As shown earlier in this book, the links between atherosclerosis, arterial stiffness, age and high BP are often difficult to establish, particularly according to age. Many atherosclerotic alterations (AA) are subclinical and difficult to define in routine clinical investigations. On the other hand, many markers have been proposed, such as defects in vascular relaxation, alterations in endotheli-um-dependent flow dilatation and/or presence of atherosclerotic plaques (see chapter by Baldewsing et al., pp 35-61, and chapter by Hayoz and Mazzolai, pp 62-75). Within the framework of antihypertensive drug therapy, it seems likely that the links between atherosclerosis and arterial stiffness should primarily be explored through a simple clinical description of CV events clearly related to AA. The principal AA are those responsible for peripheral arterial disease (see chapter by Safar, pp 199-211), coronary ischemic disease (see chapter by Kingwell and Ahimastos, pp 125-138) and carotid atherosclerotic disease (mainly stenosis of the carotid artery) (see chapter by Agabiti-Rosei and Muiesan, pp 173-186). The relation of such CV events to arterial stiffness, and potentially age and high BP, are evaluated in the following paragraphs.
In clinical medicine, the best examples associating hypertension and AA are represented by subjects with atherosclerosis of the lower limbs [15, 16]. Increased SBP and PP are commonly observed in these patients, whereas mean arterial pressure, systemic vascular resistance and ventricular ejection remain usually within the normal range. Arterial stiffness is significantly increased (see chapter by Safar, pp 199-211). This increase is exaggerated in the presence of high sodium intake and acute non-selective ^-blockade. The increased PP is significantly and independently associated with the limitation of the vasodilating arteriolar properties of the diseased limbs . This suggests that atherosclerosis, through increased arterial stiffness and wave reflections, might contribute to the elevated SBP and PP even when vascular resistance and DBP are normal. In vessels of the lower limbs, non-fibrous and non-calcified plaques contribute little to increase arterial stiffness. By contrast, in more advanced disease, atherosclerosis may contribute greatly to increased collagen content and calcifications of the arterial wall and accentuate arterial rigidity, especially in the presence of advanced age and/or hypertension.
Coronary ischemic disease has been found to be almost constantly associated with increased aortic stiffness  (see chapter by Kingwell and Ahimastos, pp 125-138). Although an increased incidence of elevated SBP has not been widely reported in populations of subjects with ischemic heart diseases, these subjects often display an increased PP and a decreased diastolic pressure-time index, probably due to aortic stiffening. Experimentally, increased aortic stiffness, which reduces DBP, participates in and aggravates the myocardial ischemia observed in the presence of stenosis of coronary arteries . Finally, even in the absence of systolic hypertension, increased stiffness is a major contributor to the evolution of coronary heart disease and predicts myocardial ischemia (see chapter by Danchin and Mourad, pp 139-149, chapter by Ver-decchia and Angeli, pp 150-159, and chapter by McEniery and Cockcroft, pp 160-172).
In contrast, with narrowed coronary arteries, stenosis of the internal carotid artery is frequently associated with systolic hypertension . In subjects with carotid endarterectomy, a significant increase of SBP variability is also observed, particularly during the night . Atherosclerotic plaques of the common carotid artery and of the carotid bifurcation are classical features of hypertensive subjects, particularly over 50 years of age . Decreased carotid distensibility, increased arterial wall thickness and calcifications are observed in uncomplicated hypertensive subjects for the same age and gender as normotensive controls . Such populations have been also the object of specific therapeutic trials (see chapter by Mackey et al., pp 234244) [22, 23].
Finally, whatever the clinical aspects of AA may be, the links of atherosclerosis with age, increased arterial stiffness and hypertension are similar in the different vascular territories and are all related by the presence of increased SBP. There is only one exception to this description, coronary ischemic disease, where the increased arterial stiffness and SBP are frequently masked by an associated reduction of ventricular ejection. Thus, the therapeutic links between AA and increased arterial stiffness are now easy to understand. The more difficult issue is how to treat systolic hypertension in the elderly. It is increased SBP. This problem must be approached cautiously. First, the principal goal of drug treatment, SBP reduction, involves a common denominator that combines several associated parameters: arterial stiffness, atherosclerosis, age and high BP. Second, to be valid in terms of AA, the reduction of SBP by drug treatment should be accompanied by the reduction of biomarkers of atherosclerosis, such as modifications in atherosclerotic plaques.
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