Laparoscopic aortobifemoral bypass in a USA academic center.

BACKGROUND: Although aortoiliac occlusive disease (AIOD) is preferentially treated endovascularly, some patients are still better served with an aortobifemoral bypass (ABF). For those patients, surgical treatment options include both standard open operations as well as laparoscopic ABF (LapABF). Several European centers perform LapABF with favorable results instead of open surgery, but this has not been widely embraced in the United States. We reviewed our ten-year experience with LapABF, evolving from a completely laparoscopic to a standardized laparoscopic-assisted approach. METHODS: A retrospective review of all laparoscopic aortic operations performed at a single US academic institution from 2005 to 2015 was completed. Demographics, co-morbidities, intraoperative parameters and clinical outcomes were recorded. Patients were excluded from consideration for laparoscopic surgery if they had previous aortic surgery, aneurysmal disease or gastrointestinal pathology (e.g. diverticulitis or an enteric stoma). RESULTS: Thirty men and sixteen women were treated, (n=46) with a mean age of 55.7 (range 38-75 years). All operations were performed by a single surgeon. LapABF was successfully completed in 95.6%. A completely laparoscopic approach was undertaken in eight patients and a laparoscopic-assisted approach was used in the remaining 38 patients. Mean follow-up was 46 months (range 1 to 131). The indication for operation was claudication (n=35, 76%), rest pain (n=8, 17%) or tissue loss (n=3, 7%). Twenty-one limbs had a history of a prior failed aortoiliac endovascular intervention (23%). Median length of stay was 6 days (range 2-30). Within 30 days there were two myocardial infarctions (4.3%), one transient ischemic attack (2.2%) and one death (2.2%). Re-intervention was performed in 12 patients over the course of the study period (26.1%). Primary, primary-assisted and secondary patency was 79.4%, 93.9% and 94.9% at 60 months, respectively. Overall mortality was 17% with a mean duration of follow-up of 60 months (range 1-116). Multivariable analysis revealed coronary artery disease (CAD; P=0.03) conferred a sixteen-fold risk for death during long-term follow-up. CONCLUSIONS: In this large US series of LapABF, we observed acceptable long-term patency, short length of stay and minimal morbidity. We suggest that this standardized approach for laparoscopic-assisted ABF is a viable option for patients with AIOD not suitable for endovascular therapy. The use of laparoscopic-assisted ABF affords practitioners the benefits of a completely laparoscopic approach while reducing the duration and complexity of the operation. Given the rate of re-interventions in the early era practitioners should be aware of the learning curve with this approach.

General outcomes and risk factors for minor and major amputations in Brazil.

Objectives Major and minor amputations are associated with significant rates of mortality. However, little is known about the impact of unplanned redo-amputation during the same hospitalization on outcomes. The objectives of this study were to identify the risk factors associated with in-hospital mortality after both major and minor amputations as well as the results of unplanned redo-amputation on outcome. Methods Retrospective study of 342 consecutive patients who were treated with lower extremity amputation in Brazil between January 2013 and October 2014. Results The in-hospital mortality rate was higher in major compared to minor amputation (25.6% vs. 4.1%; p < 0.0001). Whereas chronic kidney disease, chronic obstructive pulmonary disease, and planned staged amputation predicted in-hospital mortality after major amputation, age, and congestive heart failure predicted mortality after minor amputation. The white blood cell count predicted in-hospital mortality following both major and minor amputation. However, postoperative infection predicted in-hospital mortality only following major amputation. Conclusions In-hospital mortality was high after major amputations. Unplanned redo-amputation was not a predictor of in-hospital mortality after major or minor amputation. Planned staged amputation was associated with reduced survival after major but not minor amputation. Postoperative infection predicted mortality after major amputation. Systemic diseases and postoperative white blood cell were associated with in-hospital mortality. This study suggests a possible link between a pro-inflammatory state and increased in-hospital mortality following amputation.

Contemporary outcomes for ruptured abdominal aortic aneurysms using endovascular balloon control for hypotension.

