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J Am Coll Cardiol, 2007; 50:1-13, doi:10.1016/j.jacc.2006.12.050 (Published online 17 June 2007).
© 2007 by the American College of Cardiology Foundation
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Mechanical Factors in Arterial Aging

A Clinical Perspective

Michael F. O’Rourke, MD, DSc, FACC*,1,* and Junichiro Hashimoto, MD, PhD*,{dagger}

* St. Vincent’s Clinic/University of New South Wales, Sydney, Australia
{dagger} Tohoku University Graduate School of Pharmaceutical Science and Medicine, Sendai, Japan.


Figure 1
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Figure 1 Distributed Models of the Arterial Tree

Simple tubular models of the arterial system, connecting the heart (left) to the peripheral circulation (right) in a young (top) and old (bottom) subject. In the young subject, the tube is distensible, whereas in the old subject it is stiff. The distal end of the tube constitutes a reflection site where the pressure wave travelling down the tube is reflected back to the heart. The wave travels slowly in the young distensible tube so that the reflected wave boosts pressure in diastole when it returns to the proximal end. The wave travels faster in the old stiffer tube, returns earlier, and boosts pressure in late systole. Flow input from the heart is intermittent in both young and old subjects. In the young subject, pulsations are absorbed in the distensible tube so that outflow is steady or almost so. In the old subject with stiff tube, pulsations cannot be absorbed, and so output from tube into peripheral microvessels is pulsatile.

 

Figure 2
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Figure 2 Cartoon of Young and Old Human Aorta

Schematic diagram of the aorta section in a young (left) and old (right) human, with inset (below each) the components of the aortic wall. The wall of the older human is disorganized as a consequence of fraying and fracture of the elastic lamellae (yellow) and loss of muscle attachments (red), together with increase in collagen fibers (black) and mucoid material (green), and with foci of "medionecrosis." Drawn by O’Rourke CM, after Glagov S. Personal communication, 1994.

 

Figure 3
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Figure 3 Change in Aortic PWV With Age

Change in aortic pulse wave velocity (PWV) with age in a group of 480 normal subjects in a northern urban Chinese community with low prevalence of atherosclerosis (15). The regression line for this group (top) was significantly different from that of another normal Chinese community in Guandong (bottom) with similarly low prevalence of atherosclerosis but low salt intake and lower prevalence of hypertension (16).

 

Figure 4
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Figure 4 Changes With Age in Structural and Functional Properties of the Human Proximal Aorta and Large Muscular Arteries From 20 to 80 Years

(Left from top and down) Diameter of the ascending aorta (17), surface area of the aorta (18), carotid intima-media (IM) thickness (12), and systolic and diastolic brachial cuff pressure (27). (Right from top and down) pulsatile expansion (%) of the carotid artery and radial artery (21), ascending aortic characteristic impedance Zc (Asc. Ao. Zc) (25), and amplification of the pressure pulse between ascending aorta and radial artery (solid line [19]); and femoral artery (dashed line [20]).

 

Figure 5
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Figure 5 Aortic Impedance at Age 20 and 80 Years

Ascending aortic impedance shown schematically in a young 20-year-old and in an 80-year-old human subject showing the effect of doubling of characteristic impedance (older curve set higher) and early return of wave reflection (first minimum at double the frequency). In consequence of both, impedance modulus at heart rate frequency is increased 4-fold (4).

 

Figure 6
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Figure 6 Pressure Waveforms in Arm and Aorta of Young, Middle-Aged, and Old Subjects

Pressure waveforms measured in the radial artery (top) and synthesized for the ascending aorta (bottom) in 3 women of the same family—an 18-year-old at left, a 48-year-old at center, and a 97-year-old at right. Pulse pressure is increased almost 4-fold in the ascending aorta and 2-fold in the upper limb (4). Time calibration = 0.5 s.

 

Figure 7
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Figure 7 Aortic and LV Pressure Waves in Young and Old Subjects

Ascending aortic and left ventricular (LV) pressure waves shown schematically in a young subject at left and older subject with LV hypertrophy and diastolic LV dysfunction at right. In the older person, myocardial oxygen demands (vertically hatched area) are increased by the increase in LV and aortic systolic pressure and by the increased duration of systole. Ability for myocardial oxygen supply is reduced by shorter duration of diastole, lower aortic pressure during diastole, and increased LV pressure during diastole caused by LV dysfunction.

 

Figure 8
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Figure 8 Ill Effects of Aging

LV = left ventricular.

 

Figure 9
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Figure 9 Pulsatile Pressure Changes in the Vascular Tree

Schematic representation of pulsatile pressure change between left ventricle and capillaries of a young subject (left) and an older human with arterial stiffening (right). In the older person, pulsations are not absorbed in the large arteries and so extend down into the microcirculation.

 

Figure 10
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Figure 10 Relationship Between Augmentation of Flow and Pressure Waves in the Carotid Artery

Relationship between augmentation of simultaneously recorded flow (ordinate) and pressure (abscissa) waves in the carotid artery of 56 normal subjects age 20 to 72 years (R = 0.913, p < 0.0001). Lowest values of augmentation were seen in younger and highest values in older individuals. Inset is method used for calculating flow and pressure augmentation as late systolic augmentation ÷ pulse height (54).

 

Figure 11
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Figure 11 Relationship Between Age and Ascending Aortic Pressure Wave Augmentation

Relationship between age and ascending aortic pressure wave augmentation (A) calculated with SphygmoCor from radial artery tracings in 1,600 patients attending a cardiovascular outpatient clinic, together with values for a group of 4,001 normal U.K. men (red thin line) and women (red dashed line) from McEniery et al. (74) and 534 normal European subjects (men and women combined, thick line) from Wojciechowska et al. (75). (Inset, upper left) Method of calculating aortic pressure augmentation. AIx = augmentation index; PP = pulse pressure.

 

Figure 12
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Figure 12 Arm and Aortic Pressure Waves in Young and Old Subjects

Radial (left) and aortic (right) pressure waves in a 36-year-old man (top) and his 68-year-old father (bottom) calibrated to the same brachial cuff values of systolic and diastolic pressure. For the same brachial systolic value, difference in waveform was responsible for a 17-mm Hg lesser value of aortic pressure. Millar tonometer used for recording radial wave, SphygmoCor for analysis.

 

Figure 13
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Figure 13 Arm and Aortic Pressure Waves in Old Subject Before and After Administration of Ramipril

Radial (left) and aortic (right) pressure waves in a 68-year-old man under control conditions (top) and 2 h after administration of ramipril 10 mg orally. Ramipril caused greater (8 mm Hg) reduction of aortic than brachial systolic pressure. ACEI = angiotensin-converting enzyme inhibitor; DP = diastolic pressure; MP = mean pressure; PP = pulse pressure; SP = systolic pressure.

 




 
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