Brain natriuretic peptide as an integrator of cardiovascular stiffening in hypertension

Abstract

Background

Left ventricular (LV) diastolic dysfunction and impairment of aortic elastic properties represent common sequelae of hypertension. We investigated the relationships of these cardiovascular adaptations with brain natriuretic peptide (BNP) levels in newly-diagnosed hypertension.

Methods

200 consecutive hypertensives without LV hypertrophy (aged 52 years, 134 males, office BP = 151.4/95.5 mmHg) underwent 24 hour ambulatory BP measurement as well as aortic stiffness and LV diastolic function assessment by means of carotid-femoral pulse wave velocity (c-f PWV) measurement and Tissue Doppler Imaging (TDI), respectively. Based on BNP values patients were classified into tertiles.

Results

Hypertensives in the highest, compared to those in the lowest BNP tertile had significantly higher 24 h pulse pressure (by 6.2 mmHg, p = 0.002), lower 24 h diastolic BP (by 5.7 mmHg, p = 0.014), decreased Em/Am ratio (by 0.09, p = 0.048) and increased c-f PWV (by 0.7 m/s, p = 0.042). Moreover, hypertensives in the highest, compared with those in the lowest and the medium tertile of BNP, exhibited significantly lower Em (by 1.2 cm/s, p = 0.001 and 1 cm/s, p = 0.004, respectively) and higher E/Em ratio (by 1.3, p = 0.018 and 1.3, p = 0.014, respectively). BNP was significantly associated with E/Em ratio, 24 h pulse pressure and c-f PWV independently from age.

Conclusion

In hypertensives plasma BNP levels are associated not only with LV diastolic dysfunction but also with aortic stiffening. These findings suggest that BNP even within normal range constitutes a surrogate for cardiovascular functional impairment in the setting of essential hypertension without LV hypertrophy.

Introduction

Arterial hypertension is accompanied by augmented levels of vasoactive peptides such as brain natriuretic peptide (BNP), a reliable indicator of left ventricular (LV) pressure and/or volume overload [1], [2]. Although increased BNP levels are closely related with the impairment of LV systolic function [3], this is not always the case in the setting of hypertensive or ageing cardiovascular disease, where diastolic dysfunction may have a pivotal role [1], [4].

Increased arterial stiffness, cause and/or effect of hypertension, is an independent predictor of adverse cardiovascular events in various clinical settings. In a previous work, [5] carotid-femoral pulse wave velocity (c-f PWV), the most established measure of aortic stiffness in clinical practice, was associated with indices of LV diastolic function in the absence of LV hypertrophy. Although the pathophysiologic mechanisms underlying this relation are not yet completely elucidated, many speculations can be done, including the role of neurohumoral factors. In this concept, BNP has been associated with diverse indexes of LV diastolic performance, as well as with the severity of diastolic dysfunction [6], [7]. In the same lines, there are scarce data on the link between BNP and vascular wall properties [8].

In this study we investigated whether BNP levels are associated with aortic elastic properties in addition to LV diastolic dysfunction in newly diagnosed hypertensives without LV hypertrophy.