OBJECTIVE: Ruptured abdominal aortic aneurysm (rAAA) continues to portend significant mortality, despite ruptured endovascular aneurysm repair (rEVAR), enhanced perioperative care, and endovascular balloon control (EBC) for hypotension. We review our academic institution's experience using a protocol of EBC for all hypotensive patients, irrespective of type of repair. METHODS: A retrospective review was conducted of 66 cases of rAAA treated at a single academic institution from 2007 to 2016 using EBC for hypotensive patients. Demographics, comorbidities, intraoperative parameters, and clinical outcomes were recorded. Patients were studied with respect to hemodynamic status, rEVAR, or ruptured open aortic repair in the setting of EBC for hypotension. RESULTS: rEVAR was performed in 43 patients (65%) and ruptured open aortic repair in 23 patients (35%). rAAA was treated in 51 men (77%). Mean rAAA size was 7.6 mm, and mean age of the patients was 73 years. Perioperative survival was 82%. Overall survival at 30 days, 1 year, and 5 years was 71%, 65%, and 52%. Blood transfusion and severe hypotension were significant predictors of mortality at 30 days on multivariable analysis (odds ratio of 1.2 [P = .08] and 39 [P = .03], respectively). Severe hypotension was defined as a mean arterial blood pressure <65 mm Hg and vasopressor use and was present in 59% of the cohort. Normotension was defined as an absence of these conditions and was present in 12%, with 29% of patients exhibiting moderate hypotension. There was no difference in 30-day survival between normotensive and moderately hypotensive patients. The 30-day survival for severely hypotensive patients was 61% vs 85% for moderately hypotensive patients (P = .003), with a significant difference between groups that persisted at 1 year (85% vs 51%; P = .008) and 5 years (66% vs 51%; P = .017). CONCLUSIONS: Good midterm outcomes for moderately hypotensive and normotensive patients can be obtained using an EBC protocol for hypotension with a regionalized transport system directly to the operating room. Severely hemodynamically unstable rAAA patients still pose a significant challenge despite mitigation of hypotension by EBC, suggesting that survival may be compromised by factors other than hypotension alone. We still advocate for the use of EBC for all hypotensive patients as part of a defined rAAA protocol before definitive repair.

Effects of increased dietary cholesterol with carbohydrate restriction on hepatic lipid metabolism in Guinea pigs.

Excessive lipid accumulation within hepatocytes, or hepatic steatosis, is the pathognominic feature of nonalcoholic fatty liver disease (NAFLD), a disease associated with insulin resistance and obesity. Low-carbohydrate diets (LCD) improve these conditions and were implemented in this study to potentially attenuate hepatic steatosis in hypercholesterolemic guinea pigs. Male guinea pigs (n = 10 per group) were randomly assigned to consume high cholesterol (0.25 g/100 g) in either a LCD or a high-carbohydrate diet (HCD) for 12 wk. As compared with HCD, plasma LDL cholesterol was lower and plasma triglycerides were higher in animals fed the LCD diet, with no differences in plasma free fatty acids or glucose. The most prominent finding was a 40% increase in liver weight in guinea pigs fed the LCD diet despite no differences in hepatic cholesterol or triglycerides between the LCD and the HCD groups. Regardless of diet, all livers had severe hepatic steatosis on histologic examination. Regression analysis suggested that liver weight was independent of body weight and liver mass was independent of hepatic lipid content. LCD livers had more proliferating hepatocytes than did HCD livers, suggesting that in the context of cholesterol-induced hepatic steatosis, dietary carbohydrate restriction enhances liver cell proliferation.

A lutein-enriched diet prevents cholesterol accumulation and decreases oxidized LDL and inflammatory cytokines in the aorta of guinea pigs.

