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Left Atrial Appendage Closure versus Non-Warfarin Oral Anticoagulation in Atrial Fibrillation: 4-Year Outcomes of PRAGUE-17 Frailty and Clinical Outcomes of Direct Oral Anticoagulants Versus Warfarin in Older Adults With Atrial Fibrillation: A Cohort Study Patent Foramen Ovale Attributable Cryptogenic Embolism With Thrombophilia Has Higher Risk for Recurrence and Responds to Closure Alcohol consumption, cardiac biomarkers, and risk of atrial fibrillation and adverse outcomes Role of endothelial dysfunction in determining angina after percutaneous coronary intervention: Learning from pathophysiology to optimize treatment Stretch-induced sarcoplasmic reticulum calcium leak is causatively associated with atrial fibrillation in pressure-overloaded hearts Transcatheter Aortic Valve Implantation Represents an Anti-Inflammatory Therapy Via Reduction of Shear Stress-Induced, Piezo-1-Mediated Monocyte Activation Systematic Review and Network Meta‐Analysis Comparing Bifurcation Techniques for Percutaneous Coronary Intervention Residual Shunt After Patent Foramen Ovale Closure and Long-Term Stroke Recurrence: A Prospective Cohort Study Potential Candidates for Transcatheter Tricuspid Valve Intervention After Transcatheter Aortic Valve Replacement: Predictors and Prognosis
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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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