3. 請閱讀下列節錄文章後,說明慢性心衰竭患者合併衰弱的可能機轉(25分)
The high burden of frailty in patients with chronic HF is likely related to a coordinated multisystem dysfunction
that is precipitated by the systemic nature of HF, including systemic inflammation, high comorbidity burden,
older age, and chronic skeletal muscle abnormalities. Chronic HF accelerates the aging-assoc ciated decline in
muscle mass with relative preservation or acc cumulation of adipose, leading to higher rates of sarcopenic obesity
than with aging alone. Chronic HF is also associated with abnormal muscle composition (i.e, high levels of
intermuscular adipose tissue, shift in fiber type, reduced capillary density) that contributes to impaired
mitochondrial function in skeletal muscle, reduced exercise capacity, and physical frailty. The accelerated
changes in muscle composition and associated physical frailty in chronic HF are likely the result of an
upregulation of a proinflammatory state causing metabolic impairment, especially insulin resistance.
Comorbidities common in older patients with chronic HF are also pro-inflammatory and associated with insulin
resistance, further accelerating adverse changes in muscle composition, size, and performance. Furthermore,
hemodynamic abnormalities associated with HF can lead to tissue hypoxia, ceilular apoptosis, and
inflammation. Chronic congestion, volume overload, and hypoperfusion can also contribute to gut ischemia,
translocati tion of gut microbiome, and upregulation of inflammatory pathways. Moreover, activation of
neurohormonal pathways in chronic HP can also contribute to the pro-inflammatory state. The pro-
inflammatory state and associated metabolic impairment, coupled with chronic hypoperfusion in HF, lead to
structural and functional abnormalities in other organ systemns and contribute to global decteases in
physiological reserve and a state of heightened vulnerability.
The relation between frailty and HF is bidirectional: higher frailty contributes to worse physical functional
status, cognitive impairment, and quality of life in patients with HF through upregulation of pro-inflammatory
pathways and lower tolerance to physiological stressors. Furthermore, these chronic processes may be
exacerbated by an acute rise in inflamm natory cytokines and worse sened insulin resistance and further
compounded by profound hospital-a iated inactivity. These acute factors promote muscle loss as well as
adipocyte proliferation and lipid accumulation, which may further impair muscle function and recovery and
contribute to sustained, prolonged global decline in functional status through local and systemic inflammatory
and metabolic pathways. This may contribute to hospital-associated functional decline and a "posthospital
syndrome" such that even after resolution of decompensated HF, patients continue to have marked impairments
in physical function and a higher burden of frailty.(以上摘要修改自Pandey A, et al. Fraity is intertwined
with heart failure: mechanisms, prevalence, prognosis, assessment, and management. JACC Heart Fail.
2019:7(12):1001-1011. )
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