Arterial Stiffness Aging Arteriosclerosis and Atherosclerosis

As described earlier, age is the major determinant of increased arterial stiffness. The CV risk factors mentioned earlier contribute greatly to arterial wall stiffening, even independently of MAP level. However, the most important connection of increased arterial stiffness is atherosclerosis.

Aging, Loss of Elastin and Fatigue [2]

Central artery elasticity is critically dependent on normal content and function of the matrix protein elastin, which with a half-life of 40 years, is one of the most stable proteins in the body. Despite this stability, fatigue of elastin fibers and lamellae can occur by the sixth decade of life from the accumulated cyclic stress of more than 2 billion aorta expansions during ventricular contraction. Long-standing cyclic stress in the media of elastic-containing arteries produces fatigue and eventual fracturing of elastin along with structural changes of the ECM that include proliferation of collagen and deposition of calcium [2]. Humoral factors, cytokines, and oxidative metabolites may also play a role. This degenerative process, classically termed arteriosclerosis, is the pathologic process that results in increased central arterial stiffness. In untreated, and even long-term treated hypertensive subjects, an acceleration of the rate of development of conduit artery stiffness is observed. This process in turn may perpetuate a vicious cycle of accelerated hypertension and further increase in aortic rigidity, particularly through the associated development of vascular calcifications.

Atherosclerosis versus Arteriosclerosis

Disease processes such as diabetes, chronic renal failure and generalized atherosclerosis can accelerate aging of the aorta and central arteries with earlier development of arterial stiffness. Arteriosclerosis is often confused with atherosclerosis, but these two disease states are independent, but frequently in overlapping, conditions (table 2) [1-4]. Atherosclerosis is primarily focal, starts in the intima, and tends to be occlusive. Arteriosclerosis tends to be diffuse, starts in the media, and frequently results in a dilated and tortuous aorta. Moreover, the pathophysiology of atherosclerosis is that of inflammatory disease with lipid-containing plaques and predominantly downstream ischemic disease, which results in increased thoracic aortic stiffness and elevated left ventricle workload.

Finally, the purpose of this book is not only to give some insight into the relationship between arterial stiffness and atherosclerosis, but also to establish the possible interactions with age and high BP, and therefore to define new therapeutic perspectives for CV prevention.

Table 2. Differential features of atherosclerosis and arteriosclerosis [2]





Focal Intima


Media, adventitia Dilatory fElastin, dcollagen, Ca2+ Large artery stiffness dLeft ventricular workload

Location Geometry Pathology Physiology

Occlusive Plaque

Inflammation Ischemia

Hemodynamics f = Decrease; Î = increase.


This study was performed with the help of INSERM and GPH- CV (groupe de Pharmacologie et d'Hémodynamique Cardiovasculaire), Paris. We thank Dr. Anne Safar for helpful and stimulating discussions.


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Prof. Michel Safar

Centre de Diagnostic Hôtel-Dieu, 1, place du Parvis Notre-Dame FR-75181 Paris Cedex 04 (France)

Tel. +33 1 4234 8025, Fax +33 1 4234 8632, E-Mail [email protected]

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