The association between the extent of lipidic burden and delta-fractional flow reserve: analysis from coronary physiological and near-infrared spectroscopic measures.
Fractional flow reserve (FFR)
coronary artery disease
intravascular ultrasound
near-infrared spectroscopy (NIRS)
Journal
Cardiovascular diagnosis and therapy
ISSN: 2223-3652
Titre abrégé: Cardiovasc Diagn Ther
Pays: China
ID NLM: 101601613
Informations de publication
Date de publication:
Apr 2021
Apr 2021
Historique:
entrez:
10
5
2021
pubmed:
11
5
2021
medline:
11
5
2021
Statut:
ppublish
Résumé
Vulnerable plaque features including lipidic plaque have been shown to affect fractional flow reserve (FFR). Given that formation and propagation of lipid plaque is accompanied by endothelial dysfunction which impairs vascular tone, the degree of lipidic burden may affect vasoreactivity during hyperemia, potentially leading to reduced FFR. Our aim is to elucidate the relationship of the extent of lipidic plaque burden with coronary physiological vasoreactivity measure. We analyzed 89 subjects requeuing PCI due to angiographically intermediate coronary stenosis with FFR ≤0.80. Near-infrared spectroscopy (NIRS) and intravascular ultrasound were used to evaluate lipid-core burden index (LCBI) and atheroma volume at both target lesion (maxLCBI The averaged FFR and delta-FFR was 0.74 (0.69-0.77), and 0.17±0.05, respectively. On target lesion-based analysis, maxLCBI A greater amount of lipidic plaque burden at not only "target lesion" alone but "entire target vessel" was associated with a greater delta-FFR. The accumulation of lipidic plaque materials at both local site and entire vessel may impair hyperemia-induced vasoreactivity, which causes a reduced FFR.
Sections du résumé
BACKGROUND
BACKGROUND
Vulnerable plaque features including lipidic plaque have been shown to affect fractional flow reserve (FFR). Given that formation and propagation of lipid plaque is accompanied by endothelial dysfunction which impairs vascular tone, the degree of lipidic burden may affect vasoreactivity during hyperemia, potentially leading to reduced FFR. Our aim is to elucidate the relationship of the extent of lipidic plaque burden with coronary physiological vasoreactivity measure.
METHODS
METHODS
We analyzed 89 subjects requeuing PCI due to angiographically intermediate coronary stenosis with FFR ≤0.80. Near-infrared spectroscopy (NIRS) and intravascular ultrasound were used to evaluate lipid-core burden index (LCBI) and atheroma volume at both target lesion (maxLCBI
RESULTS
RESULTS
The averaged FFR and delta-FFR was 0.74 (0.69-0.77), and 0.17±0.05, respectively. On target lesion-based analysis, maxLCBI
CONCLUSIONS
CONCLUSIONS
A greater amount of lipidic plaque burden at not only "target lesion" alone but "entire target vessel" was associated with a greater delta-FFR. The accumulation of lipidic plaque materials at both local site and entire vessel may impair hyperemia-induced vasoreactivity, which causes a reduced FFR.
Identifiants
pubmed: 33968615
doi: 10.21037/cdt-20-1024
pii: cdt-11-02-362
pmc: PMC8102241
doi:
Types de publication
Journal Article
Langues
eng
Pagination
362-372Informations de copyright
2021 Cardiovascular Diagnosis and Therapy. All rights reserved.
Déclaration de conflit d'intérêts
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at: http://dx.doi.org/10.21037/cdt-20-1024). Kota Murai has received honoraria from Abbot, ZEON MEDICAL. Yu Kataoka serves as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from Jul 2019 to Jun 2021, and has received research support from Nipro and Abbott, and honoraria from Nipro, Abbott, Kowa, Amgen, Sanofi, Astellas, Takeda and Daiichi-Sankyo. The other author has no conflicts of interest to declare.
Références
Circulation. 2001 Oct 23;104(17):2003-6
pubmed: 11673336
JACC Cardiovasc Imaging. 2012 Mar;5(3 Suppl):S10-8
pubmed: 22421223
Nat Rev Cardiol. 2012 May 22;9(8):439-53
pubmed: 22614618
Lancet. 2019 Nov 2;394(10209):1629-1637
pubmed: 31570255
Eur Heart J. 2019 Jan 7;40(2):87-165
pubmed: 30165437
Eur Heart J. 1997 Apr;18(4):614-7
pubmed: 9129891
Heart. 2009 Sep;95(18):1525-30
pubmed: 19497916
JAMA. 2016 Dec 13;316(22):2373-2384
pubmed: 27846344
JACC Cardiovasc Interv. 2018 Oct 22;11(20):2058-2068
pubmed: 30336810
J Am Coll Cardiol. 2015 Apr 7;65(13):1273-1282
pubmed: 25835438
Circulation. 2006 Jul 25;114(4):e55-9
pubmed: 16864731
EuroIntervention. 2017 Jun 2;13(2):e185-e192
pubmed: 28134124
N Engl J Med. 2012 Sep 13;367(11):991-1001
pubmed: 22924638
J Am Coll Cardiol. 2017 May 2;69(17):2212-2241
pubmed: 28291663
Atherosclerosis. 2017 Mar;258:145-151
pubmed: 28168977
Arterioscler Thromb Vasc Biol. 2003 Feb 1;23(2):168-75
pubmed: 12588755
Atherosclerosis. 2009 Mar;203(1):178-84
pubmed: 18644595
J Am Coll Cardiol. 2018 Feb 6;71(5):499-509
pubmed: 29406855
JACC Cardiovasc Imaging. 2015 Jan;8(1):1-10
pubmed: 25592691
JACC Cardiovasc Imaging. 2008 Sep;1(5):638-48
pubmed: 19356494
JACC Cardiovasc Interv. 2013 Aug;6(8):838-46
pubmed: 23871513
Expert Rev Cardiovasc Ther. 2017 Oct;15(10):775-785
pubmed: 28846060
Circulation. 2001 Nov 13;104(20):2401-6
pubmed: 11705815
Int J Cardiovasc Imaging. 2015 Feb;31(2):247-57
pubmed: 25296909
Eur Heart J. 2013 Jul;34(27):2055-62
pubmed: 23396491
Circulation. 1992 Dec;86(6 Suppl):III12-19
pubmed: 1424046