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30-Oct-2001
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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.
