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。这样做的目的是 研究旨在确定成人冠心病的儿童标志物或特征 动脉疾病(CAD)。鉴于动脉粥样硬化的家族性， 高血压和糖尿病，这项研究是基于 假设父母有冠状动脉易患疾病的孩子早期表现出 动脉粥样硬化和血栓形成相关参数异常， 儿童时期冠心病风险的预测在黑人和黑人之间可能不同 白人，甚至可能受到成人心脏性别差异的影响 疾病。这些假设将在一个完整的混血儿群体中得到验证 路易斯安那州博加卢萨，利用资源优势和广泛的 正在进行的博加卢萨心脏研究计划的数据库。纵向 脂蛋白谱和其他危险因素变量的变化 经临床证实的父母的子女的童年和青春期 冠心病与匹配的父母未受影响的子女组的比较 CAD将通过回顾数据分析来确定。唯一的数据集 年龄在18岁到31岁之间，年龄在15岁之间的大约2000名年轻人 包括脂蛋白在内的心血管危险因素的数据范围为 可用于此目的。第二项研究将使用报告的家庭 从两次横断面调查(1987-88和1992-94)看CAD的历史 每个儿童包括3,500多名5-17岁的儿童)。这涉及到 选择至少有一个的黑人和白人家庭(N=50) 父母(年龄30至55岁)，经临床验证患有冠心病。适当地 没有家族病史的配对对照家庭将 我也学过。父母将被给予常规的心血管风险 因素检验。这些儿童(8至19岁，N=250至300人) 病例对照家系将进行深入研究，包括口腔脂肪负荷。 评价餐后富含甘油三酯的脂蛋白的试验 新陈代谢。将获得有关1)人体测量变量的数据 对体脂分布的影响，2)血清脂蛋白变量(总 胆固醇、甘油三酯、极低密度脂蛋白胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇 L、低密度脂蛋白-L：ALL、载脂蛋白A-L、载脂蛋白B、低密度脂蛋白-载脂蛋白B、载脂蛋白E、高密度脂蛋白-载脂蛋白E和低密度脂蛋白 和相关候选基因(Lp(A)、apo(A)表型和apoE 表型)，以及3)其他与动脉粥样硬化和 血栓形成(葡萄糖、胰岛素、血栓素、前列环素、von Willebrand 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)。遗传力和外显性的连锁研究 这些指标在多世代中的相关候选基因标记 家庭仍然是一个长期目标。儿童的白血球 为此目的，将收集和存储父母。理解 在混血人群中，成年冠心病的儿童期预测因素可能导致 更加合理的健康促进和疾病预防方案。

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.