Muscle in heart disease: Highlights from the European Society of Cardiology's Annual Meeting 2012

Abstract

Cardiac cachexia and alterations in muscle metabolism are a co-morbidity that can develop in advanced stages of chronic heart failure (HF). Up to 15% of ambulatory patients with HF are affected and present with a loss of different tissue types including muscle mass. Whilst cardiac cachexia has long been a neglected clinical entity, current HF guidelines of the European Society of Cardiology (ESC) include a section on weight management in patients with HF at risk of cardiac cachexia. This article highlights some recent studies of metabolic and functional alterations of the muscle in HF that were presented at the annual meeting of the ESC in August 2012 in Munich, Germany.The studies presented were focused on dysfunction of respiratory and limb skeletal musculature as well as metabolic features of myocardium in HF. Strategies improving muscle function and peak oxygen consumption in HF such as (inspiratory) muscle training and treatment of central sleep apnea by adaptive servoventilation are described. The latter shows promising results regarding HF symptoms and exercise capacity but still has to prove survival benefits in larger trials.A rat model highlights the value of microRNAs to regulate exercise-induced skeletal muscle angiogenesis. Another study provides evidence for changes in substrate utilisation depending on the functional status of mitochondria in the failing heart and points to mitochondrial dysfunction as a potential mediator of metabolic remodelling.Though treatments remain to be established, these findings may pave the way for effective therapeutic approaches to altered muscle function and cardiac cachexia.