Abstract
BACKGROUND: Thrombotic, rather than hemorrhagic, events represent a major complication of hypertension. This study aims to explore the mechanism of the hypercoagulative state in hypertension and to assess its clinical significance. HYPOTHESIS: The hypercoagulative state and even the prothrombotic state exists in patients with hypertension. This may be attributed to an impairment of the endothelium. METHODS: A total of 81 patients suffering from essential hypertension were classified into 3 groups (grade 1: n = 27; grade 2: n = 36; grade 3: n = 18) and an additional 28 nonhypertensive patients were used as the control group. This study determined the changes of platelet activation marker P-selectin (CD62P), plasma fibrinogen, plasminogen activitor inhibitor-1 (PAI-1), and endothelium function. RESULTS: The percentage of CD62P+ platelets and the concentration of plasma fibrinogen and PAI-1 in the hypertension group was significantly higher than those in the control group. These increments coincided with the elevation of blood pressure. A significant difference was found between any of the 2 hypertension subgroups in the percentages of CD62P+ platelets (P < 0.001) and the concentration of PAI-I (P < 0.05). No difference was noted between the hypertension grade 1 and 2 groups in the concentration of plasma fibrinogen (P = 0.079); however, a significant difference was found between any of the other 2 subgroups (P < 0.001). Flow-mediated dilation (FMD) in the hypertension group was significantly lower than that in the control group. CONCLUSIONS: The hypercoagulative state exists in patients with hypertension and this state was more obvious with the elevation of blood pressure and coincided with an impairment in the degree of endothelium-dependent vasodilation.