Recent Advances in Arterial Stiffness and Wave Reflection in Human Hypertension

Abstract

In recent years, great emphasis has been placed on the role of arterial stiffness and wave reflection in the development of cardiovascular (CV) diseases. Arterial stiffness and wave reflections, which are now well accepted as the most important determinants of increasing systolic and pulse pressures in aging societies, are increasingly used in the clinical assessment of patients with hypertension and various CV risk factors.1,2 This review addresses recent advances in our understanding of the role played by arterial stiffness and wave reflection in the pathophysiology and treatment of human hypertension. According to the editorial rules for “Hypertension Highlights”, and to better focus on recent research, apart from large clinical trials, only articles published during the last 2 years are quoted in this review. Research on the molecular determinants of arterial stiffness has focused for years on the structure and amount of the main load bearing proteins: elastin and collagens.3 Indeed, aging and blood pressure, the two major determinants of arterial stiffness, are associated with a number of molecular changes of the load-bearing media of elastic arteries: the orderly arrangement of elastic fibers and laminae is gradually lost over time, and thinning, splitting, fraying, and fragmentation are observed. The degeneration of elastic fibers is associated with an increase in collagenous material and in ground substance, often accompanied by calcium deposition in ground substance and in degenerate elastic fibers.4 However, quantitative changes in elastin and collagen may not explain, by themselves, paradoxical observations. For instance, the changes in arterial wall material which accompany arterial hypertrophy in animal models of essential hypertension (SHRs and SHR-SPs) and in middle-age hypertensive patients are not necessarily associated with an increased isobaric stiffness.5 We suggested5 that adaptive mechanisms may include a rearrangement of the arterial wall material through cell–matrix connections, with a …