Arterial stiffness

Last updated
Arterial stiffness
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, two of the 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 ]

Contents

Several degenerative changes that occur with age in the walls of large elastic arteries are thought to contribute to increased stiffening over time, including the mechanical fraying of lamellar elastin structures within the wall due to repeated cycles of mechanical stress; changes in the kind and increases in the content of 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). [6]

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 end stage kidney disease, [11] hypertension, [12] diabetes mellitus [13] and in the general population. [14] [15] However, at present, the role of measurement of PWV as a general clinical tool remains to be established. Devices are on the market that measure arterial stiffness parameters (augmentation index, pulse wave velocity). These include Complior, CVProfilor, PeriScope, Hanbyul Meditech, Mobil-O-Graph NG, BP Plus (Pulsecor), PulsePen, BPLab Vasotens, Arteriograph, Vascular Explorer, and SphygmoCor. [16]

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 stroke volume. Over time, this increased workload causes left ventricular hypertrophy and left ventricular remodelling, which can lead to heart failure. [20] 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. [21] This decreases the amount of time available for perfusion of cardiac tissue, which largely occurs in diastole. [17] Thus the hypertrophic heart, which has a greater oxygen demand, may have a compromised supply of oxygen and nutrients.[ citation needed ]

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 [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

  1. ↑ Winder, Nick R.; Reeve, Emily H.; Walker, Ashley E. (2021-01-01). "Large artery stiffness and brain health: insights from animal models". American Journal of Physiology. Heart and Circulatory Physiology. 320 (1): H424–H431. doi:10.1152/ajpheart.00696.2020. ISSN   0363-6135. PMC   7847068 . PMID   33164578.
  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. ↑ 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.
  4. ↑ 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.
  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. ↑ Dietz, J (2007). "Arterial stiffness and extracellular matrix". Atherosclerosis, Large Arteries and Cardiovascular Risk. Advances in Cardiology. Vol. 44. pp. 76–95. doi:10.1159/000096722. ISBN   978-3-8055-8176-9. PMID   17075200.{{cite book}}: |journal= ignored (help)
  7. 1 2 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. S2CID   199381680.
  8. ↑ 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. JSTOR   109672. S2CID   110648919.
  9. ↑ 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.
  10. ↑ Bramwell JC, Hill AV (1922). "The velocity of the pulse wave in man". Proceedings of the Royal Society of London B. 93 (652): 298–306. Bibcode:1922RSPSB..93..298C. doi:10.1098/rspb.1922.0022. JSTOR   81045. S2CID   120673490.
  11. ↑ Blacher J, Guerin AP, Pannier B, Marchais SJ, Safar ME, London GM (May 1999). "Impact of aortic stiffness on survival in end-stage renal disease". Circulation. 99 (18): 2434–9. doi: 10.1161/01.cir.99.18.2434 . PMID   10318666.
  12. ↑ Laurent S, Boutouyrie P, Asmar R, Gautier I, Laloux B, Guize L, Ducimetiere P, Benetos A (May 2001). "Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients". Hypertension. 37 (5): 1236–41. CiteSeerX   10.1.1.583.3137 . doi:10.1161/01.hyp.37.5.1236. PMID   11358934. S2CID   8417352.
  13. ↑ Cruickshank K, Riste L, Anderson SG, Wright JS, Dunn G, Gosling RG (October 2002). "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. doi: 10.1161/01.cir.0000033824.02722.f7 . PMID   12379578.
  14. ↑ Mattace-Raso FU, van der Cammen TJ, Hofman A, van Popele NM, Bos ML, Schalekamp MA, Asmar R, Reneman RS, Hoeks AP, Breteler MM, Witteman JC (February 2006). "Arterial stiffness and risk of coronary heart disease and stroke: the Rotterdam Study". Circulation. 113 (5): 657–63. doi: 10.1161/CIRCULATIONAHA.105.555235 . PMID   16461838.
  15. ↑ Willum-Hansen T, Staessen JA, Torp-Pedersen C, Rasmussen S, Thijs L, Ibsen H, Jeppesen J (February 2006). "Prognostic value of aortic pulse wave velocity as index of arterial stiffness in the general population". Circulation. 113 (5): 664–70. doi: 10.1161/CIRCULATIONAHA.105.579342 . PMID   16461839.
  16. ↑ Avolio A, Butlin M, Walsh A (2009). "Arterial blood pressure measurement and pulse wave analysis - their role in enhancing cardiovascular assessment". Physiological Measurement. 31 (1): R1–R47. doi:10.1088/0967-3334/31/1/r01. PMID   19940350. 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.
  17. 1 2 3 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.
  18. 1 2 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. S2CID   23321317.
  19. ↑ 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.
  20. ↑ 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. PMC   3621875 . PMID   22083151.
  21. ↑ 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.; Nasir, K.; Blaha, M. J. (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. PMC   3838105 . PMID   23836802.
  22. ↑ Pavelescu, Carmen (2021). "www.mdpi.com". Diagnostics (Basel, Switzerland). 12 (1). doi: 10.3390/diagnostics12010071 . PMC   8774385 . PMID   35054238.
  23. ↑ 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.

