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Introduction: Systemic ventricular end-diastolic pressure is important in patients with single ventricle heart disease. Predictors of an elevated systemic ventricular end-diastolic pressure prior to bidirectional Glenn operation have been incompletely identified., Methods: All patients who underwent bidirectional Glenn operation operation at our centre between January 2007 and March 2017 were retrospectively identified and patient variables were extracted. For patients who had undergone Fontan operation at the time of this study, post-Fontan patient variables were also extracted., Results: One-hundred patients were included with a median age at pre-bidirectional Glenn operation catheterisation of 4.5 months. In total, 71 (71%) patients had a systemic right ventricle. At the pre-bidirectional Glenn operation catheterisation, the mean systemic ventricular end-diastolic pressure was higher amongst those with systemic right ventricle compared to left ventricle (9.1 mmHg ± 2.1 versus 7.7 ± 2.7 mmHg, p < 0.01). On univariate analysis, pre-bidirectional Glenn operation systemic ventricular end-diastolic pressure was positively associated with the presence of a systemic right ventricle (p < 0.01), history of recoarctation (p = 0.03), history of Norwood operation (p = 0.04), and ventricular systolic pressure (p < 0.01). On multivariate analysis, systemic ventricular end-diastolic pressure was positively associated with the presence of a systemic right ventricle (p < 0.01) and ventricular systolic pressure (p < 0.01). Amongst those who had undergone Fontan operation at the time of study (n = 49), those with a higher pre-bidirectional Glenn operation systemic ventricular end-diastolic pressure were more likely to have experienced death, transplantation, or listed for transplantation (p = 0.02) and more likely to have had heart failure symptoms (p = 0.04) at a mean time from Fontan of 5.2 years ± 1.3., Conclusions: In patients undergoing bidirectional Glenn operation operation, the volume-loaded, pre-bidirectional Glenn operation state may expose diastolic dysfunction that has prognostic value.

Tetralogy of Fallot is characterized by a ventricular septal defect, a large, overriding aorta, subpulmonic stenosis, and right ventricular hypertrophy. These lesions can be associated with abnormal development of the pulmonary vasculature. This can include peripheral pulmonic stenosis, discontinuous pulmonary arteries, anomalous pulmonary venous return, and the development of aortopulmonary collateral vessels. Aortopulmonary collateral vessels develop to supply underperfused areas of the pulmonary bed and pose a unique and challenging problem at the time of surgical repair, which involves closure of the ventricular septal defect, relief of right ventricular outflow tract obstruction, maintenance of pulmonary valve competency when possible, and establishment of laminar pulmonary blood flow to all segments of the pulmonary bed. We describe a 36-year-old man with unrepaired tetralogy of Fallot with distinctive aortopulmonary collaterals, who underwent complete surgical repair with good outcome. Two-dimensional echocardiogram, cardiac magnetic resonance imaging, and cardiac catheterization each provided vital details allowing a stepwise approach to defining his unique anatomy for surgical correction., (© 2011 Wiley Periodicals, Inc.)

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.

The majority of primary cardiac tumors are benign; of these tumors, cardiac paragangliomas are among the rarest. We report a case of biatrial cardiac paraganglioma discovered during workup for palpitations and fatigue. The tumor involved the interatrial septum, with a lobulated portion protruding through the foramen ovale into the right atrium. The tumor was successfully excised, leading to uneventful recovery.

Stentless mitral valves have found little clinical utility to date due to difficulty in insertion. A new design for a stentless mitral valve, a modification of an existing aortic stentless prosthesis, is described. The new design mimics the native mitral physiology, and its insertion is easier than with existing stentless mitral valves. Commercially available stentless aortic valves were inserted into 2 pigs. The valves were modified so that the commissural posts were restrained. The valves were partially recessed into the left ventricular cavity, secured to the annulus, and anchored to the native papillary muscles. Both pigs were weaned from bypass successfully, and both valves functioned normally with trace regurgitation noted on echocardiography. This design affords the benefit of the reapproximation of native physiology. Preservation of papillary-annular continuity should allow maximal left ventricular function. Lack of a stent should allow avoidance of long-term anticoagulation.

