JOURNAL ARTICLE

Family history of premature cardiovascular disease as a sole and independent risk factor for increased carotid intima-media thickness

Tommaso de Giorgis, Cosimo Giannini, Antonino Scarinci, Ebe D'Adamo, Sergio Agostinelli, Francesco Chiarelli, Angelika Mohn
Journal of Hypertension 2009, 27 (4): 822-8
19516181

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-2alpha)] 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-2alpha 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-2alpha (beta = 0.905; P = 0.002; r2, 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.

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