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)

© 2022 by the American Diabetes Association
2022
Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at http://www.diabetesjournals.org/content/license.