Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study.
Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study.
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DOI：
10.1161/01.cir.96.1.308
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发表时间：
1997-07
期刊：
影响因子：
37.8
通讯作者：
S. Franklin;William Gustin;N. Wong;M. Larson;M. Weber;W. Kannel;Daniel Levy
中科院分区：
文献类型：
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作者：
S. Franklin;William Gustin;N. Wong;M. Larson;M. Weber;W. Kannel;Daniel Levy
背景：在最初的Framingham心脏研究的人群队列中，我们试图描述正常血压和未经治疗的高血压受试者的年龄相关血压变化，并推断潜在的血流动力学机制。方法和结果2036名受试者根据两年一次的血压(SBP)分为4组，分别在第10、11、12年进行一次检查。剔除接受降压药物治疗的受试者后，使用第2-16两年检查中血压正常和未接受治疗的高血压受试者长达30年的数据。对个体内血压随年龄的回归产生斜率和曲率的估计，并与四个SBP组之间使用ANOVA进行比较。30~84岁SBP呈线性上升，舒张压(DBP)和平均动脉压(MAP)同时升高，50~60岁后DBP下降，脉压(PP)急剧上升，MAP达到一渐近线。无论是舒张压的下降还是脉压的上升都不会受到后续死亡和非致命性心肌梗死或心力衰竭受试者的显著影响。在基线SBP最高的受试者中，SBP、PP和MAP与年龄相关的线性增加，以及DBP的早期上升和晚期下降是最大的；这代表了一种发散而不是平行的追踪模式。结论60岁以后DBP下降较晚，与SBP持续升高有关，不能用“耗竭性”舒张期高血压或“选择性存活”来解释，但与大动脉僵硬的增加是一致的。如果不加治疗，较高的SBP可能会加速大动脉僵硬，从而延续恶性循环。
BACKGROUND We attempted to characterize age-related changes in blood pressure in both normotensive and untreated hypertensive subjects in a population-based cohort from the original Framingham Heart Study and to infer underlying hemodynamic mechanisms. METHODS AND RESULTS A total of 2036 participants were divided into four groups according to their systolic blood pressure (SBP) at biennial examination 10, 11, or 12. After excluding subjects receiving antihypertensive drug therapy, up to 30 years of data on normotensive and untreated hypertensive subjects from biennial examinations 2 through 16 were used. Regressions of blood pressure versus age within individual subjects produced slope and curvature estimates that were compared with the use of ANOVA among the four SBP groups. There was a linear rise in SBP from age 30 through 84 years and concurrent increases in diastolic blood pressure (DBP) and mean arterial pressure (MAP); after age 50 to 60 years, DBP declined, pulse pressure (PP) rose steeply, and MAP reached an asymptote. Neither the fall in DBP nor the rise in PP was influenced significantly by removal of subsequent deaths and subjects with nonfatal myocardial infarction or heart failure. Age-related linear increases in SBP, PP, and MAP, as well as the early rise and late fall in DBP, were greatest for subjects with the highest baseline SBP; this represents a divergent rather than parallel tracking pattern. CONCLUSIONS The late fall in DBP after age 60 years, associated with a continual rise in SBP, cannot be explained by "burned out" diastolic hypertension or by "selective survivorship" but is consistent with increased large artery stiffness. Higher SBP, left untreated, may accelerate large artery stiffness and thus perpetuate a vicious cycle.