Hyperglycemia, inflammatory response and infarct size in obstructive acute myocardial infarction and MINOCA.
Aged
Aged, 80 and over
Biomarkers
/ blood
Blood Glucose
/ metabolism
Blood Platelets
C-Reactive Protein
/ metabolism
Coronary Angiography
Female
Heart Disease Risk Factors
Humans
Hyperglycemia
/ blood
Inflammation
/ blood
Inflammation Mediators
/ blood
Italy
/ epidemiology
Lymphocyte Count
Lymphocytes
Male
Middle Aged
Myocardial Infarction
/ blood
Myocardium
/ pathology
Neutrophils
Platelet Count
Predictive Value of Tests
Risk Assessment
Stroke Volume
Troponin I
/ blood
Ventricular Function, Left
Hyperglycemia
Infarct size
Inflammation
MINOCA
Obstructive acute myocardial infarction
Journal
Cardiovascular diabetology
ISSN: 1475-2840
Titre abrégé: Cardiovasc Diabetol
Pays: England
ID NLM: 101147637
Informations de publication
Date de publication:
02 02 2021
02 02 2021
Historique:
received:
23
10
2020
accepted:
20
01
2021
entrez:
3
2
2021
pubmed:
4
2
2021
medline:
6
10
2021
Statut:
epublish
Résumé
Hyperglycemia has been associated with increased inflammatory indexes and larger infarct sizes in patients with obstructive acute myocardial infarction (obs-AMI). In contrast, no studies have explored these correlations in non-obstructive acute myocardial infarction (MINOCA). We investigated the relationship between hyperglycemia, inflammation and infarct size in a cohort of AMI patients that included MINOCA. Patients with AMI undergoing coronary angiography between 2016 and 2020 were enrolled. The following inflammatory markers were evaluated: C-reactive protein, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and neutrophil-to-platelet ratio (NPR). Myocardial infarct size was measured by peak high sensitivity troponin I (Hs-TnI) levels, left-ventricular-end-diastolic-volume (LVEDV) and left ventricular ejection fraction (LVEF). The final study population consisted of 2450 patients with obs-AMI and 239 with MINOCA. Hyperglycemia was more prevalent among obs-AMI cases. In all hyperglycemic patients-obs-AMI and MINOCA-NLR, NPR, and LPR were markedly altered. Hyperglycemic obs-AMI subjects exhibited a higher Hs-TnI (p < 0.001), a larger LVEDV (p = 0.003) and a lower LVEF (p < 0.001) compared to normoglycemic ones. Conversely, MINOCA patients showed a trivial myocardial damage, irrespective of admission glucose levels. Our data confirm the association of hyperglycemic obs-AMI with elevated inflammatory markers and larger infarct sizes. MINOCA patients exhibited modest myocardial damage, regardless of admission glucose levels.
Sections du résumé
BACKGROUND
Hyperglycemia has been associated with increased inflammatory indexes and larger infarct sizes in patients with obstructive acute myocardial infarction (obs-AMI). In contrast, no studies have explored these correlations in non-obstructive acute myocardial infarction (MINOCA). We investigated the relationship between hyperglycemia, inflammation and infarct size in a cohort of AMI patients that included MINOCA.
METHODS
Patients with AMI undergoing coronary angiography between 2016 and 2020 were enrolled. The following inflammatory markers were evaluated: C-reactive protein, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and neutrophil-to-platelet ratio (NPR). Myocardial infarct size was measured by peak high sensitivity troponin I (Hs-TnI) levels, left-ventricular-end-diastolic-volume (LVEDV) and left ventricular ejection fraction (LVEF).
RESULTS
The final study population consisted of 2450 patients with obs-AMI and 239 with MINOCA. Hyperglycemia was more prevalent among obs-AMI cases. In all hyperglycemic patients-obs-AMI and MINOCA-NLR, NPR, and LPR were markedly altered. Hyperglycemic obs-AMI subjects exhibited a higher Hs-TnI (p < 0.001), a larger LVEDV (p = 0.003) and a lower LVEF (p < 0.001) compared to normoglycemic ones. Conversely, MINOCA patients showed a trivial myocardial damage, irrespective of admission glucose levels.
CONCLUSIONS
Our data confirm the association of hyperglycemic obs-AMI with elevated inflammatory markers and larger infarct sizes. MINOCA patients exhibited modest myocardial damage, regardless of admission glucose levels.
