Activation of A1, A2A, or A3 adenosine receptors attenuates lung ischemia-reperfusion injury.

OBJECTIVE: Adenosine and the activation of specific adenosine receptors are implicated in the attenuation of inflammation and organ ischemia-reperfusion injury. We hypothesized that activation of A(1), A(2A), or A(3) adenosine receptors would provide protection against lung ischemia-reperfusion injury. METHODS: With the use of an isolated, ventilated, blood-perfused rabbit lung model, lungs underwent 18 hours of cold ischemia followed by 2 hours of reperfusion. Lungs were administered vehicle, adenosine, or selective A(1), A(2A), or A(3) receptor agonists (CCPA, ATL-313, or IB-MECA, respectively) alone or with their respective antagonists (DPCPX, ZM241385, or MRS1191) during reperfusion. RESULTS: Compared with the vehicle-treated control group, treatment with A(1), A(2A), or A(3) agonists significantly improved function (increased lung compliance and oxygenation and decreased pulmonary artery pressure), decreased neutrophil infiltration by myeloperoxidase activity, decreased edema, and reduced tumor necrosis factor-alpha production. Adenosine treatment was also protective, but not to the level of the agonists. When each agonist was paired with its respective antagonist, all protective effects were blocked. The A(2A) agonist reduced pulmonary artery pressure and myeloperoxidase activity and increased oxygenation to a greater degree than the A(1) or A(3) agonists. CONCLUSION: Selective activation of A(1), A(2A), or A(3) adenosine receptors provides significant protection against lung ischemia-reperfusion injury. The decreased elaboration of the potent proinflammatory cytokine tumor necrosis factor-alpha and decreased neutrophil sequestration likely contribute to the overall improvement in pulmonary function. These results provide evidence for the therapeutic potential of specific adenosine receptor agonists in lung transplant recipients.

Elective thoracic aortic aneurysm surgery: better outcomes from high-volume centers.

BACKGROUND: Although studies have demonstrated clinical advantages in high-volume (HV) centers performing esophageal and pancreatic resections, thoracic aortic aneurysm repair has not been studied in the same fashion. We sought to determine if HV centers have better outcomes after thoracic aortic aneurysm surgery relative to lower-volume (LV) centers. STUDY DESIGN: Retrospective review of prospectively collected data pooled from the 17 institutions participating in the Virginia Cardiac Surgery Quality Initiative (VCSQI) database was performed during a 3-year period. LV centers were those that performed <40 operations during the study period, and HV centers were those that performed >80 operations. Preoperative risk factors and outcomes were compared between the 2 groups. Multivariate analysis was performed to evaluate the impact of center volume on mortality. Only elective operations were studied. RESULTS: HV centers performed 515 operations during the study period compared with 216 operations from LV centers. Perioperative mortality was significantly lower in HV centers (3.7%, n = 19) versus LV centers (8.3%, n = 18) (p = 0.02). Incidence of renal failure (HV: 4.5%; LV: 8.3%; p = 0.05) and prolonged ventilator course (HV: 16.7%; LV: 25.5%; p = 0.01) were also lower in the HV centers relative to LV centers. HV centers had higher stroke rates compared with LV centers (HV: 4.8%, LV: 1.4%; p < 0.01). Total hospital cost was $42,736 in HV centers and $51,296 in LV centers (p = 0.04). On regression analysis, LV centers were significantly associated with increased complications and mortality (all p < 0.05). CONCLUSIONS: Although LV centers had lower stroke rates, HV centers had overall better outcomes, lower mortality rates, and considerably lower cost compared with LV centers.

Elective hypothermic circulatory arrest to address aortic pathology is safe for the elderly.