Lutein has been shown to be protective against age-related macular degeneration; however, the antiinflammatory and antioxidant effects of this carotenoid in aortas are less known. Guinea pigs were fed a hypercholesterolemic diet (0.25 g cholesterol/100 g) and randomly allocated to a control group (n = 9) or a lutein group (n = 10) (0.01 g/100 g lutein) [corrected] and fed the experimental diets for 12 wk. Plasma LDL cholesterol and TG did not differ between groups; however, the lutein group had lower concentrations of medium size LDL (P < 0.05). As expected, guinea pigs from the lutein group had higher concentrations of plasma and liver lutein than those from the control group (P < 0.0001). Aortic cholesterol and malondialdehyde concentrations were lower in the lutein group (9.6 ± 2.8 mmol/g and 1.69 ± 1.35 nmol/mg protein) compared to the control group (15.5 ± 2.3 mmol/g and 2.98 ± 1.45 nmol/mg protein) (P < 0.05). Hematoxilin and eosin staining indicated that aortas from the control group presented focal intimal thickening, whereas either less thickness or no visible thickness was present in aortas from the lutein group. Oxidized LDL (oxLDL) was lower both in plasma and aorta in the lutein group compared to the control group (P < 0.001). Aortic cytokines were also lower in the lutein group (P < 0.05). Plasma lutein and oxLDL (r = -0.79; P < 0.0001) and plasma lutein and aortic oxLDL (r = -0.64; P < 0.0001) were negatively correlated. These data suggest that lutein exerts potent antioxidant and antiinflammatory effects in aortic tissue that may protect against development of atherosclerosis in guinea pigs.

The approximate entropy of the electromyographic signals of tremor correlates with the osmotic fragility of human erythrocytes.

BACKGROUND: The main problem of tremor is the damage caused to the quality of the life of patients, especially those at more advanced ages. There is not a consensus yet about the origins of this disorder, but it can be examined in the correlations between the biological signs of aging and the tremor characteristics. METHODS: This work sought correlations between the osmotic fragility of erythrocytes and features extracted from electromyographic (EMG) activity resulting from physiological tremor in healthy patients (N = 44) at different ages (24-87 years). The osmotic fragility was spectrophotometrically evaluated by the dependence of hemolysis, provided by the absorbance in 540 nm (A54o), on the concentration of NaCl. The data were adjusted to curves of sigmoidal regression and characterized by the half transition point (H50), amplitude of lysis transition (dx) and values of A540 in the curve regions that characterize the presence of lysed (A1) and preserved erythrocytes (A2). The approximate entropy was estimated from EMG signals detected from the extensor carpi ulnaris muscle during the movement of the hand of subjects holding up a laser pen towards an Archimedes spiral, fixed in a whiteboard. The evaluations were carried out with the laser pen at rest, at the center of the spiral, and in movement from the center to the outside and from outside to the center. The correlations among the parameters of osmotic fragility, tremor and age were tested. RESULTS: Negative correlations with age were found for A1 and dx. With the hand at rest, a positive correlation with H50 was found for the approximate entropy. Negative correlations with H50 were found for the entropy with the hand in movement, as from the center to the outside or from the outside to the center of the spiral. CONCLUSION: In healthy individuals, the increase in the erythrocyte osmotic fragility was associated with a decrease in the approximate entropy for rest tremor and with an increase of the entropy for movement tremor. This suggests that the neuromuscular degeneration associated with tremor entails also the mechanisms involved in the breakdown of structural homeostasis of the erythrocyte membrane.

Consuming eggs for breakfast influences plasma glucose and ghrelin, while reducing energy intake during the next 24 hours in adult men.

We hypothesized that consuming eggs for breakfast would significantly lower postprandial satiety and energy intake throughout the day. Using a crossover design, 21 men, 20 to 70 years old, consumed 2 isoenergetic test breakfasts, in a random order separated by 1 week. The macronutrient composition of the test breakfasts were as follows: (EGG, % CHO/fat/protein = 22:55:23) and (BAGEL, % CHO/fat/protein = 72:12:16). Fasting blood samples were drawn at baseline before the test breakfast and at 30, 60, 120, and 180 minutes after breakfast. After 180 minutes, subjects were given a buffet lunch and asked to eat until satisfied. Subjects filled out Visual Analog Scales (VAS) during each blood draw and recorded food intake the days before and after the test breakfasts. Plasma glucose, insulin, and appetite hormones were analyzed at each time point. Subjects consumed fewer kilocalories after the EGG breakfast compared with the BAGEL breakfast (P< .01). In addition, subjects consumed more kilocalories in the 24-hour period after the BAGEL compared with the EGG breakfast (P < .05). Based on VAS, subjects were hungrier and less satisfied 3 hours after the BAGEL breakfast compared with the EGG breakfast (P < .01). Participants had higher plasma glucose area under the curve (P < .05) as well as an increased ghrelin and insulin area under the curve with BAGEL (P < .05). These findings suggest that consumption of eggs for breakfast results in less variation of plasma glucose and insulin, a suppressed ghrelin response, and reduced energy intake.

