|
Myocardial Infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
To describe trends over time in the initiation of rosiglitazone and pioglitazone-both in the thiazolidinedione (TZD) class-and medications from the dipeptidyl peptidase-4 (DPP-4) inhibitor class before and after the FDA removed a black box warning and restricted access program for rosiglitazone regarding an increased risk of myocardial infarction.
|
30589625 |
2019 |
|
Myocardial Infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Compared with use of DPP-4 inhibitors, use of liraglutide was associated with a significantly lower risk of cardiovascular death (HR 0·78, 95% CI 0·68-0·91), but no significant differences were identified for risk of myocardial infarction (0·94, 0·84-1·06) or stroke (0·88, 0·77-1·01).
|
30527909 |
2019 |
|
Myocardial Infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Results of the current analysis showed that during a mean follow-up time period ranging from 52 to 152 weeks, the primary endpoint (cardiovascular death/non-fatal myocardial infarction (MI)/non-fatal stroke) was not significantly different in the treatment of T2DM patients with versus without DPP-4 inhibitors (OR: 0.95, 95% CI: 0.86-1.04; P = 0.26).
|
30832701 |
2019 |
|
Myocardial Infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
After the induction of myocardial infarction (MI), Fischer 344 rats with inactivating mutation of DPP-4 were orally administrated with a DPP-4 inhibitor, linagliptin (5 mg kg<sup>-1</sup>·day<sup>-1</sup>), or vehicle in drinking water for 4 weeks.
|
30638989 |
2019 |
|
Myocardial Infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
The interaction between DPP-4 inhibitor initiation and metformin was statistically significant for non-fatal MI (P = 0.008).
|
30456843 |
2019 |
|
Myocardial Infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Trials involving dipeptidyl peptidase-4 (DPP-4) inhibitors did not alter a composite MACE outcome comprising CV deaths, non-fatal myocardial infarction and non-fatal stroke; however, the possibility that some members of this class might incur a small increased risk or worsening of heart failure cannot be excluded.
|
30091169 |
2019 |
|
Myocardial Infarction
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
DPP-4 inhibition enhanced renal tubular and myocardial GLP-1 receptor expression decreased in CKD with myocardial infarction.
|
30823876 |
2019 |
|
Myocardial Infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Hazard ratios for secondary outcomes, comparing SGLT2 inhibitors with DPP4 inhibitors, were 0.99 (0.85 to 1.17) for myocardial infarction, 0.94 (0.77 to 1.15) for stroke, 0.84 (0.65 to 1.08) for cardiovascular death, and 0.80 (0.69 to 0.92) for any cause death.
|
31467044 |
2019 |
|
Myocardial Infarction
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Glucagon-like peptide-1 receptor agonists reduce atherosclerotic thromboembolic events, but have little effect on heart failure; sodium-glucose co-transporter-2 inhibitors decrease the occurrence of heart failure, but have minimal effect on myocardial infarction and stroke; and dipeptidyl peptidase-4 inhibitors do not ameliorate either atherosclerotic thromboembolic events or heart failure.
|
29532519 |
2018 |
|
Myocardial Infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
Preclinical studies revealed that dipeptidyl peptidase (DPP4) inhibition is protective during myocardial infarction.
|
30087386 |
2018 |
|
Myocardial Infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Dipeptidyl peptidase 4 inhibitors and glucagon-like peptide-1 agonists were associated with a lower risk of myocardial infarction (MI) than were sulfonylureas (odds ratio [95% credible interval] 0.41 [0.24-0.71] and 0.48 [0.27-0.91], respectively).
|
29150631 |
2017 |
|
Myocardial Infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
The relative risks of MI with SGLT2 inhibitor use were 0.77 (0.63-0.93) and 0.75 (0.60-0.94), compared with placebo and DPP4 inhibitor, respectively.
|
28542373 |
2017 |
|
Myocardial Infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this nationwide T2DM cohort, the risks of mortality and the combination of MI and ischaemic stroke were lower for patients receiving DPP-4 inhibitors than for those who did not receive such treatment.
|
27647170 |
2017 |
|
Myocardial Infarction
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Dipeptidyl peptidase-4 (DPP4) regulates blood glucose levels and inflammation, and it is also implicated in the pathophysiological process of myocardial infarction (MI).
|
28587613 |
2017 |
|
Myocardial Infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
After inducing myocardial infarction (MI), wild type (WT) and endoglin heterozygous (Eng+/-) mice were treated for 5 days with the DPP4 inhibitor Diprotin A (DipA).
|
29253907 |
2017 |
|
Myocardial Infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The risk of myocardial infarction was significantly higher for SUs compared with dipeptidyl peptidase-4 (DPP-4) inhibitors and sodium-glucose co-transporter-2 inhibitors (HR 2.54, 95% CI 1.14-6.57 and HR 41.80, 95% CI 1.64-360.4, respectively).
|
27862902 |
2017 |
|
Myocardial Infarction
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Cardiac function, angiogenesis, and VEGF expression were impaired in the diabetic TG mice, but they were ameliorated by the DPP4 inhibition to levels similar to those found in the non-diabetic TG mice.The DPP4 inhibitor ameliorated cardiac function by inhibiting the inactivation of HMGB1 in diabetic mice after MI.
|
28966327 |
2017 |
|
Myocardial Infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
The HR for the composite outcome was 0.75 (95% CI 0.72-0.79) over a median treatment duration of 1 year, but the 1-year risks of MI were 1.00 (95% CI 0.89-1.12) and 1.47 (95% CI 1.38-1.56) per 100 patients for DPP-4 inhibitors and SUs, respectively, and the corresponding stroke risks were 0.98 (95% CI 0.87-1.10) and 1.09 (95% CI 1.01-1.17).
|
28195389 |
2017 |
|
Myocardial Infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
In contrast, cardiovascular outcome trials examining the safety of the shorter-acting GLP-1R agonist lixisenatide (ELIXA trial [Evaluation of Lixisenatide in Acute Coronary Syndrom]) and the DPP-4 inhibitors saxagliptin (SAVOR-TIMI 53 trial [Saxagliptin Assessment of Vascular Outcomes Recorded in Patients With Diabetes Mellitus-Thrombolysis in Myocardial Infarction 53]), alogliptin (EXAMINE trial [Examination of Cardiovascular Outcomes With Alogliptin Versus Standard of Care in Patients With Type 2 Diabetes Mellitus and Acute Coronary Syndrome]), and sitagliptin (TECOS [Trial Evaluating Cardiovascular Outcomes With Sitagliptin]) found that these agents neither increased nor decreased cardiovascular events.
|
28847797 |
2017 |
|
Myocardial Infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In the current study we only focused on DPP4 gene to assess the association of single nucleotide polymorphisms (SNPs) in the DPP-IV gene and risk of MI in patients with CAD.
|
23122333 |
2012 |