BACKGROUND: Due to assumptions of excessive risk, hypothermic circulatory arrest (HCA) has been considered prohibitive in elderly patients. However, as more elderly patients are referred for assessment of difficult aortic valve, ascending aorta, and aortic arch pathology, the risk of HCA in these patients needs to be addressed. We hypothesized that the use of HCA would not increase mortality or complications in elderly patients compared to younger counterparts. METHODS: We retrospectively reviewed the charts of adult patients who underwent elective HCA between January 1995 and June 2007. Of 147 procedures, 45 patients were >or=75 years old. These patients were compared to their younger counterparts in terms of comorbidities, operations, and complications. RESULTS: Comparing patients >or=75 years old to their younger counterparts revealed no significant differences in outcomes including nearly identical rates of confusion (>or=75 15% vs <75 9%, p > 0.5) and stroke (>or=75 11% vs <75 7%, p > 0.2). There was also no difference in 30-day mortality (>or=75 7% vs <75 7%, p = 0.9). Lengths of hospital stays and intensive care unit stays were longer in the older patients, but this was not statistically significant. CONCLUSION: In this study, elderly patients faired well with HCA compared to younger patients. These data suggest that the use of HCA is safe in selected elderly patients. Elderly patients should be considered for indicated procedures of the aortic valve, ascending aorta, and aortic arch regardless of age.

Inflammatory lung injury after cardiopulmonary bypass is attenuated by adenosine A(2A) receptor activation.

OBJECTIVE: Cardiopulmonary bypass has been shown to exert an inflammatory response within the lung, often resulting in postoperative pulmonary dysfunction. Several studies have shown that adenosine A(2A) receptor activation attenuates lung ischemia-reperfusion injury; however, the effect of adenosine A(2A) receptor activation on cardiopulmonary bypass-induced lung injury has not been studied. We hypothesized that specific adenosine A(2A) receptor activation by ATL313 would attenuate inflammatory lung injury after cardiopulmonary bypass. METHODS: Adult male Sprague-Dawley rats were randomly divided into 3 groups: 1) SHAM group (underwent cannulation + heparinization only); 2) CONTROL group (underwent 90 minutes of normothermic cardiopulmonary bypass with normal whole-blood priming solution; and 3) ATL group (underwent 90 minutes of normothermic cardiopulmonary bypass with ATL313 added to the normal priming solution). RESULTS: There was significantly less pulmonary edema and lung injury in the ATL group compared with the CONTROL group. The ATL group had significant reductions in bronchoalveolar lavage interleukin-1, interleukin-6, interferon-gamma, and myeloperoxidase levels compared with the CONTROL group. Similarly, lung tissue interleukin-6, tumor necrosis factor-alpha, and interferon-gamma were significantly decreased in the ATL group compared with the CONTROL group. There was no significant difference between the SHAM and ATL groups in the amount of pulmonary edema, lung injury, or levels of proinflammatory cytokines. CONCLUSION: The addition of a potent adenosine A(2A) receptor agonist to the normal priming solution before the initiation of cardiopulmonary bypass significantly protects the lung from the inflammatory effects of cardiopulmonary bypass and reduces the amount of lung injury. Adenosine A(2A) receptor agonists could represent a new therapeutic strategy for reducing the potentially devastating consequences of the inflammatory response associated with cardiopulmonary bypass.

Is mitral valve repair superior to replacement in elderly patients?

