Endothelial dysfunction in adults with congenital heart disease: A systematic review and meta-analysis.

Background: Adults with congenital heart disease (ACHD) can face a lifelong risk of premature cardiovascular events. Endothelial dysfunction and arterial stiffness may be some of the key mechanisms involved. Early identification of endothelial damage in ACHD could be crucial to mitigate the adverse events.

Could SGLT2 inhibitors improve outcomes in patients with heart failure and significant valvular heart disease? Need for action.

Delivering valvular intervention for all eligible patients with valvular heart disease (VHD) in a timely manner remains a challenge. Therefore, a high number of patients with heart failure (HF) and VHD receive pharmacotherapy while awaiting intervention or as destination therapy if they are deemed inoperable. The sodium-glucose co-transporter-2 inhibitors (SGLT2i) are recommended with a class I indication for patients with chronic HF throughout the spectrum of left ventricular ejection fraction.

Atherosclerotic Risk Factor Prevalence in Adults With Congenital Heart Disease: A Meta-Analysis.

Background: The risk of atherosclerotic cardiovascular disease (ASCVD) in adults with congenital heart disease (ACHD) is comparable to that of the general population and is driven by traditional ASCVD risk factors.

Objectives: The aim of the study was to estimate the prevalence of traditional ASCVD risk factors (hypertension, dyslipidemia, diabetes mellitus [DM], obesity, smoking, and physical inactivity) in ACHD and compare it with the general population.

Methods: A systematic literature search was conducted up to May 15, 2024, to identify studies (with or without control group) reporting the prevalence of ASCVD risk factors in ACHD.

The many faces of SCN5A pathogenic variants: from channelopathy to cardiomyopathy.

The SCN5A gene encodes the alpha subunit of the cardiac sodium channel, which plays a fundamental role in the generation and propagation of the action potential in the heart muscle. During the past years our knowledge concerning the function of the cardiac sodium channel and the diseases caused by mutations of the SCN5A gene has grown. Although initially SCN5A pathogenic variants were mainly associated with channelopathies, increasing recent evidence suggests an association with structural heart disease in the form of heart muscle disease.