Thiazolidinediones and Risk of Atrial Fibrillation Among Patients with Diabetes and Coronary Disease

Pallisgaard, Jannik Langtved; Brooks, Maria M.; Chaitman, Bernard R.; Boothroyd, Derek B.; Pérez, Marco; Hlatky, Mark A.

doi:10.1016/j.amjmed.2018.02.026

Cited by 14 publications

(11 citation statements)

References 30 publications

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“…reported that the use of TZD was associated with a 24% reduction in the risk of incident AF compared with other antidiabetic drugs as second-line treatment among T2DM patients [ 38 ]. However, no significant differences in the risk of incident AF with use of TZD were reported in the PROactive, RECORD, and BARI 2D trials [ 39 – 41 ].…”

Section: Discussionmentioning

confidence: 99%

The risk of new-onset atrial fibrillation in patients with type 2 diabetes mellitus treated with sodium glucose cotransporter 2 inhibitors versus dipeptidyl peptidase-4 inhibitors

Ling

Chan

Chen

et al. 2020

Cardiovasc Diabetol

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Background Sodium glucose cotransporter 2 inhibitor (SGLT2i) reduces the risk of hard cardiovascular endpoints in type 2 diabetes mellitus (T2DM) patients with/without established cardiovascular diseases. Whether SGLT2i is associated with a lower risk of new-onset atrial fibrillation (AF) in T2DM patients is unclear. We aimed to evaluate the risk of new-onset AF associated with the use of SGLT2i compared to dipeptidyl peptidase-4 inhibitor (DPP4i) among a longitudinal cohort of diabetic patients. Methods We used medical data from a multi-center healthcare provider in Taiwan, which included a total of 15,606 and 12,383 patients treated with SGLT2i and DPP4i, respectively, from June 1, 2016 to December 31, 2018. We used propensity-score weighting to balance covariates across study groups. Patients were followed up from the drug index date until the occurrence of new-onset AF, discontinuation of the index drug, or the end of the study period, whichever occurred first. Results Overall, 55%, 45%, and 0% of the patients were treated with empagliflozin, dapagliflozin, and canagliflozin, respectively. Most patients in the DPP4i group were prescribed with linagliptin (51%), followed by sitagliptin (24%), saxagliptin (13%), vildagliptin (8%) and alogliptin (5%). The use of SGLT2i was associated with a lower risk of new-onset AF compared with DPP4i after propensity-score weighting [hazard ratio: 0.61; 95% confidential interval: 0.50–0.73; P < 0.001]. Subgroup analysis revealed that the use of SGLT2i was associated with a lower risk of new-onset AF compared with DPP4i across several subgroups including old age, female in gender, the presence of cardiovascular disease, hemoglobin A1c $$\ge$$ ≥ 8%, and chronic kidney disease. The advantage of SGLT2i over DPP4i persisted with different SGLT2i (dapagliflozin or empagliflozin) and either low- or standard-dose SGLT2i. Conclusions SGLT2i was associated with a lower risk of new-onset AF compared with DPP4i among T2DM patients in real-world practice.

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Section: Discussionmentioning

confidence: 99%

The risk of new-onset atrial fibrillation in patients with type 2 diabetes mellitus treated with sodium glucose cotransporter 2 inhibitors versus dipeptidyl peptidase-4 inhibitors

Ling

Chan

Chen

et al. 2020

Cardiovasc Diabetol

View full text Add to dashboard Cite

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“…Another prospective study, the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) study of patients with T2DM and documented coronary artery disease did not show a significant reduction in the incidence of NAF in those using metformin and/or the thiazolidinedione rosiglitazone. In the intention‐to‐treat analysis, the incidence of NAF was 87 per 1000 person‐years, with metformin and/or rosiglitazone compared to 95 per 1000 person years with insulin and/or a secretagogue (HR, 0.80; 95% CI, 0.43‐1.3; P = 0.3) . As the PROactive study, the BARI 2D study was not designed to investigate AF and, unlike the PROactive study, the thiazolidinedione rosiglitazone, and not pioglitazone, was used.…”

