P121 IDENTIFYING HAEMODYNAMIC DETERMINANTS OF PULSE PRESSURE: AN INTEGRATED NUMERICAL AND PHYSIOLOGICAL APPROACH
Purpose: Hypertension, the single biggest killer worldwide1, arises mainly as a result of an increase in central pulse pressure (PP)2, yet haemodynamic basis of that increase is still disputed. We examined the ability of a simple “reduced” model comprising a proximal characteristic impedance linked to a Windkessel element to accurately predict PP from aortic blood flow and applied the model to examine PP dependence on cardiac and vascular properties. Method: PP obtained from the model was compared with theoretical values obtained in silico and in vivo. Theoretical values were obtained using a distributed multi-segment model in a population of “virtual” subjects (n = 3,095) in which cardiovascular properties were varied over the pathophysiological range. In vivo measurements were in normotensive subject (n = 13) during modulation of physiology with vasoactive drugs with divergent actions on cardiac and cascular properties and in hypertensive subjects (n = 156). Results: PP derived from the model agreed with theoretical values (mean difference SD, −0.09±1.96 mmHg) and with measured values (−1.95±3.74 and −1.18±3.67 mmHg for normotensive and hypertensive subjects respectively). Parameters extracted from the model agreed closely with theoretical and measured physical properties. PP was seen to be determined mainly by total arterial compliance (inversely associated with arterial stiffness) and ventricular dynamics: the volume of blood ejected up to time of pulse pressure and the rate of ventricular ejection up to this point. Conclusion: Increased flow and/or volume accounted for 20.1 mmHg (52%) of the 39.0 mmHg difference in pulse pressure between the upper and lower tertiles of the hypertensive subjects..
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2017 |
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| Erschienen: |
2017 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:20 |
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| Enthalten in: |
Artery Research - 20(2017) |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Samuel Vennin [VerfasserIn] |
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| Links: |
doi.org [kostenfrei] |
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| Themen: |
Diseases of the circulatory (Cardiovascular) system |
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| doi: |
10.1016/j.artres.2017.10.103 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
DOAJ031096255 |
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| 520 | |a Purpose: Hypertension, the single biggest killer worldwide1, arises mainly as a result of an increase in central pulse pressure (PP)2, yet haemodynamic basis of that increase is still disputed. We examined the ability of a simple “reduced” model comprising a proximal characteristic impedance linked to a Windkessel element to accurately predict PP from aortic blood flow and applied the model to examine PP dependence on cardiac and vascular properties. Method: PP obtained from the model was compared with theoretical values obtained in silico and in vivo. Theoretical values were obtained using a distributed multi-segment model in a population of “virtual” subjects (n = 3,095) in which cardiovascular properties were varied over the pathophysiological range. In vivo measurements were in normotensive subject (n = 13) during modulation of physiology with vasoactive drugs with divergent actions on cardiac and cascular properties and in hypertensive subjects (n = 156). Results: PP derived from the model agreed with theoretical values (mean difference SD, −0.09±1.96 mmHg) and with measured values (−1.95±3.74 and −1.18±3.67 mmHg for normotensive and hypertensive subjects respectively). Parameters extracted from the model agreed closely with theoretical and measured physical properties. PP was seen to be determined mainly by total arterial compliance (inversely associated with arterial stiffness) and ventricular dynamics: the volume of blood ejected up to time of pulse pressure and the rate of ventricular ejection up to this point. Conclusion: Increased flow and/or volume accounted for 20.1 mmHg (52%) of the 39.0 mmHg difference in pulse pressure between the upper and lower tertiles of the hypertensive subjects. | ||
| 653 | 0 | |a Specialties of internal medicine | |
| 653 | 0 | |a Diseases of the circulatory (Cardiovascular) system | |
| 700 | 0 | |a Ye Li |e verfasserin |4 aut | |
| 700 | 0 | |a Marie Willemet |e verfasserin |4 aut | |
| 700 | 0 | |a Henry Fok |e verfasserin |4 aut | |
| 700 | 0 | |a Haotian Gu |e verfasserin |4 aut | |
| 700 | 0 | |a Peter Charlton |e verfasserin |4 aut | |
| 700 | 0 | |a Jordi Alastruey |e verfasserin |4 aut | |
| 700 | 0 | |a Phil Chowienczyk |e verfasserin |4 aut | |
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