Browse Articles

Haemophilia A is caused by variants in the gene that encodes coagulation factor VIII (FVIII). Sequencing of this gene in the 1980s was the initial step in developing replacement therapy with recombinant FVIII, and thereby removing the risk of blood-borne infections from plasma-derived FVIII.

Corey McAleese describes the study that identified the presence of metabolic heterogeneity in endothelial cells from different tissues and discusses its relevance to our current understanding of endothelial metabolism.

Milda Folkmanaite and Manuela Zaccolo highlight a study that demonstrates a role for phase-separated condensates of protein kinase A in buffering molecules of cAMP, to illustrate how phase separation of proteins in cardiac cells might contribute to the regulation of cardiac function.

In this Review, the authors describe the changes in metabolism that predispose individuals to developing atrial fibrillation (AF) and highlight the potential of available and emerging therapeutic strategies that target metabolic remodelling to treat AF.

Poscablo and colleagues identify a distinct haematopoietic platelet differentiation pathway that is enriched in ageing mice, which results in platelets that are hyper-reactive compared with canonical platelet populations.

In patients with type 2 diabetes mellitus and obesity, bariatric metabolic surgery is associated with a lower risk of the incidence of first-ever congestive heart failure than treatment with glucagon-like peptide 1 receptor agonists, according to a new study.

Data from the SEQUOIA-HCM trial show that aficamten, a cardiac myosin inhibitor, increases exercise capacity and improves quality of life in patients with symptomatic obstructive hypertrophic cardiomyopathy.

A study in Nature describes a single-cell-type strategy for vascular cell therapies that involves the artificial transplantation of mitochondria to endothelial cells, which promotes mitophagy and facilitates the formation of functional vessels in ischaemic tissue without the need for mesenchymal stromal cell support.

Activation of the bile acid receptor TGR5 inhibits CD36-mediated fatty acid uptake in cardiomyocytes and protects against cardiac lipotoxicity and the development of diabetic cardiomyopathy in mice, according to a new study.

In this Review, Adkar and Leeper describe the mechanisms of programmed cell death and efferocytosis, discuss how efferocytosis becomes impaired in atherosclerosis and other cardiometabolic diseases, and suggest potential strategies to target these pathways for the treatment of atherosclerotic cardiovascular disease.

In 1993, Lincoff and Topol claimed that the thrombolytic treatment of ST-segment elevation myocardial infarction was suboptimal in many patients and gave an ‘illusion of reperfusion’. In this Perspective article, the authors propose that a similar illusion of revascularization exists for contemporary percutaneous revascularization in patients with coronary artery disease and ischaemia, and identify how outcomes might be improved.

In the AEGIS-II trial, infusion of apolipoprotein A-I to increase cholesterol efflux capacity did not improve outcomes in patients with acute myocardial infarction.

Physiological responses to stress are thought to increase the risk of cardiovascular disease via haemodynamic, vascular and immune perturbations. In this Review, Vaccarino and Bremner focus on issues with the measurement of psychological stress and the underlying pathobiology connecting stress to the risk of cardiovascular disease.

Treatment for periodontal disease might reduce the recurrence of atrial fibrillation (AF) in patients undergoing ablation, suggesting that periodontitis is a modifiable risk factor for AF.

Findings from the ORBITA-COSMIC trial show that treatment of patients with stable coronary artery disease using a coronary sinus reducer improves angina symptoms but does not increase transmural myocardial perfusion.

In this Review, the authors discuss the receptors, ligands and interactors that regulate immune cell recruitment in atherosclerosis, describe mechanisms that promote the resolution of inflammation in atherosclerotic lesions, and highlight potential strategies to target these pathways for the treatment of atherosclerotic cardiovascular disease.

According to data from the IMPROVE-HCM trial, ninerafaxstat is well tolerated by patients with symptomatic non-obstructive hypertrophic cardiomyopathy and improves exercise performance among those who are most symptomatically limited.

Data from the DanGer Shock trial demonstrate that implantation of a microaxial flow pump in patients with ST-segment elevation myocardial infarction complicated by cardiogenic shock increases the survival rate compared with standard care alone.