160-OR: Acute Changes in Plasma Glucose Have Impact on Left Ventricular Systolic Function in Insulin-Treated Patients with Type 2 Diabetes

Abstract

Patients with type 2 diabetes (T2D) have a markedly altered cardiac metabolism and twice the risk of developing heart failure compared to individuals without diabetes. The effect of acute changes in plasma glucose (PG) on cardiac function is unclear. We evaluated the effect of acute hyperglycemia and hypoglycemia on cardiac function. Insulin-treated patients with T2D (N=21, [mean±SD] age 62.8±6.5 years, BMI 29.0±4.2 kg/m2, HbA1c 51.0±5.4 mmol/mol) and matched controls (N=21, age 62.2±8.3 years, BMI 29.2±3.5, HbA1c 34.3±3.3 mmol/l) with normal glucose tolerance underwent a 3-step glucose clamp day with 30 min of steady-state PG during each step: 1) fasting PG (FPG), 2) hyperglycemia (FPG+10 mmol/l), and 3) hyperinsulinemic hypoglycemia (PG<3.0 mmol/l). Cardiac function was evaluated during steady-state of each step by echocardiography. Acute hyperglycemia increased left ventricular ejection fraction (LVEF) from baseline in T2D patients ([mean±SEM, P-value] 4.5±1.7%, P=0.0108) whereas no change was observed in controls (2.0±1.7%, P=0.2525). Furthermore, left ventricular systolic function measured by s’ increased during hyperglycemia in both patients and controls (0.4±0.1 m/s (P=0.0007) and 0.6±0.1 m/s (P <0.0001), respectively) whereas global longitudinal strain rate only increased in the controls (-0.05±0.04 s-1 (P=0.1803) and -0.11±0.04 s-1 (P=0.0053), respectively). All measures of left ventricular systolic function increased markedly during hypoglycemia (P<0.01 for all). No significant interaction between group and PG level on cardiac function was observed. In conclusion, we demonstrate that LVEF increases during acute hyperglycemia in insulin-treated patients with T2D and that acute hypoglycemia markedly increases all measures of left ventricular systolic function. These results point to the importance of glycemia when evaluating left ventricular systolic function by echocardiography in patients with T2D. Disclosure A. Andersen: None. P.G. Jørgensen: None. J.I. Bagger: Speaker’s Bureau; Self; Novo Nordisk A/S. M. Baldassarre: None. M.B. Christensen: None. K.U. Abelin: None. U. Pedersen-Bjergaard: Advisory Panel; Self; Novo Nordisk A/S, Sanofi. Research Support; Self; Novo Nordisk A/S. J.J. Holst: Advisory Panel; Self; AstraZeneca, Merck Sharp & Dohme Corp., Novo Nordisk A/S, Zealand Pharma A/S. Other Relationship; Spouse/Partner; Antag Therapeutics. T.B. Lindhardt: None. F.K. Knop: Advisory Panel; Self; AstraZeneca, Merck Sharp & Dohme Corp., Mundipharma International, Novo Nordisk A/S, Sanofi. Consultant; Self; Carmot Therapeutics, Inc., Eli Lilly and Company, Novo Nordisk A/S. Research Support; Self; AstraZeneca, Gubra, Novo Nordisk A/S, Sanofi, Zealand Pharma A/S. Speaker’s Bureau; Self; AstraZeneca, Lupin Pharmaceuticals, Inc., Merck Sharp & Dohme Corp., Norgine B.V., Novo Nordisk A/S. T. Vilsbøll: Advisory Panel; Self; AstraZeneca, Mundipharma International, Novo Nordisk A/S, Sun Pharmaceutical Industries Ltd. Consultant; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Lilly Diabetes, Medscape, Merck Sharp & Dohme Corp., Sanofi.