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One-year outcome of a prospective trial stopping dual antiplatelet therapy at 3 months after everolimus-eluting cobalt-chromium stent implantation: ShortT and OPtimal duration of Dual AntiPlatelet Therapy after everolimus-eluting cobalt-chromium stent (STOPDAPT) trial Polymer-based or Polymer-free Stents in Patients at High Bleeding Risk Impact of Staging Percutaneous Coronary Intervention in Left Main Artery Disease: Insights From the EXCEL Trial Ticagrelor With or Without Aspirin After Complex PCI A Platelet Function Modulator of Thrombin Activation Is Causally Linked to Cardiovascular Disease and Affects PAR4 Receptor Signaling Dual Antiplatelet TherapyIs It Time to Cut the Cord With Aspirin? Does Risk of Premature Discontinuation of Dual-Antiplatelet Therapy Following PCI Attenuate With Increasing Age? Impact of SYNTAX Score on 10-Year Outcomes After Revascularization for Left Main Coronary Artery Disease Edoxaban versus Vitamin K Antagonist for Atrial Fibrillation after TAVR Stress Echocardiography and PH: What Do the Findings Mean?

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.