In-hospital arrhythmic burden reduction in diabetic patients with acute myocardial infarction treated with SGLT2-inhibitors: Insights from the SGLT2-I AMI PROTECT study.
acute myocardial infarction
atrial fibrillation
hyperglycemia
sodium-glucose cotransporter 2 inhibitors (SGLT2-i)
ventricular arrhythmias
ventricular tachycardia
Journal
Frontiers in cardiovascular medicine
ISSN: 2297-055X
Titre abrégé: Front Cardiovasc Med
Pays: Switzerland
ID NLM: 101653388
Informations de publication
Date de publication:
2022
2022
Historique:
received:
05
08
2022
accepted:
29
08
2022
entrez:
14
10
2022
pubmed:
15
10
2022
medline:
15
10
2022
Statut:
epublish
Résumé
Sodium-glucose co-transporter 2 inhibitors (SGLT2-i) have shown significant cardiovascular benefits in patients with and without type 2 diabetes mellitus (T2DM). They have also gained interest for their potential anti-arrhythmic role and their ability to reduce the occurrence of atrial fibrillation (AF) and ventricular arrhythmias (VAs) in T2DM and heart failure patients. To investigate in-hospital new-onset cardiac arrhythmias in a cohort of T2DM patients presenting with acute myocardial infarction (AMI) treated with SGLT2-i vs. other oral anti-diabetic agents (non-SGLT2-i users). Patients from the SGLT2-I AMI PROTECT registry (NCT05261867) were stratified according to the use of SGLT2-i before admission for AMI, divided into SGLT2-i users vs. non-SGLT2-i users. In-hospital outcomes included the occurrence of in-hospital new-onset cardiac arrhythmias (NOCAs), defined as a composite of new-onset AF and sustained new-onset ventricular tachycardia (VT) and/or ventricular fibrillation (VF) during hospitalization. The study population comprised 646 AMI patients categorized into SGLT2-i users (111 patients) and non-SGLT2-i users (535 patients). SGLT2-i users had a lower rate of NOCAs compared with non-SGLT2-i users (6.3 vs. 15.7%, In T2DM patients, the use of SGLT2-i was associated with a lower risk of new-onset arrhythmic events during hospitalization for AMI. In particular, the primary effect was expressed in the reduction of VAs. These findings emphasize the cardioprotective effects of SGLT2-i in the setting of AMI beyond glycemic control. Data are part of the observational international registry: SGLT2-I AMI PROTECT. ClinicalTrials.gov, identifier: NCT05261867.
Sections du résumé
Background
UNASSIGNED
Sodium-glucose co-transporter 2 inhibitors (SGLT2-i) have shown significant cardiovascular benefits in patients with and without type 2 diabetes mellitus (T2DM). They have also gained interest for their potential anti-arrhythmic role and their ability to reduce the occurrence of atrial fibrillation (AF) and ventricular arrhythmias (VAs) in T2DM and heart failure patients.
Objectives
UNASSIGNED
To investigate in-hospital new-onset cardiac arrhythmias in a cohort of T2DM patients presenting with acute myocardial infarction (AMI) treated with SGLT2-i vs. other oral anti-diabetic agents (non-SGLT2-i users).
Methods
UNASSIGNED
Patients from the SGLT2-I AMI PROTECT registry (NCT05261867) were stratified according to the use of SGLT2-i before admission for AMI, divided into SGLT2-i users vs. non-SGLT2-i users. In-hospital outcomes included the occurrence of in-hospital new-onset cardiac arrhythmias (NOCAs), defined as a composite of new-onset AF and sustained new-onset ventricular tachycardia (VT) and/or ventricular fibrillation (VF) during hospitalization.
Results
UNASSIGNED
The study population comprised 646 AMI patients categorized into SGLT2-i users (111 patients) and non-SGLT2-i users (535 patients). SGLT2-i users had a lower rate of NOCAs compared with non-SGLT2-i users (6.3 vs. 15.7%,
Conclusions
UNASSIGNED
In T2DM patients, the use of SGLT2-i was associated with a lower risk of new-onset arrhythmic events during hospitalization for AMI. In particular, the primary effect was expressed in the reduction of VAs. These findings emphasize the cardioprotective effects of SGLT2-i in the setting of AMI beyond glycemic control.
Trial registration
UNASSIGNED
Data are part of the observational international registry: SGLT2-I AMI PROTECT. ClinicalTrials.gov, identifier: NCT05261867.
