title: Association between hyperglycemia and the no-reflow phenomenon in patients with acute myocardial infarction.
abstract: OBJECTIVE
  We investigated the association between hyperglycemia and the no-reflow phenomenon in patients with acute myocardial infarction (AMI).
  
  
  BACKGROUND
  Hyperglycemia is associated with increased risks of heart failure, cardiogenic shock, and death after AMI, but its underlying mechanism remains unknown.
  
  
  METHODS
  A total of 146 consecutive patients with a first AMI were studied by intracoronary myocardial contrast echocardiography (MCE) after successful reperfusion within 24 h after symptom onset. Two-dimensional echocardiography was recorded on day 1 and three months later to determine the change in the wall motion score (DeltaWMS; sum of 16 segmental scores; dyskinesia = 4 to normokinesia = 0).
  
  
  RESULTS
  The no-reflow phenomenon was found on MCE in 49 (33.6%) of 146 patients; their glucose level on hospital admission was significantly higher than that of patients who did not exhibit this phenomenon (209 +/- 79 vs. 159 +/- 56 mg/dl; p < 0.0001). There was no difference in glycosylated hemoglobin or in the incidence of diabetes mellitus between the two subsets. The no-reflow phenomenon was more often observed in the 75 patients with hyperglycemia (>/=160 mg/dl) than in those without hyperglycemia (52.0% vs. 14.1%; p < 0.0001). Patients with hyperglycemia had a higher peak creatine kinase level (2,497 +/- 1,603 vs. 1,804 +/- 1,300 IU/l; p = 0.005) and a lower DeltaWMS (3.7 +/- 4.8 vs. 5.7 +/- 4.3; p = 0.01) than did those without hyperglycemia. The blood glucose level was an independent prognostic factor for no reflow, along with age, gender, absence of pre-infarction angina, complete occlusion of the culprit lesion, and anterior AMI.
  
  
  CONCLUSIONS
  Hyperglycemia might be associated with impaired microvascular function after AMI, resulting in a larger infarct size and worse functional recovery.
authors.affiliation: Division of Cardiology, Sakurabashi Watanabe Hospital, Osaka University, Osaka, Japan.
authors.forename: Katsuomi
authors.initials: K
authors.lastname: Iwakura
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ito
authors.forename: Masashi
authors.initials: M
authors.lastname: Ikushima
authors.forename: Shigeo
authors.initials: S
authors.lastname: Kawano
authors.forename: Atsushi
authors.initials: A
authors.lastname: Okamura
authors.forename: Katsuaki
authors.initials: K
authors.lastname: Asano
authors.forename: Tadashi
authors.initials: T
authors.lastname: Kuroda
authors.forename: Koji
authors.initials: K
authors.lastname: Tanaka
authors.forename: Tohru
authors.initials: T
authors.lastname: Masuyama
authors.forename: Masatsugu
authors.initials: M
authors.lastname: Hori
authors.forename: Kenshi
authors.initials: K
authors.lastname: Fujii
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000379:methods; D001786:Blood Glucose / Q000378:metabolism; D003326:Coronary Circulation / Q000502:physiology*; D048909:Diabetes Complications; D018450:Disease Progression; D004452:Echocardiography; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006439:Hemodynamics; D006801:Humans; D006943:Hyperglycemia / Q000150:complications* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy; D011237:Predictive Value of Tests; D020127:Recovery of Function / Q000502:physiology; D012189:Retrospective Studies; D015607:Stents
chemical_list: D001786:Blood Glucose; D006442:Glycated Hemoglobin