In seeking a cause for arteriosclerosis and an explanation for its development, one has to explain:

These issues are explicable and predictable on the basis of engineering principles of material fatigue, alluded to by Osler [1, 8] and King [10], as applied to inanimate objects, such as ships, bridges, aeroplane wing spars and even dance floors [6]. Each material object which is subjected to stretch or bending has a characteristic strain (S)/cycle number (N) or S/N curve. Natural rubber has properties similar to those of arterial elastin (indeed Osler referred to “vital rubber” as well as the effects of “wear and tear”) [1]. An S/N curve is shown in Fig. 4.2. The graph plots the properties of natural rubber in terms of the number of cycles of expansion to which it needs to be subjected in relation to the extent of strain, before fracture would be expected. The heart’s cycle is repeated some 30 million times per year and so some 1 billion times in 30 years. With the proximal thoracic aorta in youth stretching by some 15 % with each beat of the heart, one would expect that fracture of elastin fibres would begin to occur at age 30 years and progress steadily thereafter. One would also expect that peripheral muscular arteries (which dilate by <3 % at each cycle), or larger arteries such as the femoral, carotid or brachial which dilate by 3–5 % per cycle [11], would show little change in physical properties in a lifetime of 90 years.

Such an explanation fits with the disorganisation of the elastin network in the aortic media with age (Fig. 4.1), and as seen in histology and pathology texts. This is regarded as a normal aging process “physiological arteriosclerosis”, unless extreme and unless associated with areas of medionecrosis, which is the substrate for aortic weakening and aortic dissection in the elderly [1, 6].

The explanation accounts for confining this process to the media since the intima and adventitia contain no elastin fibres (and do not oppose applied stress). It accounts for distension of the aorta since fracture of structural elements causes stretch. It accounts for increased stiffness of the aorta, since cycles of stretch are transferred to and borne by the collagenous fibres in the wall which have much higher modulus of elasticity (stiffness) than elastin. Physical damage to the proximal aorta is stressed here, whereas others such as Lakatta and colleagues tend to concentrate on cellular and molecular changes with aging [12]. I favour the physical (engineering) hypothesis since it explains the issues listed above. I see the physical damage to be primary and the chemical/cellular changes to be secondary and part of the attempt to repair the damaged aorta.

Fracture of elastin elements in the aortic wall cause increase in elastic modulus. This appears to increase four- to tenfold over an average lifetime and so be greater than any other measurable effect of aging [6]. Stiffening of the aorta from change in elastic modulus increases aortic pulse wave velocity by an amount that depends on the square root of aortic modulus according to the classic Moens-Korteweg equation [6]:
where E is Young’s modulus of the wall, h is the wall thickness, r is the vessel radius and ρ is the blood density.

Hence, a ninefold increase in aortic modulus would increase aortic PWV threefold, and this explains the increase in aortic PWV with age from ~5 M/s to around 15 M/s at 90 years of age (Fig. 4.3).

Increase in aortic PWV explains another characteristic change in the pulse waveform in older persons, with wave reflection returning early and augmenting the pressure wave in late systole. This is seen in Fig. 4.4 and is the cause of the change in radial artery pulse wave described by Mahomed, Broadbent, Osler and other physicians 100 years ago [6]: “The tidal wave is prolonged and too much sustained” [7]; “The pulse is slow in its ascent, enduring, subsides slowly” [8].