Current Perspectives on Arterial Stiffness and Pulse Pressure in Hypertension and Cardiovascular Diseases

Abstract

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...

Clinical Phenotypes in Heart Failure With Preserved Ejection Fraction

“…Age also affects the vasculature 41, 42. The major effect of age on the vasculature is systolic hypertension with widening of the pulse pressure that results from age‐related increase in arterial stiffness and early wave reflections 43, 44. Arterial stiffening and early wave reflections are steady vascular features in HFpEF 45, 46, 47, 48, 49, 50, 51, 52.…”

Macro and microvasculature in hypertension: therapeutic aspects

“…With age, the reflection sites are closer to vital organs, such as the heart, brain and kidney, and even wave reflections may contribute particularly to organ damage. 1,2,24 Wave reflections may occur at any vascular site where vasomotor tone and pulsatility are still present. They disappear almost completely at pre-capillary and capillary levels (diameter: o150 mm), that is, when blood perfusion becomes almost completely steady.…”

“…1,2 When subjects are young and have quite elastic conduit arteries (low PWV), the reflected wave returns slowly towards the heart, that is, during the diastolic period. Its principal consequence is to boost coronary perfusion during this period without changing the cardiac afterload.…”

“…On the other hand, when the subjects are old and have stiff arteries, the reflected wave returns very rapidly towards the heart (high PWV), that is, during systole. 1,2 In this setting, coronary perfusion, which normally occurs only during diastole, is consistently reduced and favours coronary ischaemia. Furthermore, in the central arteries, the reflected pressure wave becomes superimposed on the forward wave during systole and causes an additive increase of SBP, called the 'augmentation pressure' (mm Hg) or 'augmentation index' (%PP).…”

“…PP and mostly systolic blood pressure (SBP) vary across the arterial tree and increase peripherally with the decline in artery diameter, the increase in arterial stiffness and the transit of wave reflections. 1,2 Anti-hypertensive therapy largely prevents the cerebral and renal complications of hypertension as well as the development of congestive heart failure. The prevention of coronary ischaemic disease is more difficult to obtain.…”