Abstract-Although central pulse pressure (PPc) is strongly related to central mean arterial pressure (MAPc), PPc predicts cardiovascular outcomes beyond MAPc. Whether modifiable risk factors for hypertension contribute to PPc and its determinants, independent of MAPc, is uncertain. In 635 randomly recruited participants, we assessed the independent relationship between 24-hour urinary sodium (Na ϩ ) or potassium (K ϩ ) excretion and brachial artery PP (in office or 24-hour; nϭ487), PPc, the forward (P1) and augmented (Paug) pressure wave components of PPc, central augmentation index, and determinants of central pressure waves, including aortic pulse wave velocity, effective reflecting distance, and reflective wave transit time. Central dynamics were determined using applanation tonometry of the carotid, femoral, and radial arteries. With adjustments for potential confounders, urinary Na ϩ /K ϩ was independently associated with in-office, central, and 24-hour PP, as well as Paug, P1, and central augmentation index (PϽ0.05 to PϽ0.005). With further adjustments for MAPc (or diastolic BP), urinary Na ϩ /K ϩ was independently associated with PPc, 24-hour PP, Paug, P1, and central augmentation index (PϽ0.05 to Pϭ0.005) but not with in-office PP, pulse wave velocity, effective reflecting distance, or reflective wave transit time. In conclusion, in a population of African ancestry, urinary salt excretion is independently related to central and 24-hour PP independent of MAPc or diastolic BP, effects that are attributed to increases in both P1 and Paug but not to pulse wave velocity. Hence, modifying salt intake could influence cardiovascular risk through effects on 24-hour and central PPs, as well as P1 and Paug, independent of steady-state pressure (MAP or diastolic BP) or pulse wave velocity. (Hypertension. 2010;56:584-590.) Key Words: pulse pressure Ⅲ arterial stiffness Ⅲ central blood pressure Ⅲ salt intake P ulse pressure (PP) predicts cardiovascular outcomes beyond other measures of blood pressure (BP), including measures of steady-state pressure, such as mean arterial pressure (MAP). [1][2][3][4][5][6][7][8][9][10][11][12][13][14] Moreover, central PP may be more closely associated with cardiovascular outcomes than peripheral PP. [15][16][17][18][19] Thus, contemporary notions of the adverse actions of BP are viewed in terms of steady-state effects, indexed by MAP, and dynamic or pulsatile effects, indexed by PP, with central PP receiving the most attention. The effects of PP independent of MAP on cardiovascular outcomes 1-14 are particularly impressive considering the close relationship between MAP and PP. Developing strategies that decrease PP, particularly central PP, without necessarily influencing MAP, is, therefore, of considerable interest, and in this regard understanding the mechanisms responsible for these changes is of importance. Although aging has been identified as the major determinant of PP, with increases in both the augmented and the forward pressure wave contributing to central PP, 20 -23 the im...

Abstract-Central aortic blood pressure (BP; BPc) predicts outcomes beyond brachial BP. In this regard, the application of a generalized transfer function (GTF) to radial pulse waves for the derivation of BPc is an easy and reproducible measurement technique. However, the use of the GTF may not be appropriate in all circumstances. Although the peak of the second shoulder of the radial waveform (P2) is closely associated with BPc, and, hence, BPc may be assessed without the need for a GTF, whether P2-derived BPc is associated with adverse cardiovascular changes independent of brachial BP is uncertain. Thus, P2-and GTF-derived aortic BPs were assessed using applanation tonometry and SphygmoCor software. Left ventricular mass was indexed for height 1.7 (nϭ678) and carotid intima-media thickness (IMT; nϭ462) was determined using echocardiography and vascular ultrasound. With adjustments for nurse-derived brachial pulse pressure (PP), P2-derived central PP was independently associated with left ventricular mass indexed for height 1.7 (partial rϭ0.18; PϽ0.0001) and IMT (partial rϭ0.40; PϽ0.0001). These relations were similar to nurse-derived brachial PP-independent relations between GTF-derived central PP and target organ changes (left ventricular mass indexed for height 1.7 : partial rϭ0.17, PϽ0.0001; IMT: partial rϭ0.37, PϽ0.0001). In contrast, with adjustments for central PP, nurse-derived brachial PP-target organ relations were eliminated (partial rϭϪ0.21 to 0.05). Twenty-four-hour, day, and night PP-target organ relations did not survive adjustments for nurse-derived brachial BP. In conclusion, central PP derived from P2, which does not require a GTF, is associated with cardiovascular target organ changes independent of brachial BP. Thus, when assessing adverse cardiovascular effects of aortic BP independent of brachial BP, P2-derived measures may complement GTF-derived measures of aortic BP. here is increasing evidence in various clinical or general populations that central aortic blood pressure (BP) predicts cardiovascular outcomes more closely or independent of BP measured at the brachial artery.

Although indices of aortic augmentation derived from radial applanation tonometry are independently associated with adverse cardiovascular effects, whether these relationships are influenced by gender is uncertain. We compared the brachial blood pressure-independent contribution of augmentation index (AIx) to variations in left ventricular mass index (LVMI) in a community sample of 808 participants, 283 of whom were men. Aortic haemodynamics were determined using radial applanation tonometry and SphygmoCor software and LVMI from echocardiography. In men, both AIx derived from aortic augmentation pressure/central aortic pulse pressure (AP/PPc; partial r = 0.17, β-coefficient ± s.e.m. = 0.55 ± 0.20, P < 0.01) and AIx derived from the second peak/first peak (P2/P1) of the aortic pulse wave (partial r = 0.21, β-coefficient ± s.e.m. = 0.42 ± 0.12, P<0.0005) were associated with LVM indexed to body surface area (LVMI-BSA). In contrast, in women, neither AIx derived from AP/PPc (partial r = -0.08, β-coefficient ± s.e.m.=-0.20 ± 0.11, P = 0.08) nor AIx derived from P2/P1 (partial r = -0.06, β-coefficient ± s.e.m. = -0.07 ± 0.05, P = 0.17) were associated with LVMI-BSA. Both the strength of the correlations (P<0.001 and P<0.0005 with z-statistics) and the slope of the AIx-LVMI relationships (P=0.001 and P<0.0005) were greater in men as compared with women. The lack of relationship between AIx and LVMI was noted in both premenopausal (n=285; AP/PPc vs. LVMI-BSA, partial r = 0.01, P = 0.95, P2/P1 vs. LVMI-BSA, partial r = 0.02, P = 0.77), and postmenopausal (n = 240; AP/PPc vs. LVMI-BSA, partial r = -0.06, P = 0.37, P2/P1 vs. LVMI-BSA, partial r = -0.03, P = 0.64) women. Similar differences were noted in the relationships between AIx and LVM indexed to height(2.7) in men and women. In conclusion, radial applanation tonometry-derived AIx may account for less of the variation in end-organ changes in women as compared with men.