virginia (CAVA) Cohort. Coronary atherosclerosis severity was quantified using the Gensini Score (GS). We employed high-dimensional single-cell transcriptome and protein methods to define how human monocytes differ in subjects with low to severe coronary artery disease. We analyzed 487 immune-related genes and 49 surface proteins at the single-cell level using Antibody-Seq (Ab-Seq). We identified six subsets of myeloid cells (cMo, iMo, nMo, plasmacytoid DC, classical DC, and DC3) at the single-cell level based on surface proteins, and we associated these subsets with coronary artery disease (CAD) incidence based on Gensini score (GS) in each subject. Only frequencies of iMo were associated with high CAD (GS > 32), adj.p = 0.024. Spearman correlation analysis with GS from each subject revealed a positive correlation with iMo frequencies (r = 0.314, p = 0.014) and further showed a robust sex-dependent positive correlation in female subjects (r = 0.663, p = 0.004). cMo frequencies did not correlate with CAD severity. Key gene pathways differed in iMo among low and high CAD subjects and between males and females. Further single-cell analysis of iMo revealed three iMo subsets in human PBMC, distinguished by the expression of HLA-DR, CXCR3, and CD206. We found that the frequency of immunoregulatory iMo_HLA-DR+CXCR3+CD206+ was associated with CAD severity (adj.p = 0.006). The immunoregulatory iMo subset positively correlated with GS in both females (r = 0.660, p = 0.004) and males (r = 0.315, p = 0.037). Cell interaction analyses identified strong interactions of iMo with CD4+ effector/memory T cells and Tregs from the same subjects. This study shows the importance of iMo in CAD progression and suggests that iMo may have important functional roles in modulating CAD risk, particularly among females.

C1q has been shown to be associated with coronary heart disease (CAD) and can co-deposit with C-reactive protein (CRP) in atherosclerotic plaques. However, few studies have been conducted between C1q, CRP parameters and CAD. The aim of this study is to explore the relationship between C1q and CRP parameters and assess their clinical significance in CAD.

238 total patients who underwent coronary artery angiography were enrolled and divided into control group (n = 65), stable CAD group (n = 47) and unstable angina group (UA group, n = 126). Patients' data were collected from self-administered questionnaires and electrical medical records. The severity of coronary stenosis was presented by Gensini score. The relationship between C1q, CRP parameters and CAD were evaluated by multivariate regression analysis and their predicting performance were assessed by ROC analysis and odds ratio analysis.

Compared with control group, C1q was showed significantly lower in stable CAD (P = 0.004) and UA groups (P = 0.008), while hsCRP was higher in UA group (P = 0.024). Serum C1q was weakly positively associated with hsCRP (r = 0.24, P < 0.001) but not correlated with Gensini score. Logistic regression identified C1q (OR: 0.87 per 10 mg/L, 95% CI: 0.79-0.95, P = 0.001) and hsCRP (OR: 1.08 mg/L, 95% CI: 1.01-1.15, P = 0.032) as independent determinants of CAD. Furthermore, combined C1q and hsCRP level showed higher discriminatory accuracy in predicting CAD than C1q (AUC: 0.676 vs 0.585, P = 0.101; NRI: 10.4%, P = 0.049; IDI: 3.9%, P < 0.001) or hsCRP (AUC: 0.676 vs 0.585, P = 0.101; NRI: 16.7%, P = 0.006; IDI: 5.8%, P < 0.001).

Reduced serum C1q and increased hsCRP are independently associated with CAD and could be potential predictors for CAD diagnosis. Furthermore, combined C1q and hsCRP showed better performance in predicting CAD than using single one.

Circulating cystatin C has been considered as an independent predictor of cardiovascular and all-cause mortality in the general population. The purpose of this study was to evaluate the prognostic value of baseline circulating cystatin C levels in patients with acute coronary syndrome (ACS) through meta-analysis.

Prospective studies about the relationship between the level of cystatin C and the prognosis of ACS patients were searched on PubMed, Web of science, Cochrane Library and Embase databases from the establishment of the databases to July 2020. The prognostic values included in this analysis covered all-cause mortality, major adverse cardiovascular events (MACE) and recurrent myocardial infarction. The effect index between cystatin C level and ACS risk was carried out by hazard ratio (HR). Stata 15.0 software was used for statistical analysis. The quality of the included literature was evaluated according to Newcastle-Ottawa Scale (NOS).

A total of 10 studies were included in this meta-analysis. The results showed that high cystatin C levels significantly predicted the all-cause mortality of ACS, HR = 2.53 (95%CI: 1.72 ~ 3.72). High cystatin C level significantly predicted MACE of patients with ACS, HR = 3.24 (95%CI: 1.30 ~ 8.07). However, it had no significant predictive significance for recurrent myocardial infarction, HR = 1.71 (95%CI:0.99 ~ 2.97).

Our meta-analysis showed that high cystatin C levels were significantly associated with the death risk and MACE in ACS patients. Therefore, cystatin C can be included in the risk stratification model to guide the treatment of high-risk ACS patients.