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(Hypertension. 1995;26:2-9.)
© 1995 American Heart Association, Inc.

Articles

Mechanical Principles in Arterial Disease

Michael O'Rourke

From the University of New South Wales, St Vincent's Hospital, Sydney, New South Wales, Australia.

Correspondence to Michael O'Rourke, MD, University of New South Wales, St Vincent's Hospital, Victoria St, Darlinghurst, New South Wales 2010, Australia.

Key Words: arteriosclerosis • compliance • atherosclerosis • wave reflection

	Introduction

Top Introduction Basic Principles Atherogenesis: Development of... Atherosclerosis: Plaque Rupture... Arteriosclerosis: Degeneration... Left Ventricular Hypertrophy... Left Ventricular Hydraulic Load Summary References

 
Arterial disease and degeneration are the major causes of cardiovascular death and disability, including myocardial and cerebral infarction, cerebral hemorrhage, and hypertensive left ventricular failure. Recent research has concentrated on chemical and molecular mechanisms: on thrombogenesis and thrombolysis, vasoactive chemicals produced by endothelial cells, and the chemical control of cardiac and vascular remodeling. There has been far less concern with details of physical factors and their relevance to atherogenesis, plaque rupture, aortic medial degeneration, and altered left ventricular hydraulic load. This is a serious anomaly, since the functions of the heart and arteries are mechanical rather than chemical: those of the heart is to contract and to generate flow; those of the arteries is to transmit blood and to cushion pulsations. Their diseases and resultant complications are mechanical as well, comprising arterial obstruction, arterial rupture, and failure of the heart as a mechanical pump. A logical approach to therapy requires consideration of mechanics and physical principles in sufficient detail to explain observed phenomena. Such an approach to arterial disease is not the role of the surgeon alone but should be taken by contemporary internists, cardiologists, and specialists in hypertensive disease. Practicing physicians need to look beyond simplistic mechanical notions and beyond simple instruments such as the cuff sphygmomanometer, which still dominates clinical practice as it has for the past 100 years. It is appropriate that they consider those recent advances in mechanical science that are as important and as far-reaching as those in chemical and molecular science but that have not yet been widely applied to assessment of cardiovascular function and disease. This symposium deals with some of these advances.

The title of this symposium, the "Second Workshop on Structure and Function of Large Arteries," is similar to another arranged by the American Heart Association on "Functional and Structural Aspects of the Vascular Wall," held in Salt Lake City, Utah, in February 1995. It is surprising that this American Heart Association–sponsored symposium deals almost exclusively with endothelium and smooth muscle in the arterial wall, making no reference at all to those elements of the wall that determine its structural integrity or its function of cushioning pulsations generated by intermittent ventricular ejection.

	Basic Principles

Top Introduction Basic Principles Atherogenesis: Development of... Atherosclerosis: Plaque Rupture... Arteriosclerosis: Degeneration... Left Ventricular Hypertrophy... Left Ventricular Hydraulic Load Summary References

 
The large arteries have two functions: to act as conduits and to act as cushions.^{1 2 3} Conduit function is to deliver blood with minimal loss of mean perfusion pressure to the tissues and organs of the body and according to need. Cushioning function smooths flow pulsations imposed by the intermittently contracting heart so that blood is directed through these organs and tissues in an almost steady stream. In experimental animals and healthy young humans, both functions are discharged with great efficiency. The mean pressure drop between the ascending aorta and a large peripheral artery in the forearm or leg is minute, perhaps only 2 to 3 mm Hg when the body is supine.^{2 4} The extra energy lost in the circulation on account of the intermittent action of the heart is normally only 10% or so greater than if the heart's output were continuous or nonpulsatile.^{1 2} Both functions, however, are disturbed by the arterial degeneration that occurs with aging and disease.

