Antihypertensive treatments obscure familial contributions to blood pressure variation
Antihypertensive treatments obscure familial contributions to blood pressure variation
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DOI：
10.1161/01.hyp.0000044938.94050.e3
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发表时间：
2003-02-01
期刊：
影响因子：
8.3
通讯作者：
Harrap, SB
中科院分区：
文献类型：
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作者：
Cui, JSS;Hopper, JL;Harrap, SB
固有血压和潜在基因型之间的联系和关联可能会受到抗高血压治疗的混淆。我们通过使用各种方法调整244名接受降压药物治疗的受试者（8.2%）的血压，估计了767个成年志愿者家庭的血压方差分量（遗传、共享环境、个体特异性）。当使用测量的压力（在每一代中按性别调整年龄）时，收缩压方差的加性遗传成分为73.9 mm Hg-2（SE，8.8），但当排除治疗受试者时下降至61.4 mm Hg-2（SE，8.0）。当用相关第95百分位数值代替治疗后的收缩压时，加性遗传成分为81.9 mm Hg-2（SE，9.5），但收缩压的个体调整范围为-53.5 mmHg至+64.5 mmHg（平均值，+17.2 mmHg）。相反，当10毫米汞柱被添加到治疗的收缩压，加性遗传成分上升到86.6转Hg-2（SE，10.1）。收缩压方差的共享环境分量和舒张压的遗传和共享环境（即家族）分量也出现了类似的变化。在任何方法中，个体特异性方差分量几乎没有变化。因此，接受治疗的受试者为血压变异的家族性成分提供了重要信息。如果接受治疗的受试者被排除在外，并且如果使用未经调整的测量压力，则该信息将被治疗效果掩盖，则该信息将丢失。加回适当的压力增量恢复家族成分，更密切地反映了预处理值，并应增加基因组连锁和连锁不平衡分析的力量。
The linkage and association between inherent blood pressure and underlying genotype is potentially confounded by antihypertensive treatment. We estimated blood pressure variance components (genetic, shared environmental, individual-specific) in 767 adult volunteer families by using a variety of approaches to adjusting blood pressure of the 244 subjects (8.2%) receiving antihypertensive medications. The additive genetic component of variance for systolic pressure was 73.9 mm Hg-2 (SE, 8.8) when measured pressures (adjusted for age by gender within each generation) were used but fell to 61.4 mm Hg-2 (SE, 8.0) when treated subjects were excluded. When the relevant 95th percentile values were substituted for treated systolic pressures, the additive genetic component was 81.9 mm Hg-2 (SE, 9.5), but individual adjustments in systolic pressure ranged from -53.5 mmHg to +64.5 mmHg (mean, +17.2 mmHg). Instead, when 10 mm Hg was added to treated systolic pressure, the additive genetic component rose to 86.6 turn Hg-2 (SE, 10.1). Similar changes were seen in the shared environment component of variance for systolic pressure and for the combined genetic and shared environmental (ie, familial) components of diastolic pressure. There was little change in the individual-specific variance component across any of the methods. Therefore, treated subjects contribute important information to the familial components of blood pressure variance. This information is lost if treated subjects are excluded and obscured by treatment effects if unadjusted measured pressures are used. Adding back an appropriate increment of pressure restores familial components, more closely reflects the pretreatment values, and should increase the power of genomic linkage and linkage disequilibrium analyses.