Section: Effect Of Drugs Used To Treat Type 2 Diabetes On Atrial Fibrmentioning

confidence: 98%

“…In the intention-to-treat analysis, the incidence of NAF was 87 per 1000 person-years, with metformin and/or rosiglitazone compared to 95 per 1000 person years with insulin and/or a secretagogue (HR, 0.80; 95% CI, 0.43-1.3; P = 0.3). 63 As the PROactive study, the BARI 2D study was not designed to investigate AF and, unlike the PROactive study, the thiazolidinedione rosiglitazone, and not pioglitazone, was used. A similar study, the RECORD study, was a prospective, blinded, placebo-controlled study of the addition of rosiglitazone to existing sulfonylurea or metformin therapy.…”

Section: Drugs That Lower Insulin Resistancementioning

confidence: 99%

Atrial fibrillation and type 2 diabetes: Prevalence, etiology, pathophysiology and effect of anti‐diabetic therapies

Bell

Goncalves

2018

Diabetes Obesity Metabolism

111

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New-onset atrial fibrillation (NAF) is increased in the type 2 diabetic patient because of the presence of the metaboli syndrome and increased sympathetic activity. This results in inflammation, endothelial dysfunction and myocardial steatosis which, in turn, lead to atrial fibrosis and dilatation. The end result is the development of structural and electrical atrial remodeling. Drugs that lower insulin resistance, particularly pioglitazone, decrease the incidence of NAF while drugs that, through hypoglycaemia, stimulate the sympathetic nervous system, insulin and secretagogues, increase the incidence of NAF. Currently there is no evidence that GLP-1 agonists, SGLT2 inhibitors and DPP-4 inhibitors either accelerate or decelerate the development of NAF.

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“…Thiazolinediones are peroxisome proliferator-activated receptor-γ agonists, which decrease glucose levels by increasing storage of fatty acids in adipocytes, also decrease incidences of atrial fibrillation onset, which might also be influenced by their anti-inflammatory actions (Chao et al, 2012 ; Pallisgaard et al, 2017 ; Zhang Z. et al, 2017 ). However, other studies have shown in patients with coronary disease, thiazolinediones have no improvements in atrial fibrillation compared with other diabetes treatments including metformin, insulin, sulfonylurea or meglitinides, suggesting that the anti-inflammatory effects of thiazolinediones does not further improve anti-arrhythmia effects of controlling glucose levels (Pallisgaard et al, 2018 ).…”

Section: The Impact Of Diabetes Therapies On Arrhythmiasmentioning

confidence: 99%

Diabetes and Arrhythmias: Pathophysiology, Mechanisms and Therapeutic Outcomes

Grisanti

2018

Front. Physiol.

111

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The prevalence of diabetes is rapidly increasing and closely associated with cardiovascular morbidity and mortality. While the major cardiovascular complication associated with diabetes is coronary artery disease, it is becoming increasingly apparent that diabetes impacts the electrical conduction system in the heart, resulting in atrial fibrillation, and ventricular arrhythmias. The relationship between diabetes and arrhythmias is complex and multifactorial including autonomic dysfunction, atrial and ventricular remodeling and molecular alterations. This review will provide a comprehensive overview of the link between diabetes and arrhythmias with insight into the common molecular mechanisms, structural alterations and therapeutic outcomes.

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Thiazolidinediones and Risk of Atrial Fibrillation Among Patients with Diabetes and Coronary Disease

Abstract: We did not find a significant reduction of atrial fibrillation incidence with use of thiazolidinediones.

Cited by 14 publications

References 30 publications

The risk of new-onset atrial fibrillation in patients with type 2 diabetes mellitus treated with sodium glucose cotransporter 2 inhibitors versus dipeptidyl peptidase-4 inhibitors

The risk of new-onset atrial fibrillation in patients with type 2 diabetes mellitus treated with sodium glucose cotransporter 2 inhibitors versus dipeptidyl peptidase-4 inhibitors

Atrial fibrillation and type 2 diabetes: Prevalence, etiology, pathophysiology and effect of anti‐diabetic therapies

Diabetes and Arrhythmias: Pathophysiology, Mechanisms and Therapeutic Outcomes

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