Dysglycemia and increased left ventricle mass in normotensive patients admitted with a first myocardial infarction: prognostic implications of dysglycemia during 14 years of follow-up.
Aged
Biomarkers
/ blood
Blood Glucose
/ metabolism
Denmark
Echocardiography
Female
Follow-Up Studies
Glucose Metabolism Disorders
/ blood
Glucose Tolerance Test
Humans
Hypertrophy, Left Ventricular
/ diagnostic imaging
Male
Middle Aged
Myocardial Infarction
/ diagnosis
Patient Admission
Prognosis
Prospective Studies
Risk Assessment
Risk Factors
Time Factors
Ventricular Function, Left
Ventricular Remodeling
All-cause mortality
Diabetes
Dysglycemia
Left ventricle mass
Major adverse cardiovascular events
Normotensive
Oral glucose tolerance test
Journal
BMC cardiovascular disorders
ISSN: 1471-2261
Titre abrégé: BMC Cardiovasc Disord
Pays: England
ID NLM: 100968539
Informations de publication
Date de publication:
02 05 2019
02 05 2019
Historique:
received:
23
11
2018
accepted:
18
04
2019
entrez:
4
5
2019
pubmed:
3
5
2019
medline:
28
1
2020
Statut:
epublish
Résumé
Left ventricle mass (LVM) can be influenced by various conditions including hypertension and/or inherent cardiomyopathies. Dysglycemia is also thought to exert an anabolic effect on heart tissue by hyperinsulinemia and thereby promoting increased LVM. The primary aim of this study was to assess the influence of dysglycemia on LVM evaluated by an oral glucose tolerance test (OGTT) in patients admitted with a first myocardial infarction (MI) without hypertension. The secondary aim was to assess the impact of dysglycemia on major adverse cardiovascular events (MACE) and all-cause mortality during long-term follow-up. Patients admitted with a first MI without known history of hypertension were included. All patients without previously known type 2 diabetes mellitus (T2DM) had a standardized 2-hour OGTT performed and were categorized as: normal glucose tolerance (NGT), impaired fasting glucose (IFG)/impaired glucose tolerance (IGT) and newly detected T2DM (new T2DM). LVM was measured by echocardiography using Devereaux formula and indexed by body surface area. Multivariate linear regression analysis was used to assess the impact of confounders (dysglycemia by OGTT, known T2DM, age, sex and type of MI) on LVM. Cox proportional hazard model was used to assess the impact of dysglycemia on all-cause mortality and a composite endpoint of MACE (all-cause mortality, MI, revascularisation due to stable angina, coronary artery bypass graft, ischemic stroke or hemorrhagic stroke). Two-hundred-and-five patients were included and followed up to 14 years. In multivariate regression analysis, LVM was only significantly increased in patients categorized as new T2DM (β = 25.3; 95% CI [7.5-43.0]) and known T2DM (β = 37.3; 95% CI [10.0-64.5]) compared to patients with NGT. Patients with new T2DM showed higher rates of MACE and all-cause mortality compared to patients with IFG/IGT and NGT; however no significantly increased hazard ratio was detected. Dysglycemia is associated with increasing LVM in normotensive patients with a first acute myocardial infarction and the strongest association was observed in patients with new T2DM and patients with known T2DM. Dysglycemia in normotensive patients with a first MI is not an independent predictor of neither MACE nor all-cause mortality during long-term follow-up compared to normotensive patients without dysglycemia.
Sections du résumé
BACKGROUND
Left ventricle mass (LVM) can be influenced by various conditions including hypertension and/or inherent cardiomyopathies. Dysglycemia is also thought to exert an anabolic effect on heart tissue by hyperinsulinemia and thereby promoting increased LVM. The primary aim of this study was to assess the influence of dysglycemia on LVM evaluated by an oral glucose tolerance test (OGTT) in patients admitted with a first myocardial infarction (MI) without hypertension. The secondary aim was to assess the impact of dysglycemia on major adverse cardiovascular events (MACE) and all-cause mortality during long-term follow-up.
METHODS
Patients admitted with a first MI without known history of hypertension were included. All patients without previously known type 2 diabetes mellitus (T2DM) had a standardized 2-hour OGTT performed and were categorized as: normal glucose tolerance (NGT), impaired fasting glucose (IFG)/impaired glucose tolerance (IGT) and newly detected T2DM (new T2DM). LVM was measured by echocardiography using Devereaux formula and indexed by body surface area. Multivariate linear regression analysis was used to assess the impact of confounders (dysglycemia by OGTT, known T2DM, age, sex and type of MI) on LVM. Cox proportional hazard model was used to assess the impact of dysglycemia on all-cause mortality and a composite endpoint of MACE (all-cause mortality, MI, revascularisation due to stable angina, coronary artery bypass graft, ischemic stroke or hemorrhagic stroke).
