Increased Excess Pressure After Creation of an Arteriovenous Fistula in End-Stage Renal Disease.


Journal

American journal of hypertension
ISSN: 1941-7225
Titre abrégé: Am J Hypertens
Pays: United States
ID NLM: 8803676

Informations de publication

Date de publication:
01 02 2022
Historique:
received: 12 04 2021
revised: 12 09 2021
accepted: 14 10 2021
pubmed: 17 10 2021
medline: 21 4 2022
entrez: 16 10 2021
Statut: ppublish

Résumé

Reservoir-wave analysis (RWA) separates the arterial waveform into reservoir and excess pressure (XSP) components, where XSP is analogous to flow and related to left ventricular workload. RWA provides more detailed information about the arterial tree than traditional blood pressure (BP) parameters. In end-stage renal disease (ESRD), we have previously shown that XSP is associated with increased mortality and is higher in patients with arteriovenous fistula (AVF). In this study, we examined whether XSP increases after creation of an AVF in ESRD. Before and after a mean of 3.9 ± 1.2 months following creation of AVF, carotid pressure waves were recorded using arterial tonometry. XSP and its integral (XSPI) were derived using RWA through pressure wave analysis alone. Aortic stiffness was assessed by carotid-femoral pulse wave velocity (CF-PWV). In 38 patients (63% male, age 59 ± 15 years), after AVF creation, brachial diastolic BP decreased (79 ± 10 vs. 72 ± 12 mm Hg, P = 0.002), but the reduction in systolic BP, was not statistically significant (133 ± 20 vs. 127 ± 26 mm Hg, P = 0.137). However, carotid XSP (14 [12-19] to 17 [12-22] mm Hg, P = 0.031) and XSPI increased significantly (275 [212-335] to 334 [241-439] kPa∙s, P = 0.015), despite a reduction in CF-PWV (13 ± 3.6 vs. 12 ± 3.5 m/s, P = 0.025). Creation of an AVF resulted in increased XSP in this population, despite improvement in diastolic BP and aortic stiffness. These findings underline the complex hemodynamic impact of AVF on the cardiovascular system.

Sections du résumé

BACKGROUND
Reservoir-wave analysis (RWA) separates the arterial waveform into reservoir and excess pressure (XSP) components, where XSP is analogous to flow and related to left ventricular workload. RWA provides more detailed information about the arterial tree than traditional blood pressure (BP) parameters. In end-stage renal disease (ESRD), we have previously shown that XSP is associated with increased mortality and is higher in patients with arteriovenous fistula (AVF). In this study, we examined whether XSP increases after creation of an AVF in ESRD.
METHODS
Before and after a mean of 3.9 ± 1.2 months following creation of AVF, carotid pressure waves were recorded using arterial tonometry. XSP and its integral (XSPI) were derived using RWA through pressure wave analysis alone. Aortic stiffness was assessed by carotid-femoral pulse wave velocity (CF-PWV).
RESURLTS
In 38 patients (63% male, age 59 ± 15 years), after AVF creation, brachial diastolic BP decreased (79 ± 10 vs. 72 ± 12 mm Hg, P = 0.002), but the reduction in systolic BP, was not statistically significant (133 ± 20 vs. 127 ± 26 mm Hg, P = 0.137). However, carotid XSP (14 [12-19] to 17 [12-22] mm Hg, P = 0.031) and XSPI increased significantly (275 [212-335] to 334 [241-439] kPa∙s, P = 0.015), despite a reduction in CF-PWV (13 ± 3.6 vs. 12 ± 3.5 m/s, P = 0.025).
CONCLUSIONS
Creation of an AVF resulted in increased XSP in this population, despite improvement in diastolic BP and aortic stiffness. These findings underline the complex hemodynamic impact of AVF on the cardiovascular system.

Identifiants

pubmed: 34655294
pii: 6398596
doi: 10.1093/ajh/hpab161
pmc: PMC8807157
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

149-155

Subventions

Organisme : CIHR
ID : NET-54008
Pays : Canada

Informations de copyright

© American Journal of Hypertension, Ltd 2021. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

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Auteurs

Mathilde Paré (M)

CHU de Québec Research Center, L'Hôtel-Dieu de Québec Hospital, Québec City, Québec, Canada.
Division of Nephrology, Department of Medicine, Faculty of Medicine, Université Laval, Québec, Québec, Canada.

Rémi Goupil (R)

Hôpital du Sacré-Cœur de Montréal, Department of Medicine, Montréal, Québec, Canada.

Catherine Fortier (C)

CHU de Québec Research Center, L'Hôtel-Dieu de Québec Hospital, Québec City, Québec, Canada.
Division of Nephrology, Department of Medicine, Faculty of Medicine, Université Laval, Québec, Québec, Canada.
INSERM-U970-Paris Cardiovascular Research Center (PARCC), Paris, France.

Fabrice Mac-Way (F)

CHU de Québec Research Center, L'Hôtel-Dieu de Québec Hospital, Québec City, Québec, Canada.
Division of Nephrology, Department of Medicine, Faculty of Medicine, Université Laval, Québec, Québec, Canada.

François Madore (F)

Hôpital du Sacré-Cœur de Montréal, Department of Medicine, Montréal, Québec, Canada.

Bernhard Hametner (B)

Center for Health & Bioresources, Department of Health and Environment, AIT Austrian Institute of Technology, Vienna, Austria.

Siegfried Wassertheurer (S)

Center for Health & Bioresources, Department of Health and Environment, AIT Austrian Institute of Technology, Vienna, Austria.

Martin G Schultz (MG)

Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia.

James E Sharman (JE)

Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia.

Mohsen Agharazii (M)

CHU de Québec Research Center, L'Hôtel-Dieu de Québec Hospital, Québec City, Québec, Canada.
Division of Nephrology, Department of Medicine, Faculty of Medicine, Université Laval, Québec, Québec, Canada.

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