Benchside to the bedside of frailty and cardiovascular aging: Main shared cellular and molecular mechanisms

Due to the impact that frailty and cardiac aging have on society and health systems, the mechanisms surrounding these conditions must be known. If the frailty and cardiovascular complications are due to numerous controllable factors or not, different strategies must be considered to improve the elderly patient's prognosis and improve their quality of life. This review aimed to investigate the main shared mechanisms of cardiac aging and frailty. MEDLINE-PubMed, Cohrane and EMBASE databases were searched to perform this review. The mesh-terms used for this search was frailty, cardiovascular disease, cardiovascular aging, or heart failure (HF). Frailty frequently coexists with heart conditions since they share predisposing pathophysiological alterations, the aging process, and elevated comorbidity burden, contributing to fast functional decline and sarcopenia. Mitochondrial dysfunctions and decreased protein synthesis lead to protein degradation, denervation, atrophy, impairment in the fatty acid oxidation, resulting in cardiomyopathy. The homeostasis of muscle metabolism deteriorates with aging, leading to a reduction in muscle quality and quantity. The installation of a low-grade and chronic inflammatory process adds to an impairment in glucose, protein and lipid metabolism, endothelial dysfunction, cardiovascular conditions, sarcopenia, and HF. The exacerbated rise in inflammatory biomarkers and impaired insulin resistance leads to worsening of the patient's general condition. The good news is that frailty is a dynamic syndrome, fluctuating between different states of seriousness but still has potential for reversibility based on physical activity, cognitive training, nutrition intervention, and a plethora of other approaches that can be performed by a multi-disciplinary team.