Background Experimental and physiologic data mechanistically implicate wave reflections in the pathogenesis of left ventricular failure and cardiovascular disease, but their association with these outcomes in the general population is unclear. Objectives To assess the relationship between central pressure profiles and incident cardiovascular events. Methods Aortic pressure waveforms were derived from a generalized transfer function applied to the radial pressure waveform recorded non-invasively from 5,960 participants in the Multiethnic Study of Atherosclerosis (MESA). The central pressure waveform was separated into forward and reflected waves using a physiologic flow waveform. Reflection magnitude (RM=[reflected/forward wave amplitude] ×100), augmentation index (AIx=[second/first systolic peak] ×100) and pulse pressure amplification (PPA=[radial/aortic pulse pressure] ×100) were assessed as predictors of cardiovascular events (CVE) and congestive heart failure (CHF) during median 7.61 years of follow-up. Results After adjustment for established risk factors, aortic AIx independently predicted hard CVE (HR per 10%-increase=1.08; 95%CI=1.01-1.14; P=0.016), whereas PPA independently predicted all CVE (HR per 10%-increase=0.82; 95%CI=0.70-0.96; P=0.012). RM was independently predictive of all CVE (hazard ratio [HR] per 10%-increase=1.34; 95%CI=1.08-1.67; P=0.009), hard CVE (HR per 10%-increase=1.46; 95%CI=1.12-1.90; P=0.006) and strongly predictive of new-onset CHF (HR per 10%-increase=2.69; 95%CI=1.79-4.04; P<0.0001), comparing favorably to other risk factors for CHF as judged by various measures of model performance, reclassification and discrimination. In a fully-adjusted model, compared to non-hypertensive subjects with low RM, the HR for hypertensive subjects with low RM, non-hypertensive subjects with high RM and hypertensive subjects with high RM were 1.81 (95%CI=0.85-3.86), 2.16 (95%CI=1.07-5.01) and 3.98 (95%CI=1.96-8.05), respectively. Conclusions Arterial wave reflections represent a novel strong risk factor for CHF in the general population.

The estimated number of hypertensives in 2008 is nearly four times higher than the last (2005) estimate of the World Health Organization Regional Office for Africa. Prevalences were significantly higher in urban than in rural populations. Population data are lacking in many countries underlining the need for national surveys.

Abstract-Central-to-peripheral amplification of the pressure pulse leads to discrepancies between central and brachial blood pressures. This amplification depends on an individual's hemodynamic and (patho)physiological characteristics. The aim of this study was to assess the magnitude and correlates of central-to-peripheral amplification in the upper limb in a healthy, middle-aged population (the Asklepios Study). Carotid, brachial, and radial pressure waveforms were acquired noninvasively using applanation tonometry in 1873 subjects (895 women) aged 35 to 55 years. Carotid, brachial, and radial pulse pressures were calculated, as well as the absolute and relative (with carotid pulse pressure as reference) amplifications. With subjects classified per semidecade of age, carotid-to-radial amplification varied from Ϸ25% in the youngest men to 8% in the oldest women. Amplification was higher in men (20Ϯ14%) than in women (13Ϯ12%; PϽ0.001) and decreased with age (PϽ0.001) in both. Amplification over the brachial-to-radial path contributed substantially to the total amplification. In univariate analysis, the strongest correlation was found with the carotid augmentation index (Ϫ0.51 in women; Ϫ0.47 in men; both PϽ0.001). In a multiple linear regression model with carotid-to-radial amplification as the dependent variable, carotid augmentation index, total arterial compliance, and heart rate were identified as the 3 major determinants of upper limb pressure amplification (R 2 ϭ0.36). We conclude that, in healthy middle-aged subjects, the central-to-radial amplification of the pressure pulse is substantial. Amplification is higher in men than in women, decreases with age, and is primarily associated with the carotid augmentation index. Key Words: cardiovascular physiology Ⅲ blood pressure Ⅲ large arteries Ⅲ wave reflection Ⅲ hemodynamics I t has long been demonstrated that, when the blood pressure waveform is measured along the arterial tree, it changes continuously in shape and amplitude. 1,2 In large-and medium-sized arteries, the systolic upstroke of the wave generally becomes steeper from the central aorta toward the periphery, whereas the amplitude also increases, mainly through an increase in the peak value (systolic blood pressure) of the waveform. Overall, the minimum (diastolic) and mean (mean blood pressure) values, and especially the difference between both, change little from one location to the other. 3 These are well-known features described in physiological textbooks, and these phenomena can be explained on the basis of wave travel and reflection. The heart generates a forward-running pressure wave, which is reflected in the periphery. The measured pressure at any location is, thus, composed of this forward component, as well as backward components, arising from reflections. 4,5 The closer the blood pressure is measured to the reflection site (ie, the further in the periphery), the earlier the forward and backward waves will interact, leading to the steeper systolic upstroke and the more peaked appearance o...

Data regarding ethnic differences in wave reflections, which markedly affect the central pressure profile, are very limited. Furthermore, because age, heart rate and body height are strong determinants of augmentation index, relating single measurements to normative data (in which augmentation index values correspond to average population values of its determinants) is challenging. We studied subject-level data from 10,550 adults enrolled in large population-based studies. In a healthy reference sample (n=3,497), we assessed ethnic differences in augmentation index (ratio of second/first systolic peaks) and generated equations for adjusted z-scores, allowing for a standardized comparison between individual augmentation index measurements and the normative population mean from subjects of the same age, gender, ethnic population, body height and heart rate. After adjustment for age, body height, heart rate and mean arterial pressure, African blacks (women:154%; men:138%) and Andean-Hispanics (women:152%; men:133%) demonstrated higher central (aortic) augmentation index values than British whites (women:140%; men:128%); whereas American Indians (women:133%; men:122%) demonstrated lower augmentation index (all P<0.0001), without significant differences between Chinese and British whites. Similar results were found for radial augmentation index. Non-linear ethnic/gender-specific equations for z-scores were successfully generated to adjust individual augmentation index values for age, body height and heart rate. Marked ethnic differences in augmentation index exist, which may contribute to ethnic differences in hypertensive organ damage. Our study provides normative data that can be used to complement the interpretation of individual hemodynamic assessments among men and women of various ethnic populations, after removing the effect of various physiologic determinants.