In of the accelerated reflected wave that arrives

In addition to the arteries being conduits through which the
blood is pumped from the heart to the various organs of the body, their elastic
recoil property has a smoothing effect on the pressure fluctuations resulting
from intermittent ventricular ejection. This ensures a steady flow of blood in
one direction into the peripheral tissues 1. The wall of the aorta allows a
significant distention during systole due to it containing a large proportion
of elastin fibres. More distal arteries are less distensible as they contain a
higher proportion of collagen fibres. This results in progressive reduction in
pulsatility through the arterial tree to the microcirculation, which works to
prevent the adverse effects of barotrauma from exposure to high systolic
pressures, especially in cerebral and renal beds.  1.

The speed by which the pulse wave generated by the
ventricular ejection travels down the arterial tree is affected by the
geometric and elastic properties of the arterial wall. Pulse wave velocity
(PWV) is a measure of this elasticity and is found to increase in parallel with
arterial stiffness. Arterial stiffness can be measured in any artery however, aortic
stiffness measured by aortic pulse wave velocity is considered the gold
standard of measurement of arterial stiffness, as it has the clearest
significance in prediction of cardiovascular events 2.

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A measurement of 17.9 m/sec indicates significant stiffening
of the elastic wall of the aorta, which is linked to many pathophysiological
changes in the circulation 1. A stiffened aorta is not able to accommodate the
large volume of blood ejected by the left ventricle 1. Cardiac afterload
increases because of the accelerated reflected wave that arrives earlier into
the central aorta during late systole, with a greater amplitude and duration.
These changes in the reflected wave characteristics and the resulting
ventricular-vascular mismatch cause a systolic pressure augmentation and a decrease
in stroke output 4. The systolic pressure overload causes left-ventricular
hypertrophy. The systolic function of hypertrophied ventricle is preserved in
this case, while the diastolic filling is affected. As the ventricular
hypertrophy progresses, progressive worsening of both systolic and diastolic
functions may occur 3. A fall in diastolic pressure results from the reduced
elastic recoil and reservoir function of the aorta 1. This decrease in
diastolic blood pressure reduces coronary artery perfusion and causes
subendocardial ischaemia which can be exacerbated by the left
ventricular-hypertrophy 5.