BACKGROUND: Mitral valve replacement is more frequently performed and perceived to be equivalent to repair in elderly patients, despite the superiority of repair in younger patients. Our objective was to compare mitral repair to replacement in elderly patients age 75 years or older. Patients younger than 75 years undergoing mitral valve surgery served as a reference population. METHODS: Consecutive elderly patients undergoing operation for mitral regurgitation at our institution from 1998 to 2006 were reviewed. Elderly patients (mean age, 78.0 +/- 2.8 years) who underwent mitral repair (n = 70) or replacement (n = 47) were compared with cohorts of young patients (mean age, 58.9 +/- 9.3 years) who underwent repair (n = 100) or replacement (n = 98) during the same period. Patient details and outcomes were compared using univariate, multivariate, and Kaplan-Meier analyses. RESULTS: Mitral replacement in elderly patients had higher mortality than repair (23.4%, 11 of 47 versus 7.1%, 5 of 70; p = 0.01) or as compared with either operation in the reference group (p < 0.0001). Postoperative stroke was higher in elderly replacement patients compared with repair (12.8%, 6 of 47 versus 0%; p = 0.003) or compared with either young cohort (p = 0.02). Compared with elderly repair patients, elderly replacement patients had more cerebrovascular disease (21.3%, 10 of 47 versus 4.3%, 3 of 70; p = 0.005) and rheumatic mitral valves (21.3%, 10 of 47 versus 0%; p = 0.0001). In the young group, overall complication and mortality were no different between replacement and repair. Long-term survival favored repair over replacement in elderly patients (p = 0.04). One elderly repair patient experienced late recurrence of persistent mitral regurgitation. CONCLUSIONS: In patients age 75 years or older, mitral repair is associated with a lower risk of mortality, postoperative stroke, and prolonged intensive care unit and hospital stay compared with mitral replacement. Mitral repair can be performed in preference over replacement even in patients older than the age of 75.

Timing of stroke after cardiopulmonary bypass determines mortality.

BACKGROUND: Stroke is an important complication of cardiopulmonary bypass (CPB). This study determined if the timing of stroke events after CPB predicted stroke-related mortality or rehabilitation needs at hospital discharge. METHODS: We performed a retrospective review of 7201 consecutive cardiac surgical patients during a 10-year period and identified 202 strokes. Postoperative stroke after CPB was classified as early (< or = 24 hours) or late (> 24 hours). Data were collected on patient characteristics, intraoperative variables and outcomes, postoperative course, stroke severity, and discharge status, including death from stroke. Logistic regression analysis was used to assess the relationship between the timing of stroke and discharge status after adjusting for clinically relevant factors. RESULTS: The stroke incidence was 2.8%. Postoperative strokes occurred within 24 hours in 22.8% (46 of 202) and after 24 hours in 77.2% (156 of 202). Factors found in logistic regression analysis to be independently associated with stroke-related death included stroke within 24 hours postoperatively (odds ratio [OR], 9.16; p < 0.0001), preoperative chronic renal insufficiency (OR, 4.46; p = 0.01), and National Institute of Health Stroke Scale (NIHSS) score (OR, 1.16 per NIHSS point increase; p < 0.0001). Among survivors, early stroke was associated with greater rehabilitation needs (p < 0.001). CONCLUSIONS: Early stroke after CPB is independently associated with higher stroke-related death and is associated with increased need for skilled rehabilitation at discharge. Neuroprotective strategies aimed at reducing early postoperative stroke may positively impact death and neurologic disability after CPB.

Cutaneous metastases in patients with rectal cancer: a report of six cases.

Cutaneous metastases from rectal cancer are rare manifestations of disseminated disease and uniformly represent dismal survival. A retrospective review of six patients with rectal cancer metastatic to the dermis was performed. The diagnosis of rectal cancer was made concurrently with the diagnosis of the dermal metastases in all six patients. A 100 per cent histopathologic concordance existed between the tissue of the dermal metastases and primary rectal tumor. The progression of systemic metastatic disease was the cause of death in 83.3 per cent of patients (5/6). No patient survived more than 7 months from the time of diagnosis. Recognition of suspicious skin lesions as possible harbingers of undiagnosed visceral malignancy is important in managing patients both with and without a history of previous cancer.

Early adenosine receptor activation ameliorates spinal cord reperfusion injury.