Background: The purpose of this study was to evaluate the role of a routine protocol for evaluation of oropharyngeal aspiration after thoracotomy for pulmonary resection., Methods: Demographic, operative, and outcomes data were collected prospectively for consecutive patients undergoing thoracotomy for pulmonary resection starting in April 2005. Starting on postoperative day one, patients underwent evaluation by a licensed speech therapist before per os intake. Patients failing clinical examination were referred for radiographic evaluation. Diets were advanced on the basis of results from both clinical and radiographic evaluation. Data analysis included descriptive statistics, Student's t test, and chi2 test when appropriate., Results: One hundred forty patients were prospectively evaluated during this period. Thirty-two patients (22.9%) failed initial clinical swallowing evaluation and were referred for dynamic videofluoroscopic esophagram. Twenty-five patients (17.8%) had evidence of potential oropharyngeal aspiration on videofluoroscopic esophagram. Only 1 patient (0.7%) aspirated after a negative clinical evaluation. Univariate risk factor analysis revealed that patients demonstrating aspiration were older (67.7 +/- 1.6 years versus 64.4 +/- 1.1 years; p = 0.10) and had a higher incidence of head and neck malignancy (p < 0.001). Patients without radiographic aspiration had a shorter median hospital stay when compared with those who did (6 days versus 5 days)., Conclusions: Aspiration after thoracotomy for pulmonary resection may affect nearly 20% of patients and is likely underrepresented in the surgical literature. The institution of a protocol to evaluate risk of aspiration has characterized patients at high risk and led to an increased awareness of the potential for aspiration after thoracotomy.

Background: ATL-146e protects the spinal cord from ischemia/reperfusion injury, presumably via adenosine A(2A) receptor activation, but this relationship remains unproven. We hypothesized that spinal cord functional and cytoarchitectural preservation from ATL-146e would be lost with simultaneous administration of the specific adenosine A(2A) antagonist ZM241385 (ZM), thus proving that adenosine A(2A) receptor activation is responsible for the protective effects of this compound., Methods: New Zealand White rabbits underwent 45 minutes of infrarenal aortic cross-clamping. Groups (n = 10) included sham, ischemia, ischemia plus ATL-146e (ATL-146E), ischemia plus ZM, or ischemia with both compounds (agonist-antagonist). Tarlov scores were recorded every 12 hours. After 48 hours, the spinal cord was fixed for histology and microtubule-associated protein 2 immunohistochemistry., Results: Tarlov scores at 48 hours were significantly better in the sham and ATL-146E groups (5.0 and 3.9, respectively) compared with the other three groups (all < or =1.3; P < .001). On hematoxylin and eosin, neuronal viability was higher in the sham, ATL-146E, and agonist-antagonist groups compared with the control and ZM groups (P < .05). Microtubule-associated protein 2 expression was preserved in the sham and ATL-146E groups but was lost in the ATL + ZM, ZM241385, and control groups., Conclusions: ATL-146e preserves the spinal cord in terms of both cytoarchitecture and function after reperfusion of the ischemic spinal cord, but this preservation is not completely blocked by competitive adenosine A(2A) receptor antagonism. Although ATL-146e does seem to partially function through activation of the adenosine A(2A) receptor, the neuroprotective mechanism may not be limited to this particular receptor.

The objective of this study is to demonstrate the effectiveness and feasibility in treating empyema after pulmonary resection with a modified Clagett procedure performed at the bedside (BMCP). A retrospective review of a single surgeon's experience at a single institution was undertaken. All operative, postoperative, and outcome data were analyzed. Follow-up data were obtained from subsequent clinic charts. Five patients, including four males, were identified who underwent BMCP after pulmonary resection. The original operative procedures included two lobectomies, one pneumonectomy, one bilobectomy, and one bilateral metastastectomy. Patients were diagnosed with an empyema (positive thoracostomy tube culture, fever, and radiographic abnormality) at a mean time of 31 days from their initial procedure. Culture results disclosed Gram-positive empyemas in all patients. Three patients underwent BMCP as an outpatient, whereas the other two had BMCP during their hospitalizations. All patients are free from complications or recurrence at a mean follow up of 11.2 months. No patient required a further procedure after BMCP. The bedside modified Clagett procedure is both safe and effective. It is a valuable option in the management of postoperative empyema because it avoids additional operative procedures. This procedure is cost-effective when compared with operative management of perioperative empyema.