Atherosclerosis is an example of disease that disturbs conduit function almost exclusively; this occurs through narrowing a major artery and causes ischemia or infarction of the organ or tissue downstream. Arteriosclerosis (stiffening and dilation of major arteries) in hypertension and with aging affects cushioning function and disturbs the heart upstream and the arteries in general by increasing pulse pressure and systolic pressure.^{2 5 6} This condition does not affect conduit function.^{2 5 6} These are two separate and distinct conditions, even though they are often seen together in older Western subjects. The first (atherosclerosis) is focal, primarily intimal, and principally occlusive. The second (arteriosclerosis) is diffuse, primarily medial, and dilatory (Fig 1). Aortic coarctation affects both conduit and cushioning function, the former by creating an impediment to blood flow into the lower body and the latter by restricting cushioning function to the proximal aorta and predominantly elastic arteries in the upper body.⁷

View larger version (7K): [in this window] [in a new window]   Figure 1. Schematic representation of atherosclerosis and arteriosclerosis. Atherosclerosis (left) is a primarily intimal disease that is patchy in location and causes narrowing of arteries and therefore interference with blood supply to tissues downstream. Arteriosclerosis (right) is a primarily medial degenerative condition that is generalized throughout the thoracic aorta and larger central elastic arteries. It causes dilation and stiffening, with impaired cushioning function, with an increased load on the left ventricle upstream.

In a symposium such as this, there is no need to consider details of peripheral resistance, since this is a property of the distal arteries and arterioles of diameter 1 mm and less.^{2 3 4} However, peripheral resistance is relevant in considering the effects of stenosis in a major artery. Such a stenosis is only relevant when the resistance created becomes a significant proportion of the total vascular resistance and therefore can account for restriction of blood flow. Conduit function is normally so efficient that such a point is not reached under basal conditions until an artery is narrowed to 20% or less of original diameter. However, such a point is reached at a lower degree of narrowing when the organ is active, so that its own peripheral arteriolar resistance is relatively low^{1 8} (Fig 2).

View larger version (13K): [in this window] [in a new window]   Figure 2. Graph shows experimentally determined relationship between coronary artery constriction (abscissa) and flow (ordinate), with basal flow (dotted line), and hyperemic flow (solid line) on the ordinate (from Gould8 ).

It is necessary to consider the details of cushioning function, since this is the major role of the large arteries and is most affected by arterial disease when it is generalized (as in arteriosclerosis) or when it involves the aorta itself (as in coarctation).

The cushioning function of an individual artery can be described in terms of stiffness, distensibility, or compliance^{2 3 9} (Table). As described in the articles that follow, one has to be careful with these terms, since the properties are different in different arteries, in the same artery at different distending pressures, and with activation of smooth muscle in the vessel wall. Both distensibility and stiffness are relative terms, with one the inverse of the other. Compliance is an absolute term, relating absolute diameter or volume change to change in pressure; hence, it is dependent on arterial caliber and is lowest in larger arteries and highest in smaller arteries. Yet none of these terms is sufficient to describe the whole arterial system, since the tubular, distributed nature of the arterial system leads to difference in absolute pressure along the arterial tree at the same point in time.^{1 2 3} The physical structure of the arterial system leads to generation of waves that travel along the arteries and that are reflected at regions of discontinuity (especially the peripheral arterioles).^{1 2 3 5 6 7} Wave travel and reflection are apparent in the secondary waves that are seen in diastole (in the young) or in systole (in older subjects)¹² (Fig 3). The major changes of the arterial pulse as seen with hypertension or aging are attributable to arterial stiffening and more rapid travel of the pulse along the major arteries and to consequent early return of wave reflection from the periphery of the body (Fig 3). This is the reason for disappearance of the reflected wave from diastole and its movement into systole, with characteristic boost to pressure in late systole.^{1 6 12 14} This was recognized as the characteristic effect of hypertension and aging, as measured by the sphygmogram in 1872, 24 years before the sphygmomanometer cuff was first introduced.¹⁵

View this table: [in this window] [in a new window]   Table 1. Indices of Arterial Stiffness

View larger version (12K): [in this window] [in a new window]   Figure 3. Simple tubular models of the systemic arterial system. Top, normal distensibility and normal pulse wave velocity; middle, decreased distensibility but normal pulse wave velocity; and bottom, decreased distensibility with increased pulse wave velocity. At left are the amplitude and contour of pressure waves that would be generated at the origin of these models by the same ventricular ejection (flow) waves. Decreased distensibility per se increases pressure wave amplitude, while increased wave velocity causes the reflected wave to return during ventricular systole (from O'Rourke et al13 ).