Identifiants
pubmed: 36237914
doi: 10.3389/fcvm.2022.1012220
pmc: PMC9551177
doi:
Banques de données
ClinicalTrials.gov
['NCT05261867']
Types de publication
Journal Article
Langues
eng
Pagination
1012220Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK020541
Pays : United States
Informations de copyright
Copyright © 2022 Cesaro, Gragnano, Paolisso, Bergamaschi, Gallinoro, Sardu, Mileva, Foà, Armillotta, Sansonetti, Amicone, Impellizzeri, Esposito, Morici, Oreglia, Casella, Mauro, Vassilev, Galie, Santulli, Pizzi, Barbato, Calabrò and Marfella.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Références
Front Cardiovasc Med. 2019 Nov 05;6:158
pubmed: 31750317
Circulation. 2020 Apr 14;141(15):1227-1234
pubmed: 31983236
Circulation. 2012 Jan 31;125(4):620-37
pubmed: 22294707
Heart Rhythm. 2021 Jul;18(7):1098-1105
pubmed: 33757845
Metabolism. 2022 Jun 19;:155243
pubmed: 35732222
J Pers Med. 2022 Feb 12;12(2):
pubmed: 35207759
Diabetologia. 2000 May;43(5):571-5
pubmed: 10855531
Front Pharmacol. 2021 Nov 15;12:777083
pubmed: 34867407
Eur Heart J. 2021 Sep 21;42(36):3727-3738
pubmed: 34448003
Life Sci. 2021 Jul 1;276:119440
pubmed: 33781832
Diabetes Obes Metab. 2018 Feb;20(2):344-351
pubmed: 28771923
J Intensive Care Med. 2009 Sep-Oct;24(5):293-316
pubmed: 19703817
ESC Heart Fail. 2018 Aug;5(4):642-648
pubmed: 30117720
Int J Mol Sci. 2021 Jul 26;22(15):
pubmed: 34360742
Eur Heart J. 2018 Jan 7;39(2):119-177
pubmed: 28886621
Diabetes Obes Metab. 2019 Feb;21(2):210-217
pubmed: 30144274
Cardiovasc Diabetol. 2018 Oct 19;17(1):136
pubmed: 30340589
Lancet Diabetes Endocrinol. 2017 Sep;5(9):709-717
pubmed: 28781064
Cardiovasc Diabetol. 2021 Oct 4;20(1):199
pubmed: 34607570
JACC Basic Transl Sci. 2020 Feb 24;5(2):180-182
pubmed: 32142070
PLoS Comput Biol. 2022 Apr 27;18(4):e1009388
pubmed: 35476614
J Am Coll Cardiol. 2022 May 24;79(20):2058-2068
pubmed: 35589167
Metabolism. 2022 Feb;127:154936
pubmed: 34801581
Cardiovasc Diabetol. 2021 May 7;20(1):100
pubmed: 33962654
Circulation. 2021 Jun;143(22):2188-2204
pubmed: 33832341
Cardiovasc Diabetol. 2022 May 15;21(1):77
pubmed: 35570280
Arrhythm Electrophysiol Rev. 2017 Aug;6(3):134-139
pubmed: 29018522
Cardiovasc Diabetol. 2020 Jun 5;19(1):73
pubmed: 32503541
N Engl J Med. 2015 Nov 26;373(22):2117-28
pubmed: 26378978
Cardiovasc Diabetol. 2022 May 18;21(1):67
pubmed: 35585590
PLoS One. 2021 Feb 19;16(2):e0244689
pubmed: 33606705
Eur J Endocrinol. 2021 Jul 21;185(2):343-353
pubmed: 34085953
Europace. 2019 Oct 1;21(10):1603-1604
pubmed: 31353412
Eur Heart J. 2021 Feb 1;42(5):373-498
pubmed: 32860505
Circulation. 2011 May 17;123(19):2094-100
pubmed: 21536994
Trends Cardiovasc Med. 2022 Apr 18;:
pubmed: 35447305
N Engl J Med. 2021 Oct 14;385(16):1451-1461
pubmed: 34449189
Cardiovasc Diabetol. 2018 Nov 17;17(1):144
pubmed: 30447687
Eur J Prev Cardiol. 2018 Mar;25(5):495-502
pubmed: 29372664
Am J Cardiol. 2012 Mar 15;109(6):805-12
pubmed: 22196782
N Engl J Med. 2019 Nov 21;381(21):1995-2008
pubmed: 31535829
Diabetes Obes Metab. 2019 May;21(5):1136-1145
pubmed: 30609272
Am Heart J. 2019 Feb;208:1-10
pubmed: 30471486
Am Heart J. 2006 Apr;151(4):806-12
pubmed: 16569539
Cardiovasc Diabetol. 2020 Nov 6;19(1):188
pubmed: 33158436
ESC Heart Fail. 2021 Oct;8(5):4346-4352
pubmed: 34382353
Cardiovasc Diabetol. 2020 Sep 25;19(1):148
pubmed: 32977831
Int J Biochem Cell Biol. 2019 Mar;108:29-33
pubmed: 30639431
Front Endocrinol (Lausanne). 2018 Jul 26;9:421
pubmed: 30093883
Circulation. 2018 Sep 25;138(13):e272-e391
pubmed: 29084731
J Am Heart Assoc. 2022 Mar 15;11(6):e024260
pubmed: 35258317
Front Cardiovasc Med. 2022 May 18;9:902923
pubmed: 35665272
Heart Rhythm. 2011 Dec;8(12):1963-8
pubmed: 21740880
Int J Mol Sci. 2022 Jan 31;23(3):
pubmed: 35163599
J Am Heart Assoc. 2021 Sep 7;10(17):e022222
pubmed: 34459238
Stroke. 2021 May;52(5):1545-1556
pubmed: 33874750