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Measuring the Interaction Between the Macro- and Micro-Vasculature
Rachel E Climie1,2,3, Antonio Gallo4,5, Dean S Picone3
1INSERM, U970, Paris Cardiovascular Research Center (PARCC), Paris Descartes University, Paris, France.
Insights
Essential hypertension causes vascular dysfunction, leading to arterial stiffening. This increases pulsatile stress on microvasculature, potentially damaging vital organs like the brain and kidneys.
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
Background:
- Essential hypertension involves macro- and microvascular dysfunction.
- Healthy arteries buffer pressure/flow pulsations, protecting the microvasculature.
- Arterial stiffening, due to aging or hypertension, impairs this buffering capacity.
Purpose of the Study:
- To review the clinical relevance of macro- and microvascular pulsatility transmission.
- To summarize methods for measuring pulsatility transmission.
Main Methods:
- Literature review of studies on arterial stiffness and pulsatility.
- Analysis of current measurement techniques for macro- and microvascular pulsatility.
Main Results:
- Arterial stiffening increases pulsatile stress on the microvasculature.
- This pulsatile stress is critical for high flow/low resistance organs (brain, kidney).
- Increased pulsatility can damage capillary networks, leading to target organ damage.
Conclusions:
- Understanding pulsatility transmission is crucial for managing hypertension.
- Arterial stiffening exacerbates pulsatile stress, contributing to organ damage.
- Accurate measurement of pulsatility transmission aids in clinical assessment.
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.
