These results indicate that the presence of atherosclerotic plaques at the spasm site is likely to be related to the occurrence of a focal vasospasm. This may support the difference of features between focal CS and diffuse CS and contribute to precise treatment for each spasm type.

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BackgroundOxidative stress is involved in the initiation and progression of atherosclerosis, and hyperglycemia is known to increase oxidative stress, which injures the endothelium and accelerates atherosclerosis. To clarify the relation between oxidative stress, diabetes mellitus (DM), and acute myocardial infarction (AMI), we evaluated and compared time-specific oxidative stress after AMI in patients with and without DM by simple measurement of derivatives of reactive oxygen metabolites (d-ROMs) levels as indices of reactive oxygen species production.MethodsSixty-eight AMI patients were enrolled (34 non-DM patients and 34 DM patients). Using the FRAS4 free radical analytical system, we measured d-ROMs levels in each patient at two time points: 1 and 2 weeks after AMI onset.Resultsd-ROM levels decreased significantly between week 1 and week 2 (from 475.4 ± 119.4 U.CARR to 367.7 ± 87.9 U.CARR, p < 0.001) in the non-DM patients but did not change in the DM patients (from 463.1 ± 109.3 U.CARR to 461.7 ± 126.8 U.CARR, p = 0.819). Moreover, significant correlation was found in the total patient group between d-ROMs levels at 1 week and N-terminal prohormone of brain natriuretic peptide (r = 0.376, p = 0.041) and between d-ROM levels at 2 weeks and 2-hour oral glucose tolerance test glucose levels (r = 0.434, p < 0.001).ConclusionsExposure to oxidative stress is greater in AMI patients with DM than AMI patients without DM. Our study results suggest that it is the continuous hyperglycemia that increases oxidative stress in these patients, causing endothelial dysfunction and accelerating atherosclerosis. However, long-term follow up study is needed to assess whether the increased oxidative stress affects patient outcomes.Electronic supplementary materialThe online version of this article (doi:10.1186/s12872-016-0259-6) contains supplementary material, which is available to authorized users.

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BackgroundHyperglycemia, 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).MethodsFifty-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.ResultsPostprandial 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).ConclusionsPostprandial 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.