Chronic heart failure (CHF) represents a major public health burden. The incidence of the disease is steadily increasing in most European countries and has been estimated to be 0.1-0.5% per year. The numbers are doubling with each decade to reach 3% in those over the age of 75. The clinical perspective remains poor, because about half of the patients with CHF die within four years of diagnosis (Remme et al., 2001). The prognosis remains poor, although the treatment of the disease has made significant advances over the last two decades. These advances have largely been made possible through a better understanding of the pathophysiology of CHF.
Members of the SICA-HF (Studies Investigating Comorbidities Aggravating Heart Failure) consortium have contributed significantly to broadening the views on CHF pathophysiology. Such findings have made novel therapeutic approaches possible, and since CHF progresses due to activation of neurohormones and pro-inflammatory cytokines, therapies to block excessive neuroendocrine activation have become a cornerstone of treatment. Indeed, beta-blockers, angiotensin receptor blockers, and aldosterone antagonists have only become part of heart failure treatment guidelines within the last 15 years.
Several subgroups of patients with CHF have received little attention so far. No treatment studies have focused on patients at the extreme ends of the body weight spectrum, i.e. patients with heart failure and obesity or patients with heart failure and cachexia. The reason is that such patients were routinely not considered to be different from patients with normal weight and that therapies that work in the one, should also work in the other. However, a wealth of data has accumulated over the last years to suggest otherwise. Unfortunately, no prospective data are available, and the available evidence stems only from retrospective analyses.