Medicine:Arterial stiffness

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Short description: Loss of elasticity in blood vessels
Not to be confused with Atherosclerosis or arteriosclerosis.
Arterial stiffness
Biological systemarteries

Arterial stiffness occurs as a consequence of biological aging, arteriosclerosis and genetic disorders, such as Marfan, Williams, and Ehlers-Danlos syndromes.[1] Inflammation plays a major role in arteriosclerosis and arterial stiffness.[2] Increased arterial stiffness is associated with an increased risk of cardiovascular events such as myocardial infarction, hypertension, heart failure, and stroke.[3][4][5] The World Health Organization identified cardiovascular disease as the leading cause of death globally in 2019.[6]

Degenerative changes that occur with age in the walls of large elastic arteries are thought to contribute to increased stiffening over time, including the disruption of lamellar elastin structures within the wall, possibly due to repeated cycles of mechanical stress; inflammation;[7] changes in arterial collagen proteins, partially as a compensatory mechanism against the loss of arterial elastin and partially due to fibrosis; and crosslinking of adjacent collagen fibers by advanced glycation endproducts (AGEs).[8]

Definition

Arterial stiffness is commonly measured as carotid–femoral pulse wave velocity (cfPWV) or brachial–ankle PWV (baPWV).[9] cfPWV is the standard for measuring large artery stiffness in Europe.[9] For baPWV, general cutoff values for cardiovascular risk assessment are <1400 cm/s for low risk, 1400–1800 cm/s for intermediate risk, and >1800 cm/s for high risk.[9] Increased cfPWV and baPWV values predict an increased risk of new-onset hypertension in apparently healthy people.[9]

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, PWV[10]) 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,[11] and is generally described by the Moens–Korteweg equation[12] or the Bramwell–Hill equation.[13] Typical values of PWV in the aorta range from approximately 5 m/s to over 15 m/s.[14]

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 end stage kidney disease,[15] hypertension,[16] diabetes mellitus[17] and in the general population.[18][19] A 2024 paper reported that the use of PWV, previously a predominantly research-focused tool, had become a marker of clinical importance.[20] Devices are available that measure arterial stiffness parameters augmentation index and pulse wave velocity, including Complior, CVProfilor, PeriScope, Hanbyul Meditech, Mobil-O-Graph NG, BP Plus (Pulsecor), PulsePen, BPLab Vasotens, Arteriograph, Vascular Explorer, and SphygmoCor.[21]

Pathophysiological consequences

The primary sites of end-target organ damage following an increase in arterial stiffness are the heart, the brain (stroke, white matter hyperintensities (WMHs)), the placenta, and the kidneys (age-related loss of kidney function).[22]

Firstly, stiffened arteries compromise the Windkessel effect of the arteries.[23] 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.[23] The increase in pulse pressure may result in increased damage to blood vessels in target organs such as the brain or kidneys.[24][25] 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.[24]

An increase in arterial stiffness also increases the load on the heart, since it has to perform more work to maintain the stroke volume. Over time, this increased workload may cause left ventricular hypertrophy and left ventricular remodelling, which can lead to heart failure.[26] The increased workload may also be associated with a higher heart rate, a proportionately longer duration of systole and a comparative reduction of duration of diastole.[27] This decreases the amount of time available for perfusion of cardiac tissue, which largely occurs in diastole.[23]

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 backward towards the heart. The speed of propagation (i.e. PWV[10]) 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.[28] Elevated PWV could represent an important parameter for identifying children with CKD and high cardiovascular risk.[29]

