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The objective of this study is to review the pathophysiologic mechanisms of arterial stiffness and their relationship with PAD, thereby providing a theoretical foundation for the clinical applications of arterial stiffness indexes. Arteriosclerosis is a term for disease of the walls of arteries that means, literally, hardening of the arteries.

It is a degenerative process of the tunica media of elastic arteries that occurs with aging and is exacerbated by cardiovascular risk factors. Atherosclerosis is a disorder that affects the artery lumens by formation of plaques in the tunica intima that are made up of deposits of fat, inflammatory cells, fibrous connective tissue, smooth muscle cells, and calcium.

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Reduction of the ankle-brachial index ABI and formation of plaques in the carotids are both associated with atherosclerosis. The pathophysiologic changes that lead to increased blood vessel rigidity can be separated into passive and active components. The passive component of arterial stiffness consists of mechanical changes to the vascular wall.

The active component comprises changes to endothelial function and smooth muscle tonus.

Applications of arterial stiffness markers in peripheral arterial disease

Changes undergone by major arteries during the cardiac cycle are part of the passive component of arterial stiffness. These changes are related to distension during systole and to elastic recoil during the diastole phase. During this process, the volume of blood ejected causes distension of large caliber arteries, in which the elastic component of the walls is fundamental. The elasticity of major arteries enables the pressure wave to be dampened, preventing the entire volume ejected from being directed to the peripheral circulation. Elastic recoil of the artery wall during diastole is responsible for maintenance of diastolic flow to many different tissues.

This element is extremely important for organs such as the myocardium and the brain, because they need perfusion to be maintained throughout the cardiac cycle. The process of adaptation to the volume ejected during systole and the elastic recoil produced during diastole primarily take place in elastic arteries such as the aorta and the carotids. The same pattern takes place in organs of the mesenteric, splenic, and renal circulation, but not in a continuous manner, since flow is regulated by mediators associated with blood volume and nutritional intake.

In the arteries of the limbs, maintenance of diastolic flow is reduced because of the greater peripheral vascular resistance and because these are muscular arteries, whose walls have a lower elastic content. Aging causes degeneration of the elastic fibers of the tunica media of major arteries. Microscopically, there is loss of internal elastic lamina, fragmentation of elastin fibers, deposition of collagen, and thickening of the media with fibrosis and calcification.

Atherosclerosis increases the process of elastic degeneration of the artery wall, since it causes interruption of the continuity of the endothelium, deposition of lipids, and formation of inflammatory mediators that exacerbate the structural derangement of the vascular wall. These changes to the wall cause it to become rigid and lead to loss of the passive control mechanism consisting of reception of the stroke volume ejected during systole and elastic recoil of the wall during diastole.

The main elements that actively influence arterial stiffness are the tonus of the smooth musculature of smooth muscle cells and the vasodilator action of nitric oxide produced by the endothelium. In addition to these, certain factors such as advanced age and hypertension cause remodeling of the vascular smooth muscle cells, altering their phenotypical expression from contractile to synthetic. As a result of these processes, the contractility of the vascular wall is lost because of degradation of elastin and collagen abnormalities.

As its availability reduces with aging and atherosclerosis, tonus increases and artery caliber decreases. After ventricular contraction, the pressure generated in the aorta travels like a wave. Pulse wave velocity measured between the carotid artery and the femoral artery is considered a predictor of cardiovascular risk and is the primary indicator of arterial stiffness.

This is because of distension of the aorta walls. The concept was developed by Otto Frank, a German physiologist, who also created a mathematical model for application to large vessels, which is used, with adaptations, to this day. In turn, elastic recoil is responsible for increasing flow during diastole. There are differences in blood pressure measured in the aorta and in the peripheral circulation, in, for example, the brachial artery. Systolic pressure SysP is lower in the central aorta, increasing as the pulse wave is transmitted to the periphery. Diastolic pressure DiaP increases less and may even reduce.

As the pulse wave travels from the heart to the peripheral arteries, PP is amplified because of wave reflection and dampened by the viscosity of the blood. The wave of the incident pulse meets increased resistance when it reaches the peripheral muscular arteries and arterioles, causing reflection waves in the direction of the heart. These pulse reflection waves occur in any segment in which there is discontinuity of flow, such as at bifurcations and, primarily, when the incident waves reach the peripheral arteries with greater resistance and lower elasticity.

Thus, to aid understanding, the waves can be designated as the incident wave or ejection wave and the reflected wave and the resulting pulse wave is the sum of the incident wave and the reflected wave Figure 3. Figure 4 illustrates the pulse wave at the root of the aorta in a scenario of increased arterial stiffness, whether due to aging or atherosclerosis.

As a result of the elevated PWV, the reflected wave arrives at the proximal aorta prematurely, at the start of systole point P1 on the graph. This early arrival of the reflected wave causes an increase in central systolic arterial blood pressure, shown at P2 on the graph. The augmentation pressure AuP is a measure of the absolute increase in pressure between two systolic peaks.