	Atherogenesis: Development of the Atherosclerotic Plaque

Top Introduction Basic Principles Atherogenesis: Development of... Atherosclerosis: Plaque Rupture... Arteriosclerosis: Degeneration... Left Ventricular Hypertrophy... Left Ventricular Hydraulic Load Summary References

 
Theories on atherogenesis must consider mechanical factors.^{1 3} In an older Western man who smokes and whose cholesterol level is high, atherosclerosis develops in the epicardial coronary arteries but not in systemic veins or in pulmonary arteries or veins of similar caliber, and not at all in the intramural coronary arteries or in the carotid artery where this artery passes through the petrous temporal bone.^{1 16 17} Clearly, tensile stress in the arterial wall is an important factor in atherogenesis. This is confirmed by the higher prevalence of atherosclerosis in hypertension. But tensile stress cannot explain all, since lesions show a predilection for certain sites, such as around orifices or just beyond bifurcations. At these sites, there are disturbances of flow patterns and alterations in shear stress (Fig 4) at the vascular interface. It is possible that such alterations in shear stress can explain localization of atherosclerosis within affected arteries. It is also possible that further disturbances created by a plaque may cause further growth of the plaque. However, the details have so far eluded us.

View larger version (24K): [in this window] [in a new window]   Figure 4. Schematic representation shows circumferential (A) and longitudinal (b) stresses in the arterial wall (top) and shearing stress at the vascular interface (bottom).

The multiplicity of theories relating shear stress to atherogenesis attests to the difficulty in gaining data on shear stress at the vascular interface.^{16 18 19} In the past, atherogenesis was related to low shear and to high shear by respected authorities.^{1 18 19} It now appears that variable shear related to secondary nonlaminar flow, and especially to pulsatile flow, is the major etiologic factor. Shearing stress may be accentuated by the presence of the plaque itself, so that the process becomes self-perpetuating. The mechanism whereby altered shear causes the development of plaque has not yet been determined, with some schools subscribing to easier entry of lipoproteins and others to deposition of platelets onto the vessel wall.^{20 21} The common factor is disturbance of the endothelial cells by the viscous drag (shearing stress) on their interface with blood.

Atherosclerosis appears to occur preferentially at sites where arteries are poorly supported or where they are subject to repetitive bending (ie, the coronaries, the femoral vessels at the groin), where an artery is dilated (the carotid bifurcation), or where a relatively narrow artery is subject to rapid and variable flow (the infrarenal aorta). All these points must give clues as to the mechanical factors that are important in atherogenesis. Factors include expansion of the wall and drag on the vascular interface, bending and flexing (coronary and femoral), presence of secondary flow (carotid), and high variable shear (abdominal aorta). The infrarenal segment of the aorta is far more susceptible to atherosclerosis than is the aorta above the renal arteries. Here the aorta is relatively narrow, so that flow velocity is relatively high, while backflow is appreciable during diastole into the renal arteries, so that shear stress is both higher and more variable than in the suprarenal aorta.³

This subject has a high priority in medical research, although it was not addressed in depth at this conference.