Right-sided aortic arch with a concomitant coarctation is an exceedingly rare congenital cardiac anomaly. We report of a 4-year-old boy who presented with a history of a stenotic bicuspid aortic valve who upon further evaluation was found to have a coarctation of a right-sided aortic arch. The frequency with which other anomalies exist in either of the above conditions requires thorough cardiac evaluation and detailed imaging. Surgical repair of this anomaly can safely be undertaken through a right thoracotomy.

Background: After pneumonectomy, the remaining lung vasculature must vasodilate to compensate for increased blood volume. We hypothesized that endothelial nitric oxide synthase (eNOS) is essential for compensatory vasodilation after pneumonectomy., Methods: Adult, wild-type C57BL6 (WT) and eNOS knockout (eNOS-/-) mice underwent left pneumonectomy and recovered under normoxic conditions. Animals were lightly anesthetized at 1, 3, 7, or 14 days after pneumonectomy, and closed chest, systolic right ventricular pressure (RVP) was recorded using fine-needle cannulation. The right ventricle to left ventricle plus septum weight ratios were measured as an index of right ventricular hypertrophy. Two additional groups of mice (WT and eNOS-/-) were recovered after pneumonectomy in inhaled nitric oxide (iNO, 10 ppm), and RVP was measured on day 7., Results: The eNOS-/- mice had significantly higher preoperative RVP than did WT (17.1 +/- 0.4 versus 14.2 +/- 0.2 cmH2O, p = 0.001). Both groups exhibited transient periods of pulmonary hypertension after pneumonectomy. On day 1, RVP was 80% above baseline in eNOS-/- mice (30.7 +/- 0.8 cmH2O) versus 42% in WT mice (20.2 +/- 0.7 cmH2O, p = 0.0001). The RVP returned to baseline in WT mice (16.3 +/- 0.2 cmH2O) but remained significantly elevated in eNOS-/- mice (28.6 +/- 0.9 cmH2O) at day 3 and at each time thereafter (p = 0.0001). The iNO significantly reduced RVP in eNOS-/- animals to 15.2 +/- 0.3 cmH2O (p = 0.0001) while having no effect in WT animals. Right ventricular hypertrophy was not observed in any group., Conclusions: Pneumonectomy results in a transient increase in RVP. Under normal circumstances, these pressures return to baseline within 3 days. The eNOS-/- mice failed to display compensatory vasodilation yet could be rescued with iNO. These results suggest that eNOS is essential for postpneumonectomy compensatory vasodilation.

Background: Paraplegia remains a devastating complication of thoracic aortic surgery, which has been attenuated by retrograde adenosine and systemic adenosine A2A receptor activation. We hypothesized that despite retrograde spinal perfusion of an adenosine A2A agonist (ATL-146e), systemic therapy produces superior spinal cord protection with reduced inflammation., Methods: Forty pigs underwent 30-minute thoracic aortic cross-clamping. Pigs received: no therapy (control); retrograde saline (retrograde control); retrograde ATL-146e; systemic ATL-146e; systemic ATL-146e with retrograde saline; or systemic and retrograde ATL-146e. Retrograde therapies were given during ischemia. Systemic ATL-146e (0.06 microg.kg(-1).min(-1)) was given intravenously for 3 hours at reperfusion. At 24 hours, motor function was assessed using the Tarlov scale. Tissue was analyzed for neuronal viability, microtubule-associated protein-2 expression, and neutrophil sequestration (myeloperoxidase activity)., Results: Four pigs received retrograde barium showing both radiographic and histologic spinal cord perfusion. Tarlov scores at 24 hours were significantly improved versus both control groups in all ATL groups except the combined ATL-146e group (all p < 0.05). Neuronal viability by hematoxylin and eosin stain was significantly preserved in systemic ATL groups compared with both control groups (all p < 0.05). Microtubule-associated protein-2 expression was significantly preserved compared with both control groups in all systemic ATL groups. Systemic ATL significantly lowered myeloperoxidase activity versus both control groups (p < 0.01)., Conclusions: Both retrograde and systemic ATL-146e therapies attenuate ischemic spinal cord injury, but combining the two routes was less effective. Given comparable results between the two routes and the simplicity of systemic delivery, peripheral venous ATL-146e at reperfusion should be preferred for spinal cord protection in thoracic aortic surgery.

