Family history of premature cardiovascular disease as a sole and independent risk factor for increased carotid intima-media thickness
Family history of premature cardiovascular disease as a sole and independent risk factor for increased carotid intima-media thickness
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DOI：
10.1097/hjh.0b013e328325d81b
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发表时间：
2009-04-01
影响因子：
4.9
通讯作者：
Mohn, Angelika
中科院分区：
文献类型：
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作者：
de Giorgis, Tommaso;Giannini, Cosimo;Mohn, Angelika
目的 本研究的目的是评估有早发性心血管疾病 (PFHPCD) 家族史的儿童的颈动脉内膜中层厚度 (cIMT) 以及 cIMT 与参与结构性血管变化的其他已知危险因素（胰岛素抵抗、氧化状态和脂质谱）之间的关系。 方法 对 24 名青春期前儿童（10 名男孩、10 名男孩、 14 名女孩（平均年龄 7.9 +/- 2.37 岁）患有 PFHPCD，并与 25 名健康青春期前儿童（11 名男孩，14 名女孩）进行比较。评估所有儿童的空腹胰岛素和血糖水平，并计算胰岛素抵抗的稳态模型评估和空腹血糖-胰岛素比值。采用高分辨率超声技术评估 cIMT。结果 与健康对照相比，PFHPCD 儿童的 cIMT 增加（P = 0.001）。 PFHPCD 儿童和对照组儿童的空腹胰岛素水平 (P = 0.416)、葡萄糖-胰岛素比值 (P = 0.454) 和胰岛素抵抗稳态模型评估 (P = 0.317) 没有显着差异。 PFHPCD 儿童的前列腺素 F-2 α 水平显着高于对照组 (P = 0.003)。为了评估 cIMT 与其他已知危险因素之间的关系，进行了多元线性回归分析。即使在调整混杂因素（年龄、性别、BMI）后，cIMT 和前列腺素 F-2 α 之间仍存在直接相关性（β = 0.905；P = 0.002；r(2), 0.63）。 结论 在青春期前就已患有 PFHPCD 的儿童中，可检测到早熟心血管风险的迹象。此外，氧化-抗氧化状态受损可能与检测到的血管壁异常有关，这表明遗传和遗传倾向在 cIMT 增加的发病机制中发挥着关键作用。 《高血压杂志》27:822-828 (C) 2009 Wolters Kluwer Health |利平科特·威廉姆斯和威尔金斯。
Objective The aim of this study was to evaluate carotid intima-media thickness (cIMT) in children with a positive family history of premature cardiovascular disease (PFHPCD) and the relationship between cIMT and other known risk factors (insulin resistance, oxidant status and lipid profile) involved in structural vascular changes.Methods Anthropometric measurements and inflammatory markers [isoprostanes (prostaglandin F-2 alpha)] were evaluated in 24 prepubertal children (10 boys, 14 girls, mean age 7.9 +/- 2.37 years) with PFHPCD and compared with 25 healthy prepubertal children (11 boys, 14 girls). Fasting insulin and glycemia levels were evaluated and homeostasis model assessment of insulin resistance and fasting glucose-insulin ratio were calculated in all children. High-resolution ultrasound technique was used to evaluate cIMT.Results Children with PFHPCD had an increased cIMT (P = 0.001) in comparison with healthy controls. No significant differences were found in terms of fasting insulin levels (P = 0.416), glucose-insulin ratio (P = 0.454) and homeostasis model assessment of insulin resistance (P = 0.317) between children with PFHPCD and controls. Prostaglandin F-2 alpha levels were significantly higher in children with PFHPCD than in controls (P = 0.003). In order to evaluate the relationship between cIMT and other known risk factors, a multiple linear regression analysis was performed. A direct correlation was found between cIMT and prostaglandin F-2 alpha (beta = 0.905; P = 0.002; r(2), 0.63) even after adjusting for confounding factors (age, sex, BMI).Conclusion Signs of precocious cardiovascular risk are detectable in children with PFHPCD already during prepuberty. Furthermore, impaired oxidant-antioxidant status would be implicated in the detected abnormalities of the vascular wall, suggesting a pivotal role of hereditary and genetic predisposition in the pathogenesis of increased cIMT. J Hypertens 27:822-828 (C) 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins.