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  • 1
    Online Resource
    Online Resource
    Intensive Treat-to-Target Statin Therapy in High-Risk Japanese Patients With Hypercholesterolemia and Diabetic Retinopathy: Report of a Randomized Study
    American Diabetes Association ; 2018
    In:  Diabetes Care Vol. 41, No. 6 ( 2018-06-01), p. 1275-1284
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 41, No. 6 ( 2018-06-01), p. 1275-1284
    Abstract: Diabetes is associated with high risk of cardiovascular (CV) events, particularly in patients with dyslipidemia and diabetic complications. We investigated the incidence of CV events with intensive or standard lipid-lowering therapy in patients with hypercholesterolemia, diabetic retinopathy, and no history of coronary artery disease (treat-to-target approach). RESEARCH DESIGN AND METHODS In this multicenter, prospective, randomized, open-label, blinded end point study, eligible patients were randomly assigned (1:1) to intensive statin therapy targeting LDL cholesterol (LDL-C) & lt;70 mg/dL (n = 2,518) or standard statin therapy targeting LDL-C 100–120 mg/dL (n = 2,524). RESULTS Mean follow-up was 37 ± 13 months. LDL-C at 36 months was 76.5 ± 21.6 mg/dL in the intensive group and 104.1 ± 22.1 mg/dL in the standard group (P & lt; 0.001). The primary end point events occurred in 129 intensive group patients and 153 standard group patients (hazard ratio [HR] 0.84 [95% CI 0.67–1.07] ; P = 0.15). The relationship between the LDL-C difference in the two groups and the event reduction rate was consistent with primary prevention studies in patients with diabetes. Exploratory findings showed significantly fewer cerebral events in the intensive group (HR 0.52 [95% CI 0.31–0.88]; P = 0.01). Safety did not differ significantly between the two groups. CONCLUSIONS We found no significant decrease in CV events or CV-associated deaths with intensive therapy, possibly because our between-group difference of LDL-C was lower than expected (27.7 mg/dL at 36 months of treatment). The potential benefit of achieving LDL-C & lt;70 mg/dL in a treat-to-target strategy in high-risk patients deserves further investigation.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc17-2224
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
    detail.hit.zdb_id: 1490520-6
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  • 2
    Online Resource
    Online Resource
    Effects of Intravenous Nicorandil Before Reperfusion for Acute Myocardial Infarction in Patients With Stress Hyperglycemia
    American Diabetes Association ; 2006
    In:  Diabetes Care Vol. 29, No. 2 ( 2006-02-01), p. 202-206
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 29, No. 2 ( 2006-02-01), p. 202-206
    Abstract: OBJECTIVE—Stress hyperglycemia increases the risk of mortality and poor outcomes in patients with acute myocardial infarction (AMI). We aimed to assess effects of intravenous nicorandil administered before reperfusion on AMI patients with stress hyperglycemia. RESEARCH DESIGN AND METHODS—This study consisted of 158 consecutive first AMI patients with stress hyperglycemia who underwent percutaneous coronary intervention (PCI) within 24 h from the onset. They were randomly assigned to receive 12 mg of nicorandil (n = 81) or a placebo (n = 77) intravenously just before reperfusion. Stress hyperglycemia was defined as a blood glucose level ≥10 mmol/l (180 mg/dl). We examined various aspects of epicardial flow and microvascular function as immediate data and major adverse cardiac events (MACEs) (coronary heart disease death or unplanned readmission due to congestive heart failure) as late-phase data. RESULTS—The incidence of slow flow after PCI was lower in the nicorandil group (13.6 vs. 27.3%, P & lt; 0.04). ST segment resolution & gt;50% was observed in 70.4 and 53.2% on nicorandil and placebo, respectively (P & lt; 0.03). Patients treated with nicorandil had a lower peak creatine kinase level (3,137 ± 2,577 vs. 4,333 ± 3,608, P & lt; 0.02). Upon Kaplan-Meier analysis, 5 years’ freedom from MACEs was 86.4% in the nicorandil group and 74.0% in the placebo (P & lt; 0.05). CONCLUSIONS—Adjunctive therapy with administration of intravenous nicorandil before reperfusion on AMI patients with stress hyperglycemia significantly improves epicardial flow and prevents the occurrence of severe microvascular reperfusion injury, resulting in better outcomes in these patients.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/diacare.29.02.06.dc05-1588