Background: Congestive heart failure (CHF) is the leading cause of hospital admissions in the United States., Methods and Results: CHF has a variety of palliative options for treatment and 1 curative one: cardiac transplantation. Palliative medical therapies are often limited in effectiveness by progression of the disease or patient intolerance. Because of limited donor availability, alternative surgical strategies are now being relied on for palliation of patients in end-stage CHF., Conclusion: In this manuscript, we review the principles, outcomes, and practices of some of these surgical strategies often used in the palliation of end-stage CHF.

Background: There is an increasing trend toward work hour restrictions for doctors world wide. These reforms have been inspired, in part, by the assertion by some that the fatigued physician is more prone to making errors. Interestingly, there is very little in the way of objective data with regard to the effects of sleep deprivation on patient outcomes. We have recently studied this in attending surgeons. The present study focused on thoracic surgical residents. Our hypothesis was that acute sleep deprivation would not lead to an increase in operative times or complications., Methods: A retrospective review of all cases performed by thoracic surgical residents at the University of Virginia from January 1994 to March of 2004 was done. Complication rates of cases performed by "sleep deprived" (SD) residents were compared with cases done when the residents were "not sleep deprived" (NSD). A resident was deemed sleep deprived if he or she performed a case the previous evening that started between 10 pm and 5 am or ended between the hours of 11 pm and 7:30 am., Results: A total of 7,323 cases were recorded in the STS database over the 10-year period examined. Two hundred and twenty-nine of these cases (3%) were performed by SD residents. Mortality rates for coronary artery bypass operations showed no significant differences (2.1% [SD = 3 of 141 patients] vs 3.1% (NSD = 143 of 4452 patients), p = 0.63). A comparison of operative, neurologic, renal, infectious, and pulmonary complications as well as cardiopulmonary bypass times, cross-clamp times, the use of blood products, and length of stay also demonstrated no significant differences between groups., Conclusions: Acute sleep deprivation in thoracic surgical residents does not affect operative efficiency, morbidity, or mortality in cardiac surgical operations.

Background: Previous formulations of cyanoacrylate, though very effective, proved to have too high a tissue reactivity to be used internally. A novel cyanoacrylate compound with less tissue reactivity was recently developed. The objective of this study was to assess this novel cyanoacrylate compound for the use as vascular suture line sealant., Materials and Methods: Twelve adult female sheep received a 6 mm PTFE interposition graft in each iliac artery, for a total of 24 grafts. Using oxidized cellulose (Surgicel) as a control, two formulations of a new cyanoacrylate compound (named "compound A" and "compound B") were assessed during this trial. Hemostatic efficiency was measured at the time of operation by the assessment of bleeding time and amount of blood loss. Long-term graft patency was assessed angiographically at 4, 6, and 18 months. Tissue reaction at 2 weeks, 1, 6, and 18 months was assessed grossly by vascular surgeons and microscopically by a blinded pathologist., Results: Average time to hemostasis was 37.6, 50.6, and 219 s in group A, group B, and oxidized cellulose control groups, respectively (P

Background: Reperfusion injury continues to significantly affect patients undergoing lung transplantation. Isolated lung models have demonstrated that adenosine A 2A receptor activation preserves function while decreasing inflammation. We hypothesized that adenosine A 2A receptor activation by ATL-146e during the initial reperfusion period preserves pulmonary function and attenuates inflammation in a porcine model of lung transplantation., Methods: Mature pig lungs preserved with Viaspan (Barr Laboratories, Pomona, NY) underwent 6 hours of cold ischemia before transplantation and 4 hours of reperfusion. Animals were treated with (ATL group, n = 7) and without (IR group, n = 7) ATL-146e (0.05 microg kg -1 . min -1 ATL-146e administered intravenously for 3 hours). With occlusion of the opposite pulmonary artery, the animal was maintained for the final 30 minutes on the allograft alone. Recipient lung physiology was monitored before tissue evaluation of pulmonary edema (wet-to-dry weight ratio), myeloperoxidase assay, and tissue tumor necrosis factor alpha by means of enzyme-linked immunosorbent assay., Results: When the ATL group was compared with the IR group, the ATL group had better partial pressure of carbon dioxide (43.8 +/- 4.1 vs 68.9 +/- 6.3 mm Hg, P < .01) and partial pressure of oxygen (272.3 +/- 132.7 vs 100.1 +/- 21.4 mm Hg, P < .01). ATL-146e-treated animals exhibited lower pulmonary artery pressures (33.6 +/- 2.1 vs 47.9 +/- 3.5 mm Hg, P < .01) and mean airway pressures (16.25 +/- 0.08 vs 16.64 +/- 0.15 mm Hg, P = .04). ATL-146e-treated lungs had lower wet-to-dry ratios (5.9 +/- 0.39 vs 7.3 +/- 0.38, P < .02), lower myeloperoxidase levels (2.9 x 10 -5 +/- 1.2 x 10 -5 vs 1.3 x 10 -4 +/- 4.0 x 10 -5 DeltaOD mg -1 . min -1 , P = .03), and a trend toward decreased lung tumor necrosis factor alpha levels (57 +/- 12 vs 96 +/- 15 pg/mL, P = .06). The ATL group demonstrated significantly less inflammation on histology., Conclusion: Adenosine A 2A activation during early reperfusion attenuated lung inflammation and preserved pulmonary function in this model of lung transplantation. ATL-146e and similar compounds could play a significant role in improving outcomes of pulmonary transplantation.

