Key result
Cardiovascular aging interacts with risk factors to promote HF, driven by oxidative stress and inflammation.
Why the study?
Heart failure usually develops in the elderly, driven by complex interactions among cardiovascular aging, risk factors, comorbidities, and cellular mechanisms that contribute to the phenotype and outcomes.
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.
Answers are grounded in this paper and cite their sources.
Does not support practice changes in elderly HF; leaves open targeted trials on aging mechanisms.
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.
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Triposkiadis et al. (2019) conducted a review in Heart failure. Cardiovascular aging was evaluated. Cardiovascular aging, driven by excessive oxidative stress and chronic low-grade inflammation, interacts with risk factors and comorbidities to contribute to the development of heart failure.
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