Low-grade inflammation and hypoadiponectinaemia have an additive detrimental effect on aortic stiffness in essential hypertensive patients.

Abstract

In this study, we investigated the combined effect of increased high-sensitivity C-reactive protein (hs-C-reactive protein) and hypoadiponectinaemia on aortic stiffness in essential hypertensive subjects. A total of 267 untreated patients with stage I-II essential hypertension underwent ambulatory BP and carotid-femoral pulse wave velocity (c-f PWV) evaluation. The distributions of hs-C-reactive protein and adiponectin were split by the median (1.3 mg/L and 7.8 microg/mL, respectively) and accordingly subjects were stratified into those with high and low values. Patients with high (n = 134) compared with those with low hs-C-reactive protein (n = 133) values exhibited greater c-f PWV levels (by 0.8 m/s, P < 0.0001), whereas patients with low (n = 133) compared with those with high (n = 134) adiponectin levels had higher c-f PWV (by 0.9 m/s, P < 0.0001). Stepwise regression analysis revealed that age, 24 h systolic BP, hs-C-reactive protein and adiponectin were independent predictors of arterial stiffness. In patients with low hs-C-reactive protein, hypoadiponectinaemia (n = 46) compared with high adiponectin (n = 87) was accompanied by increased c-f PWV (by 0.8 m/s, P < 0.0001). Similarly in patients with high hs-C-reactive protein, hypoadiponectinaemia (n = 84) compared with high adiponectin (n = 50) was related to heightened c-f PWV (by 0.7 m/s, P = 0.008). In essential hypertension, pronounced low-grade inflammation in conjunction with hypoadiponectinaemia exerts an additive detrimental effect on aortic stiffness, accelerating the vascular ageing process.