Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
The adventitia of atherosclerotic arteries is innervated by efferent and afferent neurons that form neuroimmune cardiovascular interfaces and modulate disease progression; ablating the sympathetic innervation to these regions is a potential therapeutic strategy.
The results of two early-phase trials of novel lipid-lowering agents targeting ANGPTL3 and lipoprotein(a) might help to combat the residual risk of cardiovascular events in patients treated with statins and/or PCSK9 inhibitors to lower LDL-cholesterol levels.
In patients with atrial fibrillation, treatment with asundexian, a novel, oral, small-molecule inhibitor of coagulation factor XIa, reduces the incidence of bleeding compared with standard dosing with the factor Xa inhibitor apixaban.
A strategy of treating mild chronic hypertension in pregnant women using a blood pressure target of <140/90 mmHg reduces the risk of pre-eclampsia and does not increase the risk of poor fetal growth or fetal death.
In the PROMPT-HF trial, alerts embedded within electronic health records that contained guideline-directed recommendations for patients with heart failure improved the prescription of guideline-directed medical therapy.
Use of hormone-replacement therapy (HRT) for menopausal symptoms is associated with a modest reduction in plasma lipoprotein(a) (Lp(a)) levels but is not associated with a lower Lp(a)-associated risk of coronary heart disease compared with no HRT use, according to findings presented at ACC.22.
A model generated using proteomics and machine learning that included 27 proteins was able to predict the 4-year risk of myocardial infarction, heart failure, stroke or all-cause death better than a clinical model and was sensitive to the adverse and beneficial changes in outcome.
In patients with acute myocardial infarction, the addition of the PCSK9 inhibitor alirocumab to high-intensity statin therapy leads to a greater regression of atherosclerotic plaques in non-infarct-related arteries after 52 weeks than statin therapy alone, according to findings from the PACMAN-AMI trial.
Statins increase the rate of macrophage efferocytosis through suppression of the expression of the ‘don’t-eat-me’ molecule CD47 on atherosclerotic plaque apoptotic cells, and pro-efferocytic therapies amplify the anti-atherosclerotic effects of statin treatment in an additive manner and independently of any lipid-lowering effects of statins.
The CHIEF-HF trial investigators employed a novel all-virtual study design to show that canagliflozin significantly reduces symptom burden in patients with heart failure.
A novel approach to assess the network of interactions between GATA4 and TBX5, which are both implicated in congenital heart disease, has led to the discovery of a gene with a previously unknown role in heart development.
Alterations to the composition of the gut microbiota are associated with changes in the levels of serum metabolites during the development of cardiometabolic disease, before the onset of overt ischaemic heart disease.
A new study shows that atrial fibrillation causes functional remodelling of the left ventricle via impairment of excitation–contraction coupling of ventricular cardiomyocytes, which is mediated by reduced systolic Ca2+ release and increased levels of oxidative stress.
Cardiac pacing that restores heart rate variability in the form of respiratory sinus arrhythmia improves outcomes in a sheep model of heart failure with reduced ejection fraction.
A new study describes the efficacy of novel platelet-mimicking procoagulant nanoparticles in resisting clot lysis and improving clot stability, resulting in reduced bleeding in rodent models of thrombocytopenia and haemorrhage.
A new study shows that cardiovascular diseases remodel the bone marrow vasculature, inducing endothelial dysfunction, vascular leakage, fibrosis and angiogenesis and ultimately leading to overproduction of the inflammatory leukocytes implicated in these conditions.