Related Research Articles

<span class="mw-page-title-main">Aorta</span> Largest artery in the human body

The aorta is the main and largest artery in the human body, originating from the left ventricle of the heart, branching upwards immediately after, and extending down to the abdomen, where it splits at the aortic bifurcation into two smaller arteries. The aorta distributes oxygenated blood to all parts of the body through the systemic circulation.

In medicine, a pulse represents the tactile arterial palpation of the cardiac cycle (heartbeat) by fingertips. The pulse may be palpated in any place that allows an artery to be compressed near the surface of the body, such as at the neck, wrist, at the groin, behind the knee, near the ankle joint, and on foot. The radial pulse is commonly measured using three fingers. This has a reason: the finger closest to the heart is used to occlude the pulse pressure, the middle finger is used get a crude estimate of the blood pressure, and the finger most distal to the heart is used to nullify the effect of the ulnar pulse as the two arteries are connected via the palmar arches. The study of the pulse is known as sphygmology.

<span class="mw-page-title-main">Blood pressure</span> Pressure exerted by circulating blood upon the walls of arteries

Blood pressure (BP) is the pressure of circulating blood against the walls of blood vessels. Most of this pressure results from the heart pumping blood through the circulatory system. When used without qualification, the term "blood pressure" refers to the pressure in a brachial artery, where it is most commonly measured. Blood pressure is usually expressed in terms of the systolic pressure over diastolic pressure in the cardiac cycle. It is measured in millimeters of mercury (mmHg) above the surrounding atmospheric pressure, or in kilopascals (kPa). The difference between the systolic and diastolic pressures is known as pulse pressure, while the average pressure during a cardiac cycle is known as mean arterial pressure.

<span class="mw-page-title-main">Hypertension</span> Long-term high blood pressure in the arteries

Hypertension, also known as high blood pressure, is a long-term medical condition in which the blood pressure in the arteries is persistently elevated. High blood pressure usually does not cause symptoms itself. It is, however, a major risk factor for stroke, coronary artery disease, heart failure, atrial fibrillation, peripheral arterial disease, vision loss, chronic kidney disease, and dementia. Hypertension is a major cause of premature death worldwide.

<span class="mw-page-title-main">Aortic stenosis</span> Narrowing of the exit of the hearts left ventricle

Aortic stenosis is the narrowing of the exit of the left ventricle of the heart, such that problems result. It may occur at the aortic valve as well as above and below this level. It typically gets worse over time. Symptoms often come on gradually with a decreased ability to exercise often occurring first. If heart failure, loss of consciousness, or heart related chest pain occur due to AS the outcomes are worse. Loss of consciousness typically occurs with standing or exercising. Signs of heart failure include shortness of breath especially when lying down, at night, or with exercise, and swelling of the legs. Thickening of the valve without causing obstruction is known as aortic sclerosis.

Baroreceptors are sensors located in the carotid sinus and in the aortic arch. They sense the blood pressure and relay the information to the brain, so that a proper blood pressure can be maintained.