	Atherosclerosis: Plaque Rupture and Thrombotic Occlusion

Top Introduction Basic Principles Atherogenesis: Development of... Atherosclerosis: Plaque Rupture... Arteriosclerosis: Degeneration... Left Ventricular Hypertrophy... Left Ventricular Hydraulic Load Summary References

 
It is now generally accepted that coronary occlusion is usually due to growth of an occlusive thrombus from an area where an atherosclerotic plaque has ruptured, exposing blood elements to intimal elements below the endothelium.^{22 23} Plaque rupture is the initial event. This may be silent if just a tiny thrombus is formed, may precipitate the syndrome of unstable angina or subendocardial infarction if coronary thrombus causes subocclusive narrowing, or may lead to full Q-wave transmural infarction when complete occlusion results.

The question arises as to what causes plaque rupture. If this were known, we would understand what triggers the onset of myocardial infarction and other acute coronary syndromes. There are some clues, both epidemiological and pathological. Coronary occlusion with onset of myocardial infarction can come on at any time in a susceptible person but is most common soon after waking, during the arousal response, when heart rate and blood pressure are high.²⁴ Coronary occlusion is also more common during exercise than at rest, especially if exercise is vigorous and unaccustomed.^{25 26 27} Again, these peaks correspond to increase in heart rate and blood pressure and cardiac output. From an anatomic viewpoint, plaques fracture at their edge, below the fibrous cap, where the wall of the plaque is thin and poorly supported by the soft atheromatous material below the intimal layer.^{22 23 24 25 26 27 28} This region is most susceptible to disruptive mechanical forces.²⁹ Modeling experiments have shown that mechanical shearing forces are greatest in this region of plaque.^{29 30}

Mechanical forces are definitely involved in plaque rupture, but we still cannot be certain how they are involved. Sudden rises in pressure, flow, or heart rate may increase the risk of plaque rupture 100-fold but only increase the risk of coronary occlusion from perhaps one chance per million hours to one chance per 10 000 hours, ie, to one chance per 36 million pulsatile cycles of stretch on the weakened endothelium.²⁶ The wonder is not how mechanical forces cause damage but how resilient atherosclerotic plaques are at resisting damage.

	Arteriosclerosis: Degeneration of the Arterial Media

Top Introduction Basic Principles Atherogenesis: Development of... Atherosclerosis: Plaque Rupture... Arteriosclerosis: Degeneration... Left Ventricular Hypertrophy... Left Ventricular Hydraulic Load Summary References

 
Arteriosclerosis is sometimes considered a "normal" aging phenomenon¹ but is accelerated by hypertension. Degeneration of the aortic media is associated with increased stiffness of the aorta and dilation of the aorta^{1 3} (Fig 5). Increased aortic stiffness is the basic cause of elevated pulse pressure and of increased aortic and left ventricular systolic pressure with age.⁶ The primary cause is fragmentation of elastic lamellae; these become thinned, frayed, and fractured.^{6 32 33} Fibrous remodeling appears to be a secondary event. Such elastic fiber fracture is attributable to the fatiguing effects of cyclic stress on the nonliving inert elastic fibers.^{1 3 6} The normal (adolescent) aorta and other elastic arteries expand by approximately 10% with each beat of the heart.^{34 35 36} Natural rubber, which has characteristics similar to those of elastin, fractures after approximately 10⁹ cycles of such expansion.^{37 38} At a heart rate of 60 to 70 beats per minute, this is achieved after approximately 25 to 30 years of life. In elderly persons and in older patients with long-standing hypertension, the load-bearing media of the aorta and elastic arteries is grossly disorganized and shows "faults"—areas of mucoid degeneration or medionecrosis. Such faults are the basis of aortic dissection and of aortic rupture associated with aortic dissection.^{39 40} Elastin is the most inert substance in the body. Once laid down it remains chemically unchanged for decades; it is, however, subject to the same structural physical damage as any nonliving material.^{41 42}

View larger version (14K): [in this window] [in a new window]   Figure 5. Scatterplot shows relationship between foot-to-foot pulse wave velocity (PWV) in the aorta (between carotid artery and femoral artery) and age in a group of 480 normal subjects in a population with low prevalence of hypercholesterolemia (from Avolio et al31 ).

