Influence of heart rate on FFR measurements: An experimental and clinical validation study.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
15 Oct 2020
Historique:
received: 12 05 2020
accepted: 27 05 2020
pubmed: 7 6 2020
medline: 15 5 2021
entrez: 7 6 2020
Statut: ppublish

Résumé

Functional lesion assessment in stable coronary disease is considered the gold standard. The result of fractional flow reserve (FFR) in stable coronary disease is often a decision-maker for patient qualification. Taking into account the paramount position of FFR, it is crucial to acknowledge and reduce all potential bias. In the present study, we quantified the influence of elevated HR on FFR results using a preclinical model and then validated the results in a clinical setting. The relationship between FFR and HR was first explored experimentally in a porcine model. A clinical validation study was conducted in patients with isolated moderate lesions in the left anterior descending artery (LAD) or right coronary artery (RCA). In both the experimental and clinical arms, FFR was measured at resting HR and with pacing at 100, 130, 160, and 180 (for pigs) beats per minute. In the porcine model and in the clinical settings, a significant correlation between FFR and HR was confirmed in the LAD (r = 0.89, p < .0001; r = 0.53, p = .00002), but not in the RCA (r = -0.19, p = .5; r = 0.14, p = .3). Post hoc analyses revealed that the FFR values in the LAD at 130/min and above tended to be significantly different from the baseline HR. The results of this study indicate that in an experimental setting, tachycardia might be responsible for an overestimation of FFR results in LAD lesions.

Sections du résumé

BACKGROUND BACKGROUND
Functional lesion assessment in stable coronary disease is considered the gold standard. The result of fractional flow reserve (FFR) in stable coronary disease is often a decision-maker for patient qualification. Taking into account the paramount position of FFR, it is crucial to acknowledge and reduce all potential bias.
AIMS OBJECTIVE
In the present study, we quantified the influence of elevated HR on FFR results using a preclinical model and then validated the results in a clinical setting.
METHODS AND RESULTS RESULTS
The relationship between FFR and HR was first explored experimentally in a porcine model. A clinical validation study was conducted in patients with isolated moderate lesions in the left anterior descending artery (LAD) or right coronary artery (RCA). In both the experimental and clinical arms, FFR was measured at resting HR and with pacing at 100, 130, 160, and 180 (for pigs) beats per minute. In the porcine model and in the clinical settings, a significant correlation between FFR and HR was confirmed in the LAD (r = 0.89, p < .0001; r = 0.53, p = .00002), but not in the RCA (r = -0.19, p = .5; r = 0.14, p = .3). Post hoc analyses revealed that the FFR values in the LAD at 130/min and above tended to be significantly different from the baseline HR.
CONCLUSIONS CONCLUSIONS
The results of this study indicate that in an experimental setting, tachycardia might be responsible for an overestimation of FFR results in LAD lesions.

Identifiants

pubmed: 32504716
pii: S0167-5273(20)32802-3
doi: 10.1016/j.ijcard.2020.05.089
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

13-17

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors have no conflicts of interest to declare.

Auteurs

Przemysław J Kwasiborski (PJ)

Third Department of Internal Medicine and Cardiology, Second Faculty of Medicine, Medical University of Warsaw, Warsaw, Poland. Electronic address: pkwasiborski77@gmail.com.

Wojciech Czerwiński (W)

Center for Cardiovascular Research and Development, American Heart of Poland S.A., Poland.

Paweł Kowalczyk (P)

Medical University of Warsaw, Biophysics Department, Warsaw, Poland.

Małgorzata Buksińska-Lisik (M)

Third Department of Internal Medicine and Cardiology, Second Faculty of Medicine, Medical University of Warsaw, Warsaw, Poland.

Grzegorz Horszczaruk (G)

Angiology and Hemodynamics Laboratory, MSSW, Warsaw, Poland.

Michael S Aboodi (MS)

Department of Medicine, Montefiore Medical Center, NY, USA.

Kamil Derbisz (K)

Center for Cardiovascular Research and Development, American Heart of Poland S.A., Poland.

Mariusz Hochul (M)

Center for Cardiovascular Research and Development, American Heart of Poland S.A., Poland.

Adam Janas (A)

Center for Cardiovascular Research and Development, American Heart of Poland S.A., Poland.

Andrzej Cwetsch (A)

Department of Cardiology, Military Institute of Medicine, Szaserów 128, 04-141, Warsaw 44, Poland.

Wojciech Wąsek (W)

Faculty of Medicine, University of Rzeszów, Poland.

Piotr P Buszman (PP)

Center for Cardiovascular Research and Development, American Heart of Poland S.A., Poland.

Jozef Bartunek (J)

Cardiology Department, Andrzej-Frycz Modrzewski Kraków University, Kraków, Poland.

Paweł E Buszman (PE)

Cardiovascular Center, OLV Hospital Aalst, Belgium.

Patrick W Serruys (PW)

Imperial College London, Kensington, London, UK.

Krzysztof Milewski (K)

The Jerzy Kukuczka Academy of Physical Education, Faculty of Physiotherapy, Poland.

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Classifications MeSH