Low HDL cholesterol is associated with increased atherogenic lipoproteins and insulin resistance in women classified with metabolic syndrome.

Both metabolic syndrome (MetS) and elevated LDL cholesterol (LDL-C) increase the risk for cardiovascular disease (CVD). We hypothesized that low HDL cholesterol (HDL-C) would further increase CVD risk in women having both conditions. To assess this, we recruited 89 women with MetS (25-72 y) and LDL-C ≥ 2.6 mmol/L. To determine whether plasma HDL-C concentrations were associated with dietary components, circulating atherogenic particles, and other risk factors for CVD, we divided the subjects into two groups: high HDL-C (H-HDL) (≥ 1.3 mmol/L, n = 32) and low HDL-C (L-HDL) (< 1.3 mmol/L, n = 57). Plasma lipids, insulin, adiponectin, apolipoproteins, oxidized LDL, Lipoprotein(a), and lipoprotein size and subfractions were measured, and 3-d dietary records were used to assess macronutrient intake. Women with L-HDL had higher sugar intake and glycemic load (P < 0.05), higher plasma insulin (P < 0.01), lower adiponectin (P < 0.05), and higher numbers of atherogenic lipoproteins such as large VLDL (P < 0.01) and small LDL (P < 0.001) than the H-HDL group. Women with L-HDL also had larger VLDL and both smaller LDL and HDL particle diameters (P < 0.001). HDL-C was positively correlated with LDL size (r = 0.691, P < 0.0001) and HDL size (r = 0.606, P < 0.001), and inversely correlated with VLDL size (r = -0.327, P < 0.01). We concluded that L-HDL could be used as a marker for increased numbers of circulating atherogenic lipoproteins as well as increased insulin resistance in women who are already at risk for CVD.

Low-carbohydrate diets reduce lipid accumulation and arterial inflammation in guinea pigs fed a high-cholesterol diet.

INTRODUCTION: Low-carbohydrate diets (LCD) efficiently induce weight loss and favorably affect plasma lipids, however, the effect of LCD on atherosclerosis is still argued. OBJECTIVE: To evaluate the effect of LCD on the prevention of atherosclerosis. METHODS: Twenty guinea pigs were fed either a LCD or a low-fat diet (LFD) in combination with high-cholesterol (0.25g/100g) for 12 weeks. The percentage energy of macronutrient distribution was 10:65:25 for carbohydrate:fat:protein for the LCD, and 55:20:25 for the LFD. Plasma lipids were measured using colorimetric assays. Plasma and aortic oxidized (oxLDL) were quantified using ELISA methods. Inflammatory cytokines were measured in aortic homogenates using an immunoassay. H&E stained sections of aortic sinus and Schultz stained sections of carotid arteries were examined. RESULTS: LDL cholesterol was lower in the LCD compared to the LFD group (71.9+/-34.8 vs. 81.7+/-26.9mg/dL; p=0.039). Aortic cholesterol was also lower in the LCD (4.98+/-1.3mg/g) compared to the LFD group (6.68+/-2.0mg/g); p<0.05. The Schultz staining method confirmed less aortic cholesterol accumulation in the LCD group. Plasma oxLDL did not differ between groups, however, aortic oxLDL was 61% lower in the LCD compared to the LFD group (p=0.045). There was a positive correlation (r=0.63, p=0.03) between oxLDL and cholesterol concentration in the aorta of LFD group, which was not observed in LCD group (r=-0.05, p=0.96). Inflammatory markers were reduced in guinea pigs from the LCD group (p<0.05) and they were correlated with the decreases in oxLDL in aorta. CONCLUSION: These results suggest that LCD not only decreases lipid deposition, but also prevents the accumulation of oxLDL and reduces inflammatory cytokines within the arterial wall and may prevent atherosclerosis.

