These results provide the first direct evidence that in patients with ESRD, increased aortic stiffness determined by measurement of aortic PWV is a strong independent predictor of all-cause and mainly cardiovascular mortality.

Blood pressure (BP) is a powerful cardiovascular (CV) risk factor that acts on the arterial wall and is responsible in part for various CV events, such as cerebrovascular accidents and ischemic heart disease. In clinical practice, 2 specific and arbitrary points of the BP curve, peak systolic BP (SBP) and end-diastolic BP (DBP), are used to define the CV risk factor. Because the goal of drug treatment of hypertension is to prevent CV complications, it appears likely that the totality of the BP curve, not simply 2 specific and arbitrary points, should be considered to act mechanically on the arterial wall and therefore should be used to propose an adequate definition of high BP.A current approach consists of considering the BP curve as the summation of a steady component, mean blood pressure (MBP), and a pulsatile component, pulse pressure (PP). 1 MBP, the product of cardiac output multiplied by total peripheral resistance, is the pressure for the steady flow of blood and oxygen to peripheral tissues and organs. The pulsatile component, PP, is the consequence of intermittent ventricular ejection from the heart. PP is influenced by several cardiac and vascular factors, but it is the role of large conduit arteries, mainly the aorta, to minimize pulsatility. In addition to the pattern of left ventricular ejection, the determinants of PP (and SBP) are the cushioning capacity of arteries and the timing and intensity of wave reflections. 1 The former is influenced by arterial stiffness, usually expressed in the quantitative terms of compliance and distensibility. 1 The latter result from the summation of a forward wave coming from the heart and propagating at a given speed (pulse wave velocity, or PWV) toward the origin of resistance vessels and a backward wave returning toward the heart from particular sites characterized by specific reflection coefficients. 1 Over the past few years, arterial stiffness and wave reflections have been widely investigated in old and/or hypertensive subjects for several reasons. First, whereas DBP was considered in the past as the better guide to determine disease severity, epidemiological studies have directed attention to SBP as a more informative CV risk factor, particularly in patients older than 50 years of age, and it has been shown that PP is an independent marker of CV risk, mainly for myocardial infarction. 2 Second, in subjects Ͼ50 years of age, ventricular ejection tends to be reduced, so that arterial stiffness and amplitude and timing of wave reflections become the main determinants of increased SBP and PP. Third, whereas drug control of DBP is consistently obtained in large populations of hypertensive patients, the ability to control SBP is observed much less frequently. 3 Finally, increased PP is also a predictor of CV risk in subjects with recurrent myocardial infarction and congestive heart failure. 2,4,5 From the hemodynamic factors that influence PP, 2 have been shown to independently predict CV risk: aortic stiffness, measured from aortic PWV, 6,7 and early return of...

Central haemodynamic indexes are independent predictors of future CV events and all-cause mortality. Augmentation index predicts clinical events independently of peripheral pressures, while central PP has a marginally but not significantly (P = 0.057) better predictive ability when compared with peripheral PP.

Abstract-A close relationship has been established between microvascular damage in brain and kidney and indices of age and hypertension (pulse pressure, aortic pulse wave velocity, and augmentation index). The mechanism of such association has not been established, nor has rationale for prevention and treatment of microvascular damage. A logical pathophysiological explanation can be offered on the basis of differential input impedance in the brain and kidney compared with other systemic vascular beds. Torrential flow and low resistance to flow in these organs exposes small arterial vessels to the high-pressure fluctuations that exist in the carotid, vertebral, and renal arteries. Such fluctuations, measurable as central pulse pressure, increase 3-to 4-fold with age. Exposure of small vessels to highly pulsatile pressure and flow explains microvascular damage and resulting renal insufficiency and intellectual deterioration, according to the mechanism established by Byrom Ͼ50 years ago. The logical approach to prevention and treatment requires reduction of central pulse pressure. Because the aorta and large arteries are not directly affected by drugs, this entails reduction of wave reflection by dilation of conduit arteries elsewhere in the body. This can be accomplished by regular exercise and by drugs such as nitrates, calcium channel blockers, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers. The explanation given here accounts for greater and earlier vascular damage in diabetes mellitus (relative microvascular fragility) and is similar to that given for vascular changes of pulmonary hypertension caused by ventricular septal defects and other congenital vascular shunts.