<span class="mw-page-title-main">Cardiac output</span> Measurement of blood pumped by the heart

In cardiac physiology, cardiac output (CO), also known as heart output and often denoted by the symbols , , or , is the volumetric flow rate of the heart's pumping output: that is, the volume of blood being pumped by a single ventricle of the heart, per unit time. Cardiac output (CO) is the product of the heart rate (HR), i.e. the number of heartbeats per minute (bpm), and the stroke volume (SV), which is the volume of blood pumped from the left ventricle per beat; thus giving the formula:

<span class="mw-page-title-main">Korotkoff sounds</span> Sounds listened for when taking blood pressure

Korotkoff sounds are the sounds that medical personnel listen for when they are taking blood pressure using a non-invasive procedure. They are named after Nikolai Korotkov, a Russian physician who discovered them in 1905, when he was working at the Imperial Medical Academy in St. Petersburg, the Russian Empire.

<span class="mw-page-title-main">Pulse pressure</span> Difference between systolic and diastolic blood pressure

Pulse pressure is the difference between systolic and diastolic blood pressure. It is measured in millimeters of mercury (mmHg). It represents the force that the heart generates each time it contracts. Healthy pulse pressure is around 40 mmHg. A pulse pressure that is consistently 60 mmHg or greater is likely to be associated with disease, and a pulse pressure of 50 mmHg or more increases the risk of cardiovascular disease. Pulse pressure is considered low if it is less than 25% of the systolic. A very low pulse pressure can be a symptom of disorders such as congestive heart failure.

<span class="mw-page-title-main">Afterload</span> Pressure in the wall of the left ventricle during ejection

Afterload is the pressure that the heart must work against to eject blood during systole. Afterload is proportional to the average arterial pressure. As aortic and pulmonary pressures increase, the afterload increases on the left and right ventricles respectively. Afterload changes to adapt to the continually changing demands on an animal's cardiovascular system. Afterload is proportional to mean systolic blood pressure and is measured in millimeters of mercury.

<span class="mw-page-title-main">Aortic regurgitation</span> Medical condition

Aortic regurgitation (AR), also known as aortic insufficiency (AI), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle. As a consequence, the cardiac muscle is forced to work harder than normal.

<span class="mw-page-title-main">Mean arterial pressure</span> Average blood pressure in an individual during a single cardiac cycle

In medicine, the mean arterial pressure (MAP) is an average calculated blood pressure in an individual during a single cardiac cycle. Although methods of estimating MAP vary, a common calculation is to take one-third of the pulse pressure, and add that amount to the diastolic pressure. A normal MAP is about 90 mmHg.

<span class="mw-page-title-main">Coarctation of the aorta</span> Heart defect of an abnormally narrow aorta

Coarctation of the aorta (CoA) is a congenital condition whereby the aorta is narrow, usually in the area where the ductus arteriosus inserts. The word coarctation means "pressing or drawing together; narrowing". Coarctations are most common in the aortic arch. The arch may be small in babies with coarctations. Other heart defects may also occur when coarctation is present, typically occurring on the left side of the heart. When a patient has a coarctation, the left ventricle has to work harder. Since the aorta is narrowed, the left ventricle must generate a much higher pressure than normal in order to force enough blood through the aorta to deliver blood to the lower part of the body. If the narrowing is severe enough, the left ventricle may not be strong enough to push blood through the coarctation, thus resulting in a lack of blood to the lower half of the body. Physiologically its complete form is manifested as interrupted aortic arch.

<span class="mw-page-title-main">Windkessel effect</span> Mechanism that maintains blood pressure between heart beats

Windkessel effect is a term used in medicine to account for the shape of the arterial blood pressure waveform in terms of the interaction between the stroke volume and the compliance of the aorta and large elastic arteries and the resistance of the smaller arteries and arterioles. Windkessel when loosely translated from German to English means 'air chamber', but is generally taken to imply an elastic reservoir. The walls of large elastic arteries contain elastic fibers, formed of elastin. These arteries distend when the blood pressure rises during systole and recoil when the blood pressure falls during diastole. Since the rate of blood entering these elastic arteries exceeds that leaving them via the peripheral resistance, there is a net storage of blood in the aorta and large arteries during systole, which discharges during diastole. The compliance of the aorta and large elastic arteries is therefore analogous to a capacitor ; to put it another way, these arteries collectively act as a hydraulic accumulator.