Low-carbohydrate diet disrupts the association between insulin resistance and weight gain.

The cornerstone to treat metabolic syndrome and insulin resistance is dietary intervention. Both low-carbohydrate diet (LCD) and low-fat diet (LFD) have been reported to induce weight loss and improve these conditions. One of the factors associated with a subject's adherence to the diet is satiety. The aim of this study was to evaluate the effects of LCD and LFD on body weight, appetite hormones, and insulin resistance. Twenty guinea pigs were randomly assigned to LCD or LFD (60%:10%:30% or 20%:55%:25% of energy from fat/carbohydrate/protein, respectively) for 12 weeks. Weight and food intake were recorded every week. After this period, animals were killed and plasma was obtained to measure plasma glucose and insulin, appetite hormones, and ketone bodies. Guinea pigs fed LCD gained more weight than those fed LFD. The daily amount of food intake in grams was not different between groups, suggesting that food density and gastric distension played a role in satiety. There was no difference in leptin levels, which excludes the hypothesis of leptin resistance in the LCD group. However, plasma glucagon-like peptide-1 was 47.1% lower in animals fed LCD (P < .05). Plasma glucose, plasma insulin, and insulin sensitivity were not different between groups. However, the heavier animals that were fed LFD had impairment in insulin sensitivity, which was not observed in those fed LCD. These findings suggest that satiety was dependent on the amount of food ingested. The weight gain in animals fed LCD may be related to their greater caloric intake, lower levels of glucagon-like peptide-1, and higher protein consumption. The adoption of LCD promotes a unique metabolic state that prevents insulin resistance, even in guinea pigs that gained more weight. The association between weight gain and insulin resistance seems to be dependent on high carbohydrate intake.

A-002 (Varespladib), a phospholipase A2 inhibitor, reduces atherosclerosis in guinea pigs.

BACKGROUND: The association of elevated serum levels of secretory phospholipase A2 (sPLA2) in patients with cardiovascular disease and their presence in atherosclerotic lesions suggest the participation of sPLA2 enzymes in this disease. The presence of more advanced atherosclerotic lesions in mice that overexpress sPLA2 enzymes suggest their involvement in the atherosclerotic process. Therefore, the sPLA2 family of enzymes could provide reasonable targets for the prevention and treatment of atherosclerosis. Thus, A-002 (varespladib), an inhibitor of sPLA2enzymes, is proposed to modulate the development of atherosclerosis. METHODS: Twenty-four guinea pigs were fed a high saturated fat, high cholesterol diet (0.25%) for twelve weeks. Animals were treated daily with A-002 (n = 12) or vehicle (10% aqueous acacia; n = 12) by oral gavage. After twelve weeks, animals were sacrificed and plasma, heart and aorta were collected. Plasma lipids were measured by enzymatic methods, lipoprotein particles size by nuclear magnetic resonance, aortic cytokines by a colorimetric method, and aortic sinus by histological analyses. RESULTS: Plasma total cholesterol, HDL cholesterol and triglycerides were not different among groups. However, the levels of inflammatory cytokines interleukin (IL)-10, IL-12 and granulocyte-macrophage colony-stimulating factor (GM-CSF) were significantly reduced in the treatment group. This group also had a significant 27% reduction in cholesterol accumulation in aorta compared with placebo group. Morphological analysis of aortic sinus revealed that the group treated with A-002 reduced atherosclerotic lesions by 24%. CONCLUSION: The use of A-002 may have a beneficial effect in preventing diet-induced atherosclerosis in guinea pigs.

Carbohydrate restriction reduces lipids and inflammation and prevents atherosclerosis in Guinea pigs.

