CHILDHOOD PREDICTOR OF ADULT CORONARY ARTERY DISEASE

改善心血管健康的进展在于认识到 动脉粥样硬化的发病机制始于儿童时期。的目的 研究是为了确定儿童时期的标志物或特征， 动脉疾病（CAD）。考虑到动脉粥样硬化的家族性， 原发性高血压和糖尿病，该研究基于 有冠心病倾向的父母的孩子显示出早期证据的假设 与动脉粥样硬化形成和血栓形成相关的参数异常， 儿童期CAD风险的预测因子在黑人和 白人，甚至可能受到成年人心脏性别差异的影响 疾病这些假设将在一个总的birthoracic社区进行测试， 路易斯安那州的博加卢萨，利用资源和广泛的 正在进行的博加卢萨心脏研究项目的数据库。纵向 脂蛋白谱和其他风险因素变量的变化 临床证明患有糖尿病的父母的后代的儿童期和青春期 CAD与未受影响的父母的后代的匹配组相比 将通过回顾性数据分析确定CAD。一个独特的数据集 在一组约2,000名年龄在18至31岁之间的年轻人中， 包括脂蛋白在内的心血管风险因素的数据跨度是 可用于此目的。第二项研究将使用报告的家庭 两次横断面调查（1987-88年和1992-94年）的CAD历史 每一个都包括3 500多名5至17岁的儿童）。这涉及 选择黑人和白色家庭（各N = 50）， 父母（年龄30 - 55岁）患有经临床验证的CAD。适当 没有疾病家族史的匹配对照家庭将被 也研究过。父母将被给予定期心血管风险 因子检验其中儿童（8至19岁，N = 250-300） 病例对照家庭将进行深入研究，包括口腔脂肪负荷 评价餐后富含甘油三酯脂蛋白的试验 新陈代谢.将获得1）人体测量变量相关数据 2）血清脂蛋白变量（总 胆固醇、甘油三酯、VLDL-C、LDL-C、HDL 2-C、HDL 3-C、HDL-apoE、LpA- LpA-I：All、apoA-I、apoB、LDL-apoB、apoE、HDL-apoE和LDL脂质 过氧化物酶）和相关候选基因（Lp（a）、apo（a）表型和apoE 表型），以及3）与动脉粥样硬化相关的其他变量， 血栓形成（葡萄糖、胰岛素、血栓素、前列环素、血管性血友病 因子抗原，纤维蛋白原，纤维蛋白降解产物，同型半胱氨酸，和 尿酸）。用连锁分析法研究遗传力和变异率 在这些指标的多个世代中的相关候选基因标记 家庭仍然是一个长期目标。儿童的白色血细胞 并将为此目的收集和存储父母。理解 在出生率较高的人群中，成人CAD的儿童期预测因子可导致 更合理的健康促进和疾病预防计划。

Advances toward improving cardiovascular health lie in the recognition that pathogenesis of atherosclerosis begins in childhood. The aim of this research is to identify childhood markers or traits for adult coronary artery disease (CAD). Given the familial nature of atherosclerosis, essential hypertension, and diabetes mellitus, the research is based on hypotheses that children of coronary-prone parents show early evidence of abnormalities in parameters related to atherogenesis and thrombogenesis, and that childhood predictors of CAD risk may vary between blacks and whites, and may even be influenced by gender differences of adult heart disease. These hypotheses will be tested in a total biracial community of Bogalusa, Louisiana, taking advantage of the resources and an extensive data base of the ongoing Bogalusa Heart Study program. Longitudinal changes in lipoprotein profiles and other risk factor variables during childhood and adolescence in offspring of parents with clinically proven CAD in comparison to matched group of offspring of parents unaffected by CAD will be determined by a retrospective data analysis. A unique data set of a cohort of about 2,000 young adults aged 18 to 31 years with a 15 year data span of cardiovascular risk factors including lipoproteins is available for this purpose. A second study will use reported family histories of CAD from two cross-sectional surveys (1987-88 and 1992-94 each including over 3,500 children, ages 5-17 years). This involves selection of black and white families (N = 50 each) that have at least one parent (aged 30 to 55 years) with clinically validated CAD. Appropriately matched control families with no family history of the disease will be studied as well. Parents will be given a regular cardiovascular risk factor examination. Children (aged 8 to 19 years, N = 250-300) of these case-control families will be studied in depth including an oral fat load test to evaluate the post-prandial triglyceride-rich lipoprotein metabolism. Data will be obtained on 1) anthropometric variables related to body fat distribution, 2) serum lipoprotein variables (total cholesterol, triglycerides, VLDL-C, LDL-C, HDL2-C, HDL3-C, HDL-apoE, LpA- l, LpA-l:All, apoA-l, apoB, LDL-apoB, apoE, HDL-apoE, and LDL lipid peroxides) and related candidate genes (Lp(a), apo(a) phenotypes, and apoE phenotypes), and 3) other variables related to atherosclerosis and thrombosis (glucose, insulin, thromboxane, prostacycline, von Willebrand factor antigen, fibrinogen, fibrin degradation products, homocysteine, and uric acid). The study of heritability and penetrance by linkage of relevant candidate gene markers in multiple generations of these index families remains a long-term objective. White blood cells from children and parents will be collected and stored for this purpose. Understanding childhood predictors of adult CAD in a biracial population can lead to more rational programs for health promotion and disease prevention.