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Coronary artery disease is a pathological condition in which a coronary artery is narrowed or blocked, usually as a result of atherosclerosis. Stable angina, or 'angina pectoris', is the chest pain or discomfort that can result from the impaired blood flow through the blood vessels in the heart muscle, and usually occurs after exercise or stress.
Variant-to-gene-to-program is a new approach to building maps of genome function to link risk variants to disease genes and to convergent signalling pathways in an unbiased manner; its strength is demonstrated in coronary artery disease.
Protein-protein interaction networks of coronary artery disease (CAD) risk genes in human vascular cells are enriched for genetic variants associated with CAD and can be used to guide future research into the molecular pathogenesis of CAD.
In the ORBITA-2 trial, percutaneous coronary intervention was associated with a lower angina symptom score compared with a placebo procedure in patients with stable angina who were receiving minimal or no antianginal medication.
A machine learning model trained using clinical data from electronic health records generated a novel in silico quantitative score for coronary artery disease
Previous genome-wide association studies of coronary artery disease (CAD) have discovered multiple susceptibility loci but have largely failed to uncover causal genes. A new study identifies hundreds of likely causal genes underlying the genetic risk for CAD.
Viral infections and cardiovascular disease (CVD) share a two-way connection: viral infection can raise CVD risk, and people with CVD are more prone to severe viral infection. Zhao et al. now detail a molecular mechanism whereby macrophages from patients with CVD inhibit antiviral T cell responses via immune checkpoint activation.