Menu boczne

Treść strony

Ann Acad Med Stetin, 2006; 52, 1, 51-62




Samodzielna Pracownia Zaburzeń Hemostazy

Katedry Biochemii Klinicznej i Diagnostyki Laboratoryjnej Pomorskiej Akademii Medycznej

al. Powstańców Wlkp. 72, 70-111 Szczecin

Kierownik: prof. dr hab. n. med. Maria Jastrzębska



Purpose: 1. The assessment in haemostasis system, fibrinogen, tissue plasminogen activator (t-PA) and its inhibitor type-1, von Willebrand factor and β-thromboglobulin (β-TG) levels and the changes in renin–angiotensin system (RAS), by determined angiotensin converting enzyme I (ACE) activity, in patients with essential hypertension (in relation to left ventricular hypertrophy) in comparison with normotension subjects. 2. The analysis of changes in haemostasis and RAS during treatment with perindopril in relation to left ventricular hypertrophy (group LVH+ and LVH-). 3. The assessment of haemostasis parameters levels and ACE activity in effect of treatment with perindopril in relation to ACE gene I/D polymorphism.

Material and methods: The study involved 78 male divided on two groups: cases and controls. The cases contained 44 male outpatients (25–38 years old) with untreated essential hypertension without clinical feature of coronary heart disease and 34 age- and gender- matched healthy controls.

Conclusion: 1. Untreated essential hypertension predisposes to the procoagulant state characterised by increased Fb level and suppressed of fibrinolysis. These changes not depend on ACE gene I/D polymorphism. The left ventricular hypertrophy not intensificates the procoagulant state. 2. The treatment with perindopril decreases blood pressure effectively independent of ACE gene I/D genotype and left ventricular hypertrophy. Perindopril impairs RAS activity, most in patients with ACE gene II genotype. The treatment with perindopril is only partially effective in alleviating the procoagulant state, by reducing fibrinogen level in II homozygotes due to its more potent inhibitory action on the RAS in this group. The treatment makes fibrinolysis better mainly to high t-PA levels, independently of ACE gene I/D polymorphism. 3. Left ventricular hypertrophy not differentiates the response on treatment in relation to haemostasis parameters and RAS, however there was a slight decrease in ACE activity in patients with left ventricular hypertrophy. 4. The changes in haemostasis system and ACE activity, observed during treatment, suggest the appearance of positive relation between haemostasis and RAS. Probably the antithrombotic act of perindopril is more pronounced in II genotype group.

K e y w o r d s: gene polymorphism – haemostasis – essential hypertension.

do góry