The muscular peripheral arteries do not show the same degree of medial degeneration as seen in central arteries.³⁶ The elastin components of the wall appear to be "protected" by smooth muscle and by collagenous elements. These arteries do not expand to the same degree as the central vessel; pulsatile change in diameter is approximately 5% at most, even in youth.³⁶ The same theoretical principles as referred to above predict that elastin fiber rupture in these vessels would require 3x10⁹ cycles for this degree of damage, or approximately 100 years of life.⁴³ Hence, a lower degree of expansion explains the lesser degree of degeneration in these peripheral muscular vessels. Small cerebral arteries have regions at their branch points where elastin fibers in the media are poorly supported by surrounding muscle.^{1 17} At these sites, elastin fibers may well be stretched to the same degree as in the aorta and carotid arteries and may degenerate in the same way. Such degeneration could explain development of Charcot-Bouchard aneurysms at these points of weakness and their eventual rupture, resulting in cerebral hemorrhage. A similar process may be responsible for the primarily medial damage of small cerebral arteries that is the cause of mural thrombosis and lacunar infarction in the brain.⁴⁴

	Left Ventricular Hypertrophy and Failure

Top Introduction Basic Principles Atherogenesis: Development of... Atherosclerosis: Plaque Rupture... Arteriosclerosis: Degeneration... Left Ventricular Hypertrophy... Left Ventricular Hydraulic Load Summary References

 
Left ventricular hypertrophy is a consequence of chronic sustained elevation of arterial pressure.^{45 46} Left ventricular failure may be seen alone in a young person with recent elevation of arterial pressure when such elevation is substantial, but usually presents as congestive heart failure in older persons with known long-standing hypertension and with preexisting left ventricular hypertrophy. Left ventricular failure and congestive heart failure can develop in elderly persons who are without coronary or other disease but whose arteries are stiff and whose systolic pressure has been high (but deemed normal) over many years.⁴⁶ In the chronic cases, left ventricular hypertrophy is the basis of cardiac failure and can be attributed to the effects of chronic elevation of systolic pressure in the ascending aorta and left ventricle over many years. In elderly patients without formal "hypertension," hypertrophy is attributable to progressive stiffening of the aorta and central elastic arteries, with rise in aortic and left ventricular systolic pressure attributable directly to aortic stiffness and indirectly to early return of wave reflection from peripheral sites^{6 7} (Fig 6). Progressive increase in central systolic pressure with age is underestimated from measurement of brachial systolic pressure, since the cause (arterial stiffening) also has the effect of decreasing amplification of the pressure wave (see below). Cardiac failure in hypertensive and in elderly patients can be attributed to progressive left ventricular hypertrophy with late impairment of systolic contractility⁴⁶ and also with impairment of diastolic relaxation.^{46 48} Elevation of systolic pressure in central arteries appears to be the principal and perhaps usually the only etiologic factor but also requires the passage of time. The lower the systolic boost to pressure, the longer the time; the higher the boost, the shorter the time. The basis of treatment of hypertensive heart failure is the reduction in left ventricular afterload so as to achieve reduction in aortic and left ventricular pressure together with ventricular hypertrophy⁴⁹ and improvement of both systolic and diastolic dysfunction.^{48 49 50}

View larger version (11K): [in this window] [in a new window]   Figure 6. Bottom, Diagrammatic representation of impedance modulus (ordinate) under normal conditions (lower curve) and in hypertension (upper curve), both plotted against frequency (abscissa). Top, The pressure waves (upper panel) resynthesized from impedance curves using the same ventricular ejection (flow) wave (lower panel). The causes of change in impedance curves and in impedance plots are identified as increased peripheral resistance (1), decreased aortic distensibility (2), and early return of wave reflection (3) (from O'Rourke47 ).