Identifiants
pubmed: 33530978
doi: 10.1186/s12933-021-01222-9
pii: 10.1186/s12933-021-01222-9
pmc: PMC7856791
doi:
Substances chimiques
Biomarkers
0
Blood Glucose
0
Inflammation Mediators
0
Troponin I
0
C-Reactive Protein
9007-41-4
Types de publication
Comparative Study
Journal Article
Multicenter Study
Observational Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
33Références
Diabetes Care. 2019 Oct;42(10):1946-1955
pubmed: 30796109
Integr Med Res. 2018 Jun;7(2):192-199
pubmed: 29984180
Neth Heart J. 2019 May;27(5):237-245
pubmed: 30689112
Diabetes. 2014 Jul;63(7):2474-85
pubmed: 24584550
Cardiovasc Diabetol. 2019 May 31;18(1):66
pubmed: 31151453
Cardiovasc Diabetol. 2019 Oct 31;18(1):142
pubmed: 31672144
J Intern Med. 2013 Feb;273(2):189-96
pubmed: 22742529
Ther Adv Cardiovasc Dis. 2015 Dec;9(6):412-24
pubmed: 26194489
Diabetol Metab Syndr. 2017 Mar 21;9:20
pubmed: 28344659
Am J Med Sci. 2012 Apr;343(4):321-6
pubmed: 21946827
Diabetes Res Clin Pract. 2010 Apr;88(1):97-102
pubmed: 20083319
Cardiovasc Diabetol. 2019 Mar 28;18(1):42
pubmed: 30922303
Am Heart J. 2010 Sep;160(3):412-9
pubmed: 20826247
Clin Cardiol. 2019 Jan;42(1):111-119
pubmed: 30443916
Eur Heart J. 2018 Jan 7;39(2):119-177
pubmed: 28886621
J Am Heart Assoc. 2016 Dec 16;5(12):
pubmed: 27986756
Endocrinology. 2007 Jan;148(1):241-51
pubmed: 17038556
Circulation. 2011 Aug 9;124(6):704-11
pubmed: 21768543
Int J Mol Sci. 2017 Oct 16;18(10):
pubmed: 29035323
Annu Rev Immunol. 2009;27:165-97
pubmed: 19302038
Endocrine. 2004 Mar-Apr;23(2-3):177-82
pubmed: 15146098
Lancet. 2000 Mar 4;355(9206):773-8
pubmed: 10711923
Annu Rev Pathol. 2008;3:99-126
pubmed: 18039143
Diabetes Care. 2003 Nov;26(11):3129-35
pubmed: 14578250
Cardiovasc Diabetol. 2020 Jul 4;19(1):101
pubmed: 32622355
Crit Care. 2013 Mar 06;17(2):305
pubmed: 23470218
Eur Heart J Cardiovasc Imaging. 2015 Mar;16(3):233-70
pubmed: 25712077
Sci Rep. 2017 Jan 10;7:40426
pubmed: 28071752
Diab Vasc Dis Res. 2020 Jan-Feb;17(1):1479164119883983
pubmed: 31726871
Circulation. 2008 Mar 25;117(12):1610-9
pubmed: 18299505
Cardiovasc Diabetol. 2019 Feb 28;18(1):22
pubmed: 30819191
Europace. 2020 Sep 1;22(9):1303-1310
pubmed: 32894280
Circ Res. 2010 Oct 29;107(9):1058-70
pubmed: 21030723
Am J Physiol Endocrinol Metab. 2014 Nov 15;307(10):E896-905
pubmed: 25205821
Neurosci Lett. 2000 Jan 7;278(1-2):1-4
pubmed: 10643786
Cardiovasc Diabetol. 2020 Jul 8;19(1):109
pubmed: 32641042
Circulation. 2019 Apr 30;139(18):e891-e908
pubmed: 30913893
Eur Heart J Cardiovasc Pharmacother. 2015 Oct;1(4):220-8
pubmed: 27532445
Eur Heart J Acute Cardiovasc Care. 2019 Dec;8(8):727-737
pubmed: 28777005
Ren Fail. 2012;34(2):155-9
pubmed: 22172001
Kardiol Pol. 2017;75(7):666-673
pubmed: 28394006
Diabetes Care. 2019 Jan;42(Suppl 1):S13-S28
pubmed: 30559228
Front Pharmacol. 2020 Jan 31;10:1606
pubmed: 32082147
Eur Heart J. 2009 Dec;30(23):2869-79
pubmed: 19696191
BMC Cardiovasc Disord. 2016 May 23;16:102
pubmed: 27216220
Eur J Prev Cardiol. 2020 Dec;27(19):2338-2340
pubmed: 31841054
Trends Cardiovasc Med. 2021 Jan;31(1):49-56
pubmed: 31882264
Eur Heart J. 2017 Jan 14;38(3):143-153
pubmed: 28158518
Circ Cardiovasc Imaging. 2012 Nov;5(6):708-18
pubmed: 23051889
Cardiovasc Revasc Med. 2016 Mar;17(2):119-28
pubmed: 26905055