Chronic Heart Failure and Inflammation

Heart failure (HF) is primarily a clinical diagnosis that develops secondary to either left ventricular (LV) systolic and diastolic dysfunctions. Despite significant advancements in medical therapies designed to both prevent HF development and treat HF once established, the prognosis of patients after their first hospital admission is poor. Worldwide, 2% to 17% of patients die during their first admission, with 17% to 45% mortality within 1 year of admission, and >50% mortality within 5 years. Given the staggering burden chronic HF exerts on society, in terms of not only mortality but also morbidity related to repeated and prolonged hospitalization, a greater understanding of the pathophysiological mechanisms at play merits accelerated investigation. For decades, the activation of neurohormonal and sympathetic systems dominated research in established HF, both in experimental animals and clinically in patients. Blockade of these pathways demonstrated significant beneficial outcomes in a variety of patient populations, in particular those with reduced LV systolic function. However, ≈50% of all HF admissions are in patients with HF with a preserved ejection fraction (HFpEF), and unfortunately, none of the clearly efficacious therapies that focus on neurohormonal blockade (such as angiotensin-converting enzyme inhibitors, angiotensin receptor blocker, and β-blockers) have a beneficial effect in HFpEF. Importantly, what is common to both HF with reduced EF (either from an ischemic or nonischemic cause), and patients Review