title: Contribution of the Arterial System and the Heart to Blood Pressure during Normal Aging - A Simulation Study.
abstract: 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.
authors.affiliation: Department of Medical Engineering, School of Technology and Health, KTH Royal Institute of Technology, Stockholm, Sweden.|Department of Clinical Physiology, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Elira
authors.identifier: http://orcid.org/0000-0002-9654-447X
authors.initials: E
authors.lastname: Maksuti
authors.affiliation: Departments of Physiology and Pulmonary Diseases, ICaR-VU, VU University Medical Center, Amsterdam, The Netherlands.
authors.forename: Nico
authors.initials: N
authors.lastname: Westerhof
authors.affiliation: Edwards Lifesciences BMEYE, Critical Care Noninvasive, Amsterdam, The Netherlands.|Heart Failure Research Center, Laboratory for Clinical Cardiovascular Physiology, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: Berend E
authors.initials: BE
authors.lastname: Westerhof
authors.affiliation: Department of Medical Engineering, School of Technology and Health, KTH Royal Institute of Technology, Stockholm, Sweden.|ECMO Department, Karolinska University Hospital, Stockholm, Sweden.|Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Michael
authors.initials: M
authors.lastname: Broomé
authors.affiliation: Laboratory of Hemodynamics and Cardiovascular Technology, Institute of Bioengineering, Swiss Federal Institute of Technology, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
authors.forename: Nikos
authors.initials: N
authors.lastname: Stergiopulos
mesh_terms: D000375:Aging / Q000502:physiology*; D000465:Algorithms; D001158:Arteries / Q000502:physiology*; D001794:Blood Pressure; D003198:Computer Simulation; D006321:Heart / Q000502:physiology*; D006801:Humans; D008954:Models, Biological