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von Willebrand Factor and Management of Heart Valve Disease: JACC Review Topic of the Week 6-month versus 12-month or longer dual antiplatelet therapy after percutaneous coronary intervention in patients with acute coronary syndrome (SMART-DATE): a randomised, open-label, non-inferiority trial Temporal Trends, Characteristics, and Outcomes of Infective Endocarditis After Transcatheter Aortic Valve Replacement Higher neutrophil-to-lymphocyte ratio (NLR) increases the risk of suboptimal platelet inhibition and major cardiovascular ischemic events among ACS patients receiving dual antiplatelet therapy with ticagrelor Infective Endocarditis After Transcatheter Aortic Valve Replacement Ambulatory Electrocardiogram Monitoring in Patients Undergoing Transcatheter Aortic Valve Replacement: JACC State-of-the-Art Review Relationship Between Hospital Surgical Aortic Valve Replacement Volume and Transcatheter Aortic Valve Replacement Outcomes Decline in Left Ventricular Ejection Fraction During Follow-Up in Patients With Severe Aortic Stenosis Assessment of Vascular Dysfunction in Patients Without Obstructive Coronary Artery Disease: Why, How, and When Ascending Aortic Length and Risk of Aortic Adverse Events: The Neglected Dimension
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Review ArticleVolume 75, Issue 8, March 2020

JOURNAL：J Am Coll Cardiol. Article Link

Mechanisms of Vascular Aging, A Geroscience Perspective JACC Focus Seminar

Z Ungvari, S Tarantini, F Sorond et al. Keywords: atherosclerosis; endothelial dysfunction; geroscience; microcirculation; senescence

ABSTRACT

Age-related pathological alterations of the vasculature have a critical role in morbidity and mortality of older adults. In epidemiological studies, age is the single most important cardiovascular risk factor that dwarfs the impact of traditional risk factors. To develop novel therapeutic interventions for prevention of age-related vascular pathologies, it is crucial to understand the cellular and molecular mechanisms of vascular aging. In this review, shared molecular mechanisms of aging are considered in terms of their contribution to the pathogenesis of macrovascular and microvascular diseases associated with old age. The role of cellular senescence in development of vascular aging phenotypes is highlighted, and potential interventions to prevent senescence and to eliminate senescent cells for prevention of vascular pathologies are presented. The evidence supporting a role for interorgan communication and circulating progeronic and antigeronic factors in vascular aging is discussed.
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