OBJECTIVES: Adenosine receptor activation at reperfusion has been shown to ameliorate ischemia-reperfusion injury of the spinal cord, but the effects of therapy given in response to ischemic injury are unknown. We hypothesized that adenosine receptor activation with ATL-146e would produce similar protection from ischemic spinal cord injury, whether given at reperfusion or in a delayed fashion. METHODS: Twenty-two New Zealand white rabbits were divided into three groups. All three groups, including the ischemia-reperfusion group (IR, n = 8), underwent 45 min of infrarenal aortic occlusion. The early treatment group (early, n = 8) received 0.06 mug/kg/min of ATL-146e for 3 h beginning 10 min prior to reperfusion. The delayed treatment group (delayed, n = 6) received ATL-146e starting 1 h after reperfusion. After 48 h, hind limb function was graded using the Tarlov score. Finally, lumbar spinal cord neuronal cytoarchitecture was evaluated. RESULTS: Hemodynamic parameters were similar among the groups. Hind limb function at 48 h was significantly better in the early group (3.5 +/- 1.0) compared to the IR group (0.625 +/- 0.5, P < or = 0.01). There was a trend towards better hind limb function in the early group compared to the delayed group (2.4 +/- 1.1, P = 0.08). Hind limb function was similar between delayed and IR groups. Hematoxylin-eosin spinal cord sections demonstrated preservation of viable motor neurons in the early group compared to the delayed and IR groups. CONCLUSIONS: Early therapy with ATL-146e provided better protection in this study; therefore, therapy should not be delayed until there is evidence of ischemic neurological deficit. This study suggests that adenosine receptor activation is most effective as a preventive strategy at reperfusion for optimal protection in spinal cord ischemia-reperfusion injury.

Additive protection against lung ischemia-reperfusion injury by adenosine A2A receptor activation before procurement and during reperfusion.

OBJECTIVE: Adenosine A2A receptor activation during reperfusion improves lung ischemia-reperfusion injury. In this study we sought to determine whether pretreatment of rabbits with a potent and selective adenosine A2A receptor agonist, ATL-313, before transplantation or whether adding ATL-313 to the preservation solution results in equivalent or additional protection compared with ATL-313 added during reperfusion. METHODS: An isolated, ventilated, ex vivo blood-perfused rabbit lung model was used. All groups underwent 2 hours of reperfusion after 18 hours of cold ischemia (4 degrees C). ATL-313 was administered 1 hour before ischemia intravenously, with the preservation solution, and/or during reperfusion. RESULTS: Both pretreatment of donor animals with ATL-313 or adding ATL-313 just during reperfusion improved pulmonary function, but significantly greater improvement was observed when pretreatment and treatment during reperfusion were combined (all P < .05). Myeloperoxidase levels, bronchoalveolar lavage tumor necrosis factor alpha levels, and pulmonary edema were all maximally decreased in the combined treatment group. The administration of an equimolar amount of the potent and highly selective adenosine 2A receptor antagonist, ZM 241385, along with ATL-313, resulted in the loss of protection conferred by ATL-313. CONCLUSIONS: Adenosine A2A receptor activation with ATL-313 results in the greatest protection against lung ischemia-reperfusion injury when given before ischemia and during reperfusion. Improved pulmonary function observed with adenosine A2A receptor activation was correlated with decreased bronchoalveolar lavage tumor necrosis factor alpha and decreased lung myeloperoxidase. The loss of protection observed with the concurrent administration of the adenosine A2A receptor antagonist, ZM 241385, supports that the mechanism of ATL-313 protection is specifically mediated via adenosine A2A receptor activation.

Adenosine A2A activation attenuates nontransplantation lung reperfusion injury.

