title: Mechanism and clinical significance of the prothrombotic state in patients with essential hypertension.
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.
  
  
  OBJECTIVE
  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.
authors.affiliation: Department of Cardiology, China-Japan Union Hospital, Jilin University, Jilin, China. yangping@email.jlu.edu.cn
authors.forename: Ping
authors.initials: P
authors.lastname: Yang
authors.forename: Ya-Fen
authors.initials: YF
authors.lastname: Liu
authors.forename: Li
authors.initials: L
authors.lastname: Yang
authors.forename: Qun
authors.initials: Q
authors.lastname: Wei
authors.forename: Hong
authors.initials: H
authors.lastname: Zeng
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation; D001794:Blood Pressure; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D002681:China; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D015539:Platelet Activation; D012720:Severity of Illness Index; D019851:Thrombophilia / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D013927:Thrombosis / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D014664:Vasodilation
chemical_list: D015415:Biomarkers; D019007:P-Selectin; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D005340:Fibrinogen