抄録
Cardiovascular disease (CVD) is a common problem in the elderly. In particular, the morbidity and mortality of patients with heart failure (HF) increase with age. The poor outcomes of elderly patients with HF can be explained partly by cardiac aging at the cellular and organ levels. Moreover, recent evidence has demonstrated that functional evaluation, which may reflect the status of individual aging, predicts mortality in patients with HF. Age-related changes occur throughout the body and in virtually all organ systems. Thus, we should pay more attention to geriatric conditions when treating patients with HF. Frailty represents a complex clinical syndrome that results from multiple impairments across different organs and is characterized by decreased physiological reserves and increased vulnerability to stressors. Frail patients with CVD have a worse prognosis than non-frail patients. Evidence demonstrates that frailty is an independent risk factor for incident HF among older people. The ways in which cellular senescence promotes age-related CVD and frailty remain an important issue in the biology of aging and clinical geriatrics. Senescent cells that have acquired a senescence-associated secretory phenotype (SASP) can cause local and potentially systemic inflammation. SASP might be a key phenomenon in the association between cellular senescence and the development of age-related CVD and frailty. Frailty is a dynamic and potentially reversible state; therefore, translational research efforts are focused on obtaining mechanistic insights into the pathobiology of frailty, the development of novel therapeutics, and the identification of biomarkers for frailty. This is particularly important in developed countries that are confronted with an aging society.