BACKGROUND: Lung reperfusion injury is a significant problem in cardiothoracic surgery. Previous studies have demonstrated that an adenosine A(2A) agonist can attenuate lung reperfusion injury in a lung transplantation model. There has been little work, however, examining its effects in the setting of nontransplant ischemia reperfusion. Our hypothesis was that an A(2A) agonist would attenuate lung reperfusion injury in a warm ischemia hilar clamping model. STUDY DESIGN: Sprague Dawley rats underwent 90 min of left hilar clamping followed by 4 h of reperfusion. Group 1 (n = 13) received an intravenous infusion of 0.06 ug/kg/min of ATL-146e, which was started 10 min before reperfusion. Group 2 (n = 16) received an equivalent saline infusion. A third sham group (n = 14) received the same protocol as Group 2 but no lung ischemia. RESULTS: Animals receiving ATL-146e showed significant improvements in oxygenation (Group 1: 447 +/- 26.02 mmHg versus Group 2: 223 +/- 24.46 mmHg (P < 0.001) as well as ventilation (pCO2 Group 1: 48.78 +/- 3.88 versus Group 2: 63.56 +/- 4.80 (P = 0.009)). Total protein in the bronchoalveolar lavage was significantly higher in the saline group compared with the adenosine as well as a higher proportion of neutrophils. Histological analysis demonstrated a significantly higher number of neutrophils in the IR group compared with the adenosine group. CONCLUSIONS: ATL-146e, an adenosine analogue that is a specific agonist for the A(2A) receptor, attenuates reperfusion injury in an in vivo rat lung model. Arterial blood gas measurements demonstrate a statistically significant increase in oxygenation and improved ventilation.

Obesity does not increase complications after anatomic resection for non-small cell lung cancer.

BACKGROUND: The effect of obesity on complications after resection for lung cancer is unknown. We hypothesized that obesity is associated with increased complications after anatomic resections for non-small cell lung cancer. METHODS: A review of our prospective general thoracic database identified 499 consecutive anatomic resections for non-small cell lung cancer from November 2002 to May 2006. Body mass index (BMI) was used to group patients as nonobese (BMI > 18.5 to < 30) and obese (BMI > or = 30). Patient characteristics and oncologic and operative variables were compared between groups. Multivariable logistic regression models were fit with BMI included at every level. Outcomes examined included in-hospital morbidity, mortality, length of stay, and readmission. RESULTS: Seventy-five percent (372 of 499) were nonobese, and 25% (127 of 499) were obese. Preoperative variables were similar, except for a greater incidence of diabetes mellitus (p < 0.0001) in the obese group. Overall mortality was 1.4% (7 of 499) and was not different between groups (p = 0.85). Thirty-day readmission rates (p = 0.76) and length of stay (p = 0.30) were similar. Obese patients had a higher incidence of acute renal failure (p = 0.001). A complication occurred in 33% (124 of 372) of nonobese and 31% (39 of 127) of obese patients (p = 0.59). Respiratory complications occurred in 22% (81 of 372) of nonobese and 14% (18 of 127) of obese patients (p = 0.06). Significant predictors of any complication include performance status, diffusing capacity, and tumor stage. Significant predictors of respiratory complications include performance status, diffusing capacity, chronic renal insufficiency, prior thoracic surgery, and chest wall resection. CONCLUSIONS: In contrast to our hypothesis, obesity does not increase the incidence of perioperative complications, mortality, or length of stay after anatomic resection for non-small cell lung cancer.

Reevaluating the need for left subclavian artery revascularization with thoracic endovascular aortic repair.

BACKGROUND: With increased utilization of thoracic endovascular aortic repair (TEVAR), the anatomic limitations of proximal device landing zones are being challenged. As our experience has grown with TEVAR involving exclusion of the left subclavian artery (LSA), the need for selective revascularization of the LSA appeared to be more common than we initially anticipated. We hypothesize that for patients undergoing TEVAR requiring coverage of the LSA, the need for LSA revascularization is higher than reported in the literature. METHODS: The charts of all patients undergoing TEVAR performed at a single tertiary care center from 1999 to 2006 were reviewed. The review included the preoperative radiographic evaluations, the assessment of comorbidities, the anatomic position of the proximal and distal landing zones, outcomes, complications, and the need for preoperative or postoperative subclavian artery revascularization. RESULTS: Sixty-four patients underwent TEVAR and 27 (42%) of these patients required exclusion of the LSA from the thoracic aorta. Seven of these 27 patients (25.9%) required preoperative LSA revascularization. Four patients developed late symptoms, necessitating LSA revascularization. No patients died or developed paraplegia, but three adverse neurological events occurred unrelated to the posterior fossa circulation. No patient developed any left arm disability. CONCLUSIONS: The TEVAR coverage of the LSA with selective revascularization was safe for patients, but greater than 11 of 27 (40.7%) required either preoperative or postoperative LSA revascularization. Although this study represents our early experience with TEVAR, these data suggest that selective revascularization after TEVAR exclusion of the origin of the LSA may be required more frequently than previously reported.

