Arterial stiffness
Arterial stiffness | |
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Biological system | arteries |
Arterial stiffness occurs as a consequence of biological aging and arteriosclerosis.[1] Inflammation plays a major role in arteriosclerosis development, and consequently it is a major contributor in large arteries stiffening.[2] Increased arterial stiffness is associated with an increased risk of cardiovascular events such as myocardial infarction, hypertension, heart failure and stroke, the two leading causes of death in the developed world.[3][4][5] The World Health Organization predicts that in 2010, cardiovascular disease will also be the leading killer in the developing world and represents a major global health problem.[citation needed]
Several degenerative changes that occur with age in the walls of large elastic
Background
When the heart contracts it generates a pulse or energy wave that travels through the circulatory system. The speed of travel of this pulse wave (pulse wave velocity[7] (PWV)) is related to the stiffness of the arteries. Other terms that are used to describe the mechanical properties of arteries include elastance, or the reciprocal (inverse) of elastance, compliance. The relationship between arterial stiffness and pulse wave velocity was first predicted by Thomas Young in his Croonian Lecture of 1808 [8] but is generally described by the Moens–Korteweg equation[9] or the Bramwell–Hill equation.[10] Typical values of PWV in the aorta range from approximately 5 m/s to >15 m/s.[citation needed]
Measurement of aortic PWV provides some of the strongest evidence concerning the prognostic significance of large artery stiffening. Increased aortic PWV has been shown to predict cardiovascular, and in some cases all cause, mortality in individuals with
Pathophysiological consequences of increased arterial stiffness
The primary sites of end-target organ damage following an increase in arterial stiffness are the heart, the brain (stroke, white matter hyperintensities (WMHs)), and the kidneys (age-related loss of kidney function). The mechanisms linking arterial stiffness to end-organ damage are several-fold.[citation needed]
Firstly, stiffened arteries compromise the Windkessel effect of the arteries.[17] The Windkessel effect buffers the pulsatile ejection of blood from the heart converting it into a more steady, even outflow. This function depends on the elasticity of the arteries and stiffened arteries require a greater amount of force to permit them to accommodate the volume of blood ejected from the heart (stroke volume). This increased force requirement equates to an increase in pulse pressure.[17] The increase in pulse pressure may result in increased damage to blood vessels in target organs such as the brain or kidneys.[18][19] This effect may be exaggerated if the increase in arterial stiffness results in reduced wave reflection and more propagation of the pulsatile pressure into the microcirculation.[18]
An increase in arterial stiffness also increases the load on the heart, since it has to perform more work to maintain the
Arterial stiffness may also affect the time at which pulse wave reflections return to the heart. As the pulse wave travels through the circulation it undergoes reflection at sites where the transmission properties of the arterial tree change (i.e. sites of impedance mismatch). These reflected waves propagate backwards towards the heart. The speed of propagation (i.e. PWV[7]) is increased in stiffer arteries and consequently reflected waves will arrive at the heart earlier in systole. This increases the load on the heart in systole.[22] Elevated PWV could represent an important parameter for identifying children with CKD and high cardiovascular risk.[23]
See also
Notes
- PMID 33164578.
- ^ Mozos I, Malainer C, Horbańczuk J, Gug C, Stoian D, Luca CT, Atanasov AG. Inflammatory Markers for Arterial Stiffness in Cardiovascular Diseases. Front Immunol. 2017 Aug 31;8:1058. doi: 10.3389/fimmu.2017.01058.
- ^ Demir S, Akpınar O, Akkus O, Nas K, Unal I, Molnar F, et al. The prognostic value of arterial stiffness in systolic heart failure. Cardiol J 2013; 20:665–671.
- ^ Laurent S, Boutouyrie P, Asmar R, Gautier I, Laloux B, Guize L, et al. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients. Hypertension 2001; 37:1236–1241.
- ^ Edgell H., Stickland M.K., Maclean J.E. A simplified measurement of pulse wave velocity is not inferior to standard measurement in young adults and children. Blood Press. Monit.. 2016;21(3):192-195. doi:10.1097/MBP.0000000000000183
- )
- ^ S2CID 199381680.
- S2CID 110648919.
- ^ Nichols WW, O'Rourke MF. Vascular impedance. In: McDonald's Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 4th ed. London, UK: Edward Arnold; 1998:54–97, 243–283, 347–395.
- S2CID 120673490.
- PMID 10318666.
- S2CID 8417352.
- PMID 12379578.
- PMID 16461838.
- PMID 16461839.
- S2CID 20651222. Also noted are newer pulse wave velocity measurement tools like the iHeart Internal Age device, a fingertip device that measures aortic pulse wave velocity and arterial stiffness through the pulse in the finger.
- ^ ISBN 978-1-4419-6363-5.
- ^ S2CID 23321317.
- PMID 17130269.
- PMID 22083151.
- PMID 23836802.
- PMID 35054238.
- ISBN 978-0-340-80941-9.