Thomas T van Sloten, Alfons JHM Houben, Dennis Muris, Miranda T Schram, Carla J van der Kallen, Nicolaas C Schaper, Simone J Sep, Annemarie Koster, Pie Castermans, Pieter C Dagnelie, Athanase D Protogerou, Ronald M Henry, Coen DA Stehouwer
Background and aims:
Increased arterial stiffness leads to an increased pulsatile pressure load, which may damage the microcirculation. Individuals with type 2 diabetes (T2DM) may be particularly prone to the detrimental effects of this increased pressure load, because T2DM is associated with increased microvascular perfusion, allowing pulsatile pressure to penetrate deeply into the microcirculation. The skin enables the direct measurement of microcirculatory function both at rest and during provocative stimuli. Furthermore, the cutaneous microcirculation is considered a representative vascular bed to examine generalized microvascular phenomena. The aim of the present study was therefore to evaluate, in a large population-based cohort, the association between arterial stiffness and skin microvascular function. We additionally investigated whether any such association was stronger in individuals with as compared to those without T2DM.
Material and methods:
We used cross-sectional data of The Maastricht Study (for the present analysis: n=737; age 59.7 years; 45.2% women; 28.8% T2DM (by design)). The Maastricht Study is a population-based cohort study that focuses on the pathophysiology of T2DM. Arterial stiffness was determined via carotid-femoral pulse wave velocity (cfPWV, tonometry). In addition, finger skin capillaroscopy was used to determine capillary density at baseline and during post-occlusive hyperaemic response and venous congestion. Laser Doppler flowmetry was used to assess skin microvascular flowmotion.
After adjustment for age and sex, both in individuals with and without T2DM, cfPWV was not associated with baseline capillary density, hyperaemic capillary recruitment, or capillary density during venous congestion (Table, models 1). In addition, cfPWV was not associated with microvascular flowmotion (models 1). Further adjustment for potential confounders (models 2 and 3) did not materially change these results. There was no interaction with type 2 diabetes (P for interaction, all >.13).
In the present population-based cohort study, arterial stiffness was not associated with skin microvascular function. This suggests that increased arterial stiffness does not lead to generalized microvascular dysfunction, irrespective of the presence of T2DM.