Cardiomyopathies articles from across Nature Portfolio

In this Review, Bozkurt provides an overview of the management of patients with heart failure across the full range of left ventricular ejection fraction, derived from the recommendations in the latest US and European guidelines.

Efforts to treat heart failure with antioxidants have failed. Here, authors reveal a robust sex-dependent endogenous defense against oxidative damage and demonstrate antioxidative treatment’s efficacy solely in subjects with inadequate redox capacity.

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.

Arrhythmogenic cardiomyopathy is a major cause of sudden death among young people. Three studies show that gene therapy to restore the desmosomal protein PKP2 holds promise in improving the prognosis of affected individuals.

Mosaic loss of chromosome Y (mLOY) refers to the condition in male individuals in which a detectable fraction of cells lose the Y chromosome. Prevalent in haematopoietic cells, this common somatic mutation is associated with decreased longevity and an increased risk of age-related diseases, including cardiovascular disease. Haematopoietic mLOY provides further insight into the sex-specific disparities that exist in disease susceptibility.

Treatment with the small interfering RNA patisiran preserves functional capacity and improves health status and quality of life in patients with transthyretin cardiac amyloidosis, according to data from the 12-month double-blind period of the ongoing APOLLO-B trial.

Passive stiffness measurements in heart samples of a ‘titin-cleavage’ mouse model reveal the elastic and viscous force contributions of individual myocardial components. Titin is the principal contributor to elastic forces, whereas the microtubules and titin, followed by actin, dominate the viscous force contributions; the extracellular matrix contributes at high strain.

An antibody-based therapy for transthyretin amyloid cardiomyopathy is safe, and initial findings from a phase I trial suggest that it might deplete amyloid deposits in the heart.