AIM: There is limited information on how dietary carbohydrate restriction (CR) or the combination of dietary cholesterol (chol) and CR may affect atherosclerosis development. Guinea pigs were used to evaluate the effects of chol and CR on aortic cholesterol accumulation, mechanical properties of aortas and cytokine production. METHODS: Ten male guinea pigs were fed either low (L) or high (H) chol in combination with CR or high carbohydrate (control) for 12 wk. RESULTS: Groups fed the high chol (control-H and CR-H) had significantly higher concentrations of cholesterol in aortas and higher activity of serum phospholipase A2 than the L groups. CR resulted in significantly lower concentrations of small LDL particles and aortic cytokines and chemokynes than the control groups. Aortas from the control-H and the CR-L were stiffer than those from the control-L and the CR-H groups. This finding could be explained by the reduction in arterial stiffness during the early stages of atherosclerotic. CONCLUSION: These results demonstrate that CR has a major impact on atherogenicity.

Carbohydrate restriction and dietary cholesterol distinctly affect plasma lipids and lipoprotein subfractions in adult guinea pigs.

To evaluate the effects of carbohydrate restriction (CR) and dietary cholesterol on lipoprotein metabolism, adult male guinea pigs (10 guinea pigs/diet) were fed either low (0.04 g/100 g) or high (0.25 g/100 g) amounts of dietary cholesterol, in combination with either low (10% total energy) or high (54.2% total energy) dietary carbohydrate (control groups) for a total of four groups: high carbohydrate-low cholesterol (control-L), high carbohydrate-high cholesterol (control-H), low carbohydrate-low cholesterol (CR-L) and low carbohydrate-high cholesterol (CR-H). Plasma triglyceride concentrations were lower (P<.01%), while high-density lipoprotein cholesterol concentrations were higher (P<.05) in the CR groups compared to the control groups. In contrast, high dietary cholesterol (CR-H and control-H) resulted in higher concentrations of total and low-density lipoprotein (LDL) cholesterol compared to those guinea pigs fed the low-cholesterol diets (P<.01). Dietary cholesterol significantly increased the total number of LDL particles (P<.001) and the number of small LDL (P<.001), as determined by nuclear magnetic resonance. In contrast, carbohydrate restriction (CR-L and CR-H) resulted in lower concentrations of medium very-low-density lipoprotein and small LDL particles compared to the high-carbohydrate groups. Plasma lecithin:cholesterol acyltransferase (LCAT) activity was decreased and cholesterol ester transfer protein activity was increased by dietary cholesterol, whereas carbohydrate restriction increased LCAT activity (P<.05). These findings are similar to those observed in humans, thus validating the use of adult guinea pigs to study lipid responses to carbohydrate restriction. The results also indicate that the atherogenicity of lipoproteins induced by high dietary cholesterol is attenuated by carbohydrate restriction in guinea pigs.

Dietary cholesterol from eggs increases plasma HDL cholesterol in overweight men consuming a carbohydrate-restricted diet.

Carbohydrate-restricted diets (CRD) significantly decrease body weight and independently improve plasma triglycerides (TG) and HDL cholesterol (HDL-C). Increasing intake of dietary cholesterol from eggs in the context of a low-fat diet maintains the LDL cholesterol (LDL-C)/HDL-C for both hyper- and hypo-responders to dietary cholesterol. In this study, 28 overweight/obese male subjects (BMI = 25-37 kg/m2) aged 40-70 y were recruited to evaluate the contribution of dietary cholesterol from eggs in a CRD. Subjects were counseled to consume a CRD (10-15% energy from carbohydrate) and they were randomly allocated to the EGG group [intake of 3 eggs per day (640 mg/d additional dietary cholesterol)] or SUB group [equivalent amount of egg substitute (0 dietary cholesterol) per day]. Energy intake decreased in both groups from 10,243 +/- 4040 to 7968 +/- 2401 kJ (P < 0.05) compared with baseline. All subjects irrespective of their assigned group had reduced body weight and waist circumference (P < 0.0001). Similarly, the plasma TG concentration was reduced from 1.34 +/- 0.66 to 0.83 +/- 0.30 mmol/L after 12 wk (P < 0.001) in all subjects. The plasma LDL-C concentration, as well as the LDL-C:HDL-C ratio, did not change during the intervention. In contrast, plasma HDL-C concentration increased in the EGG group from 1.23 +/- 0.39 to 1.47 +/- 0.38 mmol/L (P < 0.01), whereas HDL-C did not change in the SUB group. Plasma glucose concentrations in fasting subjects did not change. Eighteen subjects were classified as having the metabolic syndrome (MetS) at the beginning of the study, whereas 3 subjects had that classification at the end. These results suggest that including eggs in a CRD results in increased HDL-C while decreasing the risk factors associated with MetS.

