B-type natriuretic peptide and artery stiffness.

A rteries stiffen with age, largely as a consequence of structural alteration of the collagen and elastin content of the artery wall. Circulating B-type natriuretic peptide (BNP), secreted predominantly from the heart, also increases with age, probably as a consequence of left ventricular wall stress induced by a rise in impedance to ejection or structural changes in the myocardium including age-related loss of myocytes. It is not surprising, therefore, that arterial stiffness and BNP are correlated. A correlation between large artery stiffness, defined by a pulse-wave velocity measurement, and BNP assessed by the Shionogi method in 725 healthy Japanese men, is reported by Yambe et al in this issue of the Journal. Based on the mechanisms identified above, it is hardly surprising that these vascular and cardiac measurements are correlated. Indeed the very low correlation coefficient (r 0.12; r 0.014) suggests that the measurements are mechanistically related to a minimal extent at most. The methods used in this study require further analysis. Artery stiffness can refer to any segment of the arterial tree from the root of the aorta to the capillary beds. The arterial system is obviously complex, with multiple parallel channels; and the stiffening that may occur has quite distinct causes in different segments. In the aorta and large conduit arteries, in which pulse-wave velocity is measured, the main cause of stiffening is a structural change related to fragmentation of elastin, which is very compliant, and to growth of collagen, which is stiff. These are changes related to the aging process. The large arteries are not very responsive to vasoactive substances secreted by the endothelium. In contrast, the small arteries that characterize branch points and the precapillary microcirculation are particularly sensitive to nitric oxide secreted from the endothelium. Stiffening of these vessels is characteristic of endothelial dysfunction that eventually will facilitate structural changes in the small arteries as well as the large conduit arteries. The pulsewave velocity studies reported by Yambe et al were derived by an unusual method of identifying the difference between aortic-to-femoral and aortic-to-brachial time delays. These velocities nonetheless define a stiffness parameter limited to the proximal conduit arteries.