• Cristiana Catena, Gianluca Colussi, Valentina Fagotto, and Leonardo A Sechi.
• Department of Experimental and Clinical Medical Sciences, Hypertension Unit, Internal Medicine, University of Udine, 33100 Udine, Italy.
• J Res Med Sci. 2017 Jan 1; 22: 57.

BackgroundA prothrombotic state is associated with the presence and severity of organ damage in hypertensive patients. In these patients, evidence of subclinical carotid functional changes anticipates major cardiovascular events. The aim of this study was to investigate the association of hemostatic markers with carotid artery stiffness in hypertension.Materials And MethodsIn 116 untreated essential hypertensive patients recruited at a referral center in the University of Udine, we assessed common carotid artery stiffness by B-mode ultrasonography and measured plasma fibrinogen, D-dimer, plasminogen activator inhibitor-1 (PAI-1), and homocysteine by the currently available methods. For statistical reasons, the patients were divided according to the median value of each index of carotid stiffness, and continuous variables were further analyzed by univariate correlation and stepwise multivariate regression analysis.ResultsPAI-1 levels were significantly higher in patients with low coefficient of distensibility (P = 0.018) and high Young's elastic modulus (P = 0.012), whereas no association of fibrinogen, D-dimer, and homocysteine levels was observed with carotid coefficient of distensibility, Young's elastic modulus, and β-stiffness. On univariate analysis, Young's elastic modulus was significantly and positively correlated with PAI-1 levels (r = 0.286, P = 0.002), a correlation that on multivariate regression resulted to be independent of other confounders (β = 0.289, P = 0.028).ConclusionAn independent association of plasma PAI-1 levels with carotid artery stiffness suggests a possible contribution of decreased fibrinolytic activity to the early functional abnormalities of arterial vessels in hypertensive patients. This contribution might be relevant for subsequent development of hypertension-related cardiovascular complications.

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