Frailty assessment and candidate optimization before cardiothoracic transplantation

Figures

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  Figure 1. Clinical trajectories of frail and nonfrail patients in response to stressors. Frail patients (red line) have extremely limited physiologic reserve and may not be able to recover from a physiologic insult (e.g., disease exacerbation, major transplant surgery) while non-frail patients may tolerate the physiologic insult and can recover without decompensating into critical illness (green line). The dotted lines represent the uncertainty in the prognosis of frail patients, which can vary according to the type of frailty (mainly disease-related versus age- or comorbidity-dependent) from deterioration leading to death to marked improvement. Prehabilitation or treatment of secondary frailty may theoretically allow for recuperation of physiologic reserve, facilitating recovery (purple arrow). Adapted from “Frailty in the End-Stage Lung Disease or Heart Failure Patient,” Bottiger et al, J Cardiothorac Vasc Anesth, Volume 33, Issue 5, 1382-1392, 2019 May, with permission.

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  Figure 2. Biomarker changes associated with physical frailty. The clinical risk factors for physical frailty are listed on the left, while biomarkers are based on the pathobiological cascade mapped in the figure. Markers of inflammation seem to be the most relevant to mortality risk, with IL-6 and CRP being consistent between LTx and HTx populations. Persistent inflammation fuels cellular senescence, then upends neurohormonal balance (relative GH excess, low IGF-1, insulin and GH resistance, ↑ cortisol/DHEA). This catabolic state drives muscle wasting (sarcopenia), blunted ventilatory response, exercise intolerance, and chronotropic incompetence that contribute to cachexia. CXCL10: interferon-inducible protein-10, DHEA: dehydroepiandrosterone, FGF-21/23: Fibroblast growth factor 21/23, GDF-15: Growth differentiation factor 15, GH: growth hormone, IGF-1: insulin-like growth factor-1, IL-1Ra: Interleukin-1 receptor antagonist, IL-6: interleukin 6, TNF-α: tumor necrosis factor, TNF-R1: TNF receptor-1.