	Left Ventricular Hydraulic Load

Top Introduction Basic Principles Atherogenesis: Development of... Atherosclerosis: Plaque Rupture... Arteriosclerosis: Degeneration... Left Ventricular Hypertrophy... Left Ventricular Hydraulic Load Summary References

 
The pressure load generated by the heart is usually assessed through measurement of arterial pressure in the brachial artery by sphygmomanometry. The hydraulic load and its change under different conditions are usually determined from mean pressure (gauged as diastolic plus one third pulse pressure) and peripheral resistance.

This practice is unduly simplistic and quite unsatisfactory, first because it fails to consider the differences in pressure between central and peripheral arteries, and second because it ignores the effects of altered large artery properties and of altered cushioning function of left ventricular load.^{1 3}

Amplification of the arterial pressure pulse between central and peripheral arteries is well established^{1 2 3} and is described in standard physiological textbooks. In older humans, such amplification may be relatively small in absolute terms and may under some circumstances warrant the assumption that central aortic and brachial systolic pressures are identical.³ But such is not the case in disease,^{1 3} with vasodilator drug therapy,⁵¹ or with exercise.⁵² In the presence of heart failure with hypotension, differences as high as 20 mm Hg have been described¹ ; similar differences are frequently seen during use of vasodilator therapy,⁵¹ and differences up to 80 mm Hg have been observed with exercise.⁵² Clearly, account must be taken of pressure wave transmission from ascending aortic to brachial artery when assessing left ventricular load.

The resistance to mean flow from the heart is just one component of left ventricular hydraulic load. Since the greatest fall in mean pressure occurs in tiny peripheral vessels where blood flow is nonpulsatile, this component of left ventricular load is principally a property of peripheral arterioles.^{1 2 3} The other component of load is a consequence of the heart's intermittent output and therefore of pulsatile flow in the aorta and major arteries. The entire hydraulic load can be expressed as input impedance of the systemic circulation.^{1 2 3 53} Impedance is determined from the harmonic components of pressure and flow waves measured in the ascending aorta and takes the form of a graph of modulus and phase plotted against frequency (Fig 7). Peripheral resistance is the modulus of impedance at zero frequency and is determined from the mean (zero frequency) components of aortic pressure and aortic flow.

View larger version (20K): [in this window] [in a new window]   Figure 7. Line graphs show ascending aortic impedance in a group of six patients with heart failure before () and during () nitroprusside infusions. The vasodilator decreased peripheral resistance, indicating arteriolar dilation, and decreased modulus and phase of impedance at low frequency (<3 Hz), indicating decrease in wave reflection. However, it did not alter characteristic impedance (modulus at high frequency), suggesting no change in properties of the proximal aorta (from Merillon et al54 ).

Characteristic changes in ascending aortic impedance have been described with aging and in hypertension^{1 3 54 55} and are illustrated diagrammatically in Fig 6. Increase in peripheral resistance is attributable to increased arteriolar tone (or to decreased number of arterioles). Increase in impedance modulus at high frequencies is attributable to increased stiffness of the proximal aorta, while the shift of the whole curve to the right is attributable to early return of wave reflection (and due indirectly to increased arterial stiffening).^{1 6} The principal effect of aging and hypertension is to increase the modulus of impedance at heart rate frequency. This effect is substantial and explains the change in amplitude and shape of the aortic pressure wave and the greater energy expenditure in generating pulsatile flow.^{6 7} In heart failure, there are relatively minor changes in ascending aortic impedance, implying that the quite gross alterations in aortic flow and pressure waves are due to change in left ventricular ejection properties.^{56 57} However, therapeutic maneuvers as used in heart failure have quite marked effects on ascending aortic impedance, sometimes without any significant alteration in measured peripheral resistance.^{56 57 58 59} Drugs such as nitroglycerin and dobutamine decrease wave reflection from peripheral sites and can thereby cause marked reduction in impedance modulus at and about heart rate frequency.^{56 57 59} Such impedance changes readily explain reduction in aortic systolic pressure and pulse pressure and therefore reduction in left ventricular hydraulic load as brought about by these vasodilator agents. Such reduction in left ventricular hydraulic load is often not apparent from measurements of peripheral resistance or from measurement of systolic pressure in a peripheral artery.^{51 60 61}

