White-coat hypertension contributes to the presence of carotid arteriosclerosis
White-coat hypertension contributes to the presence of carotid arteriosclerosis
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DOI：
10.1291/hypres.27.739
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发表时间：
2004-10-01
影响因子：
5.4
通讯作者：
Saito, Y
中科院分区：
文献类型：
--
作者：
Nakashima, T;Yamano, S;Saito, Y
目前尚不清楚白大衣高血压是否与血管器官损伤（如颈动脉硬化）相关，就像持续性高血压一样。因此，我们比较了血压正常、持续高血压或白大褂高血压的日本人颈动脉硬化的进展。共有30名白大衣高血压患者（平均年龄58岁）、30名未经治疗且颈动脉无斑块形成的持续性高血压患者（平均年龄54岁）和30名血压正常的患者（平均年龄58岁）参加了本研究。白大褂组和持续高血压组的临床血压相匹配，但他们的动态血压不同。相反，白大褂高血压和正常血压的受试者在动态血压方面是匹配的，但他们的临床血压不同。b超测量颈动脉内内侧厚度，计算颈总动脉横截面积。这三组在年龄、性别比例、身高、实验室数据和吸烟发生率方面相似。持续高血压患者的体重和体重指数明显高于正常血压或白大衣高血压患者。白大褂患者和持续高血压患者的内膜-内侧厚度和颈动脉横截面积相似，明显高于血压正常者。总的来说，这些发现表明，白大褂高血压以与持续高血压相似的方式导致了受试者颈动脉硬化的存在。因此，在进行白大褂高血压的临床评估时，应考虑到靶器官的潜在损害。
It remains unclear whether white-coat hypertension is associated with vascular organ damage (e.g., carotid arteriosclerosis) in the same way sustained hypertension is. We therefore compared the progression of carotid arteriosclerosis among Japanese individuals showing normal blood pressures, sustained hypertension or white-coat hypertension. A total of 30 subjects (mean age, 58 years) with white-coat hypertension, 30 (mean age, 54 years) with untreated sustained hypertension who had no plaque formation in the carotid arteries, and 30 normotensive subjects (mean age, 58 years) were enrolled in this study. The white-coat and sustained hypertensive subjects were matched with respect to their clinical blood pressures, but their ambulatory blood pressures differed. Conversely, white-coat hypertensive and normotensive subjects were matched with respect to ambulatory blood pressures, but their clinical blood pressures differed. Carotid intimal-medial thickness was measured by B-mode ultrasonography, and the cross-sectional area of the common carotid artery was calculated. The three groups were similar with respect to age, sex ratio, height, laboratory data and the incidence of smoking. Body weights and body mass indexes were significantly higher among patients with sustained hypertension than among either normotensive or white-coat hypertensive patients. Intimal-medial thicknesses and carotid cross-sectional areas were similar in patients with white-coat and sustained hypertension and significantly higher than in normotensive subjects. Collectively, these findings suggest that white-coat hypertension contributed to the presence of carotid arteriosclerosis in our subjects in a manner similar to sustained hypertension. Thus, clinical evaluation of white-coat hypertension should be conducted with the potential for target organ damage in mind.