M Joubert1, J Hardouin2, D Legallois3, K Blanchart4, N Elie5, M Nowoczyn6, P Croisille7, L Coulbault8, C Bor-Angelier9, S Allouche10, A Manrique11. 1. Diabetes Care Unit, Caen University Hospital, Caen, France; EA4650 Normandie université, GIP Cyceron, 14000 Caen, France. Electronic address: dr.michaeljoubert@gmail.com. 2. Diabetes Care Unit, Caen University Hospital, Caen, France; EA4650 Normandie université, GIP Cyceron, 14000 Caen, France. Electronic address: hardouin-j@chu-caen.fr. 3. Cardiology Unit, Caen University Hospital, 14033 Caen, France; EA4650 Normandie université, GIP Cyceron, 14000 Caen, France. Electronic address: legallois-da@chu-caen.fr. 4. Cardiology Unit, Caen University Hospital, 14033 Caen, France; EA4650 Normandie université, GIP Cyceron, 14000 Caen, France. Electronic address: blanchart-k@chu-caen.fr. 5. CMABIO-HIQ Facility, SF4206 ICORE, IBFA, University of Caen, 14000 Caen, France. Electronic address: nicolas.elie@unicaen.fr. 6. Biochemistry Unit, Caen University Hospital, 14000 Caen, France; EA4650 Normandie université, GIP Cyceron, 14000 Caen, France. Electronic address: nowoczyn-m@chu-caen.fr. 7. Radiology Department, Saint-Etienne University Hospital, 42000 Saint-Etienne, France; CREATIS CNRS UMR5220 Inserm U1044, Lyon University, 69000 Lyon, France. Electronic address: pierre.croisille@creatis.univ-lyon1.fr. 8. Biochemistry Unit, Caen University Hospital, 14000 Caen, France; EA4650 Normandie université, GIP Cyceron, 14000 Caen, France. Electronic address: coulbault-l@chu-caen.fr. 9. Pathology Department, F.-Baclesse Cancer Center, 14000 Caen, France. Electronic address: c.bor-angelier@baclesse.fr. 10. Biochemistry Unit, Caen University Hospital, 14000 Caen, France; EA4650 Normandie université, GIP Cyceron, 14000 Caen, France. Electronic address: allouche-s@chu-caen.fr. 11. Nuclear Medicine Department, Caen University Hospital, 14033 Caen, France; EA4650 Normandie université, GIP Cyceron, 14000 Caen, France. Electronic address: manrique@cyceron.fr.
Abstract
AIMS: In addition to hyperglycaemia, glycaemic variability seems to be associated with poor outcomes after acute myocardial infarction. This study explored the impact of glycaemic variability in diabetic Wistar rats subjected to myocardial ischaemia/reperfusion. METHODS: Animals with streptozotocin-induced diabetes received insulin either to maintain stable hyperglycaemia (Dh group) or to generate glycaemic variability (Dv). After experimental myocardial ischaemia/reperfusion was surgically induced, 7T cardiac magnetic resonance imaging (CMR) was performed at weeks 1 (w1) and 3 (w3). RESULTS: Twenty-six rats were randomized [sham group (S): n=5; control group (C): n=7; Dh group: n=6; and Dv group: n=8]. The mean amplitude of glucose reflecting glycaemic variability was higher in the Dv than in the Dh group (9.1±2.7mmol/L vs 5.9±1.9mmol/L; P<0.05). CMR assessment at w3 revealed ventricular enlargement in both Dh and Dv groups compared with the C and S groups (end-diastolic volume: 1.60±0.22 and 1.36±0.30mL/kg compared with 1.11±0.13 and 0.87±0.11mL/kg, respectively; P<0.05). Circumferential strain was altered between w1 and w3 in the remote area only in the Dv group, resulting in a lower value in this group than in the S, C and Dh groups (-0.11±0.01 vs -0.17±0.05, -0.15±0.03 and -0.16±0.03, respectively; P<0.05). In addition, at w3, oedema was also higher in the remote area in the Dv than in the C group (18.3±4.9ms vs 14.5±1.7ms, respectively; P<0.05). CONCLUSION: In the context of experimental myocardial ischaemia/reperfusion, our results suggest that glycaemic variability might have a potentially deleterious impact on myocardial outcomes beyond the classical glucose metrics.
AIMS: In addition to hyperglycaemia, glycaemic variability seems to be associated with poor outcomes after acute myocardial infarction. This study explored the impact of glycaemic variability in diabeticWistar rats subjected to myocardial ischaemia/reperfusion. METHODS: Animals with streptozotocin-induced diabetes received insulin either to maintain stable hyperglycaemia (Dh group) or to generate glycaemic variability (Dv). After experimental myocardial ischaemia/reperfusion was surgically induced, 7T cardiac magnetic resonance imaging (CMR) was performed at weeks 1 (w1) and 3 (w3). RESULTS: Twenty-six rats were randomized [sham group (S): n=5; control group (C): n=7; Dh group: n=6; and Dv group: n=8]. The mean amplitude of glucose reflecting glycaemic variability was higher in the Dv than in the Dh group (9.1±2.7mmol/L vs 5.9±1.9mmol/L; P<0.05). CMR assessment at w3 revealed ventricular enlargement in both Dh and Dv groups compared with the C and S groups (end-diastolic volume: 1.60±0.22 and 1.36±0.30mL/kg compared with 1.11±0.13 and 0.87±0.11mL/kg, respectively; P<0.05). Circumferential strain was altered between w1 and w3 in the remote area only in the Dv group, resulting in a lower value in this group than in the S, C and Dh groups (-0.11±0.01 vs -0.17±0.05, -0.15±0.03 and -0.16±0.03, respectively; P<0.05). In addition, at w3, oedema was also higher in the remote area in the Dv than in the C group (18.3±4.9ms vs 14.5±1.7ms, respectively; P<0.05). CONCLUSION: In the context of experimental myocardial ischaemia/reperfusion, our results suggest that glycaemic variability might have a potentially deleterious impact on myocardial outcomes beyond the classical glucose metrics.