Last update:

   30-Oct-2001
 

Arch Hellen Med, 2000, 17(Supplement):124-128

ORIGINAL PAPER

Hemostatic balance disturbances in hypertensive patients
and prehypertensive individuals

C. TSOUKALA, Th. MAKRIS, A. HATZIZACHARIAS, A. GIALERAKI,
P. CRESPI, G. ANASTASIADIS, V. VOTTEAS, M. KYRIAKIDIS, T. MANDALAKI
2nd Regional Blood Transfusion and Haemophilia Center, Department of Cardiology,
"Laikon" General Hospital, Athens, Greece

OBJECTIVE It is generally accepted that arterial hypertension (AH) is a clinical syndrome accompanied by anatomic, functional, metabolic and hemostatic disturbances. Hemostatic imbalance, as a result of endothelial dysfunction may lead to thrombotic events in hypertensives. It is also suggested that endothelial damage may preceed establishment of AH and be included in its pathogenesis. The aim of the current study was to evaluate the hemostatic balance in hypertensive patients and normotensives who turned to hypertensives over a period of 5 years.
METHODS Hemostatic parameters were studied in 83 patients with mild or moderate hypertension prior to the administration of any treatment and in 42 healthy volunteers matched for age, sex, body mass index and other risk factors.
RESULTS It was found that fibrinogen, PAI, and t-PA: Ag were significantly increased, while á2-antiplasmin was decreased in hypertensives, when compared to healthy controls (327.75±51.36 vs 272.84±46.8 mg/dL, P<0.0001, 11.8±10.9 vs 7.91±5.5 IU/mL, P<0.05, 8.81±3.32 vs 5.76±2.54 ng/mL, P<0.001, 98.71±15.4 vs 107.84±17.52, P<0.05, respectively). Moreover statistically significant decrease of thrombodulin levels (32.5±9.7 vs 45.6±15.2 ng/mL, P<0.001) and increased levels of TFPI (103.3±28.3 vs 91.8±24.4 ng/mL, P<0.05) were observed in hypertensives versus controls.
CONCLUSIONS These findings suggest both disturbance in hemostatic balance and endothelial dysfunction. Additionally, 450 normotensives were followed for a period of 2–8 years. During this period, 65 developed AH while 385 remained normotensive. Fibrinogen, PA-1 and t-PA: Ag levels, at entry of the study, were significantly higher in the individuals who developed AH in comparison to the individuals who remained normotensive (270±44 vs 290±50 mg/dL, P<0.01, 7.6±4.8 vs 9.9±6.8 IU/mL, P<0.01 êáé 6.7±2.8 vs 7.8±3.1 ng/mL, P<0.01, respectively). Our findings also strengthen the hypothesis that endothelial dysfunction may preceed and be involved in the pathogenesis of AH.

Key words: Arterial hypertension, á2-antiplasmin, Fibrinogen, PAI-1, TFPI, Thrombomodulin, t-PA Ag.


© 2001, Archives of Hellenic Medicine