377-P: Exercise-Related Hypoglycemia Induces Hypercoagulable Changes in Patients with Type 1 Diabetes

Abstract

Diabetes is a hypercoagulable state predisposing to cardiovascular disease. Physical exercise can improve cardiovascular health but may also cause hypoglycemia in insulin-treated patients. We compared hemostatic profiles of patients with type 1 diabetes (T1D) with healthy controls and delineated hemostatic changes of hypoglycemia, induced with or without exercise, in patients with T1D. Thromboelastography (TEG®6s) was used to compare hemostatic profiles of patients with T1D (N=15, (mean±SD) age 29.4±8.1 years, HbA1c 6.8±0.5%, diabetes duration 13.1±6.2 years, BMI 23.7±2.0 kg/m2) with individually matched healthy controls (N=15) . In addition, the patients with T1D underwent (randomized, crossover design) two separate hyperinsulinemic euglycemic-hypoglycemic clamp days. During decline in plasma glucose and the initial 15 min of hypoglycemia, the subjects were either resting or performing moderate-intensity exercise. TEG was performed at baseline euglycemia and after 15 min and 60 min of hypoglycemia. Compared with healthy controls, patients with T1D were more hypercoagulable with shorter R-time (P<0.001) and K-time (P=0.019) and an increased Angle-value (P=0.009) . Clot maximum amplitude (MA) , functional fibrinogen (MA-FF) , and fibrinolysis (LY-30) were similar in the two groups. In patients with T1D, exercise-related hypoglycemia induced hypercoagulable changes with decreased K-time (P=0.005) , increased Angle-value (P=0.049) , and increased MA (P<0.001) after 15 min of hypoglycemia. These changes were not compensated by an increased fibrinolysis. In contrast, hypoglycemia induced at rest resulted in decreased K-time (P=0.03) and increased MA-FF (P=0.02) only after 60 min, along with increased LY-30 (P=0.02) . In conclusion, patients with T1D have a more hypercoagulable profile than healthy controls, and exercise-related hypoglycemia induces coagulation without a compensatory fibrinolytic activity, which may increase susceptibility for thrombosis. Disclosure P.G.Hagelqvist: None. A.Andersen: n/a. K.Maytham: None. S.Engberg: Employee; Novo Nordisk A/S. U.Pedersen-bjergaard: Advisory Panel; Novo Nordisk A/S, Sanofi. P.I.Johansson: None. F.K.Knop: Advisory Panel; Boehringer Ingelheim International GmbH, Eli Lilly and Company, Merck Sharp & Dohme Corp., Novo Nordisk, Sanofi, ShouTi, Zucara Therapeutics, Consultant; AstraZeneca, Eli Lilly and Company, Novo Nordisk, Pharmacosmos A/S, Sanofi, ShouTi, Zealand Pharma A/S, Zucara Therapeutics, Research Support; AstraZeneca, Novo Nordisk, Sanofi, Zealand Pharma A/S, Speaker's Bureau; AstraZeneca, Bayer AG, Boehringer Ingelheim International GmbH, Eli Lilly and Company, Novo Nordisk, Sanofi, Stock/Shareholder; Antag Therapeutics. T.Vilsbøll: Consultant; AstraZeneca, Bristol-Myers Squibb Company, Eli Lilly and Company, Gilead Sciences, Inc., GlaxoSmithKline plc., Merck Sharp & Dohme Corp., Mundipharma, Novo Nordisk, Sun Pharmaceutical Industries Ltd. Funding Independent research fund Denmark (1030-00256B) Grosserer L.F. Foghts Fund (21.761)