The augmentation index AIx measures the percentage of the pressure increase that is caused by the premature arrival of the reflected wave and is expressed as the ratio of PAo and PP multiplied by The larger the reflected pulse waves, as in cases with elevated arteriolar tonus or arterial obstruction, the higher the AIx. Therefore, AIx is considered an indirect indicator of arterial stiffness and a predictor of cardiovascular events.

Young people have high arterial elasticity. Since PWV is low in these cases, the reflected pulse wave arrives at the thoracic aorta during diastole. It therefore contributes to increase diastolic flow and maintain constant flow in the coronary and cerebral arteries. With aging, PWV increases because of the reduced elasticity of major arteries. As a result, the reflected wave arrives at the root of the aorta during systole, increasing AIx Figure 5. Heart rate is an important modulator of PAo.

Under low heart rate conditions, widening of the cardiac cycle and longer ejection time cause the reflected wave to arrive at the proximal aorta during systole, increasing both PAo and AIx. During tachycardia, the reflected pulse wave arrives at the root of the aorta during diastole. AIx 75 is AIx corrected to a heart rate of 75 beats per minute.

In addition to heart rate, other factors modulate pulse wave reflections and central aortic pressure. Inhibition of angiotensin II, calcium channel blockers and administration of insulin reduce pulse wave reflections and central systolic pressure. Over recent decades, it has been shown that central pulse pressure Cpp is associated with increased cardiovascular risk.

Both elevated Cpp and elevated peripheral pulse pressure are associated with increased risk of coronary disease in middle-aged adults and the elderly. Elevated Cpp is associated with hypertrophy of the left ventricle and carotid atherosclerosis. Elevated arterial stiffness is a current concept that is foregrounded in studies of cardiovascular diseases because it is an early predictor of arterial hypertension and atherosclerosis. It is a biomarker that has been associated with increased mortality and damage to target organs responsible for cardiac diseases, stroke, and renal failure.

There is currently considerable research interest in investigation of arterial stiffness as a potential therapeutic target for prevention or treatment of cardiovascular diseases. Many different studies have demonstrated that increased PWV is associated with increased risk of cardiovascular events such as coronary disease, stroke, and terminal kidney disease.

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The association between arterial stiffness and hypertension has been studied in depth. Especially in young people, identification of increased arterial stiffness is an early opportunity to modify lifestyle habits and prevent irreversible deterioration of blood vessels. Arterial stiffness increases afterload on the left ventricle, contributes to ventricular remodeling, and reduces its mechanical efficiency.

Thus, arterial stiffness is associated with diastolic ventricular dysfunction, which increases filling pressures and overload on the atria, contributing to hypertrophy, fibrosis, and atrial fibrillation. It is important to highlight that arterial stiffness is directly associated with increased risk of heart failure. The kidneys are organs that are exposed to high blood flow, because the pressures at the level of the glomerulus are similar to those in the aorta, due to the characteristics of renal microvasculature.

Increased aortic rigidity exposes the renal glomerulus to excessive pressures and, over time, leads to proteinuria and impaired filtration function. In common with the kidneys, the brain is a high-flow organ and is dependent on diastolic flow. The low resistance of cerebral arteries facilitates penetration of pulse waves to the microvasculature.

In this case, transmission of the pulse wave energy, which is increased in situations of elevated arterial stiffness, contributes to cerebral microinfarcts that are not recognized clinically, but which, over the long term, can lead to cognitive deficits and dementia. The same mechanism that increases pulsatility in cerebral arteries also links aortic rigidity to hemorrhagic strokes.

It is possible to measure PWV using catheters in the aorta, but invasive measurement has little practical applicability. Studies employing central pressure measurements are only conducted in humans in clinical trial settings and for validation of noninvasive methods. Measurements of arterial stiffness and inference of central pressure levels are performed using mathematical models. Equipment used to determine the measurements for rigidity indexes can be classified into four categories: devices that employ tonometry to measure pulse waves, devices with cuffs that capture the pulse wave by oscillometry, ultrasound-based measurements, and measurements using magnetic resonance imaging MRI.

The instrument employs a probe to measure pressure tonometry at two sites; generally over the cervical carotid artery and the femoral artery at the inguinal level, where the pulse is detectable. The device is synchronized using an electrocardiogram, and pulse waves are measured throughout the cardiac cycle. Distance is measured manually from the suprasternal angle to the femoral artery. After measuring arterial blood pressure, the cuff is inflated to diastolic pressure for approximately 10 seconds to capture pulse waves. A mathematical model is then used to estimate a series of hemodynamic parameters, including measures of reflection waves, pressure, and AIx The device has been validated for measurement of PWV by comparison with invasive and noninvasive tests.

The distensibility of the arteries and the characteristics of flow curves can be easily accessed at the cervical carotid, the brachial artery, and the femoral artery, in the groin.

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