Arterial stiffness

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Arterial stiffness occurs as a consequence of biological aging and arteriosclerosis. Increased arterial stiffness is associated with an increased risk of cardiovascular events such as myocardial infarction and stroke, the two leading causes of death in the developed world. The World Health Organisation predicts that in 2010, cardiovascular disease will also be the leading killer in the developing world and represents a major global health problem.

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 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).[1]

Background

The arteries were once considered by the ancient Greeks as inert conduits within which air flowed; William Harvey is generally credited with being the first to describe the circulation of the blood through them. 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 or PWV) is related to the stiffness of the arteries. Other terms that are used to described 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 [2] but is generally described by the Moens–Korteweg equation[3] or the Bramwell–Hill equation.[4] Typical values of PWV in the aorta range from approximately 5 m/s to >15 m/s.

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 renal failure,[5] hypertension,[6] diabetes mellitus[7] and in the general population.[8][9] 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 the Complior, CVProfilor, PeriScope, Hanbyul Meditech, Mobil-O-Graph NG, Pulsecor, PulsePen, BPLab Vasotens, Arteriograph, and SphygmoCor.[10]

The pathophysiology of arterial stiffness

The primary sites of end-target organ damage following an increase in arterial stiffness are the heart, brain (stroke, white matter hyperintensities (WMHs)), and kidneys (age-related loss of renal function). The mechanisms linking arterial stiffness to end-organ damage are several-fold.

Firstly, stiffened arteries interrupt the Windkessel effect of the arteries. This function describes how arteries can be exposed to pulsatile ejections of blood from the heart at one end and convert it into a steady, even flow at the other end. This function is made possible because arteries are compliant and are readily able to expand due to pressure, but they also possess the ability to recoil.

Thus, stiffened arteries require a greater amount of force to cause them to expand and take up the blood ejected from the heart. This increased force requirement is provided by the heart, which begins to contract harder to accommodate the artery. Over time, this increased load placed on the heart causes left ventricular hypertrophy and eventually left ventricular failure. Causing further damage is the increased time required for systole and the reduction of diastole. This reduction in both time and pressure during diastole decreases the amount of perfusion for cardiac tissue. Thus the heart, which is becoming hypertrophic (and with therefore a greater oxygen demand) is starved of oxygen and nutrition, adding to cardiac damage.

Arterial stiffness also repositions the site of pulse wave reflections. These reflections are an inevitable phenomenon of any conduit system with geometric discontinuity. As pressure waves travel down and through a tube of decreasing diameter, a reflected wave of energy is created. Within a young person, these reflected waves arrive at the heart during late systole to diastole, thus contributing to the magnitude of diastole via constructive wave interference. However, stiffened arteries equate to an earlier reduction in the diameter of the artery, thus establishing the point of wave reflection at an earlier point along the arterial tree. Therefore, the reflected wave arrives at the heart closer to systole, increasing its magnitude through constructive wave interference. Once again, this increase in systole places a greater load on the heart, causing it to become hypertrophic.

See also

Notes

  1. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  2. ↑ Young T: On the function of the heart and arteries: The Croonian lecture. Phil Trans Roy Soc 1809;99:l-31
  3. ↑ 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.
  4. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  5. ↑ Blacher et al.,Circulation. 1999; 99: 2434–2439
  6. ↑ Laurent et al., Hypertension. 2001; 37: 1236–1241
  7. ↑ Cruickshank et al., Circulation. 2002; 106: 2085–2090
  8. ↑ Mattace-Raso et al. Circulation. 2006;113:657-663
  9. ↑ Hansen et al., Circulation. 2006;113:664-670
  10. ↑ Avolio, A.; Butlin, M. & Walsh, A. Arterial blood pressure measurement and pulse wave analysis - their role in enhancing cardiovascular assessment. Physiol Meas, 2009, 31, R1-R47
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