What Are Elastic Arteries
Elastic arteries are the large, central vessels (primarily the aorta and its major branches) characterized by a unique medial layer containing 60-80 concentric elastic lamellae that enable them to cyclically distend during systole and recoil during diastole, thereby performing the critical "windkessel" function that reduces cardiac workload and maintains continuous blood flow to organs. 1
Structural Composition
The defining feature of elastic arteries is their highly organized ultrastructure:
- The medial layer contains 60-80 concentric elastic lamellae in the human ascending aorta, interdigitated with connective tissue layers containing smooth muscle cells (SMCs) 1
- This microstructure gradually disappears as arteries transition peripherally, with elastic lamellae decreasing in number and SMC content increasing in medium-sized and smaller vessels 1
- The elastic fibers consist of elastin (the core component), fibrillin microfibrils (providing scaffolding), and associated proteins essential for cross-linking 1
Functional Mechanics
The mechanical behavior of elastic arteries arises from two key components:
- Elastin provides intrinsic distensibility at physiological pressures, allowing the vessel to stretch and store elastic energy 1
- Wavy, undulating collagen fibers helically spiral along the artery and are progressively recruited at higher pressures, creating the characteristic nonlinear mechanical response 1
This design enables the windkessel function: elastic arteries cyclically distend to store blood and elastic energy during systole, then release this energy to promote blood flow during diastole, reducing cardiac workload and dampening pulsatile flow to distal organs 1
Critical Clinical Implications
A crucial caveat: elastin is only deposited during fetal growth and infancy and is never renewed thereafter 1. This has profound consequences:
- Elastin has a half-life of 40-50 years, inherently predisposing elastic arteries to stiffening in late life 1
- As elastin degrades, load shifts to stiffer collagen components, increasing arterial stiffness 1
- Loss of windkessel function forces more blood to travel longer distances during systole, requiring higher driving pressures and increasing cardiac energy demands 1
- This leads to widened pulse pressure and increased mechanical stress on vessels and organs, strongly associating with organ damage in the heart, kidney, and brain 1
Geographic Distribution
The composition changes dramatically from central to peripheral circulation:
- Central elastic arteries (aorta, major branches) have maximal elastic lamellae content 1
- Peripheral arteries have much lower elastin content and are less susceptible to age-related stiffening 1
- This creates a "stiffness gradient" that decreases with aging, altering arterial hemodynamics and pressure wave transmission 1