In recent years, our fundamental knowledge of atherosclerosis in the human being has dramatically increased, not only from a better understanding of the pathophysiological information, but also from the clinical use of new hypolipidemic agents which are so very different from the traditional therapeutic mechanisms directed toward atherosclerotic disease. This advance was exceedingly important for all clinical investigators since their clinical approach to atherosclerotic disease has changed, particularly regarding its links with hypertension and the aging process.
Moreover, as a consequence of new epidemiological findings, we have divided the well-established vascular 'diseases' into two pedagogic categories: those related to cardiovascular risk factors (hypertension, diabetes mellitus, dyslipidemia, obesity and smoking) and those related to specific clinical events affecting the target organ circulations (i.e., brain, kidney, heart, and lower limbs). Furthermore, because of increased longevity in recent years, a dissociation of atherosclerosis from the effects of aging per se has been a major effort in presenting the concept of this textbook. Another important point needed to be clarified: in understanding the different clinical and hemodynamic features of atherosclerosis, it was important to present a current means of evaluating cardiovascular risk as well as a practical rationale for developing a therapeutic strategy.
Finally, in arriving at a dissociation and understanding of the mechanisms of hypertensive disease and of the aging process, the structural and functional changes of the vessels of each must be recognized as clearly as possible with respect to how they involve the totality of the arterial and arteriolar system. Thus, it is necessary to comprehend both the aging phenomenon and the pathophysiology of hypertension and their respective global impacts on arterial stiffness, especially involving the aorta and its major large arterial branches. In this regard, the clinical aspects of arterial stiffness have been widely developed in hypertensive subjects over the last 10 years. In contrast, in patients with atherosclerosis, the distribution of arterial rigidity on large vessels is much more patchy and predominates in certain arteries - for example the coronary arteries and at the level of the arterial bifurcations. In these vessels, non-fibrous and non-calcified plaques do not necessarily contribute to increased vessel stiffness. Therefore, the problem of arterial rigidity in atherosclerosis is more difficult to resolve than in hypertension. For these reasons, the principal purpose of this book was to respond to the following questions: In which conditions does the atherosclerosis process contribute to the development of vascular stiffness and to vascular calcifications since both of these factors independently participate in determining cardiovascular risk and, possibly, in modifying therapeutic strategy?
This book is composed of four sections. First, the definition and measurement of arterial stiffness are described with respect to the pathophysiological aspects of atherosclerosis. Second, the mechanisms underlying arterial stiffness are described successively in the major territories involved with atherosclerosis, particularly the coronary arteries. Third, arterial stiffness is discussed with respect to its relation with other cardiovascular factors such as diabetes mellitus or hyperlipidemia. Finally, in the fourth section the therapeutic means of approaching arterial stiffness are analyzed in detail. We hope this approach to the effects of arterial stiffness involving hypertension, atherosclerosis, and aging is now better understood and that it will, in turn, result in a more clearly developed concept for therapy in the future.
Michel E. Safar, Paris
Edward D. Frohlich, New Orleans, La.
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