RESULTS
Two-hundred-and-five patients were included and followed up to 14 years. In multivariate regression analysis, LVM was only significantly increased in patients categorized as new T2DM (β = 25.3; 95% CI [7.5-43.0]) and known T2DM (β = 37.3; 95% CI [10.0-64.5]) compared to patients with NGT. Patients with new T2DM showed higher rates of MACE and all-cause mortality compared to patients with IFG/IGT and NGT; however no significantly increased hazard ratio was detected.
CONCLUSIONS
Dysglycemia is associated with increasing LVM in normotensive patients with a first acute myocardial infarction and the strongest association was observed in patients with new T2DM and patients with known T2DM. Dysglycemia in normotensive patients with a first MI is not an independent predictor of neither MACE nor all-cause mortality during long-term follow-up compared to normotensive patients without dysglycemia.
Identifiants
pubmed: 31046690
doi: 10.1186/s12872-019-1084-5
pii: 10.1186/s12872-019-1084-5
pmc: PMC6498536
doi:
Substances chimiques
Biomarkers
0
Blood Glucose
0
Types de publication
Comparative Study
Journal Article
Observational Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
103Références
PLoS One. 2015 Nov 16;10(11):e0142045
pubmed: 26571120
Echocardiography. 2016 Sep;33(9):1284-9
pubmed: 27109543
Pharmacoeconomics. 2015 Aug;33(8):811-31
pubmed: 25787932
J Cardiovasc Dis Res. 2011 Jan;2(1):50-6
pubmed: 21716753
Diabetes Care. 2016 Dec;39(12):e212-e213
pubmed: 27679584
Diabetes Care. 2011 Jun;34(6):1406-11
pubmed: 21515837
Int J Cardiol. 2009 Jul 10;135(3):323-30
pubmed: 18929416
BMC Cardiovasc Disord. 2018 Aug 9;18(1):162
pubmed: 30092757
Circulation. 2000 Oct 31;102(18):2233-8
pubmed: 11056098
Lancet. 2016 Apr 9;387(10027):1513-1530
pubmed: 27061677
J Am Coll Cardiol. 2013 Apr 23;61(16):1698-706
pubmed: 23500236
Atherosclerosis. 2015 Aug;241(2):579-87
pubmed: 26115069
J Am Geriatr Soc. 1999 Jun;47(6):727-9
pubmed: 10366175
J Cardiovasc Magn Reson. 2009 Apr 24;11:9
pubmed: 19393079
Heart. 2008 Jul;94(7):874-8
pubmed: 17932091
J Hum Hypertens. 2015 Jan;29(1):1-6
pubmed: 24804791
JACC Cardiovasc Imaging. 2009 Oct;2(10):1159-66
pubmed: 19833304
Circulation. 2009 Oct 20;120(16):1640-5
pubmed: 19805654
Eur Heart J. 2016 Jan 14;37(3):267-315
pubmed: 26320110
Diab Vasc Dis Res. 2015 Jan;12(1):23-32
pubmed: 25311248
Cardiovasc Diabetol. 2012 Dec 27;11:155
pubmed: 23270530
Circulation. 2003 Jan 28;107(3):448-54
pubmed: 12551870
Int J Cardiol. 2016 Jul 1;214:310-5
pubmed: 27085117
Diabetologia. 2017 Sep;60(9):1704-1711
pubmed: 28664298
Nutr Metab Cardiovasc Dis. 2012 Jul;22(7):561-6
pubmed: 21944738
J Hypertens. 2009 Dec;27(12):2458-64
pubmed: 19654559
J Am Coll Cardiol. 2008 Apr 8;51(14):1342-8
pubmed: 18387434
Clin Exp Hypertens. 2015;37(8):674-9
pubmed: 26151825
Am J Hypertens. 2014 Aug;27(8):1079-86
pubmed: 24610896
PLoS One. 2018 Apr 13;13(4):e0194446
pubmed: 29652881
Eur J Echocardiogr. 2010 Sep;11(8):677-82
pubmed: 20378683
Obes Surg. 2016 Nov;26(11):2772-2778
pubmed: 27156853
Int J Cardiol. 2012 Aug 23;159(2):107-11
pubmed: 21392830
Eur J Endocrinol. 2007 Jul;157(1):63-8
pubmed: 17609403
Diabet Med. 1998 Jul;15(7):539-53
pubmed: 9686693
Hypertension. 1996 Aug;28(2):159-68
pubmed: 8707376
Acta Cardiol. 2006 Aug;61(4):398-405
pubmed: 16970048
Int J Cardiol. 2016 Oct 15;221:114-21
pubmed: 27423078
Medicine (Baltimore). 2018 Jan;97(4):e9748
pubmed: 29369222
J Heart Valve Dis. 2015 May;24(3):272-9
pubmed: 26901894
JACC Cardiovasc Imaging. 2009 May;2(5):592-9
pubmed: 19442946
Diab Vasc Dis Res. 2014 May;11(3):133-73
pubmed: 24800783