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. 2023 Aug 21;30(11):1101-1117.
doi: 10.1093/eurjpc/zwad028.

Vascular ageing: moving from bench towards bedside

Affiliations

Vascular ageing: moving from bench towards bedside

Rachel E Climie et al. Eur J Prev Cardiol. .

Erratum in

Abstract

Prevention of cardiovascular disease (CVD) remains one of the largest public health challenges of our time. Identifying individuals at increased cardiovascular risk at an asymptomatic, sub-clinical stage is of paramount importance for minimizing disease progression as well as the substantial health and economic burden associated with overt CVD. Vascular ageing (VA) involves the deterioration in vascular structure and function over time and ultimately leads to damage in the heart, brain, kidney, and other organs. Vascular ageing encompasses the cumulative effect of all cardiovascular risk factors on the arterial wall over the life course and thus may help identify those at elevated cardiovascular risk, early in disease development. Although the concept of VA is gaining interest clinically, it is seldom measured in routine clinical practice due to lack of consensus on how to characterize VA as physiological vs. pathological and various practical issues. In this state-of-the-art review and as a network of scientists, clinicians, engineers, and industry partners with expertise in VA, we address six questions related to VA in an attempt to increase knowledge among the broader medical community and move the routine measurement of VA a little closer from bench towards bedside.

Keywords: Ageing; Cardiovascular disease prevention; Vascular damage.

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Conflict of interest statement

Conflict of interest: None declared.

Figures

Figure 1
Figure 1
Mechanisms of vascular ageing comprising of arteriosclerotic and atherosclerotic processes. The figure depicts structural and mechanical changes, as well as major biochemical derangements contributing to vascular ageing processes. VA miRNAs, micro-ribonucleic acids of vascular ageing; NO, nitric oxide; GF, growth factors; MMP, matrix metalloproteinase; AGEs, advanced glycation end-products; SOD, superoxide dismutase; TNF-α, tumour necrosis factor-alpha; hs-CRP, high-sensitivity C-reactive protein; Il-6, interleukin-6; ICAM, intercellular adhesion molecule; RBCs, red blood cells; Ox LDL, oxidized low-density lipoprotein.
Figure 2
Figure 2
How to measure vascular age. The vascular ageing process can impact different arterial characteristics: pulse wave velocity and features, arterial dynamic or geometrical parameters, pulse pressure, and vessel structural composition. Alterations of these properties can be assessed by processing images or signals obtained using various technologies. CAC, coronary artery calcification; CT, computed tomography; MRI, magnetic resonance imaging; PG, plethysmography.
Figure 3
Figure 3
Relationship between vascular ageing measures with chronological ageing. aoPWV, aortic pulse wave velocity; cfPWV, carotid-femoral pulse wave velocity; baPWV, brachial-ankle pulse wave velocity; CAVI, cardio-ankle vascular index; afVWV, aorto-femoral volume wave velocity; cb/crPWV, carotid-brachial/radial PWV; ftPWV, finger-to-toe pulse wave velocity; est aoPWV, estimated aortic pulse wave velocity; scalesPWV, pulse wave velocity derived with bathroom scales; bPP, brachial pulse pressure; cPP, central pulse pressure; AIx, augmentation index; AP, augmentation pressure; Pb, backward wave amplitude; RM, reflection magnitude; PPG RI, photoplethysmogram-based reflection index; car Dist, carotid artery distensibility; car IMT, carotid intima-media thickness; car plaque, carotid plaque; CAC, coronary artery calcification; ABI, ankle-brachial index; FMD, flow-mediated dilation; ao diam, aortic diameter; ao/LA inflamm, large artery inflammation (positron emission tomography).
Figure 4
Figure 4
Factors contributing to why some people display early vascular ageing (EVA) compared to others. IFG, impaired fasting glucose; IGT, impaired glucose tolerance.

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