Clinical Studies
Chinese Adults Are Less Susceptible Than Whites to Age-Related Endothelial Dysfunction

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Abstract

Objectives. We sought to assess the effects of aging on the endothelial physiology of a group of Chinese adults.

Background. Several studies have documented an association between aging and progressive arterial endothelial dysfunction in white subjects. We hypothesized that age-related endothelial dysfunction, an important event in atherosclerosis, might be less marked in southern Chinese subjects, in whom the prevalence of coronary heart disease is only ∼20% of that in industrialized countries.

Methods. We studied endothelial function in 76 healthy adults aged 16 to 70 years: 38 Chinese from a village of 3,000 people in southern China and 38 white subjects from Sydney, Australia. In each ethnic group, there were 19 younger persons (16 to 40 years) and 19 older adults (55 to 70 years). None had evidence of diabetes, hypertension or clinical vascular disease or had ever been regular cigarette smokers. With the use of high resolution external vascular ultrasound, brachial artery diameter was measured at rest, after flow increase (causing endothelium-dependent dilation) and after sublingual nitroglycerin (an endothelium-independent dilator).

Results. Endothelium-dependent dilation was similar in young Chinese (mean ± SD 8.3 ± 2.5%), young whites (7.9 ± 2.0%) and older Chinese (6.8 ± 2.9%), but it was significantly impaired in older whites (1.8 ± 2.5%, p < 0.001 by analysis of variance). On multivariate analysis, older age was associated with impaired endothelium-dependent dilation (p < 0.001) (independent of the effects of serum cholesterol, gender and vessel size) in the white but not in the Chinese subjects (p = 0.83). Nitroglycerin-induced dilation was not significantly different with aging in either ethnic group.

Conclusions. Endothelium-dependent dilation is similar in the arteries of healthy young Chinese and white adults. With older age, however, Chinese subjects are less susceptible to impaired endothelial function.

(J Am Coll Cardiol 1997;30:113–8)

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Ms. Robinson and Dr. Adams are supported by the National Heart Foundation of Australia; Dr. McCrohon by the University of Sydney; and Dr. Celermajer by The Medical Foundation, University of Sydney, Sydney, Australia. This study was supported in part by grants from the National Health and Medical Research Council and the National Heart Foundation, Australia; the Atherosclerosis Research Trust, Acuson, Mountainview, California; the U.S.–China Industrial Exchange (Chindex, Beijing, People’s Republic of China), which provided ultrasound equipment and technical support in Shek Kei Village, People’s Republic of China; and the Cardiac Research Fund of the Chinese University of Hong Kong, Hong Kong.