Background: Ischemia-reperfusion (IR) injury negatively impacts patient outcome in lung transplantation. Clinically, we observed that lung transplant patients with ischemia-reperfusion injury tend to have cardiac dysfunction. Previous studies have shown that ATL-146e (4-{3-[6-amino-9-(5-ethylcarbamoyl-3,4-dihydroxy-tetrahydro-furan-2-yl)-9H-purin-2-yl]-prop-2-ynyl}-cyclohexanecarboxylic acid methyl ester), a selective adenosine A2A receptor agonist, reduces lung inflammation after ischemia-reperfusion. We hypothesized that pulmonary ischemia-reperfusion causes secondary heart dysfunction and ATL-146e will improve this dysfunction., Methods: We utilized an in vivo rabbit lung ischemia-reperfusion model. The Sham group underwent 120 minutes single lung ventilation. The IR and ATL groups underwent 90 minutes right lung ischemia with 30 minutes right lung reperfusion. The ATL-146e was given intravenously to the ATL group during reperfusion. Cardiac output and arterial blood gases were monitored, and neutrophil sequestration was measured by myeloperoxidase activity., Results: Upon reperfusion, cardiac output (mL/min) significantly dropped in the IR and ATL groups. By 15 minutes reperfusion, cardiac output in the ATL group improved significantly over the IR group and remained significant thereafter. Lung myeloperoxidase activity was significantly reduced by ATL-146e. Although never hypoxemic, arterial oxygenation was lower in the IR and ATL groups while central venous pressures and mean arterial pressures were similar among groups. A separate experiment demonstrated that reperfusion with the antioxidant N-(2-mercaptopropionyl)glycine prevented cardiac dysfunction., Conclusions: Pulmonary ischemia-reperfusion causes cardiac dysfunction independent of preload, afterload, and oxygenation. The ATL-146e improves this dysfunction presumably by the antiinflammatory effects of adenosine A2A receptor activation on neutrophils. One likely mechanism involves the release of oxidants from the ischemic lung upon reperfusion, which has immediate negative effects on the heart.

Pulmonary ischemia-reperfusion injury is complex and involves many cell types and mechanisms of action. Van Putte and coworkers have attempted to provide insight into and describe some of the complex components of this process. Their study describes two new components of the multifaceted process of reperfusion injury. The time-dependent course of neutrophil activation and the discovery of programmed cell death in reperfused lung tissue are two new pieces of a complex puzzle.

