Epidemiological studies have demonstrated inconsistent associations between drinking water magnesium levels and risk of mortality from coronary heart disease (CHD); thus, a meta-analysis was performed to assess the association between them. Relevant studies were searched by the databases of Cochrane, EMBASE, PubMed and Web of Knowledge. Pooled relative risks (RR) with their 95% CI were calculated to assess this association using a random-effects model. Finally, nine articles with 10 studies involving 77,821 CHD cases were used in this study. Our results revealed an inverse association between drinking water magnesium level and CHD mortality (RR = 0.89, 95% CI = 0.79–0.99, I² = 70.6). Nine of the 10 studies came from Europe, and the association was significant between drinking water magnesium level and the risk of CHD mortality (RR = 0.83, 95% CI = 0.69–0.98). In conclusion, drinking water magnesium level was significantly inversely associated with CHD mortality.

Liquid–liquid phase separation (LLPS) is a biochemical process in cells that can drive proteins, RNA, and other molecules to concentrate into droplets. These droplets do not have a lipid membrane but rather exist as distinct organelles relative to the surrounding environment, and act as biochemical reaction chambers. In recent years, significant progress has been made in the study of LLPS, especially in the neurodegenerative disease, cancer, and virology fields, but little is known about LLPS in cardiovascular disease (CVD). In this review, we discuss the current understanding of the mechanism and biological functions of LLPS, particularly its roles in regulating CVD.

Background: Vascular calcification during aging is highly prevalent in patients with cardiovascular disease; however, there is still no improvement in clarifying the development of vascular calcification. FOSL1 is a transcription regulator belonging to the AP-1 family, which has a unique function in vascular senescence, but its role in vascular calcification needs to be further explored. Methods: Primary mouse vascular smooth muscle cells were isolated and used to construct a calcification model in vitro. Seven-week-old male C57BL/6 mice were used to build the vitD3-induced calcification model in vivo. qRT-PCR and western blot were used to verify the expression of FOSL1 and other genes expressed in vascular smooth muscle cells and aortas. The level of calcification was determined by Alizarin Red S (ARS) staining and the calcium content assay. The level of cellular GSH was detected by the GSH assay kit. Results: Here, we report that FOSL1 was up-regulated after high-calcium/phosphate treatment in both the in vivo and in vitro vascular calcification models. Functional studies have shown that the reduction of FOSL1 attenuates ferroptosis and calcification in vascular smooth muscle cells, as indicated by ARS staining, calcium content assay, and western blot. The inhibition of FOSL1 downregulated the expression of bone-related molecules including Msh Homeobox 2 (MSX2) and tumor necrosis factor receptor superfamily, member 11b/osteoprotegerin (OPG), suggesting that FOSL1 promoted osteogenic differentiation of vascular smooth muscle cells. Furthermore, we found that the ferroptosis-inducing drug erastin can significantly accelerate calcification in the aortic ring while Ferrostatin-1 (fer-1), a drug to protect cells from ferroptosis, can alleviate calcification. Further experiments have shown that inhibiting FOSL1 can promote the expression of ferroptosis-related genes and attenuate calcification. Functionally, cellular GSH levels were increased after the reduction of FOSL1. Conclusions: In this study, we observed a significant protective effect when we reduced the expression of FOSL1 during vascular calcification, and this effect might regulate ferroptosis to a great extent.

Background: Retinal microvasculature has been associated with coronary artery disease (CAD), but the exact contributory role in coronary total occlusion (CTO) is unclear. We aimed to investigate whether retinal vasculature is associated with CTO and could provide incremental value in the assessment of CTO.Methods: A total of 218 CAD patients including 102 CTO and 116 non-CTO were enrolled. Retinal vasculature was measured by optical coherence tomography angiography (OCTA) for all patients. Receiver operating characteristic (ROC) curve was used to assess the performance of retinal vasculature in differentiating CTO from non-CTO patients.Results: In non-CTO CAD patients, vessel density (VD) of mean superficial capillary plexus (SCP) and parafovea SCP were 49.85 and 52.56%, respectively; in CTO patients, VD of mean SCP and parafovea SCP were 47.77, and 49.58%, respectively. After multiple adjustment, VD in the SCP was significantly lower in CTO patients compared to non-CTO patients. VD of superior hemi in the parafovea SCP combined with the clinical variates showed the best ability to predict CTO from CAD with an area under the curve (AUC) of 0.812 (specificity of 89.0% and sensitivity of 65.9%).Conclusions: In CTO patients, retinal VD was significantly decreased, and microvascular damage might specifically target to arterioles than capillaries. Retinal vasculature could thus be a surrogate for detecting the microvascular damage and assist in the assessment of CTO patients. OCTA examination could be suggested to monitor the process of coronary arteries lesions.

Objectives To investigate the role of pulmonary artery pressure (PAP) in predicting in-hospital death after valve replacement surgery in middle-aged and aged patients with rheumatic mitral disease. Design An observational study. Setting Guangdong General Hospital, China. Participants 1639middle-aged and aged patients (mean age 57±6 years) diagnosed with rheumatic mitral disease, undergoing valve replacement surgery and receiving coronary angiography and transthoracic echocardiography before operation, were enrolled. Interventions All participants underwent valve replacement surgery and received coronary angiography before operation. Primary and secondary outcome measures In-hospital death and 1-year mortality after operation. Methods Included patients were divided into four groups based on the preoperative PAP obtained by echocardiography: group A (PAP≤30 mm Hg); group B (>30 mm Hg50 mm Hg70 mm Hg). The relationship between PAP and in-hospital death and cumulative rate of 1-year mortality was evaluated. Results In-hospital mortality rate increased gradually but significantly as the PAP level increased, with 1.9% in group A (n=268), 2.3% in group B (n=771), 4.7% in group C (n=384) and 10.2% in group D (n=216) (p70 mm Hg was an independent predictor of in-hospital death (OR=2.93, 95% CI 1.61 to 5.32, p52.5 mm Hg had a sensitivity of 60.3% and specificity of 67.7% in predicting in-hospital death (area under the curve=0.672, 95% CI 0.602 to 0.743, p52.5 mm Hg had higher 1-year mortality after operation than those without (log-rank=21.51, p<0.001). Conclusions PAP could serve as a predictor of postoperative in-hospital and 1-year mortality after valve replacement surgery in middle-aged and aged patients with rheumatic mitral disease.