Frailty assessment in the cardiovascular care of older adults

Abstract

Due to the aging and increasingly complex nature of our patients, frailty has become a high-priority theme in cardiovascular medicine. Despite the recognition of frailty as a pivotal element in the evaluation of older adults with cardiovascular disease (CVD), there has yet to be a road map to facilitate its adoption in routine clinical practice. Thus, we sought to synthesize the existing body of evidence and offer a perspective on how to integrate frailty into clinical practice. Frailty is a biological syndrome that reflects a state of decreased physiological reserve and vulnerability to stressors. Upward of 20 frailty assessment tools have been developed, with most tools revolving around the core phenotypic domains of frailty-slow walking speed, weakness, inactivity, exhaustion, and shrinking-as measured by physical performance tests and questionnaires. The prevalence of frailty ranges from 10% to 60%, depending on the CVD burden, as well as the tool and cutoff chosen to define frailty. Epidemiological studies have consistently demonstrated that frailty carries a relative risk of >2 for mortality and morbidity across a spectrum of stable CVD, acute coronary syndromes, heart failure, and surgical and transcatheter interventions. Frailty contributes valuable prognostic insights incremental to existing risk models and assists clinicians in defining optimal care pathways for their patients. Interventions designed to improve outcomes in frail elders with CVD such as multidisciplinary cardiac rehabilitation are being actively tested. Ultimately, frailty should not be viewed as a reason to withhold care but rather as a means of delivering it in a more patient-centered fashion.

Keywords: cardiovascular disease; elderly; frailty.

Copyright © 2014 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Figures

Figure 1. Two of the Pathways Leading Toward the Phenotype of Frailty

(Left) The age-associated activation of inflammatory cells and decline in androgen hormones upset the balance between catabolic and anabolic stimuli, respectively, leading to a decline in muscle mass and composition known as sarcopenia. This detrimental response is aggravated in patients with insulin resistance and metabolic syndrome. Addition of bed rest and malnutrition initiates a vicious cycle of further decline in muscle mass, limiting the necessary mobilization of amino acids in times of stress. (Right) The accumulation of subclinical impairments in multiple organ systems resulting from cardiovascular disease, lifelong “wear and tear,” and/or genetic predispositions lead to decreased homeostatic reserve and resiliency to stressors. Other pathophysiological pathways have been proposed. Biological pathways may manifest clinically as slow walking speed, weakness, weight loss, physical inactivity, and exhaustion—termed the phenotype of frailty. CRP = C-reactive protein; IL = interleukin; TNF = tumor necrosis factor.