Background: There has been an increasing trend towards the mandatory reduction in work hours for physicians because of the fear that sleep-deprived (SD) surgeons are more prone to make mistakes. We hypothesized that sleep deprivation would not be associated with increased morbidity or mortality in cardiac operations., Methods: A retrospective review was done of all cases performed by all attending cardiac surgeons from January 1994 to April 2003. Complication rates of cases performed by SD surgeons were compared with cases done when the surgeons were not sleep-deprived (NSD). A surgeon was deemed sleep deprived if he or she performed a case the previous evening that started between 10:00 pm and 5:00 am, or ended between the hours of 11:00 pm and 7:30 am., Results: A total of 6,751 cases were recorded in the Society of Thoracic Surgeons database over the 9-year period examined. Of these, 339 cases (5%) were performed by SD surgeons, and 6,412 (95%) cases were performed by NSD surgeons. Mortality rates for coronary artery bypass operations showed no significant differences (1.7% [SD = 4/223] vs 3.1% [NSD = 133/4206)] p = 0.34). Operative (p = 0.47), pulmonary (p = 0.60), renal (p = 0.93), neurologic (p = 0.11), and infectious (p = 0.87) complications of all cases also failed to show any statistically significant differences in any group. Perfusion times, cross-clamp times, and the use of blood products were also similar between groups., Conclusions: Sleep deprivation does not affect operative morbidity or mortality in cardiac surgical operations. These data do not support a need for work hour restrictions on surgeons.

Background: ATL-146e is an adenosine A(2A) agonist that has recently been demonstrated to improve neurological outcome in spinal cord injury in animals. In the current study, we extended the treatment paradigm and tested neurobehavioral functioning out to 1 week after injury to assess if early neurological improvement is sustained long term by an adenosine analogue., Materials and Methods: New Zealand White rabbits (3.0-3.5 kg) sustained mid-thoracic blunt spinal cord injury using a weight-drop model (10 g weight dropped from 6 cm directly onto dura). Animals received either (1) 3 h iv infusion of saline carrier (Trauma, N = 21); (2) 3 h iv infusion of 0.06 microg/kg/min ATL-146e followed by intraperitoneal bolus of 10.8 microg/kg ATL-146e at 3 h postinjury (ATL, N = 14); or (3) 3 h iv infusion of 0.06 microg/kg/min ATL-146e followed by intraperitoneal bolus injection of 10.8 microg/kg ATL-146e at 3, 12, and 24 h postinjury (ATL-PLUS, N = 11). Fourteen animals underwent sham injury. Hemodynamic parameters were monitored and hind limb motor functioning was assessed by Tarlov scores (0 = paralyzed to 5 = normal hop) for 7 days after injury., Results: ATL-146e significantly improved Tarlov scores of ATL-146e groups compared with saline-treated controls (P < 0.01 12, 24, 36, and 48 h). Control animals, severely neurologically impaired at 48 h (Tarlov 1.61 +/- 0.35), were euthanized early due to ethical concerns, thus not permitting later statistical comparisons. Early neurological improvements in both ATL-146e-treated groups were sustained longer term (7 day mean Tarlov, SHAM 4.9 +/- 0.30, ATL 5.0 +/- 0, ATL-PLUS 4.25 +/- 0.31)., Conclusions: ATL-146e given immediately after blunt spinal cord trauma significantly improves neurological outcome, which is sustained through 7 days. Early adenosine A2A receptor agonism may be critical since additional IP administration afforded no further neurological improvement. The current data further support the potential clinical utility of adenosine A(2A) agonists in the treatment of spinal cord injury.

Objective: To compare the outcomes of mitral repair and replacement in revascularized patients with ischemic mitral regurgitation., Summary Background Data: Combined coronary bypass (CABG) and mitral procedures have been associated with the highest mortality (>10%) in cardiac surgery. Recent studies have suggested that mitral valve replacement (MVR) with sparing of the subvalvular apparatus had comparable results to mitral repair when associated with CABG., Methods: Over the past 7 years, 54 patients had CABG/mitral repair versus 56 who had CABG/MVR with preservation of the subvalvular apparatus. The groups were similar in age at 69.2 years in the replacement group versus 67.0 in the repair group. We compared these 2 groups based on hospital mortality, incidence of complications including nosocomial infection, neurologic decompensation (stroke), pulmonary complication (pneumonia, atelectasis, and prolonged ventilation), and renal complications (acute renal failure or insufficiency)., Results: The mitral repair group had a hospital mortality of 1.9% versus 10.7% in the replacement group (P = 0.05). Infection occurred in 9% of repairs compared with 13% of replacements (P = 0.59). The incidence of stroke was no different between groups (2 of 54 repairs vs. 2 of 56 replacements, P = 1.00). Pulmonary complication rate was 39% in repairs versus 32% in replacements (P = 0.59). Worsening renal function occurred in 15% of repairs versus 18% of replacements (P = 0.67)., Conclusions: Mitral repair is superior to mitral replacement when associated with coronary artery disease in terms of perioperative morbidity and hospital mortality. Although preservation of the subvalvular apparatus with MVR has a theoretical advantage in terms of ventricular function, mitral repair clearly adds a survival benefit in patients with concomitant ischemic cardiac disease.

