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Low‑Shear Stress Promotes Atherosclerosis via Inducing Endothelial Cell Pyroptosis Mediated by IKKε/STAT1/NLRP3 Pathway Disturbed shear stress promotes atherosclerosis through TRIM21-regulated MAPK6 degradation and consequent endothelial inflammation Paclitaxel-Coated Balloon for the Treatment of Small Vessel In-Stent Restenosis: A Subgroup Analysis of the AGENT IDE Randomized Trial

Review ArticleVolume 74, Issue 6, 13 August 2019, Pages 804-813

JOURNAL:J Am Coll Cardiol. Article Link

Cardiovascular Aging and Heart Failure: JACC Review Topic of the Week

F Triposkiadis, A Xanthopoulos, J Butler et al. Keywords: aging; amyloidosis; comorbidities; heart failure; risk factors

ABSTRACT


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.