Ultra-high sensitivity cardiac troponin-I concentration and left ventricular structure and function in women with ischemia and no obstructive coronary artery disease.
Cardiomyocyte injury
Diastolic strain
Ischemia and no obstructive coronary artery disease (INOCA)
Left ventricular dysfunction
Left ventricular mass
Ultra-high sensitivity cardiac troponin
Journal
American heart journal plus : cardiology research and practice
ISSN: 2666-6022
Titre abrégé: Am Heart J Plus
Pays: United States
ID NLM: 101779333
Informations de publication
Date de publication:
Jan 2022
Jan 2022
Historique:
entrez:
5
7
2022
pubmed:
6
7
2022
medline:
6
7
2022
Statut:
ppublish
Résumé
Women are disproportionally impacted by ischemia and no obstructive coronary artery disease (INOCA), and such women are at increased risk of developing heart failure with preserved ejection fraction (HFpEF), however the mechanisms linking these conditions remain poorly understood. The aim of this study was to determine whether ultra-high sensitivity cardiac troponin I (u-hscTnI), an indicator of cardiomyocyte injury, is associated with abnormalities in myocardial perfusion and left ventricular (LV) structure and function in women with INOCA. 327 women with INOCA enrolled in the Women's Ischemia Syndrome Evaluation-Coronary Vascular Dysfunction (WISE-CVD) study underwent vasodilator stress cardiac magnetic resonance imaging (CMRI) and u-hscTnI measurements (Simoa HD-1 Analyzer, Quanterix Corporation). Multivariable linear regression was used to evaluate associations between u-hscTnI concentrations and myocardial perfusion (MPRI), LV mass index and feature-tracking derived strain measures of LV function. u-hscTnI concentrations were quantifiable in 100% of the cohort and ranged from 0.004 to 79.6 pg/mL. In adjusted models, u-hscTnI was associated with LV mass index (+2.03; 95% CI 1.17, 2.89; Together, these findings support cardiomyocyte injury as a putative pathway towards adverse LV remodeling and dysfunction; however, further research is needed to define the specific mechanism(s) driving myocellular injury in INOCA.
Identifiants
pubmed: 35784010
doi: 10.1016/j.ahjo.2022.100115
pmc: PMC9246284
mid: NIHMS1793529
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : NHLBI NIH HHS
ID : K23 HL151867
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL146158
Pays : United States
Organisme : NIA NIH HHS
ID : U54 AG065141
Pays : United States
Déclaration de conflit d'intérêts
Declaration of competing interest Dr. Bairey Merz serves as Board of Director for iRhythm, fees paid through CSMC from Abbott Diagnostics and Sanofi.
Références
J Invasive Cardiol. 2018 Nov;30(11):406-410
pubmed: 30373950
J Am Coll Cardiol. 2006 Feb 7;47(3 Suppl):S4-S20
pubmed: 16458170
Atherosclerosis. 2014 Sep;236(1):207-14
pubmed: 25075937
Circ Cardiovasc Imaging. 2014 May;7(3):510-6
pubmed: 24633782
Eur Heart J. 2020 Jul 1;41(25):2366-2375
pubmed: 32221588
Am J Physiol Heart Circ Physiol. 2016 Jan 1;310(1):H14-9
pubmed: 26519031
Am J Cardiol. 2017 Jun 15;119(12):2017-2020
pubmed: 28477861
Clin Chem. 2019 Mar;65(3):484-489
pubmed: 30626631
Clin Chem. 2015 Oct;61(10):1283-91
pubmed: 26283690
Am Heart J. 2020 Feb;220:224-236
pubmed: 31884245
JACC Cardiovasc Imaging. 2010 Oct;3(10):1030-6
pubmed: 20947048
Circ Cardiovasc Imaging. 2015 Apr;8(4):
pubmed: 25801710
Eur Heart J. 2013 Aug;34(30):2354-61
pubmed: 23644181
Am J Cardiol. 2001 Apr 15;87(8):937-41; A3
pubmed: 11305981
Biomarkers. 2018 Dec;23(8):725-734
pubmed: 29976112
J Am Coll Cardiol. 2013 Aug 13;62(7):632-40
pubmed: 23644085
J Am Heart Assoc. 2020 Aug 18;9(16):e017221
pubmed: 32757795
Clin Chem Lab Med. 2015 Apr;53(5):635-52
pubmed: 25252753
Int J Cardiol. 2021 Mar 15;327:25-30
pubmed: 33202262
Eur J Clin Invest. 2015 Aug;45(8):842-9
pubmed: 26077878
Circulation. 2017 Mar 14;135(11):1075-1092
pubmed: 28289007
J Cardiovasc Magn Reson. 2009 Dec 21;11:55
pubmed: 20025732
Eur Heart J. 2018 Mar 7;39(10):840-849
pubmed: 29293969
J Am Coll Cardiol. 1998 Nov;32(5):1454-9
pubmed: 9809962
J Am Heart Assoc. 2018 Feb 21;7(5):
pubmed: 29467150
Am Heart J. 2001 May;141(5):735-41
pubmed: 11320360
Circulation. 2011 Apr 5;123(13):1367-76
pubmed: 21422391
JACC Heart Fail. 2018 Mar;6(3):187-197
pubmed: 29331272
Clin Biochem. 2015 Mar;48(4-5):358-9
pubmed: 25482854
N Engl J Med. 2009 Dec 24;361(26):2538-47
pubmed: 19940289
Arterioscler Thromb Vasc Biol. 2020 Dec;40(12):3015-3021
pubmed: 33028098
Eur Heart J. 2018 Oct 1;39(37):3439-3450
pubmed: 30165580
J Am Coll Cardiol. 2019 Dec 10;74(23):2858-2873
pubmed: 31806129
Circulation. 2001 Aug 7;104(6):735-40
pubmed: 11489784
Clin Chem. 2010 Aug;56(8):1357-9
pubmed: 20525763
JAMA. 2010 Dec 8;304(22):2503-12
pubmed: 21139111
JAMA Cardiol. 2019 Oct 1;4(10):997-1006
pubmed: 31483438
Biochem Med (Zagreb). 2018 Oct 15;28(3):030501
pubmed: 30429666
Clin Cardiol. 2017 May;40(5):300-306
pubmed: 28004395
J Am Coll Cardiol. 2006 Feb 7;47(3 Suppl):S21-9
pubmed: 16458167
Circulation. 2018 Feb 20;137(8):874-876
pubmed: 29459474
Int J Cardiol. 2016 Nov 15;223:936-939
pubmed: 27589041
J Am Coll Cardiol. 2008 Dec 16;52(25):2148-55
pubmed: 19095132
Anatol J Cardiol. 2015 Mar;15(3):264-5
pubmed: 25880185
Circulation. 2017 Apr 18;135(16):1494-1505
pubmed: 28159799
Circulation. 2007 Sep 11;116(11):1242-9
pubmed: 17698733
Hypertension. 2001 Dec 1;38(6):1406-12
pubmed: 11751726
BMJ Case Rep. 2010 Jul 15;2010:
pubmed: 22752944