Acute coronary syndromes articles from across Nature Portfolio

Boccella, Yu and colleagues reveal that the transmembrane protein ANTXR1 regulates post-infarction fibrotic remodeling, and its inhibition blocks collagen turnover and improves heart function.

New evidence from five randomized trials suggests that withholding β-blockers after myocardial infarction (MI) is safe for carefully selected, low-risk patients. However, even if β-blockers are not required to treat ventricular dysfunction, hypertension or arrhythmias, it might still be wiser to continue treatment during the vulnerable period immediately after MI and withdraw treatment several months later.

In patients with residual inflammation after acute myocardial infarction, antibody-mediated antagonism of the oxidized LDL receptor LOX1 does not induce significant regression of noncalcified atherosclerotic plaque volume over the course of 9 months compared with placebo, according to the GOLDILOX-TIMI 69 trial.

In the mouse ischaemic myocardium, neutrophils promote ventricular tachycardia via the secretion of resistin-like molecule-γ, according to a new study published in Science.

Routine screening for Helicobacter pylori infection during hospitalization for myocardial infarction does not reduce the risk of upper gastrointestinal bleeding, according to findings from the HELP-MI SWEDEHEART trial, although secondary and subgroup analyses suggest potential clinically meaningful benefits.

Immunomodulatory approaches have gained momentum in cardiology. A report now highlights how low-dose interleukin-2 treatment expands regulatory T cells, reducing inflammation, in patients with acute coronary syndrome, shedding light on T cell antigen specificity and differentiation in cardiovascular disease.