Intracoronary Saline‐Induced Hyperemia During Coronary Thermodilution Measurements of Absolute Coronary Blood Flow: An Animal Mechanistic Study

Background Absolute hyperemic coronary blood flow and microvascular resistances can be measured by continuous thermodilution with a dedicated infusion catheter. We aimed to determine the mechanisms of this hyperemic response in animal. Methods and Results Twenty open chest pigs were instrumented wit...

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Main Authors: Julien Adjedj, Fabien Picard, Carlos Collet, Patrick Bruneval, Stephane Fournier, Alain Bize, Lucien Sambin, Alain Berdeaux, Olivier Varenne, Bernard De Bruyne, Bijan Ghaleh
Format: Article
Language:English
Published: Wiley 2020-08-01
Series:Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Subjects:
Online Access:https://www.ahajournals.org/doi/10.1161/JAHA.120.015793
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author Julien Adjedj
Fabien Picard
Carlos Collet
Patrick Bruneval
Stephane Fournier
Alain Bize
Lucien Sambin
Alain Berdeaux
Olivier Varenne
Bernard De Bruyne
Bijan Ghaleh
author_facet Julien Adjedj
Fabien Picard
Carlos Collet
Patrick Bruneval
Stephane Fournier
Alain Bize
Lucien Sambin
Alain Berdeaux
Olivier Varenne
Bernard De Bruyne
Bijan Ghaleh
author_sort Julien Adjedj
collection DOAJ
description Background Absolute hyperemic coronary blood flow and microvascular resistances can be measured by continuous thermodilution with a dedicated infusion catheter. We aimed to determine the mechanisms of this hyperemic response in animal. Methods and Results Twenty open chest pigs were instrumented with flow probes on coronary arteries. The following possible mechanisms of saline‐induced hyperemia were explored compared with maximal hyperemia achieve with adenosine by testing: (1) various infusion rates; (2) various infusion content and temperature; (3) NO production inhibition with L‐arginine methyl ester and endothelial denudation; (4) effects of vibrations generated by rotational atherectomy and of infusion through one end‐hole versus side‐holes. Saline infusion rates of 5, 10 and 15 mL/min did not reach maximal hyperemia as compared with adenosine. Percentage of coronary blood flow expressed in percent of the coronary blood flow after adenosine were 48±17% at baseline, 57±18% at 5 mL/min, 65±17% at 10 mL/min, 82±26% at 15 mL/min and 107±18% at 20 mL/min. Maximal hyperemia was observed during infusion of both saline at body temperature and glucose 5%, after endothelial denudation, l‐arginine methyl ester administration, and after stent implantation. The activation of a Rota burr in the first millimeters of the epicardial artery also induced maximal hyperemia. Maximal hyperemia was achieved by infusion through lateral side‐holes but not through an end‐hole catheter. Conclusions Infusion of saline at 20 mL/min through a catheter with side holes in the first millimeters of the epicardial artery induces maximal hyperemia. The data indicate that this vasodilation is related neither to the composition/temperature of the indicator nor is it endothelial mediated. It is suggested that it could be elicited by epicardial wall vibrations.
