The apolipoprotein B/A1 ratio is associated with reactive oxygen metabolites and endothelial dysfunction in statin-treated patients with coronary artery disease.

AIM: The prognostic significance of the apolipoprotein B/A1 (ApoB/A1) ratio in statintreated patients with coronary artery disease (CAD) is unknown. We aimed to evaluate the association of the ApoB/A1 ratio with oxidative stress and endothelial dysfunction in these patients. METHODS: We enrolled 62 consecutive statin-treated patients who underwent percutaneous coronary intervention (PCI). Their lipid profiles, diacron-reactive oxygen metabolites (d-ROMs), as a marker of oxidative stress, flow-mediated dilatation (FMD), as a marker of vascular endothelial function, and C-reactive protein (CRP) levels, as a marker of inflammation, were measured. RESULTS: Our study population comprised 44 men and 18 women (mean age, 70.5 ± 2.5 years). The ApoB/A1 ratio was positively correlated with the results of the d-ROMs test (p=0.004, r=0.36) and CRP level (p=0.02, r=0.30) and negatively correlated with the %FMD (p=0.005, r=-0.40). A multivariate logistic regression analysis showed that the most powerful predictive factor for the d-ROMs was the ApoB/A1 ratio (p=0.026). We therefore divided patients into two groups according to the cutoff point reported by the INTERHEART study: a low ApoB/A1 ratio (<0.641, n=26) and a high ApoB/A1 ratio (>0.641, n=36). The patients with a high ApoB/A1 ratio had higher levels of d-ROMs and CRP, and tended to have a lower %FMD. CONCLUSION: The ApoB/A1 ratio was associated with the d-ROMs, a marker of oxidative stress, endothelial dysfunction and inflammation, and could be useful as a residual atherosclerotic risk marker to help prevent CAD in statin-treated patients.

Possible association between non-invasive parameter of flow-mediated dilatation in brachial artery and whole coronary plaque vulnerability in patients with coronary artery disease.

BACKGROUND: Despite being a relatively widely-used non-invasive parameter of endothelial dysfunction, little is known regarding the relationship between flow-mediated dilatation (FMD) and coronary plaque vulnerability in patients with coronary artery disease (CAD). METHODS: 111 CAD patients (age; 68.9 ± 9.3) who underwent both coronary intervention and FMD were enrolled. Spectral analyses of intravascular ultrasound radiofrequency data for both culprit and non-culprit lesions were performed using Virtual Histology software. Plaque burden was described based on fibrotic, fibro-fatty, dense calcium, and necrotic core (NC) components, and thin-cap fibroatheroma (TCFA) was defined as focal NC rich (> 10%) plaques touching the lumen with a percent-plaque volume exceeding 40%. RESULTS: Averaged %FMD was 2.86 ± 2.03% (median 2.27%, 25th 1.40%, 75th 4.20%). NC volumes were negatively correlated with log%FMD for both culprit and non-culprit lesions (P = 0.001, r = 0.31 and P = 0.03, r = 0.21, respectively). We divided the patients into three tertiles according to %FMD; 38 were lower (≤ 1.75%), 41 were middle (> 1.75%, but ≤ 3.5%), and 32 were upper tertile (> 3.5%). The prevalence rate of TCFA increased with decreasing %FMD tertile and the incidence of major adverse cardiac events was significantly higher in lower %FMD tertile. Multivariate logistic regression analyses showed that the most powerful predictive factor for TCFA was log%FMD (P < 0.0001), and ROC curve analysis identified %FMD of < 2.81% (AUC = 0.82, sensitivity: 91.2%, specificity: 66.7%) as the optimal cut-off point for predicting the presence of TCFA. CONCLUSIONS: Impaired endothelial function in brachial arteries may be associated with whole coronary plaque vulnerability and poor clinical outcome in patients with CAD.

Comparisons of detailed arterial healing response at seven months following implantation of an everolimus- or sirolimus-eluting stent in patients with ST-segment elevation myocardial infarction.

BACKGROUND: The difference of arterial healing response following everolimus-eluting stent (EES) or sirolimus-eluting stent (SES) implantation in patients with ST-segment elevated myocardial infarction (STEMI) has not been compared in detail. METHODS: Thirty-five patients with STEMI were randomly implanted with an EES or SES (23 EES, 12 SES). At seven months, neointimal thickness (NIT) and strut malapposition were evaluated by optical coherence tomography (OCT) and the grade and heterogeneity of neointimal coverage (NIC) and development of intra-stent thrombi were evaluated by angioscopy. RESULTS: No significant differences were noted in clinical events experienced by the two groups, although one patient with an EES died following a papillary muscle rupture and one patient with a SES experienced sub-acute stent thrombosis. On OCT, although the EES implants showed a greater NIT than the SES implants (94.8 ± 88.8 µm vs 65.6 ± 63.3 µm, P<0.0001), both the EES and SES showed an excellent suppression of neointimal proliferation in the culprit lesion of STEMI. The frequency of uncovered and malapposed struts of EES was significantly lower than that of SES (2.7% vs. 15.7%, P<0.0001, 0.7% vs. 2.3%, P<0.0001, respectively). The ratio of stents fully covered with neointima of EES group was significantly higher than that of SES group (P=0.04). Angioscopic analysis also showed greater dominant NIC grade with homogenous NIC in EES than in SES (P=0.03, P=0.0002, respectively). The incidence of massive intra-stent thrombus of EES was lower than that of SES (P=0.05). CONCLUSION: For patients with STEMI, EES may promote better arterial healing response than SES.

Effect of 3-month repeated administration of miglitol on vascular endothelial function in patients with diabetes mellitus and coronary artery disease.

Repeated postprandial hyperglycemia may play an important role in the development of atherosclerosis by suppressing vascular endothelial function. Although miglitol suppresses the elevation of blood glucose levels shortly after a meal more than other α-glucosidase inhibitors, the effect of 3-month repeated administration of miglitol on endothelial dysfunction is unknown. Fifty patients with type 2 diabetes and coronary artery disease were enrolled in the present study. The patients were randomly divided into 2 groups, the first treated with miglitol and the second with voglibose for 3 months. Blood chemistry (lipid and blood glucose profiles, glycosylated hemoglobin, 1,5-anhydroglucitol, serum insulin levels, and C-reactive protein) and flow-mediated dilatation were measured at the beginning and end of the trial period. Patient characteristics and blood chemistry of the 2 groups were similar at the beginning of the trial. At the end of the trial, glycosylated hemoglobin decreased in the 2 groups, but the improvements in 1,5-anhydroglucitol in the miglitol group were significantly higher than in the voglibose group. Insulin resistance index, C-reactive protein, and percentage flow-mediated dilatation were also improved in the miglitol group but not in the voglibose group. In conclusion, 3-month repeated administration of miglitol improved vascular endothelial dysfunction by strongly suppressing postprandial hyperglycemia. Miglitol may have antiatherogenic effects in patients with type 2 diabetes and coronary artery disease.