The quantifiable measure of the elasticity and distensibility of the arterial walls, representing their ability to expand and recoil in response to changes in blood pressure during the cardiac cycle. Optimal vascular compliance is essential for buffering the pulsatile flow from the heart, ensuring a smooth, steady blood flow to peripheral tissues, and maintaining healthy blood pressure. A reduction in compliance, or arterial stiffening, is a hallmark of cardiovascular aging and a predictor of adverse cardiac events.
Origin
The concept is rooted in hemodynamics and cardiovascular physiology, applying principles of physics to the circulatory system. The clinical measurement of compliance, often through pulse wave velocity (PWV), became a key diagnostic tool in the late 20th century. The recognition that hormonal balance, particularly nitric oxide and estrogen signaling, profoundly affects vessel wall elasticity integrated this concept into the domain of hormonal health.
Mechanism
Vascular compliance is primarily determined by the structural integrity and composition of the arterial wall, specifically the ratio of elastin to collagen fibers and the functional tone of the vascular smooth muscle cells. Endothelial cells release vasoactive substances, such as nitric oxide, which promote smooth muscle relaxation and increase compliance. Conversely, chronic inflammation and hormonal shifts can lead to collagen deposition and reduced nitric oxide bioavailability, resulting in arterial stiffening and diminished compliance.
Personalized hormone protocols support cardiovascular health by restoring the biological signals that maintain vascular function and metabolic efficiency.
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