Hypertension is often associated with undesirable changes in platelet function.59 It has been suggested that abnormalities of the coagulation/fibrinolytic system may predispose to a procoagulant state, which increases the risk of cardiovascular disease.60
Although many factors are involved in the regulation of fibrinolytic balance and haemostatic function, there is considerable evidence that the renin-angiotensin system plays an important role.60
Makris et al (2004) compared the effects of eprosartan and losartan on the plasma levels of various markers of haemostatic/fibrinolytic and endothelial function in 86 hypertensive patients.60 Plasma levels of these markers were measured before and after 6 months of treatment with eprosartan 600mg/day or losartan 100mg/day.
Both drugs gave significant reductions in systolic and diastolic blood pressure compared with pretreatment, but eprosartan was statistically significantly superior to losartan in lowering systolic blood pressure (-18.0 versus -10.9mmHg reduction from pretreatment baseline, respectively).
Compared with pretreatment values, both drugs induced significant reductions in plasminogen activator inhibitor-1 (PAI-1), fibrinogen and thrombomodulin, and an increase in tissue plasminogen activator inhibitor (tPA) antigen. However, the favourable modification of these parameters was significantly greater in the eprosartan than in the losartan group (figure 26).
Figure 26: Percentage change in haemodynamic and haemostatic factors after six months of treatment with eprosartan or losartan compared with baseline. Differences between eprosartan and losartan were statistically significant. Adapted from 60
Labios et al (2004) demonstrated that eprosartan normalised markers of platelet function in a study of 30 patients with mild-to-moderate hypertension who received eprosartan 600mg/day.59 Blood pressure measurements and platelet function changes were assessed at baseline and after 4 and 8 weeks of eprosartan therapy.
Eprosartan treatment produced statistically significant reductions in SBP and DBP at the study endpoint compared with pretreatment baseline. There was also a significant reduction in the number of platelet microparticles after blood shear exposure (p<0.01) and after exposure to calcium-ion ionophore activation (p<0.05). Eprosartan also reduced the trend for platelets to be more readily activated in hypertensive patients compared with a group of normotensive controls.