Arterial stiffness and hypertension: chicken or egg?
Arterial stiffness and hypertension: chicken or egg?
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DOI：
10.1161/hypertensionaha.114.03449
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发表时间：
2014-08
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通讯作者：
Mitchell GF
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作者：
Mitchell GF
Mitchell动脉僵硬度与PP中的高血压211，与老年人主要收缩期高血压的高发病率相关。在同一队列中（Fracket Heart研究），上述关于动脉僵硬度和高血压事件之间关系的研究之一也检查了初始血压和CFPWV评估的动脉僵硬度进展之间的关系。15作者发现CFPWV的初始值与随后的刚度进展密切相关。然而，在考虑CFPWV的初始值后，没有血压分量（收缩压、舒张压或平均值）进入未来刚度的模型。15这些结果支持了主动脉僵硬可能先于并可能促成高血压发展的假设。最近的几项纵向研究评价了进行性主动脉硬化的相关性，发现初始血压和进行性主动脉硬化之间的关系结果不一。15，21-25 Wildman等人22在一个相对较小（n= 152）和年轻（20-40岁）的birthday队列中评估了2年随访期间CFPWV的变化，发现黑人的加速硬化与基线或各种肥胖指标的变化相关。然而，血压组分的基线和变化与僵硬进展无关。Benetos等人21对一组持续血压正常和持续接受治疗的高血压志愿者进行了6年的随访，发现基线年龄、心率和接受治疗的高血压与多变量模型中的CFPWV进展相关，而基线收缩压和舒张压水平与CFPWV进展无关。相比之下，Birru等人，25 El Khoutian等人，23和AlGhatrif等人24在多变量模型中发现了基线收缩压与PWV进展之间的关系，尽管El Khoutian等人似乎没有在其模型中纳入基线CFPWV术语。上述关于基线血压和动脉僵硬度加速进展之间关系的混合结果表明，这种关系似乎足够温和，难以一致地检测。一些基础和临床研究已经证明，通常通过破坏主动脉壁中的弹性蛋白而直接增加主动脉僵硬度的损伤与随后的高血压发展相关。在弹性蛋白表达受损的小鼠模型中进行的研究表明，在收缩压增加之前，主动脉硬度增加，直径早期减小，并且随后的收缩压增量与主动脉中的弹性蛋白含量成反比。[26]同样，患有威廉姆斯综合征（弹性蛋白单倍不足）的儿童在相对年轻的时候动脉僵硬度就增加了，早在发生高血压之前。[27]通过引入人类弹性蛋白基因的异位拷贝来增加弹性蛋白的表达可以挽救弹性蛋白缺陷小鼠的动脉表型。28服用高剂量的维生素D3和尼古丁的组合或华法林和维生素K的组合会导致主动脉中膜弹性钙化、主动脉硬化、PWV和PP增加以及单纯收缩期高血压，而平均动脉压没有先前的增加。29，30最近，在引入高脂肪、高蔗糖饮食后的早期（1个月），在收缩压升高之前（6个月时发生），仅改变饮食即可增加主动脉PWV。31高脂肪，高…
Mitchell Arterial Stiffness and Hypertension 211 in PP that is associated with high incidence of predominantly systolic hypertension in older people. One of the foregoing studies of relationships between arterial stiffness and incident hypertension also examined, in the same (Framingham Heart Study) cohort, relationships between initial blood pressure and progression of arterial stiffness as assessed by CFPWV. 15 The authors found that the initial value of CFPWV was strongly associated with subsequent stiffness progression. However, after accounting for the initial value of CFPWV, no blood pressure component (systolic, diastolic, or mean) entered the model for future stiffness. 15 These results provide support for the hypothesis that aortic stiffness may antedate and may contribute to the development of hypertension. Several recent longitudinal studies evaluated the correlates of progressive aortic stiffening and found mixed results with respect to relationships between initial blood pressure and progressive aortic stiffening. 15, 21–25 Wildman et al22 evaluated change in CFPWV during 2 years of follow-up in a relatively small (n= 152) and young (20–40 years old) biracial cohort and found accelerated stiffening in blacks and in association with baseline or change in various measures of adiposity. Baseline and change in blood pressures components were not, however, related to stiffness progression. Benetos et al21 examined a cohort of persistently normotensive and persistently treated hypertensive volunteers followed up for 6 years and found that baseline age, heart rate, and the presence of treated hypertension were associated with CFPWV progression in a multivariable model, whereas baseline levels of systolic blood pressure and diastolic blood pressure were not related to CFPWV progression. In contrast, Birru et al, 25 El Khoudary et al, 23 and AlGhatrif et al24 found relationships between baseline systolic blood pressure and progression of PWV in multivariable models although El Khoudary et al seem to have not included a term for baseline CFPWV in their model. The foregoing mixed results about relationships between baseline blood pressure and accelerated progression of arterial stiffness suggest that the relationship seems to be sufficiently modest that it is difficult to detect consistently. Several basic and clinical studies have demonstrated that insults that increase aortic stiffness directly, generally by disrupting elastin in the aortic wall, are associated with subsequent development of hypertension. Studies performed in mouse models of impaired elastin expression have shown that aortic stiffness is increased and diameter is reduced early, before the increase in systolic pressure and that subsequent increments in systolic pressure are inversely proportional to elastin content in the aorta. 26 Similarly, children with Williams syndrome (elastin haploinsufficiency) have increased arterial stiffness at a relatively young age, well before the development of hypertension. 27 Increasing elastin expression through introduction of an ectopic copy of the human elastin gene can rescue the arterial phenotype in elastin-deficient mice. 28 Administration of a high-dose combination of vitamin D3 and nicotine or a combination of warfarin and vitamin K produces aortic medial elastocalcinosis, stiffening of the aorta, increased PWV and PP, and isolated systolic hypertension with no antecedent increase in mean arterial pressure. 29, 30 Recently, alterations in diet alone were shown to increase aortic PWV early (1 month) after introduction of a high-fat, high-sucrose diet, before an increase in systolic blood pressure, which occurred at 6 months. 31 High-fat, high …