Volume 17 Issue 3, March 2020

Levels of non-HDL cholesterol in the blood are strongly linked with long-term risk of cardiovascular disease, according to a new risk evaluation study that followed-up almost 400,000 individuals without cardiovascular disease at baseline for a median of 13.5 years.

Deficiency in the orphan G protein-coupled receptor 146 (GPR146) decreases blood lipid levels and protects against atherosclerosis in mice independently of LDL receptor activity, according to a new study.

Intravenous infusion of a platelet-derived growth factor promoted wound healing and increased survival in a pig model of myocardial infarction.

The Apple Heart Study demonstrates that the Apple Watch can detect atrial fibrillation inferred from the smartwatch heart-rate sensor with a high positive predictive value. However, we must now contend with many clinically relevant unknowns that were not addressed by the study, such as the ramifications of a false-positive result.

Clonal haematopoiesis of indeterminate potential (CHIP) commonly occurs as a result of mutations in transcriptional regulators and is associated with a doubling of the risk of atherosclerotic cardiovascular disease. Jaiswal and Libby propose that CHIP contributes to the increased inflammation seen in ageing and thereby explains some of the age-related risk of cardiovascular disease.

Rheumatic heart disease is a complication of group A streptococcal infection and rheumatic fever. In this Review, Muhamed and colleagues assess the emerging role of genome-wide association studies in detecting loci associated with genetic susceptibility to rheumatic heart disease.

Although saphenous vein grafts (SVGs) are the most commonly used conduit in coronary artery bypass graft surgery, vein graft failure (VGF) occurs in almost half of all patients with SVGs by 10 years after surgery. In this Review, Caliskan and colleagues discuss approaches to prevent saphenous VGF, including optimal harvesting techniques and intraoperative preservation strategies.

In this Review, Cai and colleagues discuss the complex crosstalk between different oxidase systems and the consequences of this crosstalk in mediating cardiovascular disease processes, focusing on the central role of particular NADPH oxidase isoforms activated in specific cardiovascular diseases.