Hemostasis in normotensive and hypertensive men: results of the PROCAM study. The prospective cardiovascular Münster study.
BACKGROUND
The greater than normal cardiovascular risk of hypertensive patients could be partly due to an impairment of hemostatic balance found in such individuals.


OBJECTIVE
To examine the relationship between hemostatic variables and blood pressures in 1950 apparently healthy male participants in the prospective cardiovascular Münster study aged 40-65 years.


METHODS
Blood pressure and other variables were determined, including fibrinogen level, coagulation factor VII clotting activity, protein C level, antithrombin III level, plasminogen activator inhibitor-1 level, euglobulin fibrinolytic activity, and von Willebrand factor level.


RESULTS
Age-adjusted mean values of coagulation factor VII clotting activity, plasminogen activator inhibitor-1 level, antithrombin III level, and protein C level in hypertensives and borderline hypertensives were significantly higher than those in normotensive men (e.g. for hypertensive versus normotensive men, coagulation factor VII clotting factor activity 111.5 versus 106.1%, plasminogen activator inhibitor-1 level 5.05 versus 3.22 arbitrary units/ml, and protein C level 111.1 versus 107.0%, P < 0.05-0.01). For most of the hemostatic variables we found positive bivariate correlations to blood pressure (P < or = 0.05). Exceptions were von Willebrand factor level (no correlation to blood pressure), and euglobulin fibrinolytic activity (a negative correlation to systolic blood pressure and no correlation to diastolic blood pressure). Significance persisted in the multiple logistic regression analysis with the exception of the relationships between systolic and diastolic blood pressures and fibrinogen level as well as euglobin fibrinolytic activity after adjustment for age. After adjustment for age and body mass index significance for relationships between systolic blood pressure and coagulation factor VII clotting activity as well as protein C level was also lost.


CONCLUSIONS
We conclude that the greater than normal cardiovascular risk of hypertensive patients is partly due to an imbalance in hemostasis.
Junker
R
R
Institut für Klinische Chemie und Laboratoriumsmedizin, Westfälische Wilhelms-Universität Münster, Germany. junker@uni-muenster.de
Heinrich
J
J
Schulte
H
H
Erren
M
M
Assmann
G
G
D000328:Adult; D000990:Antithrombin III / Q000378:metabolism; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000209:etiology; D005167:Factor VII / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D005858:Germany; D006487:Hemostasis; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011446:Prospective Studies; D011486:Protein C / Q000378:metabolism; D012016:Reference Values; D012307:Risk Factors; D012712:Serum Globulins / Q000378:metabolism; D014841:von Willebrand Factor / Q000378:metabolism
D017395:Plasminogen Activator Inhibitor 1; D011486:Protein C; D012712:Serum Globulins; D014841:von Willebrand Factor; D000990:Antithrombin III; D005167:Factor VII; D005340:Fibrinogen