Cardiac contractility is a key factor in determining pulse pressure and its peripheral amplification

TY - JOUR

T1 - Cardiac contractility is a key factor in determining pulse pressure and its peripheral amplification

AU - Piccioli, Francesco

AU - Li, Ye

AU - Valiani, Alessandro

AU - Caleffi, Valerio

AU - Chowienczyk, Philip

AU - Alastruey, Jordi

N1 - Funding Information: AV was funded by FIR 2020 of the University of Ferrara. VC was funded by MIUR FFABR 2017. PC and JA acknowledge support from the EPSRC [EP/K031546/1], the BHF [PG/17/50/32903], the Wellcome/EPSRC Centre for Medical Engineering at King’s College London [WT 203148/Z/16/Z], the Department of Health through the National Institute for Health Research (NIHR) Cardiovascular MedTech Co-operative at Guy’s and St Thomas’ NHS Foundation Trust (GSTT) [MIC-2016-019], and the comprehensive Biomedical Research Centre and Clinical Research Facilities awards to Guy’s and St Thomas’ NHS Foundation Trust in partnership with King’s College London and King’s College Hospital NHS Foundation Trust. Publisher Copyright: 2023 Piccioli, Li, Valiani, Caleffi, Chowienczyk and Alastruey.

PY - 2023

Y1 - 2023

N2 - Background: Arterial stiffening and peripheral wave reflections have been considered the major determinants of raised pulse pressure (PP) and isolated systolic hypertension, but the importance of cardiac contractility and ventricular ejection dynamics is also recognised. Methods: We examined the contributions of arterial compliance and ventricular contractility to variations in aortic flow and increased central (cPP) and peripheral (pPP) pulse pressure, and PP amplification (PPa) in normotensive subjects during pharmacological modulation of physiology, in hypertensive subjects, and in silico using a cardiovascular model accounting for ventricular–aortic coupling. Reflections at the aortic root and from downstream vessels were quantified using emission and reflection coefficients, respectively. Results: cPP was strongly associated with contractility and compliance, whereas pPP and PPa were strongly associated with contractility. Increased contractility by inotropic stimulation increased peak aortic flow (323.9 ± 52.8 vs. 389.1 ± 65.1 ml/s), and the rate of increase (3193.6 ± 793.0 vs. 4848.3 ± 450.4 ml/s 2) in aortic flow, leading to larger cPP (36.1 ± 8.8 vs. 59.0 ± 10.8 mmHg), pPP (56.9 ± 13.1 vs. 93.0 ± 17.0 mmHg) and PPa (20.8 ± 4.8 vs. 34.0 ± 7.3 mmHg). Increased compliance by vasodilation decreased cPP (62.2 ± 20.2 vs. 45.2 ± 17.8 mmHg) without altering (Formula presented.), pPP or PPa. The emission coefficient changed with increasing cPP, but the reflection coefficient did not. These results agreed with in silico data obtained by independently changing contractility/compliance over the range observed in vivo. Conclusions: Ventricular contractility plays a key role in raising and amplifying PP, by altering aortic flow wave morphology.

AB - Background: Arterial stiffening and peripheral wave reflections have been considered the major determinants of raised pulse pressure (PP) and isolated systolic hypertension, but the importance of cardiac contractility and ventricular ejection dynamics is also recognised. Methods: We examined the contributions of arterial compliance and ventricular contractility to variations in aortic flow and increased central (cPP) and peripheral (pPP) pulse pressure, and PP amplification (PPa) in normotensive subjects during pharmacological modulation of physiology, in hypertensive subjects, and in silico using a cardiovascular model accounting for ventricular–aortic coupling. Reflections at the aortic root and from downstream vessels were quantified using emission and reflection coefficients, respectively. Results: cPP was strongly associated with contractility and compliance, whereas pPP and PPa were strongly associated with contractility. Increased contractility by inotropic stimulation increased peak aortic flow (323.9 ± 52.8 vs. 389.1 ± 65.1 ml/s), and the rate of increase (3193.6 ± 793.0 vs. 4848.3 ± 450.4 ml/s 2) in aortic flow, leading to larger cPP (36.1 ± 8.8 vs. 59.0 ± 10.8 mmHg), pPP (56.9 ± 13.1 vs. 93.0 ± 17.0 mmHg) and PPa (20.8 ± 4.8 vs. 34.0 ± 7.3 mmHg). Increased compliance by vasodilation decreased cPP (62.2 ± 20.2 vs. 45.2 ± 17.8 mmHg) without altering (Formula presented.), pPP or PPa. The emission coefficient changed with increasing cPP, but the reflection coefficient did not. These results agreed with in silico data obtained by independently changing contractility/compliance over the range observed in vivo. Conclusions: Ventricular contractility plays a key role in raising and amplifying PP, by altering aortic flow wave morphology.

UR - http://www.scopus.com/inward/record.url?scp=85164566593&partnerID=8YFLogxK

U2 - 10.3389/fcvm.2023.1197842

DO - 10.3389/fcvm.2023.1197842

M3 - Article

SN - 2297-055X

VL - 10

JO - Frontiers in Cardiovascular Medicine

JF - Frontiers in Cardiovascular Medicine

M1 - 1197842

ER -