Measuring the Interaction Between the Macro- and Micro-Vasculature

Abstract

Structural and functional dysfunction in both the macro- and microvasculature are a feature of essential hypertension. In a healthy cardiovascular system, the elastic properties of the large arteries ensure that pulsations in pressure and flow generated by cyclic left ventricular contraction are dampened, so that less pulsatile pressure and flow are delivered at the microvascular level. However, in response to aging, hypertension, and other disease states, arterial stiffening limits the buffering capacity of the elastic arteries, thus exposing the microvasculature to increased pulsatile stress. This is thought to be particularly pertinent to high flow/low resistance organs such as the brain and kidney, which may be sensitive to excess pressure and flow pulsatility, damaging capillary networks, and resulting in target organ damage. In this review, we describe the clinical relevance of the pulsatile interaction between the macro- and microvasculature and summarize current methods for measuring the transmission of pulsatility between the two sites.

Vasculo-Neuronal Coupling and Neurovascular Coupling at the Neurovascular Unit: Impact of Hypertension

“…Moreover, hypertension results in increase wall stiffness of larger vessels (i.e., posterior cerebral artery) and increased wall stress and wall thickness of parenchymal arteriole (Diaz-Otero et al, 2016). While few have addressed the importance of understanding the relationship between the macro-and micro-vasculature, these questions are emerging (Climie et al, 2019) and constitute new paradigms toward the development of new therapeutic targets addressing the impact of cardiovascular disease on cognitive function.…”

Renal resistive index as a novel biomarker for cardiovascular and kidney risk reduction in type II diabetes

“…1,5,6 To this point, aortic stiffening results in propagation of excessive pulsatile (kinetic) energy into peripheral organs, such as the kidney, where there is high flow but low precapillary resistance or impedance. 7,8 The difference in the velocities between the central arterial tree and the end organ is measured as a resistivity index (RI) as evaluated by the indirect analysis of intrarenal circulation though the study of arterial flow as determined by Doppler sonography. Over time, this persistent excess pulsatile wave (increased pulsatility) to the end organ contributes to alterations in autoregulatory mechanisms, which include increases in myogenic tone, abnormal wall remodeling, and strain.…”

“…These processes are especially deleterious to high flow, low impedance circulatory beds such as the kidney microcirculation. 8 Therefore, the kidney is highly susceptible to excess pulsatile flow and of aortic vascular stiffness from the central aorta that can lead to glomerular injury and albuminuria. 9 Its diagnostic utility has been further examined in both acute and chronic settings in clinical practice.…”

Clinical application of pulsatility index

“…The natural pulsations in pressure caused by each contraction of the left ventricle are largely diminished thanks to elasticity of large arteries. As the aorta expands, it stores a portion of the stroke volume, so that the microvasculature is less exposed to pulsatile stress [6]. Thus, the elasticity of blood vessels allows for blunting down harmful pulsations in the large arteries before they reach end-organ microcirculation [6].…”

“…As the aorta expands, it stores a portion of the stroke volume, so that the microvasculature is less exposed to pulsatile stress [6]. Thus, the elasticity of blood vessels allows for blunting down harmful pulsations in the large arteries before they reach end-organ microcirculation [6]. However, from early on in childhood, arterial walls continually increase in stiffness through the loss of elastic fibers.…”