Relationship between low-grade inflammation and arterial stiffness in patients with essential hypertension

Abstract

Background: Arterial stiffness is an independent cardiovascular risk factor in hypertensive individuals. Inflammation is associated with increased arterial stiffness and is implicated in the pathogenesis of hypertension.

Objectives: To examine whether low-grade inflammation contributes to arterial stiffness and wave reflections independently of blood pressure, in patients with essential hypertension and in controls.

Methods: We studied 235 consecutive patients with uncomplicated, never-treated essential hypertension and 103 sex- and age-matched controls. The level of inflammation was evaluated with high-sensitivity C-reactive protein (hsCRP) and serum amyloid A (SAA). Arterial stiffness was assessed with carotid-femoral (c-f) and carotid-radial (c-r) pulse wave velocity (PWV), and wave reflections with augmentation index (AIx).

Results: In the hypertensive group, in multiple regression analysis, both PWVc-f and PWVc-r were independently correlated with log hsCRP (beta = 0.56, P = 0.006 and beta = 0.45, P = 0.016, respectively), whereas no correlation was found between PWV and log SAA (P = NS). No significant correlation was observed between heart-rate-corrected AIx and log hsCRP (P = NS) and log SAA (P = 0.07) in the same group. Similarly, in the control group, an independent association was observed between PWVc-f and PWVc-r with log hsCRP (beta = 0.68, P = 0.05 and beta = 0.74, P = 0.05 respectively), but not with log SAA (P = NS). Furthermore, no significant association was shown between heart-rate-corrected AIx and log hsCRP or log SAA (P = NS) in the control group.

Conclusions: In hypertensive individuals, hsCRP is related to PWV, a direct marker of arterial stiffness, but not to AIx, a measure of wave reflections. Whether inflammation might act as a pathogenetic or modulating factor in arterial stiffening in chronic hypertension has to be confirmed.