Ferreira I, et al. - The clinicians examined the hypothesis that whether vascular inflammation and endothelial dysfunction contribute to arterial stiffening and hypertension. The involvement of vascular endothelial dysfunction and inflammation was supported in the development of premature arterial stiffening and hypertension in type 1 diabetes.

• The researchers investigated the course, tracking and temporal inter-relationships of BP, specifically pulse pressure (a marker of arterial stiffening) and hypertension in an inception cohort of 277 individuals with type 1 diabetes.
• They also examined the following biomarkers of systemic and vascular inflammation/endothelial dysfunction: C-reactive protein (CRP), soluble intracellular adhesion molecule-1 (sICAM-1), soluble vascular cellular adhesion molecule-1 (sVCAM-1) and soluble E-selectin (sE-selectin).
• They measured these biomarkers and other risk factors at baseline and repeatedly up to 20 years after the onset of type 1 diabetes.
• They examined data with generalized estimating equations including adjustments for age, sex, smoking status, BMI, HbA_1c, serum creatinine, total cholesterol, urinary AER, insulin treatment dose and mean arterial pressure.

• The researchers noted increases in all biomarkers except sE-selectin, which decreased over time.
• In this study, levels differed from baseline at 2–4 years and preceded the increase in pulse pressure, which occurred at 8–10 years after the onset of type 1 diabetes.
• At baseline and throughout the 20-year follow-up, higher levels of sICAM-1 and sVCAM-1 were significantly associated with higher (changes in) pulse pressure at subsequent time points, but not CRP or sE-selectin.
• At baseline and during follow-up, higher levels of sVCAM-1 were also significantly correlated with the prevalence (OR 3.60 [95% CI 1.36, 9.53] and OR 2.28 [1.03, 5.25], respectively) and incidence (OR 2.89 [1.08, 7.75] and OR 3.06 [1.01, 9.26], respectively) of hypertension.
• Furthermore, they examined the longitudinal associations between BP or hypertension as determinants of subsequent (changes in) levels of CRP, sICAM-1, sVCAM-1 and sE-selectin.
• However, they did not find evidence to support a reverse causality hypothesis.