Plasma brain natriuretic peptide: a biochemical marker of effective blood pressure management?

OBJECTIVE: To investigate plasma brain natriuretic peptide (BNP) concentrations in association with blood pressure (BP) at baseline and after antihypertensive drug treatment. PATIENTS AND METHODS: We prospectively examined 186 individuals with newly diagnosed essential hypertension without target organ damage, whose mean age was 48.7 +/- 10.9 years. Treatment initiation began with irbesartan 150 mg/day and was doubled at 4 weeks in cases of inadequate BP control. If indicated, at 8-week-follow-up hydrochlorothiazide 12.5 mg alone or with amlodipine 5-10 mg was added. BNP levels were measured at baseline and after 3 months of antihypertensive treatment. RESULTS: At baseline plasma BNP levels were found to be related to systolic BP (r = 0.27, P < 0.001), independent of age, sex, smoking status, BMI and left ventricular mass index estimated by echocardiography (beta = 11.81, SE = 3.82, P = 0.002). Additionally, higher BNP concentrations were observed in patients with stage 2 hypertension compared with those with stage 1 (median 38.9 vs. 29.9 pg/ml, P = 0.022). Multivariate analysis showed a positive association between BNP and systolic BP variability (beta = 0.03, SE = 0.01, P = 0.034). At follow-up, 64.7% of the participants who had achieved BP control showed decreased BNP levels in contrast to those with poor BP control (median change -14.5 vs. -1.3 and median range from -34.4 to -4.4 vs. -9.6 to 10.9, respectively, P < 0.001). CONCLUSION: In this hypertensive population, increased BNP concentrations are associated with higher BP levels and systolic BP variability. The fall of BNP observed in those who achieved BP control indicates that BNP could be used as a biochemical marker of effective BP control and target organ protection.

Increased plasma plasminogen activator inhibitor-1 levels: a possible marker of hypertensive target organ damage.

High plasma plasminogen-activator inhibitor-1 (PAI-1) concentrations have been reported in coronary artery disease and stroke. We therefore, prospectively studied the association of PAI-1 with early target organ damage in patients with arterial hypertension has not been clearly established. We therefore investigated 136 subjects, 64 males and 72 females, mean age 50.0 +/- 12.3 years, with newly diagnosed essential hypertension who were free of cardiovascular events and were not receiving any antihypertensive medication. Plasma PAI-1 levels were measured by an ELISA method (STAGO). The study population was divided into two groups, group A with PAI-1 levels below 40 ng/mL and group B with more than 40 ng/mL. The left ventricular mass was calculated according to the formula of Devereux and was normalized by the individual's body surface area (LVM/BSA). Carotid intima-media thickness (IMT) was determined by ultrasonography. Microalbuminuria was assessed by an immunoturbidimetric method (SERA-PAK). Group A consisted of 89 individuals with hypertension (65.4%), 41 males and 48 females and group B of 47 individuals with hypertension (34.6%), 21 males and 26 females. Individuals in group B exhibited significantly higher LVM/BSA than individuals in group A (155.9 +/- 23.1 g/m2 vs. 129.7 +/- 32.2g/m2, respectively, p = 0.004) and increased IMT (0.97 +/- 0.20mm vs. 0.87 +/- 0.21 mm, respectively, p < 0.001). Microalbumin excretion rate was greater in group B than group A (70.9 +/- 84.4 mg/24 hrs vs. 20.9 +/- 45.1 mg/24 hrs, respectively, p = 0.002). In conclusion, elevated PAI-1 levels are associated with target organ damage in subjects with newly diagnosed arterial hypertension. Thus, it can be postulated that this fibrinolytic inhibitor may characterize hypertensives in the early stages of the atherothrombotic process.