Outcomes after non-cardiac surgery: Mortality, complications, disability, and rehospitalization

In the last 25 years, the number of patients aged ≥75 years undergoing non-cardiac surgery has greatly increased. In elderly patients, frailty is significantly associated with an increased risk of adverse events, functional decline, procedural complications, prolonged hospitalization, and mortality. The relationship between frailty and increased mortality and morbidity requires an appropriate tool of assessment to accurately quantify the patient's clinical and perioperative conditions. The preoperative evaluation of elderly patients candidate for non-cardiac surgery should include assessment of frailty, sarcopenia and malnutrition, as these are related to high surgical risk. For colon-rectal surgery as also for gastric cancer surgery, especially early gastric cancer, the introduction of laparoscopy has yielded considerable benefits in terms of short-term postsurgical outcomes, e.g. lower rate of intraprocedural bleeding and reduced length of hospital stay. Despite the progress made in preoperative assessment, surgical procedures and postoperative management, the improvement of outcomes after non-cardiac surgery in elderly patients remains a challenge and calls for future, well-designed clinical studies.</p

evolution of surgical techniques for a progressive risk reduction

Advanced age is a strong predictor of high perioperative mortality in surgical patients and patients aged 75 years and older have an elevated surgical risk, much higher than that of younger patients. Progressive advances in surgical techniques now make it possible to treat high-risk surgical patients with minimally invasive procedures. Endovascular techniques have revolutionized the treatment of several vascular diseases, in particular carotid stenosis, aortic pathologies, and severely incapacitating intermittent claudication or critical limb ischemia. The main advantages of the endovascular approach are the low complication rate, high rate of technical success and a good clinical outcome. Biliary stenting has improved the clinical status of severely ill patients with bile duct stricture before major surgery, and represents a good palliative therapy in the case of malignant biliary obstruction

Alirocumab therapy in individuals with type 2 diabetes mellitus and atherosclerotic cardiovascular disease:analysis of the ODYSSEY DM-DYSLIPIDEMIA and DM-INSULIN studies

Background Individuals with diabetes often have high levels of atherogenic lipoproteins and cholesterol reflected by elevated low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), apolipoprotein B (ApoB), and LDL particle number (LDL-PN). The presence of atherosclerotic cardiovascular disease (ASCVD) increases the risk of future cardiovascular events. We evaluated the efficacy and safety of the proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor, alirocumab, among individuals with type 2 diabetes (T2DM), high LDL-C or non-HDL-C, and established ASCVD receiving maximally tolerated statin in ODYSSEY DM-DYSLIPIDEMIA (NCT02642159) and DM-INSULIN (NCT02585778). Methods In DM-DYSLIPIDEMIA, individuals with T2DM and mixed dyslipidemia (non-HDL-C ≥ 100 mg/dL; n = 413) were randomized to open-label alirocumab 75 mg every 2 weeks (Q2W) or usual care (UC) for 24 weeks, with UC options selected before stratified randomization. In DM-INSULIN, insulin-treated individuals with T2DM (LDL-C ≥ 70 mg/dL; n = 441) were randomized in a double-blind fashion to alirocumab 75 mg Q2W or placebo for 24 weeks. Study participants also had a glycated hemoglobin < 9% (DM-DYSLIPIDEMIA) or < 10% (DM-INSULIN). Alirocumab dose was increased to 150 mg Q2W at week 12 if week 8 LDL-C was ≥ 70 mg/dL (DM-INSULIN) or non-HDL-C was ≥ 100 mg/dL (DM-DYSLIPIDEMIA). Lipid reductions and safety were assessed in patients with ASCVD from these studies. Results This analysis included 142 DM-DYSLIPIDEMIA and 177 DM-INSULIN participants with ASCVD, including 95.1% and 86.4% with coronary heart disease, and 32.4% and 49.7% with microvascular diabetes complications, respectively. At week 24, alirocumab significantly reduced LDL-C, non-HDL-C, ApoB, and LDL-PN from baseline versus control. This translated into a greater proportion of individuals achieving non-HDL-C < 100 mg/dL (64.6% alirocumab/23.8% UC [DM-DYSLIPIDEMIA]; 65.4% alirocumab/14.9% placebo [DM-INSULIN]) and ApoB < 80 mg/dL (75.1% alirocumab/35.4% UC and 76.8% alirocumab/24.8% placebo, respectively) versus control at week 24 (all P < 0.0001). In pooling these studies, 66.4% (alirocumab) and 67.0% (control) of individuals reported treatment-emergent adverse events. The adverse event pattern was similar with alirocumab versus controls. Conclusions Among individuals with T2DM and ASCVD who had high non-HDL-C/LDL-C levels despite maximally tolerated statin, alirocumab significantly reduced atherogenic cholesterol and LDL-PN versus control. Alirocumab was generally well tolerated

International Conference New Trends in Water and Environmental Engineering for Safety and Life: Eco-compatible Solutions for Aquatic Environments

