The ‘skeletal muscle hypothesis in heart failure’ revised

This editorial refers to ‘Muscle wasting in patients with chronic heart failure: results from the studies investigating co-morbidities aggravating heart failure (SICA-HF)’, by S. Fulster et al. , doi:10.1093/eurheartj/ehs381 Understanding the genesis of the symptoms which commonly limit exercise tolerance in disease states remains one of the major challenges facing scientists and clinicians involved in the care of patients with chronic heart failure (CHF). In contrast to the traditional vision that saw a malfunction of the heart as a pump as the leading cause, in the last 20 years there has been mounting evidence that the complex pathophysiology of CHF begins with an abnormality of the heart as a ‘ primum movens ’, but involves adaptive changes in many body organs and systems, including the cardiovascular, musculoskeletal, renal, neuroendocrine, haemostatic, immune, and inflammatory systems. These changes play key roles in the HF syndrome and its progression.1 Three of these systems have been considered of particular significance, as they constitute universal mechanisms that relate to survival of the species and they are conserved in evolution: the neurohormonal system maintaining blood pressure and/or peripheral perfusion in the optimal range, the immune system protecting the body from the intrusion of external microorganisms, and the haemostatic mechanisms limiting excessive bleeding.2 The preservation of arterial perfusion pressure is a fundamental necessity for the maintenance of the blood supply to the vital organs and systems. During evolution, specific mechanisms have been developed to achieve this aim even in highly unfavourable environmental conditions. A key role is played by the autonomic nervous system in controlling homeostasis, with major effects on the heart and blood vessels, and indirect modulation of blood volume …