We conclude that determination of the carotid IMT and of the ACE I/D polymorphism do not permit discrimination of the cardiovascular risk in children of parents with or without premature stroke.
A family history of cardiovascular disease predicts cardiovascular risk in the next generation, which is either the result of inherited traits or certain living habits in some families. The aim of our study was to evaluate both variables and particularly the role of one of the possible genetic risk factors--angiotensin-converting enzyme (ACE) gene polymorphism. History and anthropometric and biochemical parameters, ACE gene polymorphism and carotid wall thickness--intima media thickness (IMT) were studied in two groups of children: in children whose parents had a stroke before the age of 45 years and in children without a positive family history. The preliminary results of the present study failed to confirm our hypothesis that ACE gene polymorphism is a cardiovascular risk factor in children of parents with premature stroke.
Aim: To determine some common cardiovascular risk factors, alterations in the measurements of intima‐media thickness (IMT) and the distribution of the angiotensin‐converting enzyme (ACE) polymorphism in children of parents with premature stroke, and to investigate the cardiovascular risk of these children and the potential need for some preventive measures.Methods: A family history of cardiovascular disease represents a cardiovascular risk factor in the offspring. This association has not yet been clearly determined for cerebrovascular accidents. New technology allows us to investigate the risk for cardiovascular disease at an early presymptomatic stage. We applied the measurement of IMT of carotid arteries by ultrasound imaging and the determination of the ACE insertion/deletion (I/D) polymorphism in blood to evaluate the predisposition for cerebrovascular disease in the offspring of patients with previous stroke. We investigated 58 subjects whose parents had experienced a cerebrovascular accident before the age of 45 y and compared them with a matched control group whose parents had not suffered a stroke. Results: The results of IMT at various sites of the carotid arteries and the genotype distribution of the ACE gene were not significantly different between the study group and the control group. In addition, no differences were found in the serum levels of lipid fractions or other biochemical variables.
Conclusion: We conclude that determination of the carotid IMT and of the ACE I/D polymorphism do not permit discrimination of the cardiovascular risk in children of parents with or without premature stroke.
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