A change in perspective: results for ischemic mitral valve repair are similar to mitral valve repair for degenerative disease.

BACKGROUND: Although the benefits of mitral valve repair for degenerative disease are well established, many consider surgery for functional ischemic mitral regurgitation (MR) less amenable to operative treatment. We hypothesized that mitral valve repair for ischemic MR results in outcomes similar to those for mitral valve repair for degenerative MR. METHODS: Retrospective review of nonemergent mitral valve repairs for an 8-year period revealed 105 patients with functional ischemic MR, of whom 39 were treated for severe tethering (ischemic group), and 245 patients with degenerative MR (degenerative group). RESULTS: Patients in the ischemic group had more comorbidities (p < 0.01) and worse preoperative left ventricular dysfunction (ejection fraction < or = 0.29) compared with patients in the degenerative group; (ischemic, 37.1% [39 of 105] versus degenerative, 2.0% [5 of 245]; p < 0.01). Immediate postrepair transesophageal echocardiogram revealed a 0 to 1+ MR in all patients in both groups (not significant). The hospital mortality rate was 1.9% (2 of 105) in the ischemic group and 1.2% (3 of 245) in the degenerative group (p = 1.00). The 5-year survival rate was 83.9% in the ischemic group and 94.3% in the degenerative group (p < 0.01). Five-year freedom from reoperation for recurrent MR was 100% and 97.5% in the ischemic and degenerative groups, respectively (p = 0.14). Postoperative renal failure and stroke rates were similar between both groups (not significant). The incidence of moderate or greater MR after more than 1 year of follow-up was similar between groups (not significant). CONCLUSIONS: Despite the multiple comorbidities that afflict patients with ischemic MR, mitral valve repair for ischemic and degenerative disease produces comparable and satisfactory outcomes. An aggressive approach to repair of functional ischemic MR, including treatment of tethering, leads to durable results.

Pulmonary macrophage inhibition and inhaled nitric oxide attenuate lung ischemia-reperfusion injury.

BACKGROUND: Lung ischemia-reperfusion injury (LIRI) is postulated to occur biphasically. Donor pulmonary macrophages mediate early injury, and neutrophil-dependent injury predominates in the later phase of LIRI. We hypothesized that the biphasic response to LIRI would be attenuated by the administration of gadolinium, a known pulmonary macrophage inhibitor, and inhaled nitric oxide (NO), a pulmonary vasodilator that also interferes with neutrophil chemotaxis. METHODS: Using our isolated, ventilated, blood-perfused rabbit lung model, study groups (n = 10 per group) underwent two hours of reperfusion after 18 hours of cold ischemia (4 degrees C). Lungs received gadolinium alone, or inhaled NO in the presence or absence of macrophage inhibition with gadolinium. RESULTS: Compared with control animals, pulmonary macrophage inhibition with the concurrent administration of inhaled NO increased lung compliance (p < 0.01) and oxygenation (p = 0.03), while also decreasing pulmonary artery pressure (p < 0.01), myeloperoxidase content by 63% (p < 0.01), wet to dry ratios by 23% (p < 0.01), and lung tissue (p < 0.01) and bronchoalveolar lavage tumor necrosis factor-alpha (TNF-alpha) protein levels (p < 0.01). CONCLUSIONS: The severity of LIRI was most significantly reduced by the inhibition of pulmonary macrophages and the concomitant use of inhaled NO. Pulmonary macrophages, likely through the elaboration of proinflammatory cytokines such as TNF-alpha, not only cause early injury themselves but also prime cells such as neutrophils to injure lungs in the later stages of LIRI. The LIRI was effectively blunted by the reduction of macrophage-dependent injury by gadolinium while inhaled NO also attenuated injury by reducing pulmonary hypertension and minimizing neutrophil sequestration.

