title: Chronic metformin treatment is associated with reduced myocardial infarct size in diabetic patients with ST-segment elevation myocardial infarction.
abstract: OBJECTIVE
  Increased myocardial infarct (MI) size is associated with higher risk of developing left ventricular dysfunction, heart failure and mortality. Experimental studies have suggested that metformin treatment reduces MI size after induced ischaemia but human data is lacking. We aimed to investigate the effect of metformin on MI size in patients presenting with an acute MI.
  
  
  METHODS
  All consecutive patients (n = 3,288) presenting to our hospital with ST-segment elevation myocardial infarction (STEMI) undergoing primary PCI between January 2004 and December 2010 were included in this retrospective analysis. Patients with diabetes were divided according to metformin versus non-metformin based pharmacotherapy. MI size was estimated using peak values of serum creatine kinase (CK), myocardial band of CK (CK-MB), and troponin-T.
  
  
  RESULTS
  We identified 677 (20.6 %) patients with diabetes, of whom 189 (27.9 %) were treated with metformin. Chronic metformin treatment was associated with lower peak levels of CK (1,101 vs. 1,422 U/L, P = 0.005), CK-MB (152 vs. 182 U/L, P = 0.018) and troponin-T (2.5 vs. 4.0 ng/L, P = 0.021) compared to non-metformin using diabetics. After adjustment for age, sex, TIMI flow post PCI, and previous MI, the use of metformin treatment remained an independent predictor of smaller MI size. Patient with diabetes treated with metformin had even smaller MI size than patients without diabetes.
  
  
  CONCLUSIONS
  Chronic metformin treatment is associated with reduced MI size compared to non-metformin based strategies in diabetic patients presenting with STEMI. Metformin might have additional beneficial effects beyond glucose lowering efficacy.
authors.affiliation: Department of Cardiology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB, PO Box 30.001, Groningen, The Netherlands, c.p.h.lexis@umcg.nl.
authors.forename: Chris P H
authors.initials: CP
authors.lastname: Lexis
authors.forename: Wouter G
authors.initials: WG
authors.lastname: Wieringa
authors.forename: Bart
authors.initials: B
authors.lastname: Hiemstra
authors.forename: Vincent M
authors.initials: VM
authors.lastname: van Deursen
authors.forename: Erik
authors.initials: E
authors.lastname: Lipsic
authors.forename: Pim
authors.initials: P
authors.lastname: van der Harst
authors.forename: Dirk J
authors.initials: DJ
authors.lastname: van Veldhuisen
authors.forename: Iwan C C
authors.initials: IC
authors.lastname: van der Horst
mesh_terms: D000368:Aged; D052279:Creatine Kinase, MB Form / Q000378:metabolism; D003920:Diabetes Mellitus / Q000473:pathology*; D004562:Electrocardiography / Q000379:methods; D005260:Female; D006801:Humans; D008297:Male; D008687:Metformin / Q000627:therapeutic use*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000473:pathology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D012189:Retrospective Studies; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology; D020107:Troponin T / Q000378:metabolism
chemical_list: D020107:Troponin T; D008687:Metformin; D052279:Creatine Kinase, MB Form