This review highlights the cellular and molecular mechanisms of cardiovascular aging, such as oxidative stress and inflammation, that contribute to the development of heart failure in the elderly.
Heart failure (HF) is a clinical syndrome that usually develops in the elderly. Complex interactions of the cardiovascular aging process with risk factors (obesity, hypertension, and atherosclerosis), comorbidities (anemia, chronic kidney disease, diabetes, and so on), and disease modifiers (sex, genes, others) contribute to the development of HF phenotype and outcome. A conglomerate of cellular and molecular mechanisms underlies the effects of aging on cardiovascular function, the most important being excessive oxidative stress and chronic low-grade inflammation superimposed on the limited cardiac regeneration capacity. Notably, a sizeable percentage of elderly HF patients have cardiac amyloidosis, an HF precipitator. This review summarizes the current published data on the mechanisms of cardiovascular aging as they contribute to the development of HF phenotype and outcome.
Triposkiadis et al. (Thu,) studied this question.