Central aortic blood pressure is the blood pressure at the root of aorta. Studies have shown the importance of central aortic pressure, especially as compared to peripheral blood pressure, and its implications in assessing the efficacy of antihypertensive treatment with respect to cardiovascular risk factors, kidney disease, and mortality. There is an emerging movement for clinicians to begin using central aortic blood pressure, instead of peripheral blood pressure, as a guide for clinical decisions.

<span class="mw-page-title-main">Pathophysiology of hypertension</span>

Pathophysiology is a study which explains the function of the body as it relates to diseases and conditions. The pathophysiology of hypertension is an area which attempts to explain mechanistically the causes of hypertension, which is a chronic disease characterized by elevation of blood pressure. Hypertension can be classified by cause as either essential or secondary. About 90–95% of hypertension is essential hypertension. Some authorities define essential hypertension as that which has no known explanation, while others define its cause as being due to overconsumption of sodium and underconsumption of potassium. Secondary hypertension indicates that the hypertension is a result of a specific underlying condition with a well-known mechanism, such as chronic kidney disease, narrowing of the aorta or kidney arteries, or endocrine disorders such as excess aldosterone, cortisol, or catecholamines. Persistent hypertension is a major risk factor for hypertensive heart disease, coronary artery disease, stroke, aortic aneurysm, peripheral artery disease, and chronic kidney disease.

Pulse wave velocity (PWV) is the velocity at which the blood pressure pulse propagates through the circulatory system, usually an artery or a combined length of arteries. PWV is used clinically as a measure of arterial stiffness and can be readily measured non-invasively in humans, with measurement of carotid to femoral PWV (cfPWV) being the recommended method. cfPWV is highly reproducible, and predicts future cardiovascular events and all-cause mortality independent of conventional cardiovascular risk factors. It has been recognized by the European Society of Hypertension as an indicator of target organ damage and a useful additional test in the investigation of hypertension.

<span class="mw-page-title-main">Heart failure with preserved ejection fraction</span> Medical condition

Heart failure with preserved ejection fraction (HFpEF) is a form of heart failure in which the ejection fraction – the percentage of the volume of blood ejected from the left ventricle with each heartbeat divided by the volume of blood when the left ventricle is maximally filled – is normal, defined as greater than 50%; this may be measured by echocardiography or cardiac catheterization. Approximately half of people with heart failure have preserved ejection fraction, while the other half have a reduction in ejection fraction, called heart failure with reduced ejection fraction (HFrEF).

<span class="mw-page-title-main">Blood pressure measurement</span> Techniques for determining blood pressure

Arterial blood pressure is most commonly measured via a sphygmomanometer, which historically used the height of a column of mercury to reflect the circulating pressure. Blood pressure values are generally reported in millimetres of mercury (mmHg), though modern aneroid and electronic devices do not contain mercury.

<span class="mw-page-title-main">Wave intensity analysis</span> Method in the dynamics of blood flow

Wave intensity analysis provides a method to calculate the properties of arterial waves that give rise to arterial blood pressure, based on measurements of pressure, P, and velocity, U, waveforms. Wave intensity analysis is applicable to the evaluation of circulatory physiology and quantifying the pathophysiology of disorders such as coronary artery disease. The method is based on discrete, successive wave fronts (wavelets) and is carried out in the time domain. These wavelets travel forward and backwards in the arteries with amplitudes and . The wave intensity, , of a particular wavelet is defined asIt is related to sound intensity in acoustics and describes the power per unit area carried by the wavelet. From the theory discussed below, there is a relationship between the pressure amplitude and the velocity amplitude of a waveletwhere ρ is the density of blood and c is the wave speed of the wavelet. From these equations, generally known as the water hammer equations, it follows that the wave intensity for forward wavelets and for backward wavelets . The ability to determine the direction of a wavelet from its sign is the basis of the practical utility of wave intensity analysis.

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.