Inflammation may play a central role in the pathophysiology of heart failure with preserved ejection fraction (HFpEF).1 IL (interleukin)-6 is the principal stimulus to the hepatic synthesis of CRP (C-reactive protein) and high circulating concentrations of both IL-6 and CRP have been associated with the development of HFpEF.2–5 However, robust data specifically addressing the association between circulating levels of IL-6 and prognosis for patients with HFpEF are limited.6–8. Here, CRP is linked to heart failure.