A simplified approach to degenerative disease: triangular resections of the mitral valve.

BACKGROUND: Only 40% of patients with mitral valve (MV) regurgitation undergo operative repair rather than replacement. Quadrangular resection combined with ring annuloplasty has been the most common method of repair for degenerative posterior leaflet disease. Techniques such as sliding annuloplasty and artificial chord usage have increased the complexity of repair. These techniques have been perceived to be difficult and have possibly reduced the incidence of MV repair. We present our experience with a simplified approach to MV repair utilizing a triangular resection and larger rings. METHODS: Retrospective review of all MV repairs over a 7-year period (1999 to 2006) revealed 154 patients who underwent triangular resection for degenerative disease. Patients who underwent ring annuloplasty without leaflet resection and patients who had artificial chords or quadrangular resections were excluded. RESULTS: Of 154 patients who underwent triangular resection, isolated posterior leaflet resection was performed on 130 patients. Isolated anterior and combined anterior and posterior leaflet triangular resections were performed on 16 and 8 patients, respectively. Thirty-day postoperative mortality was 0%. Five-year freedom from reoperation for recurrent mitral regurgitation was 99.0%. No patients who had intended leaflet resection were converted to MV replacement. Intraoperative transesophageal echocardiogram revealed trace to 1+ mitral regurgitation. Mild systolic anterior motion was noted in 7.1% of cases initially, but resolved with volume loading in all. CONCLUSIONS: Triangular leaflet resection of the mitral valve produces durable results and can be safely and efficiently performed with minimal morbidity and mortality. This technique should allow increased utilization of MV repair for degenerative disease.

Endoscopic versus open saphenous vein harvest for femoral to below the knee arterial bypass using saphenous vein graft.

BACKGROUND: Although the use of endoscopic vein harvest (EVH) in coronary artery bypass grafting is accepted, few studies have documented the implementation of EVH in peripheral vascular disease surgery. We hypothesized that EVH improves outcomes compared with open vein harvest (OVH) in patients undergoing femoral to below the knee arterial bypass surgery. METHODS: The charts of 144 consecutive patients undergoing infrainguinal bypass surgery over the course of 27 months were reviewed. A femoral to below the knee arterial bypass with saphenous vein was done in 88 patients (29 had EVH, 59 had OVH). The preoperative characteristics evaluated were age, gender, renal function, history of diabetes, hypertension, tobacco use, and previous infrainguinal bypass surgery on the affected side. End points included wound complications, length of hospital stay, operative time, angiographic and operative interventions for graft occlusion, patency rates, limb salvage, acute renal failure, myocardial infarction, and death. RESULTS: Patient characteristics and demographics were similar in the EVH and OVH groups. No operative intervention for occlusion was required in the EVH group (0/29) compared with 13.4% in the OVH group (8/59) (P = .03). At the mean follow-up time of 21 months, primary patency rate was 92.8% in the EVH group and 80.6% in the OVH group (P = .12). No significant differences were found between the EVH and OVH groups in postoperative complications, length of hospital stay, operative time, patency rates, limb salvage, and death. CONCLUSION: Despite our initial concerns of damaging the venous conduit with a minimally invasive approach to saphenous vein harvest, EVH in our experience has resulted in a trend toward improved patency rates and decreased infectious wound complications while affording the benefit of improved cosmesis. An endoscopic approach results in smaller incisions, decreased interventions for occlusion, and improved outcomes compared with OVH. EVH is the procedure of choice for harvesting saphenous vein for femoral to below the knee arterial bypass surgery.

