|Risk factors and carotid atherosclerosis in hypertensive and control subjects|
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The arterial wall consists of three anatomically distinct layers: intima, media and adventitia, which are separated by two thin elastic layers, inner and outer, respectively. Atherosclerosis is a disease of intima. Atherosclerotic changes in the arterial wall can be divided into five categories (Stary et al. 1995). Stage I and II changes include intimal thickening and formation of foam cells (i.e. macrophages with accumulation of cholesterol), stage III preatheroma with accumulation of extracellulary lipids, stages IV and V plaque (atheroma) formation and stage VI complicated lesions. Carotid artery atherosclerosis is a common feature, which is developmentally and anatomically is indistinguishable from atherosclerosis in the other arteries. In population, the main risk factors of carotid artery atherosclerosis are the same as those of other atherosclerotic diseases, namely high blood pressure, smoking, hypercholesterolemia and aging (Berglund et al. 1994).
B-mode ultrasonography is nowadays commonly accepted as a noninvasive, safe, inexpensive and reliable method for measuring the IMT (i.e. intimal plus medial thickness) of large arteries located close to the skin, such as the carotid and femoral arteries. An increase in the IMT of the carotid arteries measured by ultrasonography is considered to reflect early atherosclerosis, although it might also reflect adaptation to other factors, such as hypertension. Several aspects of evidence, however, suggest a true correlation between an increase of ultrasonographic IMT and atherosclerosis. First, several conventional cardiovascular risk factors are associated with IMT in both men and women (Salonen & Salonen 1990, Bonithon-Kopp et al. 1991). Secondly, there is a strong correlation between increases in carotid IMT and CHD as determined by angiography or the disease history (Salonen & Salonen 1991, Wofford et al. 1991), and finally, increased IMT has been shown to be successfully reduced by lipid-lowering therapy (Mack et al. 1993, Wendelhag et al. 1995). In accordance, the progression of IMT has been shown to be associated with age, plasma LDL cholesterol level and smoking (Salonen & Salonen 1990). Furthermore, the IMT values of CCA measured ultrasonographically and microscopically show a close correlation (Pignoli et al. 1986).
In the Cardiovascular Health Study (O’Leary et al. 1992), detectable carotid stenosis was present in 75% of men and 62% of women, although the prevalence of ≥ 50% stenosis was low, 7% in men and 5% in women aged ≥ 65 years. On average, IMT of CCA increased by 0.01 mm for both men and women each year beyond age 65, and IMT of ICA increased by 0.02 mm (O’Leary et al. 1992). In the ARIC study, similar estimates were obtained for IMT of CCA but IMT of ICA increased by 0.01 mm/year for women and 0.014 mm/year for men. In the carotid bifurcation, IMT increased by 0.015 mm/year in women and 0.018 mm/year in men (Howard et al. 1993). Interestingly, in the Cardiovascular Health Study, IMT of CCA and IMT of ICA had slightly different predictive values for the presence of CHD and stroke. Each of the wall thickness measures showed an increase of about 20% in the risk of CHD or stroke for a 1 SD change independently of each other (O’Leary et al. 1992).
Studies based on carotid artery ultrasonography use both near-wall and far-wall measurements, although the near-wall IMT may be difficult to define, due to the echogenic structure of adventitia, which may make impossible to define the adventitia-media interface (Wendelhag et al. 1991). This is in contrast to the far wall, where the media-adventitia interface is usually easy to detect. Wong et al. (1993) and Wikstrand & Wendelhag (1994) concluded that only the far-wall IMT can be accurately measured by ultrasonography. If near-wall measurements are used, however, these measurements ought to be presented separately.
Recently, prospective follow-up results of the relationship between IMT and the risk of stroke and myocardial infarction have been reported (Bots et al. 1997). The mean duration of follow-up was 2.7 years in the Rotterdam Study. The unadjusted odds ratio for stroke per standard deviation increase (0.163 mm) of IMT was 1.41 (95% CI, 1.25 to 1.82). For myocardial infarction, an odds ratio of 1.43 (95% CI, 1.16 to 1.78) was found, but additional adjustment for several cardiovascular risk factors attenuated the association to a nonsignificant level. The large ARIC study yielded very similar but more consistent hazard risk ratios of incident CHD, and the association remained significant after adjustment for other CHD risk factors (Chambless et al. 1997). In a Finnish study (Salonen & Salonen 1991), for each millimeter increase of IMT, the risk of acute coronary event rose 2.14-fold (95% CI, 1.08 to 4.26), although the mean follow-up was about 1 year.
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