Maksuti Elira, Westerhof Nico, Westerhof Berend E, Broomé Michael, Stergiopulos Nikos
Department of Medical Engineering, School of Technology and Health, KTH Royal Institute of Technology, Stockholm, Sweden.
Department of Clinical Physiology, Karolinska Institutet, Stockholm, Sweden.
PLoS One. 2016 Jun 24;11(6):e0157493. doi: 10.1371/journal.pone.0157493. eCollection 2016.
During aging, systolic blood pressure continuously increases over time, whereas diastolic pressure first increases and then slightly decreases after middle age. These pressure changes are usually explained by changes of the arterial system alone (increase in arterial stiffness and vascular resistance). However, we hypothesise that the heart contributes to the age-related blood pressure progression as well. In the present study we quantified the blood pressure changes in normal aging by using a Windkessel model for the arterial system and the time-varying elastance model for the heart, and compared the simulation results with data from the Framingham Heart Study. Parameters representing arterial changes (resistance and stiffness) during aging were based on literature values, whereas parameters representing cardiac changes were computed through physiological rules (compensated hypertrophy and preservation of end-diastolic volume). When taking into account arterial changes only, the systolic and diastolic pressure did not agree well with the population data. Between 20 and 80 years, systolic pressure increased from 100 to 122 mmHg, and diastolic pressure decreased from 76 to 55 mmHg. When taking cardiac adaptations into account as well, systolic and diastolic pressure increased from 100 to 151 mmHg and decreased from 76 to 69 mmHg, respectively. Our results show that not only the arterial system, but also the heart, contributes to the changes in blood pressure during aging. The changes in arterial properties initiate a systolic pressure increase, which in turn initiates a cardiac remodelling process that further augments systolic pressure and mitigates the decrease in diastolic pressure.
在衰老过程中,收缩压随时间持续升高,而舒张压在中年后先升高然后略有下降。这些血压变化通常仅用动脉系统的变化(动脉僵硬度和血管阻力增加)来解释。然而,我们推测心脏也对与年龄相关的血压进展有影响。在本研究中,我们使用动脉系统的Windkessel模型和心脏的时变弹性模型来量化正常衰老过程中的血压变化,并将模拟结果与弗雷明汉心脏研究的数据进行比较。代表衰老过程中动脉变化(阻力和僵硬度)的参数基于文献值,而代表心脏变化的参数则通过生理规则(代偿性肥大和舒张末期容积的保留)计算得出。仅考虑动脉变化时,收缩压和舒张压与人群数据不太相符。在20至80岁之间,收缩压从100 mmHg升高至122 mmHg,舒张压从76 mmHg降至55 mmHg。当同时考虑心脏适应性变化时,收缩压和舒张压分别从100 mmHg升高至151 mmHg,从76 mmHg降至69 mmHg。我们的结果表明,不仅动脉系统,而且心脏也对衰老过程中的血压变化有影响。动脉特性的变化引发收缩压升高,进而引发心脏重塑过程,这进一步增加了收缩压并减轻了舒张压的下降。