Malnutrition after vascular surgery: are patients with chronic renal failure at increased risk?

BACKGROUND: The deleterious effects of perioperative malnutrition on recovery after general surgery are established. Since the effects of perioperative malnutrition on recovery after vascular surgery are not known, we examined the effects of nutritional status, and risk factors predictive of malnutrition, on outcome after vascular surgery. METHODS: The records of all open index vascular cases (abdominal aortic aneurysm [AAA] repair, carotid endarterectomy [CEA], lower extremity bypass) performed at the Veterans Affairs (VA) Connecticut between July 2004 and June 2005 were reviewed. The primary outcome was mortality; secondary outcomes included infection and nutritional risk index (NRI) scores. RESULTS: Sixty-eight open vascular cases were performed during the study period. Nutritional depletion developed in 55% of patients and was more likely in patients undergoing AAA (85%) or bypass (77%) than CEA (30%; P = .0005). Patients who developed malnutrition had similar mortality as patients who did not develop postoperative malnutrition (6.1% vs. 3.7%; P = .68); however, malnourished patients had higher rates of postoperative infection (24.2% vs. 3.7%; P = .03). Chronic renal failure was the only patient-associated risk factor predictive of postoperative nutritional depletion (odds ratio 5.9, confidence interval 1.0 to 33.6; P = .04). CONCLUSIONS: Patients undergoing major open vascular surgery have high rates of postoperative malnutrition, with patients undergoing AAA repair having the highest rates of postoperative malnutrition and infection. Patients with chronic renal failure undergoing vascular surgery are associated with increased risk for postoperative malnutrition and may be a group to target for perioperative risk factor modification and nutritional supplementation.

Hospital-based factors predict outcome after carotid endarterectomy.

OBJECTIVE: Patient, hospital, and surgeon factors affect outcome after carotid endarterectomy (CEA). The nature and importance of hospital-specific factors, especially those unrelated to procedural volume, that affect post-CEA outcome remains poorly defined. We used a statewide database to determine the impact of several hospital-associated factors on outcome after CEA. METHODS: Hospital factors were established by telephone survey and validated by repeated survey as well as by the Connecticut Hospital Association, Connecticut state, and individual hospital internet Websites. All CEA in Connecticut non-federal hospitals between 1991 and 2002 were examined, including perioperative mortality, stroke, and cardiac complications. Multivariable logistic regression was used to analyze data. RESULTS: There were 14,288 CEAs performed with 0.5% mortality, 1.3% stroke, and 2.4% cardiac complications. The only hospital factor independently predictive of perioperative mortality was few number of hospital beds (less than 132 beds; odds ratio (OR) 2.78, P = 0.032). Factors predictive of perioperative stroke included few number of beds (OR 1.96, P = 0.001) and absence of a critical pathway (OR 1.39, P = 0.038). Factors predictive of perioperative cardiac complications included few number of beds (OR 3.01, P = 0.003), absence of a critical pathway (OR 1.50, P = 0.001), and absence of dedicated vascular recovery beds (OR 1.35, P = 0.03). Combined mortality, stroke, or cardiac complications were independently predicted by few hospital beds (OR 4.58, P = 0.002), absence of a critical pathway (OR 1.81, P < or = 0.0001), or inability to perform cardiac angiography (OR 3.92, P = 0.024). CONCLUSIONS: Hospital-based factors, such as greater bed capacity, use of critical pathways, ability to perform cardiac angiography, or presence of a dedicated vascular recovery unit predict reduced perioperative mortality, stroke and cardiac complications from CEA. These results suggest that hospital-associated factors do impact surgical outcome and that surgeons need to optimize these factors, extrinsic to the patient and surgeon, to provide maximal quality of care.