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Valsartan is safe and effective in improving cardiac structure and function in patients with early-stage hypertrophic cardiomyopathy, according to results from the phase II VANISH trial.
Human genetic studies combined with biotechnological advances have guided and accelerated the development of PCSK9-targeting therapies. In this Clinical Outlook, we highlight present and future approaches for PCSK9 inhibition to reduce LDL-cholesterol levels and the risk of atherosclerotic cardiovascular disease.
A form of adenine base editing has been used in mouse embryos to correct a genetic variant associated with hypertrophic cardiomyopathy. This approach is potentially safer than other forms of germline gene editing, which carry a risk of off-target editing and the introduction of indels.
Precision medicine envisages a changed paradigm for health care through better understanding of individual disease susceptibility and prognosis, enabling more personalized treatment. Enabling technologies such as the health digital twin are rapidly evolving, presenting important challenges and opportunities to be tackled within local contexts.
Mice deficient in type 2 innate lymphoid cells have a greater accumulation of inflammatory macrophages and poorer cardiac function after myocardial infarction compared with control mice, indicating a role for this subset of lymphocytes in regulating inflammatory pathways in the injured heart.
Two new studies show that pharmacological blood pressure (BP) reduction is effective in older individuals and that a more intensive treatment with a lower BP threshold reduces the incidence of cardiovascular events in older patients with hypertension.
In a clinical first, empagliflozin treatment cuts the risk of cardiovascular death and hospitalization compared with placebo in patients with heart failure with preserved ejection fraction.
The STROKESTOP trial and The LOOP study used different approaches to screen for atrial fibrillation, with the aim of initiating oral anticoagulation to prevent stroke and death.
In the SSaSS trial, substituting regular table salt (100% sodium chloride) with an alternative containing 25% potassium chloride reduced the rate of stroke, major cardiovascular events and all-cause death.
In the QUARTET trial, initial treatment with a single pill containing quarter doses of four antihypertensive drugs achieved and maintained a greater blood-pressure-lowering effect than initial monotherapy with full-dose irbesartan.
Delivery of automated external defibrillators with drones to the scene of an out-of-hospital cardiac arrest is feasible and can be faster than an ambulance, according to findings from a pilot clinical study.
Influenza vaccination shortly after a myocardial infarction or in high-risk coronary heart disease reduces the risk of future cardiovascular events, according to findings from the IAMI trial.
Ablation plus cardiac resynchronization therapy is superior to pharmacological therapy in reducing mortality in patients with atrial fibrillation and a narrow QRS complex who were hospitalized with heart failure.
Data from the MASTER DAPT trial indicate that the duration of dual antiplatelet therapy can be abbreviated in patients at high risk of bleeding undergoing implantation of a drug-eluting stent, resulting in a reduction in bleeding risk without an increase in ischaemic events.
Dietary supplementation with NAD+ precursors or ketone esters has been shown to improve mitochondrial function in preclinical models of heart failure with either reduced or preserved ejection fraction. Both supplementation approaches hold promise but are in the early stages of development as clinical therapies for heart failure.
Atherosclerosis causes myocardial infarction, ischaemic cardiomyopathy, many ischaemic strokes and jeopardized limbs. Despite enormous progress, atherosclerosis has become the major cause of death worldwide. This Comment intertwines clinical and basic advances in atherosclerosis to illustrate their interdependence, which provides a template for a way forwards to conquer the scourge of atherosclerotic cardiovascular disease.
High levels of extracellular glucose induce trained immunity in macrophages, promoting a pro-atherosclerotic phenotype that persists even after normalization of glucose levels.
