The pressures of aging.

A ortic stiffness has re-emerged over the past 20 years as an important predictor of cardiovascular outcome. Despite this, we still know relatively little about the pathophysiological processes underlying large artery stiffening (ie, arteriosclero-sis). In previous editorials, 1,2 we emphasized that arterioscle-rosis is a distinct pathophysiological entity, separate from atherosclerosis, and should not be considered as an inevitable part of aging. Although potential risk factors for arterioscle-rosis have been identified from cross-sectional observations, there is a general lack of consistency between studies. 3 This no doubt reflects methodological differences, often small sample sizes, bias, (un)known confounders (variably adjusted for), and reverse causality. Longitudinal observations deal with some of these limitations and, therefore, provide a better framework for investigating the drivers of arteriosclerosis and identifying potential stiffening risk factors. For the past 10 years, very few longitudinal studies, with repeated measurement of aortic pulse wave velocity (aPWV), the currently accepted gold standard clinical measure of aortic stiffness, have been published. They range in size from 112 to 1759 subjects, with 2 to 7 years of follow-up. 4–7 Therefore, it is particularly pleasing to see new data from the Baltimore Longitudinal Study of Ageing (BLSA). 8 Although not particularly large, the BLSA has the added advantage of repeated measures of aPWV for a 9-year average follow-up period, in men and women, and across a wide age range. The headline findings are that initial systolic pressure and age are the main driving forces of arterial stiffening, that older men compared with women have a steeper rise in aPWV, and that traditional cardiovascular risk factors, other than systolic pressure and waist circumference, have little impact on arteriosclerosis. Increasing aortic stiffness acutely results in a rise in pulse and systolic pressures, leading some to view systolic hyper-tension as a consequence of aortic stiffening. Indeed, aPWV is increased in subjects with systolic hypertension, even after adjusting for differences in mean arterial pressure 9 ; and in the BLSA and Framingham Heart Study, aPWV predicts the change in systolic pressure with aging and development of hypertension. 7,10 However, others think that elevated systolic (and pulse) pressure promotes degeneration of the arterial wall and thus aortic stiffening, as seen in these recent data from the BLSA. Other longitudinal studies are unhelpful in this respect, with 2 reporting that baseline systolic pressure is positively associated with aortic stiffening and 2 finding no such association. However, these hypotheses should not …