Diabetes & Vascular Disease Research最新文献

Objective: To compare fetal and neonatal cardiac morphology in fetuses of mothers with gestational diabetes mellitus (GDM) with the controls.

Patients and methods: Pregnant women at average risk of GDM underwent 100-g, 3-h-OGTT at 24-28 weeks of gestation for diagnosis of GDM. Both GDM group and the control group underwent fetal echocardiography at 32-36 weeks to assess cardiac dimensions. The neonates underwent echocardiography within 48 h after birth to assess cardiac morphology.

Results: A total of 154 pregnant women were recruited, including 60 in the GDM group and 94 in the control group. All of the study group were well controlled for GDM. Most baseline characteristics of both groups were comparable. All obstetric outcomes were not significantly different between the two groups. Morphological cardiac dimensions in the fetuses and newborns of both groups were also not significant different. Subgroup analysis in the study group showed no significantly different in cardiac morphology between the group with diet control and that of insulin control.

Conclusion: Fetal and neonatal cardiac morphologic changes among mothers with well-controlled GDM are not significantly different from those in the controls. It is possible that good control of maternal blood glucose can prevent fetal and neonatal cardiac abnormalities.

Background: Diabetes type 2 is one of the strongest risk factors affecting coronary artery disease (CAD) and is also a marker of poor short and long-term prognosis in subjects with acute coronary syndrome (ACS) treated with percutaneous coronary intervention (PCI) with subsequent drug-eluting stent (DES) implantation. Chronic local vascular inflammation along with endothelial dysfunction is postulated to be the pathophysiological background of unfavorable results. The second generation of metallic magnesium BRS -Magmaris (Biotronik, Berlin, Germany) had been introduced to clinical practice to overcome these limitations.

Methods: We evaluated 2-years clinical outcomes after Magmaris BRS implantation in NSTE-ACS diabetic (n-72) and non-diabetic (n-121) cohorts.

Results: No significant differences between diabetic and non-diabetes cohorts were noticed in terms of Primary Outcome (cardiac death, myocardial infarction, stent thrombosis) (8.1% vs 3.3% p = 0.182) and Principal secondary outcome - TLF- target lesion failure (9.5% vs 3.3% p = 0.106) at 2-years follow-up.

Conclusions: 2-years outcome suggests good safety and efficacy of the magnesium BRS (Magmaris) in NSTE- ACS and concomitant DM. Nevertheless, there is a strong need for large multicenter, randomized, prospective studies for a full assessment of this novel device in diabetic patients with ACS.

Aims: To analyze the association between hemoglobin glycation index (HGI) and the long-term prognosis of patients with coronary artery disease (CAD) after percutaneous coronary intervention (PCI).

Methods: Predicted glycated hemoglobin (HbA1c) level was calculated using an established formula and HGI represented the difference between laboratory measured HbA1c and predicted HbA1c. A total of 1780 patients were stratified into three subgroups (HGI < -0.4, -0.4 ≦ HGI < 0.12 and HGI ≧ 0.12). The primary endpoints included all-cause mortality (ACM) and cardiac mortality (CM). The secondary endpoints were major adverse cardiac events (MACEs) and major adverse cardiac and cerebrovascular events (MACCEs).

Results: ACM occurred in 54 patients: 22 (3.7) in the low-HGI subgroup, 8 (1.3) in the moderate-HGI subgroup and 24 (4.1) in the high-HGI subgroup (p = .012). After adjusting for the traditional clinical prognostic factors, multivariate Cox regression analysis showed that patients in both the low and high HGI subgroups had significantly increased risk of ACM as compared with patients in the moderate HGI subgroup (hazard ratio [HR] = 4.979, 95% confidence interval [CI]: 1.865-13.297, p = .001 and HR = 2.918, 95% CI: 1.075-7.922, p = .036). However, we did not find significant differences in the incidence of CM, MACEs and MACCEs.

Conclusion: HGI can predicts risk for long-term mortality in patients undergoing PCI. This index could be helpful for the effective clinical management of the CAD population.

Background: Advanced glycation end products (AGEs) impair vascular physiology in Diabetes mellitus (DM). However, the underlying mechanisms remain unclear. Vascular large conductance calcium-activated potassium (BK) channels play important roles in coronary arterial function.Purpose: Our study aimed to investigate the regulatory role of AGEs in BK channels.Research Design: Using gavage of vehicle (V, normal saline) or aminoguanidine (A) for 8 weeks, normal and diabetic rats were divided into four groups: C+V group, DM+V group, C+A group, and DM+A group.Study Sample: Coronary arteries from different groups of rats and human coronary smooth muscle cells were used in this study.Data Collection and Analysis: Data were presented as mean ± SEM (standard error of mean). Student's t-test was used to compare data between two groups. One-way ANOVA with post-hoc LSD analysis was used to compare data between multiple groups.Results: Compared to the C+V group, vascular contraction induced by iberiotoxin (IBTX), a BK channel inhibitor, was impaired, and BK channel densities decreased in the DM+V group. However, aminoguanidine administration reduced the impairment. Protein expression of BK-β1, phosphorylation of adenosine 5'-monophosphate-activated protein kinase (AMPK), and protein kinase B (PKB or Akt) were down-regulated, while F-box protein 32 (FBXO32) expression increased in the DM+V group and in high glucose (HG) cultured human coronary smooth muscle cells. Treatment with aminoguanidine in vitro and in vivo could reverse the above protein expression. The effect of aminoguanidine on the improvement of BK channel function by inhibiting the generation of AGEs was reversed by adding MK2206 (Akt inhibitor) or Compound C (AMPK inhibitor) in HG conditions in vitro.Conclusions: AGEs aggravate BK channel dysfunction via the AMPK/Akt/FBXO32 signaling pathway.