Greenfield Jerry R, Samaras Katherine, Campbell Lesley V, Jenkins Arthur B, Kelly Paul J, Spector Tim D, Hayward Christopher S
Department of Endocrinology, St. Vincent's Hospital, Sydney, Australia.
J Am Coll Cardiol. 2003 Jul 16;42(2):264-70. doi: 10.1016/s0735-1097(03)00631-4.
We sought to examine associations between the augmentation index (AI) and metabolic, adiposity, and lifestyle factors, independent of genetic influences, and to determine whether gene-environment interactions modulate these relationships.
Reported associations between AI, an index of systemic arterial stiffness, and metabolic, adiposity, and lifestyle factors remain contradictory. The modulating effect of genetic risk is unknown.
We studied 684 female twins (age 18 to 71 years); AI was derived from the pressure waveform measured at the radial artery by applanation tonometry. Percentage of total body fat (TBF) and percentage of central abdominal fat (CAF) were assessed by dual-energy X-ray absorptiometry.
In univariate analysis, age-adjusted AI was significantly associated with fasting triglyceride levels (r = 0.1, P = 0.03), apolipoprotein-B/A1 (r = 0.1, P = 0.04), percentage of TBF (r = 0.11, P = 0.006), and percentage of CAF (r = 0.11, P = 0.004). In co-twin case-control (monozygotic twin) analysis, a 3.1% absolute within-pair difference in percentage of CAF accounted for a 6% within-pair difference in AI, independent of genetic effects. Smokers and subjects with alcohol intakes >15 U/week had higher AI than nonsmokers (p = 0.01) and nondrinkers (p = 0.02), respectively. Forty percent of the variance in AI was explained by age, central mean arterial pressure, heart rate, height, percentage of CAF, and smoking. In gene-environment interaction analysis, subjects at high genetic risk of increased AI participating in regular leisure-time physical activity had AI values similar to low genetic risk subjects.
Central abdominal adiposity is a significant determinant of AI in female twins, independent of hemodynamic, lifestyle, and, importantly, genetic effects. Smoking is associated with increased AI, even after controlling for abdominal obesity and other AI determinants. Physical activity reduces genetic predisposition to increased AI.
我们旨在研究增强指数（AI）与代谢、肥胖及生活方式因素之间的关联，排除基因影响，并确定基因 - 环境相互作用是否会调节这些关系。
作为全身动脉僵硬度指标的AI与代谢、肥胖及生活方式因素之间的关联报道相互矛盾。基因风险的调节作用尚不清楚。
我们研究了684名女性双胞胎（年龄18至71岁）；AI通过应用压平式眼压计测量桡动脉压力波形得出。通过双能X线吸收法评估全身脂肪百分比（TBF）和腹部中央脂肪百分比（CAF）。
在单变量分析中，年龄校正后的AI与空腹甘油三酯水平（r = 0.1，P = 0.03）、载脂蛋白B/A1（r = 0.1，P = 0.04）、TBF百分比（r = 0.11，P = 0.006）和CAF百分比（r = 0.11，P = 0.004）显著相关。在同卵双胞胎病例对照分析中，CAF百分比3.1%的绝对配对内差异导致AI出现6%的配对内差异，不受基因效应影响。吸烟者和每周酒精摄入量>15单位的受试者的AI分别高于非吸烟者（p = 0.01）和不饮酒者（p = 0.02）。AI变异的40%可由年龄、中心平均动脉压、心率、身高、CAF百分比和吸烟来解释。在基因 - 环境相互作用分析中，具有高AI遗传风险且参与定期休闲体育活动的受试者的AI值与低遗传风险受试者相似。
腹部中央肥胖是女性双胞胎AI的重要决定因素，不受血流动力学、生活方式影响，重要的是不受基因效应影响。即使在控制腹部肥胖和其他AI决定因素后，吸烟仍与AI升高有关。体育活动可降低AI升高的遗传易感性。
