A novel radiomics-based technique for identifying vulnerable coronary plaques: a follow-up study.

BACKGROUND: Previous reports have suggested that coronary computed tomography angiography (CCTA)-based radiomics analysis is a potentially helpful tool for assessing vulnerable plaques. We aimed to investigate whether coronary radiomic analysis of CCTA images could identify vulnerable plaques in patients with stable angina pectoris. METHODS: This retrospective study included patients initially diagnosed with stable angina pectoris. Patients were randomly divided into either the training or test dataset at an 8 : 2 ratio. Radiomics features were extracted from CCTA images. Radiomics models for predicting vulnerable plaques were developed using the support vector machine (SVM) algorithm. The model performance was assessed using the area under the curve (AUC); the accuracy, sensitivity, and specificity were calculated to compare the diagnostic performance using the two cohorts. RESULTS: A total of 158 patients were included in the analysis. The SVM radiomics model performed well in predicting vulnerable plaques, with AUC values of 0.977 and 0.875 for the training and test cohorts, respectively. With optimal cutoff values, the radiomics model showed accuracies of 0.91 and 0.882 in the training and test cohorts, respectively. CONCLUSION: Although further larger population studies are necessary, this novel CCTA radiomics model may identify vulnerable plaques in patients with stable angina pectoris.

Research progress on the role of exosomes in obstructive sleep apnea-hypopnea syndrome-related atherosclerosis.

Cardiovascular disease (CVD) is a leading cause of mortality worldwide. Atherosclerosis, a multifactorial disease with complicated pathogenesis, is the main cause of CVD, underlying several major adverse cardiovascular events. Obesity is the main cause of obstructive sleep apnea (OSA) and a significant risk for atherosclerosis. OSA is an independent risk factor for CVD. Recent research has focused on understanding the underlying molecular mechanisms by which OSA influences atherosclerosis pathogenesis. The role of exosomes in this process has attracted considerable attention. Exosomes are a type of extracellular vesicles (EV) that are released from many cells (both healthy and diseased) and mediate cell-to-cell communication by transporting microRNAs (miRNAs), proteins, mRNAs, DNA, or lipids to target cells, thereby modulating the functions of target cells and tissues. Intermittent hypoxia in OSA alters the exosomal carrier in circulation and promotes the permeability and dysfunction of endothelial cells, which have been associated with the pathogenesis of atherosclerosis. This review discusses the potential roles of exosomes and exosome-derived molecules in the development and progression of OSA-related atherosclerosis. Additionally, we explore the possible mechanisms underlying OSA-related atherosclerosis and provide new insights for the development of novel exosome-based therapeutics for OSA-related atherosclerosis and CVD.

Stem cell-derived exosomes in the treatment of acute myocardial infarction in preclinical animal models: a meta-analysis of randomized controlled trials.

BACKGROUND: Exosomes (EXOs) derived from stem cells have become a potential new treatment for acute myocardial infarction (AMI). However, their impact is still not fully understood. Therefore, we performed this meta-analysis to systematically review the efficacy of EXOs on AMI in preclinical animal models. METHODS: We searched PubMed, EMBASE, and the Web of Science from September 1, 1980 to September 1, 2021, to retrieve the studies reporting the therapeutic effects of EXOs on AMI animal models. Secondary endpoints include the fractional shortening (FS), infarct size (IS), fibrosis area (FA), the TNF-α, IL-6 and IL-10 levels, the apoptosis rate and the number of autophagic vesicles. Two authors independently screened the articles based on inclusion and exclusion criteria. All statistical analyses were conducted using Stata14.0. RESULTS: Ten studies satisfied the inclusion criteria. Pooled analyses demonstrated that the levels of LVEF (WMD = 3.67%; 95% CI 2.28-5.07%; P = 0.000), FS (WMD = 3.69%; 95% CI 2.06-5.33%; P = 0.000), IS (WMD = -4.52%, 95% CI - 7.14 to - 1.9%; P = 0.001), and FA (WMD = -7.04%, 95% CI - 8.74 to - 5.34%; P = 0.000), TNF-α (WMD = -3.09, 95% CI - 5.47 to - 0.72; P = 0.011), TL-6 (WMD = -6.34, 95% CI - 11.2 to - 1.49; P < 0.01), TL-10 (WMD = 6.37, 95% CI 1.53-11.21; P = 0.01), the apoptosis rate (WMD = -8.23, 95% CI - 15.29 to - 1.17; P = 0.000), and the number of autophagic vesicles (WMD = -4.52, 95% CI - 7.43 to - 1.62; P = 0.000). Subgroup analysis showed that the EXOs were derived from HMSCs. Subgroup analysis showed that the EXOs derived from HMSCs, and that exosome therapy immediately after myocardial infarction can better improve the LVEF. CONCLUSIONS: EXOs therapy has the potential to improve cardiac function, fibrogenesis, and inflammatory response, as well as reducing cell apoptosis and autophagy in preclinical AMI animal models. This can inform future human clinical trials of EXOs.