See also

References

  1. ↑ Laurent, Stéphane; Boutouyrie, Pierre; Lacolley, Patrick (June 2005). "Structural and Genetic Bases of Arterial Stiffness". Hypertension 45 (6): 1050–1055. doi:10.1161/01.HYP.0000164580.39991.3d. PMID 15851625. https://www.ahajournals.org/doi/10.1161/01.HYP.0000164580.39991.3d. 
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ 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
  6. ↑ "Cardiovascular diseases (CVDs)" (in en). https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds)#:~:text=Cardiovascular%20diseases%20(CVDs)%20are%20the,counselling%20and%20medicines%20can%20begin.. 
  7. ↑ Halsey, Gregory; Sinha, Dipasha; Dhital, Saphala; Wang, Xiaoying; Vyavahare, Naren (2023-06-01). "Role of elastic fiber degradation in disease pathogenesis". Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1869 (5). doi:10.1016/j.bbadis.2023.166706. ISSN 0925-4439. PMID 37001705. 
  8. ↑ Dietz, J (2007). "Arterial stiffness and extracellular matrix". Atherosclerosis, Large Arteries and Cardiovascular Risk. Advances in Cardiology. 44. pp. 76–95. doi:10.1159/000096722. ISBN 978-3-8055-8176-9. 
  9. ↑ 9.0 9.1 9.2 9.3 Mancia, Giuseppe; Kreutz, Reinhold; Brunström, Mattias; Burnier, Michel; Grassi, Guido; Januszewicz, Andrzej; Muiesan, Maria Lorenza; Tsioufis, Konstantinos et al. (December 2023). "2023 ESH Guidelines for the management of arterial hypertension The Task Force for the management of arterial hypertension of the European Society of Hypertension: Endorsed by the International Society of Hypertension (ISH) and the European Renal Association (ERA)" (in en-US). Journal of Hypertension 41 (12): 1874–2071. doi:10.1097/HJH.0000000000003480. ISSN 0263-6352. PMID 37345492. https://journals.lww.com/jhypertension/fulltext/2023/12000/2023_esh_guidelines_for_the_management_of_arterial.2.aspx. 
  10. ↑ 10.0 10.1 Nabeel, P. M.; Kiran, V. Raj; Joseph, Jayaraj; Abhidev, V. V.; Sivaprakasam, Mohanasankar (2020). "Local Pulse Wave Velocity: Theory, Methods, Advancements, and Clinical Applications". IEEE Reviews in Biomedical Engineering 13: 74–112. doi:10.1109/RBME.2019.2931587. ISSN 1937-3333. PMID 31369386. Bibcode: 2020IRBE...13...74N. 
  11. ↑ Young (1809). "On the function of the heart and arteries: The Croonian lecture". Philos Trans R Soc 99: 1–31. doi:10.1098/rstl.1809.0001. 
  12. ↑ 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.
  13. ↑ "The velocity of the pulse wave in man". Proceedings of the Royal Society of London B 93 (652): 298–306. 1922. doi:10.1098/rspb.1922.0022. Bibcode: 1922RSPSB..93..298C. 
  14. ↑ The Reference Values for Arterial Stiffness' Collaboration (2010-10-01). "Determinants of pulse wave velocity in healthy people and in the presence of cardiovascular risk factors: 'establishing normal and reference values'" (in en). European Heart Journal 31 (19): 2338–2350. doi:10.1093/eurheartj/ehq165. ISSN 1522-9645. PMID 20530030. PMC 2948201. https://academic.oup.com/eurheartj/article/31/19/2338/441416. 
  15. ↑ "Impact of aortic stiffness on survival in end-stage renal disease". Circulation 99 (18): 2434–9. May 1999. doi:10.1161/01.cir.99.18.2434. PMID 10318666. 
  16. ↑ "Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients". Hypertension 37 (5): 1236–41. May 2001. doi:10.1161/01.hyp.37.5.1236. PMID 11358934. 
  17. ↑ "Aortic pulse-wave velocity and its relationship to mortality in diabetes and glucose intolerance: an integrated index of vascular function?". Circulation 106 (16): 2085–90. October 2002. doi:10.1161/01.cir.0000033824.02722.f7. PMID 12379578. 
