Sex and gender in myocardial hypertrophy

Heart failure (HF) is one of the leading causes of cardiovascular mortality and morbidity in the western world. It affects men at younger age than women. Women develop more frequently diastolic HF, associated with the major risk factors diabetes and hypertension and men more frequently systolic HF due to coronary artery disease. Under stress, male hearts develop more easily pathological hypertrophy with dilatation and poor systolic function than female hearts. Women with aortic stenosis have more concentric hypertrophy with better systolic function, less upregulation of extracellular matrix genes and better reversibility after unloading. Stressed female hearts, from mice and men, maintain energy metabolism better than male hearts and are better protected against calcium overload. Estrogens and androgens and their receptors are present in the myocardium and lead to coordinated regulation of functionally relevant pathways. Collagen synthesis and degradation as well as mitochondrial energy metabolism have been identified as most prominent sources for sex differences in experimental and clinical HF. In addition, men with end‐stage cardiomyopathy have more frequently auto‐antibodies than women. Expensive and invasive therapies like advanced pacemakers and transplantation are underused in women. In spite of worse diagnostics and therapy, prognosis is better in women than in men.