In this paper design criteria of pool and weir, orifice and vertical slot fishways are proposed. Each criterion is based on the need to conciliate the hydraulic lows controlling flow conditions in the manufact and the biological exigencies of the fish species for which the fishway is designed. These exigencies mainly regard the minimum ecological discharge and water depth and velocity suitable for the aquatic ecosystem preservation, the minimum acceptable size of a pool, enough to remove any possible cause of delay in the fish migration, orifice size and shape

The vascular effects of L-arginine in humans: the role of endogenous insulin

This study aimed at evaluating whether increased availability of the natural precursor of nitric oxide, L-arginine, could influence systemic hemodynamic and rheologic parameters in humans and whether the effects of L-arginine are mediated by endogenous insulin. 10 healthy young subjects participated in the following studies: study I, infusion of L-arginine (1 g/min for 30 min); study II, infusion of L-arginine plus octreotide (25 �g as i.v. bolus � 0.5 �g/min) to block endogenous insulin and glucagon secretion, plus replacement of basal insulin and glucagon; study III, infusion of L-arginine plus octreotide plus basal glucagon plus an insulin infusion designed to mimic the insulin response of study I. L-Arginine infusion significantly reduced systolic (11�3, mean�SE) and diastolic (8�2 mmHg, P � 0.001) blood pressure, platelet aggregation (20�4%), and blood viscosity (1.6�0.2 centipois, P � 0.01), and increased leg blood flow (97�16 ml/min), heart rate, and plasma catecholamine levels (P � 0.01). In study II, plasma insulin levels remained suppressed at baseline; in this condition, the vascular responses to L-arginine were significantly reduced, except for plasma catecholamines which did not change significantly. In study III, the plasma insulin response to L-arginine was reestablished; this was associated with hemodynamic and rheologic changes following L-arginine not significantly different from those recorded in study I. These findings show that systemic infusion of L-arginine in healthy subjects induces vasodilation and inhibits platelet aggregation and blood viscosity. These effects are mediated, in part, by endogenou

Vascular Effects of L -Arginine The Vascular Effects of L -Arginine in Humans The Role of Endogenous Insulin

Abstract This study aimed at evaluating whether increased availability of the natural precursor of nitric oxide, L -arginine, could influence systemic hemodynamic and rheologic parameters in humans and whether the effects of L -arginine are mediated by endogenous insulin. 10 healthy young subjects participated in the following studies: study I, infusion of L -arginine (1 g/min for 30 min); study II, infusion of L -arginine plus octreotide (25 g as i.v. bolus ϩ 0.5 g/min) to block endogenous insulin and glucagon secretion, plus replacement of basal insulin and glucagon; study III, infusion of L -arginine plus octreotide plus basal glucagon plus an insulin infusion designed to mimic the insulin response of study I. L -Arginine infusion significantly reduced systolic (11 Ϯ 3, mean Ϯ SE) and diastolic (8 Ϯ 2 mmHg, P Ͻ 0.001) blood pressure, platelet aggregation (20 Ϯ 4%), and blood viscosity (1.6 Ϯ 0.2 centipois, P Ͻ 0.01), and increased leg blood flow (97 Ϯ 16 ml/min), heart rate, and plasma catecholamine levels ( P Ͻ 0.01). In study II, plasma insulin levels remained suppressed at baseline; in this condition, the vascular responses to L -arginine were significantly reduced, except for plasma catecholamines which did not change significantly. In study III, the plasma insulin response to L -arginine was reestablished; this was associated with hemodynamic and rheologic changes following L -arginine not significantly different from those recorded in study I. These findings show that systemic infusion of L -arginine in healthy subjects induces vasodilation and inhibits platelet aggregation and blood viscosity. These effects are mediated, in part, by endogenous released insulin

Glucose "peak" and glucose "spike" : impact on endothelial function and oxidative stress

Aim: Data suggest that 2 h hyperglycaemia during an OGTT is less predictive for cardiovascular disease of the glucose "spike" (the difference between the baseline glucose level and the "peak" hyperglycaemia during the test). Methods: A euinsulinemic hyperglycaemic clamp at 10 and 15 mmol/l glucose, with or without vitamin C, was given in increasing steps in diabetic and nor-Mal subjects. Moreover, a hyperglycaemic clamp, 10 mmol/l, was performed in two groups of diabetic patients with different levels of fasting glycaemia. in both the experiments flow mediated dilation and nitrotyrosine were measured. Results: Glucose at 10 and 15 mmol/l resulted in a concentration-dependent induction of endothelial dysfunction and oxidative stress. Vitamin C counterbalanced this effect. The increase of glycaemia to 10 mmol/l induced a significant endothelial dysfunction and increased nitrotyrosine in both the groups of diabetics with different fasting glycaemia. However, when the delta (the difference between the basal value and the peak value) for endothelial function and nitrotyrosine was evaluated, patients with lower basal values showed a worse outcome. Conclusions: Our data suggest that at the same level of hyperglycaemia the grading of the endothelial dysfunction is almost super imposable, but clearly worse in terms of delta from fasting glycaemia. (C) 2008 Elsevier Ireland Ltd. All rights reserved