Abstract
SummaryFrailty, a clinical syndrome that typically occurs in older adults, implies a reduced ability to tolerate biological stressors. Frailty accompanies many age‐related diseases but can also occur without overt evidence of end‐organ disease. The condition is associated with circulating inflammatory cytokines and sarcopenia, features that are shared with heart failure (HF). However, the biological underpinnings of frailty remain unclear and the interaction with HF is complex. Here, we describe the inflammatory pathophysiology that is associated with frailty and speculate that the inflammation that occurs with frailty shares common origins with HF. We discuss the limitations in investigating the pathophysiology of frailty due to few relevant experimental models. Leveraging current therapies for advanced HF and current known therapies to address frailty in humans may enable translational studies to better understand the inflammatory interactions between frailty and HF.
Highlights
25% of older patients with heart failure (HF) exhibit evidence of frailty, a clinical syndrome characterized by reduced tolerance to biological stressors (Boxer et al 2008; Dodson & Chaudhry 2012)
We describe the underlying inflammatory phenotype associated with frailty and speculate how it may be linked to the inflammatory phenotype that occurs with HF
The Toll-like receptor (TLR) and inflammasome pathways are activated by host derived proteins in addition to microbial motifs leading to sterile inflammation, which is defined as inflammation without microbes (Shen et al 2013)
Summary
As the number of people over 65 year of age grows, so too will the rate of cardiovascular diseases in the population. It is possible that there may be two forms of frailty, one associated with aging and resultant sarcopenia and anorexia but without evidence of end-organ disease, and the other more common form, which occurs in the setting of comorbidities or severe illnesses (Fried et al 2001). End organ disease such as HF exacerbates frailty. The inflammasome is known to be activated by bacteria (e.g., salmonella) and viruses (e.g., influenza) (Lamkanfi & Dixit 2014) The RIG-I like receptors (RLR) respond to intracellular nucleic acids in the context of viral infections (e.g., influenza virus) to produce type 1 interferons (IFN) (Yoneyama et al 2015)
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