Abstract
Arterial stiffness (AS) integrates the cumulative burden of known and unknown cardiovascular risk factors on the elastic wall of large arteries along the lifespan of an individual. As a marker of vascular aging, AS is an independent predictor of cardiovascular events and improves cardiovascular risk prediction when added to the Framingham Risk Score. In addition, AS may affect the microvasculature and promote the development of microvascular complications. Its impact on both the macro- and microvasculature has led to the concept that the arterial wall itself should be considered as a target organ. Here, we review the biological and clinical consequences of AS on the macro- and microvasculature and the measurement of AS in routine clinical practice. We also discuss the pathophysiological mechanisms underpinning AS development using diabetes and, in particular, type 1 diabetes, as a disease model with a high risk of cardiovascular events and microvascular complications that are accelerated by AS.
Highlights
IntroductionPublisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations
This score requires 10 clinical variables, and we proposed to simplify the assessment of CV risk by evaluating of carotidfemoral PWV (cfPWV), with the caveat that further evaluation will be needed in appropriate prospective cohorts
The gold standard for measuring Arterial stiffness (AS) is the assessment of cfPWV, which can be typically measured in clinical practice by applanation tonometry. cfPWV has been demonstrated to improve the CV risk prediction when combined with the Framingham Risk
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. How well these scores perform in daily clinical practice is unclear [6], and the use of other CV biomarkers has been proposed to improve upon CV risk predictions. One such biomarker is arterial stiffness (AS), which is considered as the central paradigm of vascular aging [7]. There is accumulating evidence supporting the concept that AS underpins the development of complications at the microvasculature level [9,10] Against this background, the present review will focus on: (1) the biological and clinical consequences of AS on both macro- and microvasculature; (2) the measurement of AS in daily clinical practice; (3) the pathophysiological mechanisms implicated in AS development; (4) AS in the context of. While it is known that AS may affect almost (if not all) all chronic conditions, some of them among the most prevalent worldwide (e.g., obesity, hypertension) [11,12], this review will focus on T1D because of its high risk of both CV events and microvascular complications
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
