title: Miglitol improves postprandial endothelial dysfunction in patients with acute coronary syndrome and new-onset postprandial hyperglycemia.
abstract: BACKGROUND
  Hyperglycemia, a risk factor for development of cardiovascular disease, causes endothelial dysfunction. Alpha-glucosidase inhibitors (α-GIs) improve postprandial hyperglycemia (PPHG) and may have favorable effects on associated cardiovascular disease. Effects of α-GIs in patients with acute coronary syndrome (ACS) and PPHG remain unclear; thus, we assessed the effect of α-GI miglitol on endothelial function in such patients by digital reactive hyperemia peripheral arterial tonometry (RH-PAT).
  
  
  METHODS
  Fifty-four patients with ACS who underwent primary percutaneous coronary intervention were enrolled in the study: 36 with new-onset PPHG and 18 with normal glucose tolerance. Eighteen PPHG patients were given 50 mg of miglitol with each meal for 1 week. Endothelial function was assessed on the basis of the RH-PAT index (RHI) before and after the 1-week miglitol treatment. The other 18 PPHG patients and the 18 NGT patients were not given any anti-diabetic agent for 1 week, and endothelial function was assessed.
  
  
  RESULTS
  Postprandial RHI decreased significantly in patients with PPHG. Miglitol improved PPHG significantly; postprandial RHI also improved (p = 0.007). Significant inverse correlation was found between the postprandial change in RHI and postprandial fasting-to-60-minutes surge in glucose (r = -0.382, p = 0.009). Moreover, the improvement in endothelial function correlated with the reduced postprandial glucose surge achieved with miglitol (r = -0.462, p = 0.001).
  
  
  CONCLUSIONS
  Postprandial changes in glucose are related to endothelial dysfunction in ACS. Miglitol-based improvement in PPHG appears to improve endothelial function. The effect of miglitol on glucose-dependent endothelial function might improve outcomes of ACS.
authors.affiliation: Division of Cardiology, Department of Medicine, Nihon University School of Medicine, 30-1 Ohyaguchi Kamicho, Itabashi-ku, Tokyo 173-8610, Japan.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Kitano
authors.forename: Masaaki
authors.initials: M
authors.lastname: Chiku
authors.forename: Yuxin
authors.initials: Y
authors.lastname: Li
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Okumura
authors.forename: Daisuke
authors.initials: D
authors.lastname: Fukamachi
authors.forename: Tadateru
authors.initials: T
authors.lastname: Takayama
authors.forename: Takafumi
authors.initials: T
authors.lastname: Hiro
authors.forename: Satoshi
authors.initials: S
authors.lastname: Saito
authors.forename: Atsushi
authors.initials: A
authors.lastname: Hirayama
mesh_terms: D017485:1-Deoxynojirimycin / Q000031:analogs & derivatives* / Q000627:therapeutic use; D054058:Acute Coronary Syndrome / Q000150:complications / Q000628:therapy*; D000368:Aged; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000188:drug therapy*; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D008297:Male; D008365:Manometry; D008875:Middle Aged; D062645:Percutaneous Coronary Intervention; D019518:Postprandial Period; D016896:Treatment Outcome
chemical_list: D007004:Hypoglycemic Agents; C045621:miglitol; D017485:1-Deoxynojirimycin