Leeds Institute of Cardiovascular & Metabolic Medicine, University of Leeds, Leeds, LS2 9JT, UK.
Published: October 2020
AI Article Synopsis
Article Abstract
China is experiencing rapid urbanization and industrialization with correspondingly high levels of air pollution. Although the harm of PM has been long reported, it is only quite recently that there is increasing concern in China for its possible adverse health effects on cardiovascular disease. We reviewed the epidemiologic evidence of potential health effects of PM on cardiovascular disease reported from recent studies in China (2013 onwards). There is clear evidence for the contribution of PM to cardiovascular outcomes, including mortality, ischemic heart disease, and stroke from studies based in various regions in China. This evidence adds to the global evidence that PM contributes to adverse cardiovascular health risk and highlights the need for improved air quality in China.
Background: Adults with congenital heart disease (ACHD) can face a lifelong risk of premature cardiovascular events. Endothelial dysfunction and arterial stiffness may be some of the key mechanisms involved. Early identification of endothelial damage in ACHD could be crucial to mitigate the adverse events.
Background: Computational modeling indicated that pathological high shear stress (HSS; 100 dyn/cm) is generated in pulmonary arteries (PAs; 100-500 µm) in congenital heart defects causing PA hypertension (PAH) and in idiopathic PAH with occlusive vascular remodeling. Endothelial-to-mesenchymal transition (EndMT) is a feature of PAH. We hypothesize that HSS induces EndMT, contributing to the initiation and progression of PAH.
Background: Women who had preeclampsia (a history of preeclampsia) have a >4-fold risk of developing cardiovascular disease compared with women who had an uncomplicated pregnancy (history of healthy pregnancy). Despite the remission of clinical symptoms after pregnancy, vascular endothelial dysfunction persists postpartum, mediated in part by exaggerated Ang II (angiotensin II)-mediated constriction. However, the role of vasodilatory ATRs (Ang II type 2 receptors) in this dysfunction is unknown.
Transcription factors collaborate with epigenetic regulatory factors to orchestrate cardiac differentiation for heart development, but the underlying mechanism is not fully understood. Here, we report that GATA-6 induces cardiac differentiation but peroxisome proliferator-activated receptor α (PPARα) reverses GATA-6-induced cardiac differentiation, possibly because GATA-6/PPARα recruits the polycomb protein complex containing EZH2/Ring1b/BMI1 to the promoter of the cardiac-specific α-myosin heavy chain (α-MHC) gene and suppresses α-MHC expression, which ultimately inhibits cardiac differentiation. Furthermore, Ring1b ubiquitylates PPARα and GATA-6.
Endovascular repair has significantly improved the treatment of aortic aneurysms, particularly in older and high-risk patients. However, many studies have not found significant differences in long-term outcomes when comparing open and endovascular repair methods. Additionally, endovascular repair is associated with a higher rate of aortic-related reinterventions compared to open repair (OR), sometimes necessitating late open surgical conversion (LOSC).
