title: Acute-phase glucose fluctuation is negatively correlated with myocardial salvage after acute myocardial infarction.
abstract: BACKGROUND
  It remains unclear whether glycemic fluctuation immediately after acute myocardial infarction (AMI) can affect myocardial damage. This study investigated the impact of glucose fluctuation on myocardial salvage following successful recanalization of primary AMI.
  
  
  RESULTS
  A total of 36 consecutive patients with AMI were studied. Glycemic variability, as indicated by the mean amplitude of glycemic excursion (MAGE), was measured on a continuous glucose monitoring system. Three subsets (CD14(+)CD16(-), CD14(++)CD16(+) and CD14(+-)CD16(+)) were measured on flow cytometry 1, 2, 3, 4 and 5 days after AMI onset. A 2-h oral glucose test was performed in 23 patients who had no previous diagnosis of diabetes and/or glycated hemoglobin <6.5%, after the onset of AMI at 2 weeks. Plasma active glucagon-like peptide (GLP)-1 level was measured in each sample. The extent of myocardial salvage 7 days after AMI was evaluated on cardiovascular magnetic resonance imaging. MAGE and the peak CD14(+)CD16(-) monocyte level were significantly negatively correlated with myocardial salvage index (MSI). MAGE was significantly correlated with peak CD14(+)CD16(-) monocyte level. Of interest, plasma GLP-1 level was significantly positively correlated with MSI and significantly negatively correlated with MAGE.
  
  
  CONCLUSIONS
  Glucose fluctuations during the acute phase of AMI affect MSI, indicating that manipulation of glucose variability from peak to nadir might be a potential therapeutic target for salvaging ischemic damage.
authors.affiliation: Departments of Cardiovascular Medicine, Wakayama Medical University.
authors.forename: Ikuko
authors.initials: I
authors.lastname: Teraguchi
authors.forename: Toshio
authors.initials: T
authors.lastname: Imanishi
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Ozaki
authors.forename: Takashi
authors.initials: T
authors.lastname: Tanimoto
authors.forename: Minoru
authors.initials: M
authors.lastname: Ueyama
authors.forename: Makoto
authors.initials: M
authors.lastname: Orii
authors.forename: Yasutsugu
authors.initials: Y
authors.lastname: Shiono
authors.forename: Kunihiro
authors.initials: K
authors.lastname: Shimamura
authors.forename: Kohei
authors.initials: K
authors.lastname: Ishibashi
authors.forename: Takashi
authors.initials: T
authors.lastname: Yamano
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Ino
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Yamaguchi
authors.forename: Kumiko
authors.initials: K
authors.lastname: Hirata
authors.forename: Takashi
authors.initials: T
authors.lastname: Kubo
authors.forename: Tokio
authors.initials: T
authors.lastname: Sanke
authors.forename: Takashi
authors.initials: T
authors.lastname: Akasaka
mesh_terms: D000368:Aged; D001786:Blood Glucose / Q000378:metabolism*; D005260:Female; D005434:Flow Cytometry; D058851:GPI-Linked Proteins; D052216:Glucagon-Like Peptide 1 / Q000097:blood*; D006801:Humans; D018950:Lipopolysaccharide Receptors; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D009203:Myocardial Infarction / Q000097:blood* / Q000628:therapy*; D017452:Receptors, IgG; D013997:Time Factors
chemical_list: D001786:Blood Glucose; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D018950:Lipopolysaccharide Receptors; D017452:Receptors, IgG; D052216:Glucagon-Like Peptide 1