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spelling doaj.art-6c56784db948496b9c8fb7811614f1b52022-12-21T23:46:22ZengWileyJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease2047-99802020-08-0191510.1161/JAHA.120.015793Intracoronary Saline‐Induced Hyperemia During Coronary Thermodilution Measurements of Absolute Coronary Blood Flow: An Animal Mechanistic StudyJulien Adjedj0Fabien Picard1Carlos Collet2Patrick Bruneval3Stephane Fournier4Alain Bize5Lucien Sambin6Alain Berdeaux7Olivier Varenne8Bernard De Bruyne9Bijan Ghaleh10Department of Cardiology Institut Arnault Tzanck Saint Laurent du Var FranceFaculté de Médecine Paris Descartes Université Paris Descartes Paris FranceCardiovascular Center Aalst, OLV Clinic Aalst BelgiumUMR 970 Inserm Paris Cardiovascular Research Center Hôpital Européen Georges Pompidou Paris FranceDepartment of Cardiology Lausanne University Center Hospital Lausanne SwitzerlandU955‐IMRB Equipe 03 Inserm UPEC Ecole Nationale Vétérinaire d’Alfort Maisons‐Alfort FranceU955‐IMRB Equipe 03 Inserm UPEC Ecole Nationale Vétérinaire d’Alfort Maisons‐Alfort FranceU955‐IMRB Equipe 03 Inserm UPEC Ecole Nationale Vétérinaire d’Alfort Maisons‐Alfort FranceFaculté de Médecine Paris Descartes Université Paris Descartes Paris FranceDepartment of Cardiology Lausanne University Center Hospital Lausanne SwitzerlandU955‐IMRB Equipe 03 Inserm UPEC Ecole Nationale Vétérinaire d’Alfort Maisons‐Alfort FranceBackground Absolute hyperemic coronary blood flow and microvascular resistances can be measured by continuous thermodilution with a dedicated infusion catheter. We aimed to determine the mechanisms of this hyperemic response in animal. Methods and Results Twenty open chest pigs were instrumented with flow probes on coronary arteries. The following possible mechanisms of saline‐induced hyperemia were explored compared with maximal hyperemia achieve with adenosine by testing: (1) various infusion rates; (2) various infusion content and temperature; (3) NO production inhibition with L‐arginine methyl ester and endothelial denudation; (4) effects of vibrations generated by rotational atherectomy and of infusion through one end‐hole versus side‐holes. Saline infusion rates of 5, 10 and 15 mL/min did not reach maximal hyperemia as compared with adenosine. Percentage of coronary blood flow expressed in percent of the coronary blood flow after adenosine were 48±17% at baseline, 57±18% at 5 mL/min, 65±17% at 10 mL/min, 82±26% at 15 mL/min and 107±18% at 20 mL/min. Maximal hyperemia was observed during infusion of both saline at body temperature and glucose 5%, after endothelial denudation, l‐arginine methyl ester administration, and after stent implantation. The activation of a Rota burr in the first millimeters of the epicardial artery also induced maximal hyperemia. Maximal hyperemia was achieved by infusion through lateral side‐holes but not through an end‐hole catheter. Conclusions Infusion of saline at 20 mL/min through a catheter with side holes in the first millimeters of the epicardial artery induces maximal hyperemia. The data indicate that this vasodilation is related neither to the composition/temperature of the indicator nor is it endothelial mediated. It is suggested that it could be elicited by epicardial wall vibrations.https://www.ahajournals.org/doi/10.1161/JAHA.120.015793absolute coronary flowadenosinecoronary hyperemiacoronary thermodilutionendothelial shear stressrotational atherectomy
spellingShingle Julien Adjedj
Fabien Picard
Carlos Collet
Patrick Bruneval
Stephane Fournier
Alain Bize
Lucien Sambin
Alain Berdeaux
Olivier Varenne
Bernard De Bruyne
Bijan Ghaleh
Intracoronary Saline‐Induced Hyperemia During Coronary Thermodilution Measurements of Absolute Coronary Blood Flow: An Animal Mechanistic Study
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
absolute coronary flow
adenosine
coronary hyperemia
coronary thermodilution
endothelial shear stress
rotational atherectomy
title Intracoronary Saline‐Induced Hyperemia During Coronary Thermodilution Measurements of Absolute Coronary Blood Flow: An Animal Mechanistic Study
title_full Intracoronary Saline‐Induced Hyperemia During Coronary Thermodilution Measurements of Absolute Coronary Blood Flow: An Animal Mechanistic Study
title_fullStr Intracoronary Saline‐Induced Hyperemia During Coronary Thermodilution Measurements of Absolute Coronary Blood Flow: An Animal Mechanistic Study
title_full_unstemmed Intracoronary Saline‐Induced Hyperemia During Coronary Thermodilution Measurements of Absolute Coronary Blood Flow: An Animal Mechanistic Study
title_short Intracoronary Saline‐Induced Hyperemia During Coronary Thermodilution Measurements of Absolute Coronary Blood Flow: An Animal Mechanistic Study
title_sort intracoronary saline induced hyperemia during coronary thermodilution measurements of absolute coronary blood flow an animal mechanistic study
topic absolute coronary flow
adenosine
coronary hyperemia
coronary thermodilution
endothelial shear stress
rotational atherectomy
url https://www.ahajournals.org/doi/10.1161/JAHA.120.015793
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