Social Support and Self-Efficacy as Mediating Factors Affecting the Association Between Depression and Medication Adherence in Older Patients with Coronary Heart Disease: A Multiple Mediator Model with a Cross-Sectional Study.

PURPOSE: Medication non-adherence is a major public health issue. Recent evidence suggests that depression, inadequate social support, and lower levels of self-efficacy are associated with poor medication adherence. However, the mechanism underlying the association among depression, social support, self-efficacy and medication adherence is unclear. This study aims to examine the mediating role of social support and self-efficacy between depression and medication adherence in older patients with coronary heart disease. PATIENTS AND METHODS: Data were collected from 238 hospitalized older patients with coronary heart disease. Depression, social support, self-efficacy, and medication adherence were assessed using structured questionnaires. A serial multiple mediation model was tested using the PROCESS macro for SPSS. RESULTS: A total of 238 older patients with CHD with a mean age of 70.5 years were involved in this cross-sectional study. Depression was negatively correlated with medication adherence in older patients with coronary heart disease. Social support and self-efficacy were positively associated with medication adherence, and fully mediated the relationship between depression and medication adherence. Three mediation paths were included in the model: (a) social support, (b) chain combination of social support and self-efficacy, and (c) self-efficacy. CONCLUSION: Social support and self-efficacy explain the association of depression and medication adherence in older CHD patients and may be the keys target for enhanced intervention to improve medication adherence in older CHD patients with depression.

Biodegradable Biomaterial Arterial Stent in the Treatment of Coronary Heart Disease.

This study aims to evaluate the clinical application value of two materials, drug-eluting stent, and biodegradable stent, in the treatment of coronary heart disease. The results show that the therapeutic effects of drug-eluting stents and biodegradable stents are similar. Both treatment methods have high safety and effectiveness. The ideal coronary artery stent should have good biocompatibility, safety, and possibility.

Abnormal expression of long non-coding RNA rhabdomyosarcoma 2-associated transcript (RMST) participates in the pathological mechanism of atherosclerosis by regulating miR-224-3p.

Study shows that long non-coding RNA (lncRNA) plays a regulatory role in cardiovascular diseases, and the mechanism of rhabdomyosarcoma 2-associated transcript (RMST) in atherosclerosis (AS) is still unclear. This study aimed to evaluate the expression of RMST and its possible role in the occurrence of AS. RMST and miR-224-3p level in serum and human umbilical vein endothelial cells (HUVECs) were determined by real-time quantitative PCR (RT-qPCR). In vitro atherosclerotic cell model was achieved by treating HUVECs with ox-LDL. Receiver operating characteristic (ROC) curve assessed the diagnostic value of RMST in AS, and Pearson correlation coefficient estimated the correlation of RMST with carotid intima-media thickness (CIMT) and carotid-femoral pulse wave velocity (cfPWV). Cell counting kit-8 (CCK-8) assay and Enzyme-linked immunosorbent assay (ELISA) were performed to evaluate the effect of RMST on cell viability and inflammatory response. The luciferase analysis was used to validate the relationship between RMST and miR-224-3p. The results showed that in serum and HUVECs, RMST levels were increased, while miR-224-3p level was decreased. ROC curve suggested that RMST had clinical diagnostic value for AS. Besides, CIMT and cfPWV were positively correlated with RMST levels, respectively. In HUVECs, RMST-knockdown notably improved the cell viability and inhibited the production of inflammatory factors. Moreover, miR-224-3p was the target of RMST. In conclusion, RMST has the potential to be a diagnostic marker for AS. RMST-knockdown contributes to the enhancement of cell viability and the inhibition of inflammatory response, which may provide new insights into the conquest of AS.