Thoracic aortic endografting is the treatment of choice for elderly patients with thoracic aortic disease.

OBJECTIVE: To assess the effect of age on outcomes following thoracic aortic endografting. SUMMARY BACKGROUND DATA: Endograft therapy for thoracic aortic disease is rapidly evolving. This therapy is less invasive, and elderly patients with significant medical comorbidities are more frequently referred for endografting. We hypothesized that elderly patients over the age of 75 have worse outcomes after thoracic endografting than patients under the age of 75. METHODS: We retrospectively reviewed the charts of the first 42 patients who underwent endografting for thoracic aortic pathology. Charts were reviewed for demographics, comorbid conditions, perioperative complications and death, endoleaks, and results at 3, 6, and 12 months. Preexisting medical conditions were also evaluated to determine if any patient characteristics were associated with adverse outcomes. Perioperative morbidity included cardiac, pulmonary, renal, hemorrhagic, and neurologic (stroke and spinal cord injury) complications. RESULTS: Twenty-four patients were under the age of 75, and 18 patients were 75 or older. Baseline demographics and comorbidities were similar between the 2 groups. There were no differences in operative time, length of stay, perioperative mortality, or the incidence of significant complications between the 2 age groups. Gender, however, was associated with a statistically significant difference between the occurrence of complications, with more women experiencing complications than men (P = 0.026, relative risk = 2.36). One patient (age >75 years) in the entire cohort of 42 (2.4%) suffered a spinal cord injury. At 3 months, endoleaks were more common in the older age group (P = 0.059). CONCLUSION: Endograft therapy for thoracic aortic disease can be performed safely in elderly patients with no significant increase in perioperative morbidity or mortality compared with younger patients. Female gender is associated with a higher likelihood of perioperative complications, regardless of age. The overall incidence of spinal cord injury is very low. Endograft therapy, when anatomically possible, is the treatment of choice for thoracic aortic disease in elderly patients.

Does the addition of glutamine to enteral feeds affect patient mortality?

OBJECTIVE: Studies have failed to consistently demonstrate improved survival in intensive care unit (ICU) patients receiving immune-modulating nutrient-enhanced enteral feeds when compared with standard enteral feeds. The objective was to study in a prospective fashion the effects of adding glutamine to standard or immune-modulated (supplemented with omega-3 fatty acids, beta-carotene, and amino acids such as glutamine and arginine) tube feeds. DESIGN: Prospective, unblinded study using sequential allocation. SETTING: A university surgical trauma ICU. PATIENTS: All surgical and trauma patients admitted to the surgical trauma ICU at a university hospital over a 3-yr period who were to receive enteral feeds (n = 185). INTERVENTIONS: Sequential assignment to three isocaloric, isonitrogenous diets was performed as follows: standard 1-kcal/mL feeds with added protein (group 1), standard feeds with the addition of 20-40 g/day (0.6 g/kg/day) glutamine (group 2), or an immune-modulated formula with similar addition of glutamine (group 3). The goal for all patients was 25-30 kcal/kg/day and 2 g/kg/day protein. MEASUREMENTS AND MAIN RESULTS: Patients were followed until discharge from the hospital. The primary end point was in-hospital mortality, and multiple secondary end points were recorded. In-hospital mortality for group 1 was 6.3% (four of 64) vs. 16.9% (ten of 59, p = .09) for group 2 and 16.1% (ten of 62, p = .09) for group 3. After controlling for age and severity of illness, the difference in mortality between patients receiving standard tube feeds and all patients receiving glutamine was not significant (p < or = .11). There were no statistically significant differences between the groups for secondary end points. CONCLUSIONS: The addition of glutamine to standard enteral feeds or to an immunomodulatory formula did not improve outcomes. These findings suggest that enteral glutamine should not be routinely administered to patients with surgical critical illness.