Pulse pressure (PP), a marker of arterial system properties, has been linked to cardiovascular (CV) complications. We examined (a) association between unit changes of PP and (i) composite CV outcomes and (ii) development of left-ventricular hypertrophy (LVH) and (b) effect of mean arterial pressure (MAP) control on rate of change in PP. We studied 1094 nondiabetics with nephrosclerosis in the African American Study of Kidney Disease and Hypertension. Subjects were randomly assigned to usual MAP goal (102–107？mmHg) or a lower MAP goal (≤92？mmHg) and randomized to beta-blocker, angiotensin converting enzyme inhibitor, or calcium channel blocker. After covariate adjustment, a higher PP was associated with increased risk of CV outcome (RR = 1.28, CI = 1.11–1.47, ) and new LVH (RR = 1.26, CI = 1.04–1.54, ). PP increased at a greater rate in the usual than in lower MAP groups (slope ± SE: 1.08 ± 0.15 versus 0.42 ± 0.15 mmHg/year, ), but not by the antihypertensive treatment assignment. Observations indicate that control to a lower MAP slows the progression of PP, a correlate of cardiovascular remodeling and complications, and may be beneficial to CV health. 1. Introduction Population and hospital-based studies [1, 2] have demonstrated that persistently elevated blood pressure (BP) levels increase the risk of cardiovascular (CV) events and subsequent CV mortality. Though the precise mechanisms of this association are still being investigated, several studies have detected a direct link between increased BP variability and target-organ damage [3–7]. The major target organs for the complications of elevated BP are the kidneys, heart, brain, and the arterial system. Study of the character of vascular alterations and the time course of such alterations is important to better understand the mechanism of hypertensive process. Retta and Randall [8] have suggested that target-organ damage is the result of an integrated effect of BP level as a function of time, whether it is continuously elevated or intermittent increases of pressure. Arterial stiffness is linked with changes in BP profile, characterized by isolated increase in systolic pressure and/or increase in pulse pressure (PP). Increased PP can result from an increase in systolic pressure and/or a decrease in diastolic pressure, which is typical for advanced arteriosclerosis and is responsible for the diastolic pressure stabilization or decline observed in aging [9]. Investigations in hypertension have generally focused on the steady components of blood pressure, such as mean arterial pressure (MAP), which is
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