  18. ↑ "Arterial stiffness and risk of coronary heart disease and stroke: the Rotterdam Study". Circulation 113 (5): 657–63. February 2006. doi:10.1161/CIRCULATIONAHA.105.555235. PMID 16461838. 
  19. ↑ "Prognostic value of aortic pulse wave velocity as index of arterial stiffness in the general population". Circulation 113 (5): 664–70. February 2006. doi:10.1161/CIRCULATIONAHA.105.579342. PMID 16461839. 
  20. ↑ Pilz, Niklas; Heinz, Viktor; Ax, Timon; Fesseler, Leon; Patzak, Andreas; Bothe, Tomas Lucca (17 July 2024). "Pulse Wave Velocity: Methodology, Clinical Applications, and Interplay with Heart Rate Variability". Reviews in Cardiovascular Medicine 25 (7). doi:10.31083/j.rcm2507266. ISSN 1530-6550. PMID 39139426. 
  21. ↑ "Arterial blood pressure measurement and pulse wave analysis - their role in enhancing cardiovascular assessment". Physiological Measurement 31 (1): R1–R47. 2009. doi:10.1088/0967-3334/31/1/r01. PMID 19940350.  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.
  22. ↑ Chirinos, Julio A.; Segers, Patrick; Hughes, Timothy; Townsend, Raymond (2019-09-03). "Large-Artery Stiffness in Health and Disease: JACC State-of-the-Art Review". Journal of the American College of Cardiology 74 (9): 1237–1263. doi:10.1016/j.jacc.2019.07.012. ISSN 0735-1097. PMID 31466622. 
  23. ↑ 23.0 23.1 23.2 Nicolaas Westerhof; Nikolaos Stergiopulos; Mark I.M. Noble (2 September 2010). Snapshots of Hemodynamics: An Aid for Clinical Research and Graduate Education. Springer Science & Business Media. pp. 181–. ISBN 978-1-4419-6363-5. https://books.google.com/books?id=fqWIm8RmVYsC&pg=PA181. 
  24. ↑ 24.0 24.1 Mitchell, Gary F. (2015). "Arterial stiffness". Current Opinion in Nephrology and Hypertension 24 (1): 1–7. doi:10.1097/MNH.0000000000000092. ISSN 1062-4821. PMID 25470012. 
  25. ↑ Fernandez-Fresnedo, G.; Rodrigo, E.; de Francisco, A. L. M.; de Castro, S. S.; Castaneda, O.; Arias, M. (2006). "Role of Pulse Pressure on Cardiovascular Risk in Chronic Kidney Disease Patients". Journal of the American Society of Nephrology 17 (12_suppl_3): S246–S249. doi:10.1681/ASN.2006080921. ISSN 1046-6673. PMID 17130269. 
  26. ↑ Cheng, S.; Vasan, R. S. (2011). "Advances in the Epidemiology of Heart Failure and Left Ventricular Remodeling". Circulation 124 (20): e516–e519. doi:10.1161/CIRCULATIONAHA.111.070235. ISSN 0009-7322. PMID 22083151. 
  27. ↑ Whelton, S. P.; Blankstein, R.; Al-Mallah, M. H.; Lima, J. A. C.; Bluemke, D. A.; Hundley, W. G.; Polak, J. F.; Blumenthal, R. S. et al. (2013). "Association of Resting Heart Rate With Carotid and Aortic Arterial Stiffness: Multi-Ethnic Study of Atherosclerosis". Hypertension 62 (3): 477–484. doi:10.1161/HYPERTENSIONAHA.113.01605. ISSN 0194-911X. PMID 23836802. 
  28. ↑ Pavelescu, Carmen (2021). "www.mdpi.com". Diagnostics (Basel, Switzerland) 12 (1). doi:10.3390/diagnostics12010071. PMID 35054238. 
  29. ↑ Wilmer W. Nichols; Michael F. O'Rourke (25 February 2005). McDonald's Blood Flow in Arteries 5Ed: Theoretical, experimental and clinical principles. Taylor & Francis. ISBN 978-0-340-80941-9. https://books.google.com/books?id=F8RpQgAACAAJ. 

Filip, Cristina; Cirstoveanu, Cătălin; Bizubac, Mihaela; Berghea, Elena Camelia; Căpitănescu, Andrei; Bălgrădean, Mihaela; Pavelescu, Carmen; Nicolescu, Alin et al. (29 December 2021). "Pulse Wave Velocity as a Marker of Vascular Dysfunction and Its Correlation with Cardiac Disease in Children with End-Stage Renal Disease (ESRD)". Diagnostics 12 (1): 71. doi:10.3390/diagnostics12010071. ISSN 2075-4418. PMID 35054238. 



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