Lieb Wolfgang, Pencina Michael J, Wang Thomas J, Larson Martin G, Lanier Katherine J, Benjamin Emelia J, Levy Daniel, Tofler Geoffrey H, Meigs James B, Newton-Cheh Christopher, Vasan Ramachandran S
Framingham Heart Study, 73 Mount Wayte Ave, Framingham, MA 01702-5803, USA.
Hypertension. 2008 Aug;52(2):381-6. doi: 10.1161/HYPERTENSIONAHA.108.113589. Epub 2008 Jun 23.
Children of parents with hypertension are at increased risk of developing high blood pressure. We hypothesize that circulating concentrations of putative biomarkers (that may play a role in development of high blood pressure) are higher in nonhypertensive offspring of parents with hypertension. We compared concentrations of 4 different biomarkers (urinary albumin:creatinine ratio, circulating C-reactive protein, aldosterone:renin ratio, and plasminogen activator inhibitor-1) in nonhypertensive Framingham offspring study participants with none (n=233), 1 (n=474), or both (n=322) parents with hypertension. Parental hypertension was defined as onset before age 60 years, based on longitudinal observations of the original Framingham cohort. Serum C-reactive protein concentrations were higher in nonhypertensive offspring with 1 (median: 1.7; Q1 to Q3: 0.8 to 3.6 mg/L) or both parents with hypertension (median: 1.8; Q1 to Q3: 0.7 to 3.6 mg/L) compared with offspring without parental hypertension (median: 1.4; Q1 to Q3: 0.7 to 3.2 mg/L). In multivariable analyses, parental hypertension was associated with higher serum C-reactive protein concentration in offspring (15% increase per parent with hypertension; P=0.004). Prospectively, the relation of parental hypertension to longitudinal changes in blood pressure in the nonhypertensive offspring was attenuated on adjustment for C-reactive protein (P=0.04 for attenuation). The levels of the other biomarkers evaluated did not significantly differ in offspring according to parental hypertension status. In conclusion, serum C-reactive protein concentrations are higher in nonhypertensive offspring of parents with hypertension. These data suggest that inflammation may partly mediate the familial influences on hypertension risk.
父母患有高血压的子女患高血压的风险增加。我们假设,在父母患有高血压的非高血压后代中,假定生物标志物(可能在高血压发展中起作用)的循环浓度更高。我们比较了弗雷明汉心脏研究中无高血压父母(n = 233)、有1位高血压父母(n = 474)或有2位高血压父母(n = 322)的非高血压参与者体内4种不同生物标志物(尿白蛋白:肌酐比值、循环C反应蛋白、醛固酮:肾素比值和纤溶酶原激活物抑制剂-1)的浓度。根据对原始弗雷明汉队列的纵向观察,父母高血压定义为发病年龄在60岁之前。与无父母高血压的后代(中位数:1.4;第一四分位数至第三四分位数:0.7至3.2 mg/L)相比,有1位(中位数:1.7;第一四分位数至第三四分位数:0.8至3.6 mg/L)或2位父母患有高血压的非高血压后代的血清C反应蛋白浓度更高(中位数:1.8;第一四分位数至第三四分位数:0.7至3.6 mg/L)。在多变量分析中,父母高血压与后代血清C反应蛋白浓度升高相关(每位患有高血压的父母血清C反应蛋白浓度增加15%;P = 0.004)。前瞻性研究发现,在调整C反应蛋白后,父母高血压与非高血压后代血压纵向变化之间的关系减弱(减弱的P值为0.04)。根据父母高血压状态,所评估的其他生物标志物水平在后代中无显著差异。总之,父母患有高血压的非高血压后代的血清C反应蛋白浓度更高。这些数据表明,炎症可能部分介导了家族因素对高血压风险的影响。