The concepts of vascular impedance in general and of ascending aortic impedance in particular are well accepted as describing pressure-flow relationships and hydraulic load.^{1 2 3} Impedance is the description of pressure-flow relationship as a transfer function. The same principles can be applied in relating pressure to pressure at different sites. This is of particular value in expressing the relationship of brachial or radial pressure to pressure in the ascending aorta. Transfer functions have been described for the relationship between ascending aortic pressure and brachial artery pressure by O'Rourke,⁶² Lasance et al,⁶³ and Karamanoglu et al.⁶⁴ In contrast to ascending aortic impedance, which varies considerably with age, mean arterial pressure, and drug therapy, the transfer function for pressure wave transmission in the upper limb appears to be surprisingly consistent, at least over that frequency range (1 to 5 Hz) (Fig 8) that contains most of the energy of the ascending aortic pressure pulse⁶⁴ (Fig 9). This point has been exploited by us to derive ascending aortic pressure from the pressure wave recorded in the radial or brachial arteries, under a variety of conditions,^{6 9} with the use of a generalized transfer function for aorta-radial or aorta-brachial pressure waves. The contour and amplitude of ascending aortic pressure waves derived from such generalized transfer functions are very similar to those recorded directly or inferred indirectly from carotid tracings.⁶⁴ This method has not yet been fully validated but does constitute a step toward better assessment of the ascending aortic pressure wave than that recorded in a peripheral artery.

View larger version (12K): [in this window] [in a new window]   Figure 8. Line graph shows relationship between modulus of transfer function and frequency for pressure between the brachial artery and ascending aorta under control conditions () and with nitroglycerin (NTG) (). Dotted line represents the average of the two results (modified from Karamanoglu et al64 ).

View larger version (12K): [in this window] [in a new window]   Figure 9. Graphs show transfer function between the ascending aorta (AA) and brachial artery (BA) (A) and the ascending aortic pressure pulse power spectrum for the first six harmonics (B) in an adult human. Despite change in heart rate, virtually all power of the waves was at frequencies <4 Hz.

	Summary

Top Introduction Basic Principles Atherogenesis: Development of... Atherosclerosis: Plaque Rupture... Arteriosclerosis: Degeneration... Left Ventricular Hypertrophy... Left Ventricular Hydraulic Load Summary References

 
Like other scientific advances, developments in mechanics and engineering principles provide new insights into the genesis of arterial disease and the ill effects of such disease on the heart. The development of atherosclerotic plaques and of complicated lesions is related to tensile stress in the arterial wall and to shear stress at the vascular interface. Thrombotic occlusion of a narrowed artery is initiated by tearing of the intima consequent on such stress. Mechanical degeneration of the aorta with dilation and stiffening is attributable to the fatiguing effects of cyclic stress, acting over decades. Left ventricular load and its change with age and hypertension are explicable on the basis of vascular properties, expressed as vascular impedance. Changes in vascular impedance with aging, blood pressure, and drug therapy explain alteration in left ventricular load and in arterial pulse wave contour under different conditions. Differences between central and peripheral upper limb arterial pressure waves can be described in terms of transfer functions. Relative stability of transfer functions in the upper limb enables aortic pressure wave contour and amplitude to be determined with reasonable accuracy from the peripheral pressure pulse. While peripheral resistance can be determined with ease and expressed simply, measures of arterial stiffness and distensibility are more complicated and require consideration of site, distending pressure, vascular tone, and the distributed nature of the vascular tree, together with finite wave travel and wave reflection.

	References

Top Introduction Basic Principles Atherogenesis: Development of... Atherosclerosis: Plaque Rupture... Arteriosclerosis: Degeneration... Left Ventricular Hypertrophy... Left Ventricular Hydraulic Load Summary References

 
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