Introduction & Objective: Prediabetes (PRE) and type 2 diabetes (T2D) associate with excess risk and worse outcome of myocardial infarction (MI). Increased endogenous glucose production (EGP) contributes to hyperglycemia in critical illness, however, if elevated EGP associates with worsening of the prognosis is yet unclear. We hypothesized that (i) people with recent MI show greater insulin resistance and EGP compared to event-free people and (ii) impairment of left ventricular ejection fraction (EF) after MI correlates with higher fasting EGP.

Methods: Participants of the DIabetes and ST-segment elevation MI study (DISTEMI) underwent comprehensive phenotyping at 6-12 weeks after MI (MI+, n=95) and were compared to event-free participants of the German Diabetes Study (GDS) with comparable age, sex, BMI and HbA1c (MI-, n=78). Whole-body insulin sensitivity and EGP were assessed by hyperinsulinemic-euglycemic clamps and stable isotope dilution. EF was quantified by MRI.

Results: Insulin sensitivity was about 18% lower in MI+ than MI- (p<0.001), predominantly in MI+ with PRE (7.4±1.9 vs. 9.1±2.4 mg*kg-1*min-1, p<0.05) or T2D (4.5±1.4 vs. 6.3±1.9 mg*kg-1*min-1, p<0.001). EGP was similar between MI+ and MI- (1.79±0.25 vs. 1.79±0.24 mg*kg-1*min-1, p=0.74). Independently of glucose tolerance, EF was comparable between MI+ and MI- (57±11 vs. 57±7%, p=0.85), but correlated inversely with EGP (r=-0.41, p<0.01) in MI+ with PRE (r=-0.53, p=0.01) and -by trend- in MI+ with T2D (r=-0.60, p=0.07) but not in glucose tolerant MI+ and MI- (p=0.34 and p=0.61).

Conclusion: After myocardial infarction, people with dysglycemia show greater insulin resistance but similar fasting endogenous glucose production compared to event-free people. However, they exhibit increased fasting glucose production at decreased cardiac function, suggesting an important role of antihyperglycemic treatment for cardio-protective prevention in the post-infarction setting.

Disclosure

C. Möser: None. V. Schrauwen-Hinderling: None. S. Trenkamp: None. G. Heilmann: None. P. Bobrov: None. V. Burkart: None. R. Wagner: Speaker's Bureau; Sanofi. Advisory Panel; Lilly Diabetes. Speaker's Bureau; Boehringer-Ingelheim, Novo Nordisk. J. Szendroedi: None. M. Kelm: Research Support; Edwards Lifesciences Coroporation, Microvision Medical, B.Braun, IPP Med GmbH - Institut für Pharmakologie u. präventive Medizin GmbH, Mars Scientific Advisory Council (MSAC). Other Relationship; Bayer Inc., Abiomed. Board Member; ESC-European Society of Cardiology, DGIM-Deutsche Geselleschaft für Innere Medizin, DSHF-Deutsche Stiftung für Herzforschung, DGK-Deutsche Gesellschaft für Kardiologie. Other Relationship; Kel Con GmbH, diaplan. M. Roden: Advisory Panel; Eli Lilly and Company. Research Support; Boehringer-Ingelheim. Advisory Panel; Novo Nordisk. Research Support; Novo Nordisk. Advisory Panel; TARGET PharmaSolutions, Inc. Speaker's Bureau; AstraZeneca.

© 2024 by the American Diabetes Association
2024
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