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Two studies now report that TET2-driven clonal haematopoiesis of indeterminate potential (CHIP) is associated with poor prognosis in patients with heart failure (HF) and preserved ejection fraction and that DNMT3A CHIP driver mutations promote dysregulated gene expression profiles that are associated with inflammation in monocytes in the setting of HF.
The link between migraine and cardiovascular disease is complex and involves overlapping mechanisms, such as endovascular disturbances. Challenges in measuring migraine, in distinguishing between causation and prediction, and in the understanding of clinical implications highlight the need for further research to guide treatment and cardiovascular risk assessment for the millions of individuals living with migraine.
In patients with heart failure (HF) with preserved ejection fraction and obesity, treatment with the glucagon-like peptide 1 receptor agonist semaglutide (2.4 mg) leads to large reductions in HF-related symptoms and physical limitations, improves exercise function and decreases body weight compared with placebo, according to the STEP-HFpEF trial.
In this Review, the authors discuss the clinical and experimental data on immunomodulatory effects of evidence-based treatments for heart failure and their primary mechanisms of action, and highlight potential therapeutic targets and opportunities for the development and application of novel immunomodulatory treatments for heart failure.
An interaction between blood vessels and nerve fibres in the heart contributes to the decline in nerve density in the ageing left ventricle, potentially increasing susceptibility to arrhythmias.
The FIRE trial showed that complete revascularization improves outcomes in older patients with myocardial infarction (MI) and multivessel disease compared with culprit-lesion-only revascularization, whereas the MULTISTARS AMI trial reported that immediate multivessel revascularization is non-inferior to staged revascularization in patients with ST-segment elevation MI.
In the CASTLE HTx trial, patients with symptomatic atrial fibrillation and end-stage heart failure who underwent catheter ablation and received medical therapy had improved outcomes compared with patients who received medical therapy only.
New data from the ECLS-SHOCK trial and a meta-analysis indicate that the routine use of venoarterial extracorporeal membrane oxygenation does not increase survival in patients with myocardial infarction-related cardiogenic shock.
Two clinical trials presented at the ESC Congress 2023 provide conflicting evidence on the use of optical coherence tomography to guide percutaneous coronary intervention.
According to data from the COP-AF trial, anti-inflammatory therapy with colchicine does not reduce the risk of perioperative atrial fibrillation or myocardial injury in patients undergoing major non-cardiac thoracic surgery.
Novel non-steroidal mineralocorticoid receptor antagonists (MRAs) have improved pharmacological properties compared with steroidal MRAs. Among the non-steroidal MRAs, finerenone has been approved for patients with chronic kidney disease who have diabetes mellitus and has demonstrated favourable safety and promising early results in patients with heart failure.
In patients with an acute myocardial infarction, disrupted circadian rhythms during the initial days in the cardiac intensive care unit, caused by factors such as noise, excessive night-time light and frequent patient–staff interactions, can have devastating effects on cardiac repair and long-term prognosis. Providing care that aligns with the patient’s natural circadian rhythms is critical for optimum long-term recovery. Incorporating ‘circadian medicine’ into clinical practice will provide important health-care benefits.
Unloading left atrial hypertension by catheter-based, transvenous creation of atrial shunts is being explored to treat heart failure. So far, trials including sham control have demonstrated safety and efficacy in lowering left-sided cardiac filling pressures. Ongoing trials will determine the effect on clinical outcomes.
In the REPRIEVE trial, pitavastatin treatment in patients with human immunodeficiency virus (HIV) infection without pre-existing cardiovascular disease prevented cardiovascular events compared with placebo.
A new study reveals that the disrupted sleep patterns that are frequently observed in patients with cardiac disease are driven by immune-mediated sympathetic denervation and dysfunction of the pineal gland, which leads to a decrease in the circulating levels of melatonin and subsequent sleep disruption.
Some species have a greater capacity for cardiac regeneration than others. In this Review, Weinberger and Riley summarize the diverse array of vertebrates that have been studied for their cardiac regenerative potential and the core mechanisms that regulate cardiac regeneration across vertebrate species.
In this Review, Marsan et al. discuss the different clinical scenarios in which valvular heart diseases and cardiomyopathies coexist, either as the cause of one another or because of a common aetiology, to highlight the need for an improved classification of these diseases with potential repercussions in clinical management and personalized treatment.
In the infarcted heart, pericytes have crucial roles in inflammatory signalling, angiogenesis, and scar formation and stabilization. In this Review, Avolio and colleagues discuss the numerous roles of cardiac pericytes in homeostasis and disease and describe the potential of pericyte-based therapy for restoring the perivascular niche after myocardial infarction.
A study shows that macrophages undergo substantial expansion in the diseased atria of patients with atrial fibrillation (AF), and identifies two potential immunotherapy targets for the treatment of AF.
In failing cardiomyocytes, depletion of carnitine acetyltransferase promotes cholesterol catabolism via the bile acid synthesis pathway. The intracellular accumulation of bile acid intermediates induces the release of mitochondrial DNA into the cytosol, triggering type I interferon responses and AIM2 inflammasome activation, thereby contributing to chronic myocardial inflammation and heart failure progression.
