Cardiovascular Risk Factors Atherosclerosis and Pulse Pressure

Jacques Amar Bernard Chamontin

Service de Médecine Interne et d'hypertension artérielle, CHU Toulouse, France

Abstract

Blood pressure is a complex phenomenon that can be divided into two components: a steady and a pulsatile component. The pulsatile component is estimated by the pulse pressure which is mainly influenced by the large artery stiffness. The purpose of this review was to describe the relation between pulse pressure, cardiovascular risk factors and atherosclerosis. Epidemiological studies have shown positive correlations between pulse pressure and smoking or glucose metabolism impairment. More controversial data have been reported on the relation between blood lipids and large artery stiffness or pulse pressure. In cross-sectional studies, carotid, aortic and coronary plaques were associated with aortic stiffness, particularly echogenic or ulcerative plaques, and in a longitudinal study, the progression of atherosclerosis is accompanied by an increase in pulse pressure. From a pathophysiological point of view, the deleterious influence of most risk factors on endo-thelial function and the development of atheroma are likely to contribute to these relations. Furthermore, with respect to the connections observed between C-reactive protein, most cardiovascular risk factors, atherosclerotic diseases and pulse pressure, subclinical inflammation might also underlie these relations.

Copyright © 2007 S. Karger AG, Basel

There is impressive body of evidence of relationships between blood pressure, other cardiovascular risk factors and atherosclerosis: numerous studies have indicated that hypertensive subjects have an atherogenic lipoprotein profile [1] and impaired glucose metabolism [2] and elevated blood pressure is an established risk factor for atherosclerotic diseases. Blood pressure is a complex phenomenon that can be divided into two components: a steady and a pulsatile component [3]. The steady component is determined exclusively by cardiac output and vascular resistance. The pulsatile component represents the varia-

Table 1. Stepwise multiple regression analysis between pulse pressure and clinical and lipid variables [from 9]

Mean blood pressure Apoprotein B

Coefficient ± SEM

G.2268G.G7S S.S24±2.346

S.S3 G.GG4

6.16 G.G14

tion of the pressure curve around the steady component, and it is mainly influenced by the large artery stiffness. The pulsatile component is estimated by the pulse pressure which is the difference between systolic and diastolic blood pressure. The purpose of this review was to describe the relation between pulse pressure, cardiovascular risk factors and atherosclerosis.

Epidemiological Aspects

Relation between Pulse Pressure and Cardiovascular Risk Factors

Lipids

Numerous studies have examined the relation between cholesterol and large arteries stiffness in various populations. Divergent results have been reported. In asymptomatic normotensive patients, no relation [4], reduced [5] and increased arterial stiffness [6] with elevated total or LDL cholesterol have been successively described. In asymptomatic men with elevated cholesterol [ 7], no significant correlation was observed between carotid femoral pulse wave velocity - a surrogate marker of aortic stiffness - and total or LDL cholesterol. However, a positive link was observed in this population between HDL3 subfraction and aortic stiffness. In hypertensive patients with a low prevalence of known symptomatic atheromatous disease, Dart et al. [8] failed to find any significant correlation between total cholesterol and large arteries stiffness in older subjects (65-84 years).

Fewer studies have assessed the relation between pulse pressure and blood lipids. A weak but significant association has been reported between pulse pressure and apoprotein B in a population-based study conducted in Haute Garonne, a French region with a low cardiovascular risk (table 1) [9]. Furthermore, this association remained significant after adjustment for mean blood pressure. In agreement with these data, a correlation between cholesterol and pulse pressure have been reported in 18,336 men aged 40-69 years, who were followed up for a mean period of 9.5 years in a French cohort [10] and in 2,207

Fig. 1. Rest blood pressure of the brachial artery after placebo administration and after atorvastatin treatment. The top portion of each bar represents systolic blood pressure; the white band in the middle represents mean arterial pressure, and the base portion of each bar represents diastolic blood pressure. Values are mean ± SEM. * p < 0.05 for systolic, diastolic and mean blood pressure [from 13].

Fig. 1. Rest blood pressure of the brachial artery after placebo administration and after atorvastatin treatment. The top portion of each bar represents systolic blood pressure; the white band in the middle represents mean arterial pressure, and the base portion of each bar represents diastolic blood pressure. Values are mean ± SEM. * p < 0.05 for systolic, diastolic and mean blood pressure [from 13].

treated hypertensive patients in the USA [ 11]. However, no significant link with total cholesterol was observed in apparently healthy subjects in epidemiological studies conducted in Chicago in apparently healthy subjects [12]. Interestingly, in a randomized, cross-over design, controlled trial [13] comparing the effect of atorvastatin to placebo, it was found that intensive cholesterol reduction with atorvastatin over 3 months reduced large artery stiffness and blood pressure (fig. 1) in normocholesterolemic patients with stage I isolated systolic hypertension. However, blood pressure reduction does not occur with statin treatment in hypercholesterolemic normo tensive patients [14]. In patients with controlled hypertension who were also hypercholesterolemic, divergent results have been reported: two studies [15, 16] found no change in blood pressure under statin therapy whereas others [17] demonstrated that additional statin therapy led to greater reduction in blood pressure.

In summary, divergent results have been reported on the relation between both pulse pressure and aortic stiffness and lipids. It is possible that in the older population, subjects with elevated cholesterol and large artery stiffness are underrepresented because of such subjects having died contributing to these discrepancies. Also, the major determinants of artery stiffness, namely older age and hypertension, when present, may reduce the potential role of other factors. However, beyond these hypotheses, these discrepancies suggest

Table 2. Cross-sectional associations of pulse pressure, systolic pressure, and diastolic pressure with HbA1c and Amadori albumin [from 21]

Early glycation Pulse pressure Systolic pressure Diastolic pressure products mm Hg mm Hg mm Hg

Table 2. Cross-sectional associations of pulse pressure, systolic pressure, and diastolic pressure with HbA1c and Amadori albumin [from 21]

Early glycation Pulse pressure Systolic pressure Diastolic pressure products mm Hg mm Hg mm Hg

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