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2006
    detail.hit.zdb_id: 1490520-6
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  • 3
    Online Resource
    Online Resource
    Therapeutic Neovascularization Using Cord Blood–Derived Endothelial Progenitor Cells for Diabetic Neuropathy
    American Diabetes Association ; 2005
    In:  Diabetes Vol. 54, No. 6 ( 2005-06-01), p. 1823-1828
    Details
    In: Diabetes, American Diabetes Association, Vol. 54, No. 6 ( 2005-06-01), p. 1823-1828
    Abstract: Diabetic neuropathy is based on the impairment of nerve blood flow and the metabolic disorder. Although the vasodilating agents and anticoagulants improve nerve function and symptoms in diabetic neuropathy, more effective treatments are needed. Because endothelial progenitor cells (EPCs) have been identified in adult human peripheral blood, many studies have shown that transplantation of EPCs improves circulation to ischemic tissues. In this study, we have demonstrated that therapeutic neovascularization using human umbilical cord blood–derived EPCs reversed diabetic neuropathy. EPCs were isolated and expanded on day 7 of culture from cord blood mononuclear cells. Unilateral intramuscular injection of EPCs into hindlimb skeletal muscles significantly ameliorated impaired sciatic motor nerve conduction velocity and sciatic nerve blood flow in the EPC-injected side of streptozotocin-induced diabetic nude rats compared with the saline-injected side of diabetic nude rats. Histological study revealed an increased number of microvessels in hindlimb skeletal muscles in the EPC-injected side of diabetic rats. These findings suggest that transplantation of EPCs from cord blood may be a useful treatment for diabetic neuropathy.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diabetes.54.6.1823
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2005
    detail.hit.zdb_id: 1501252-9
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  • 4
    Online Resource
    Online Resource
    Stress Augments Insulin Resistance and Prothrombotic State
    American Diabetes Association ; 2012
    In:  Diabetes Vol. 61, No. 6 ( 2012-06-01), p. 1552-1561
    Details
    In: Diabetes, American Diabetes Association, Vol. 61, No. 6 ( 2012-06-01), p. 1552-1561
    Abstract: Stressors contribute to thrombosis and insulin resistance. Since obesity-related adipose inflammation is also involved in these pathological states, we assumed that stress correlates with adipose inflammation. Male mice were subjected to 2-week intermittent restraint stress. Expression of plasma lipids, monocyte/macrophage markers (CD11b, CD68, and F4/80), proinflammatory cytokines (monocyte chemoattractant protein-1 [MCP-1], tumor necrosis factor-α, and interleukin-6), adiponectin, heat shock protein 70.1 (HSP70.1), and coagulation factors (plasminogen activation inhibitor-1 [PAI-1] and tissue factor [TF]) in blood and inguinal white adipose tissue (WAT) was determined using immunohistochemistry, enzyme-linked immunosorbent assay, and RT-PCR, respectively. Glucose metabolism was assessed by glucose tolerance tests (GTTs) and insulin tolerance tests, and expression of insulin receptor substrate-1 (IRS-1) and glucose transporter 4 (GLUT4) in WAT. To examine effects of MCP-1 blockade, animals were treated with control or neutralizing antibody, or transplanted with control or 7ND (dominant-negative form of MCP-1)-overexpressing adipose-derived stromal cells (ADSCs). Stress increased monocyte accumulation, free fatty acids, proinflammatory cytokine, and HSP70.1 and reduced adiponectin. Adipose stromal cells highly expressed MCP-1. The stress-induced adipose inflammation increased PAI-1 and TF but did not give rise to thrombus formation. Without any changes in GTT, stress worsened insulin sensitivity and decreased IRS-1 and GLUT4 in WAT. Neutralizing antibody and 7ND-ADSCs reversed stress-induced adipose inflammation, procoagulant state, and insulin resistance. Stress evoked adipose inflammation to increase coagulation factors and impair insulin sensitivity through adipose-derived MCP-1.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db11-0828
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2012
    detail.hit.zdb_id: 1501252-9
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