OBJECTIVE -Hyperglycemia is associated with poor clinical outcomes and mortality in myocardial infarction, stroke, and general hospital patients. However, there are few data regarding the effect of hyperglycemia on outcomes in patients receiving total parenteral nutrition (TPN), a therapy that predisposes patients to hyperglycemia. The aim of this study was to determine whether elevated blood glucose levels are associated with adverse outcomes in patients receiving TPN. RESEARCH DESIGN AND METHODS-A retrospective analysis was undertaken from the medical records of 111 patients (122 treatment episodes) receiving TPN. All patients had blood drawn daily for the measurement of blood glucose levels. Outcome measures were assessed as a function of mean daily blood glucose levels while receiving TPN.RESULTS -Increased blood glucose levels were associated with an increased risk of cardiac complications (odds ratio 1.61, 95% CI 1.09 -2.37, P ϭ 0.02), infection (1.4, 1.08 -1.82, P ϭ 0.01), systemic sepsis (1.36, 1.00 -1.86, P ϭ 0.05), acute renal failure (1.47, 1.00 -2.17, P ϭ 0.05), and death (1.77, 1.23-2.52, P Ͻ 0.01). When the data were examined by quartiles of blood glucose levels, the mortality of subjects in the highest quartile was 10.9 times (95% CI 2.0 -60.5, P Ͻ 0.01) that of subjects in the lowest quartile, and the risk of developing any complication was 4.3 times higher (1.4 -13.1, P Ͻ 0.01). These effects were independent of age, sex, or prior diabetes status.CONCLUSIONS -Hyperglycemia is a predictor of poor outcomes in patients receiving TPN. The confirmation of a relation between blood glucose levels and adverse outcomes provides support for tight glycemic control in these patients. Diabetes Care 28:2367-2371, 2005H yperglycemia is associated with adverse outcomes in critically ill patients. A number of studies have demonstrated a relation between blood glucose levels and mortality after myocardial infarction (1) and stroke (2). Among hospitalized patients in general, those with hyperglycemia have a higher mortality rate than those with normal glucose levels (3). Hyperglycemia has been associated with increased infection rates in patients after cardiothoracic (4 -6) or general (7) surgery. Recent randomized controlled trials in intensive care settings (8) and myocardial infarction (9) have also demonstrated that glucose control with insulin therapy can reduce mortality.One group of patients who should be particularly susceptible to hyperglycemia are those who require total parenteral nutrition (TPN). These patients are often critically ill and are administered preparations with a high glucose content. The combination of these two factors leads to a high frequency of hyperglycemia in a particularly vulnerable population. Central vein catheter infections have been observed to be five times more prevalent in diabetic patients than in the general TPN population (10). However, to date, the potential for hyperglycemia to result in other adverse outcomes in patients receiving TPN has not been systematically exami...
The 5-year results of the COBEST demonstrated that the CS has an enduring patency advantage over the BMS in both the short and long terms. Furthermore, the CS showed acceptable patency rates for the treatment of more severe TASC C and D lesions, and patients who received a CS required fewer revascularization procedures. However, the choice of stent did not affect the rate of major limb amputations.
The iron-binding protein lactoferrin (Lf) is a constituent of neutrophil secondary granules and is discharged into the surrounding medium when neutrophils are activated. Lf released from neutrophils phagocytosing opsonized particles inhibits proliferation of mixed lymphocyte cultures (MLC) and has also been shown to inhibit granulopoiesis, suppress antibody production, and regulate natural killer cell activity. All of these processes are controlled by cytokines, suggesting that Lf may modulate immune responses by inhibiting cytokine activity. When MLC were cultured in round-bottomed wells to crowd the cells together, Lf, 50% saturated with iron, inhibited both proliferation and interleukin-2 (IL-2) release into the supernatants. Inhibition was concentration-dependent and lost at concentrations of Lf greater than 10(-12) mol/L. Lf at 10(-10) mol/L inhibited release of tumor necrosis factor-alpha (TNF) and interleukin- 1 beta (IL-1) into MLC supernatants, as well as inhibiting IL-2 release. TNF in the supernatant was significantly reduced at 5 and 24 hours, becoming less and losing significance by 72 hours. IL-1 in the supernatant was not significantly reduced at 5 and 24 hours, becoming significant at 48 and 72 hours. IL-2 was significantly reduced at 48 and 72 hours and followed the same time course as proliferation. Inhibition was blocked by specific antiserum to Lf, but not by a preimmune serum. Lf, 10(-10) mol/L, also inhibited the production of TNF (49.15% +/- 7.98%; n = 10, P = .032) and IL-1 (42.67% +/- 6.72%; n = 6, P = .032) from endotoxin-stimulated mononuclear cells. As with MLC, inhibition was dose-dependent and abrogated by specific antiserum. Lf did not block the biological action of TNF, IL-1, or IL-2 in specific assays using cytokine-sensitive cell lines. These data suggest that Lf, released from activated neutrophils, acts as a negative feedback mechanism to prevent recruitment and activation of leukocytes in sites of inflammation.
Summary. Background: Experimental animal studies have shown that the intimal hyperplasia (IH) responsible for occlusion after successful revascularization procedures may be partially caused by a bone marrow-derived cell that migrates to the site of vascular injury. Concurrent studies have demonstrated an extensive role in wound healing for the circulating fibrocyte. Objectives: We aimed to trace the path of the circulating cell that contributes to IH and determine if it is the fibrocyte. Methods and results: We established an in vitro model whereby purified monocytes from six healthy human volunteers were cultured into fibrocytes. These cells were morphometrically similar to the vascular smooth muscle cell (VSMC) found in IH and expressed alpha-smooth muscle actin (a-SMA) as well as CD34, CD45 and Collagen I (Col I), markers indicative of the fibrocyte. In an in vivo ovine carotid artery synthetic patch graft model, carboxyfluorescein diacetate, succinimidyl ester (CFSE) labeled circulating leukocytes were observed throughout the graft as well as in the neointima in 18 sheep. These cells were shown to produce collagen and a-SMA at 1, 2 and 4 weeks. These cells then underwent immunohistochemical analysis and were found to express a set of markers unique to the fibrocyte (CD34, CD45, Vimentin and a-SMA) and also to double stain for CD34 and a-SMA. Conclusions: IH in an ovine carotid artery patch graft model is partially derived from a hematopoietic circulating progenitor cell that acquires mesenchymal features as it matures at the site of injury.
Peripheral artery disease affects >200 million people worldwide and is associated with significant limb and cardiovascular morbidity and mortality. Limb revascularization is recommended to improve function and quality of life for symptomatic patients with peripheral artery disease with intermittent claudication who have not responded to medical treatment. For patients with critical limb ischemia, the goals of revascularization are to relieve pain, help wound healing, and prevent limb loss. The baseline risk of cardiovascular and limb-related events demonstrated among patients with stable peripheral artery disease is elevated after revascularization and related to atherothrombosis and restenosis. Both of these processes involve platelet activation and the coagulation cascade, forming the basis for the use of antiplatelet and anticoagulant therapies to optimize procedural success and reduce postprocedural cardiovascular risk. Unfortunately, few high-quality, randomized data to support use of these therapies after peripheral artery disease revascularization exist, and much of the rationale for the use of antiplatelet agents after endovascular peripheral revascularization is extrapolated from percutaneous coronary intervention literature. Consequently, guideline recommendations for antithrombotic therapy after lower limb revascularization are inconsistent and not always evidence-based. In this context, the purpose of this structured review is to assess the available randomized data for antithrombotic therapy after peripheral arterial revascularization, with a focus on clinical trial design issues that may affect interpretation of study results, and highlight areas that require further investigation.
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