Objective: A central role of macrophages in initiating lung ischemia-reperfusion injury is emerging. Tumor necrosis factor-alpha is a proinflammatory cytokine secreted mainly by macrophages under various conditions. We hypothesized that tumor necrosis factor-alpha from resident lung cells is a key initiating factor in pulmonary ischemia-reperfusion injury., Methods: We used an isolated, buffer-perfused lung system to explore the role of tumor necrosis factor-alpha production by resident lung cells in pulmonary ischemia-reperfusion injury. Lungs from wild-type mice and tumor necrosis factor-alpha-deficient mice were subjected to 60 minutes of ischemia followed by 60 minutes of reperfusion. Histologic injury scores and measurements of lung compliance, airway resistance, mean pulmonary artery pressure, vascular reactivity, and wet lung weight index were obtained and compared using repeated-measures analysis of variance., Results: Lungs from tumor necrosis factor-alpha-deficient mice showed significantly less injury in all physiologic parameters throughout the entire 60 minutes of reperfusion compared with lungs from wild-type mice (P <.001). The most notable effects were observed in pulmonary artery pressure and airway resistance. Vascular reactivity (acute vasoconstrictive episodes per 60 minutes) was also blunted in the lungs from tumor necrosis factor-alpha-deficient mice compared with the lungs from wild-type mice (5.8 responses/hour vs 1.2 responses). Histologic injury scores and wet lung weight index were significantly reduced in lungs from tumor necrosis factor-alpha-deficient mice., Conclusions: By using the advantages of a nonblood-perfused system, we have focused our investigation on resident lung cells. Our results demonstrate that resident cell-produced tumor necrosis factor-alpha is a key initiating factor in acute lung ischemia-reperfusion injury.

Background: Coronary artery bypass is an acceptable therapy in patients with ischemic cardiomyopathy. However, it has been demonstrated that patients with increased left ventricular volume have a worse outcome than patients with normal ventricular volume. Our hypothesis was that ventricular restoration plus coronary artery bypass provides improved outcome compared with coronary artery bypass alone in ischemic cardiomyopathy with ventricular enlargement., Methods: A retrospective analysis was performed of patients with ischemic cardiomyopathy (ejection fraction <30%) who underwent operation between 1998 and 2002. Patients with enlarged ventricles (end-diastolic dimension > or =6.0 cm) who underwent either coronary artery bypass alone or coronary artery bypass with ventricular restoration were compared. Preoperative and postoperative ejection fraction, morbidity, mortality, and freedom from heart failure (hospitalization secondary to heart failure) were assessed., Results: Ninety-five patients were included in the study. Thirty-nine patients had coronary artery bypass alone, whereas 56 patients had ventricular restoration with coronary artery bypass. Both groups demonstrated an improved postoperative ejection fraction; however, the improvement was significantly greater in the ventricular restoration plus coronary artery bypass group (P <.01). There were no hospital deaths in either group; however, late mortality was higher in the coronary artery bypass group. Freedom from heart failure was achieved in all but 2 of the ventricular restoration plus coronary artery bypass patients (2/56, or 3.6%) versus 7 in the coronary artery bypass group (7/39, or 18%). The combined outcomes of freedom from failure and late mortality were significantly improved in the ventricular restoration plus coronary artery bypass group (P <.05)., Conclusions: Ventricular restoration affords significant improvement in ejection fraction compared with coronary artery bypass alone, without added mortality. Most importantly, left ventricular restoration reduces late morbidity and mortality compared with coronary artery bypass alone in patients with large ventricles.

Background: Ventricular reconstruction using the Dor technique has been demonstrated to improve outcome in patients with dilated left ventricles. It has been suggested that a beating heart approach improves ventricular function by allowing the surgeon to palpate that part of the ventricle to exclude., Methods: We performed a retrospective analysis of patients who underwent an endoventricular circular patch plasty (Dor procedure) between 1998 and 2001. All patients who received ventricular restoration, with or without revascularization or valve repair, were included in the analysis. Discrete left ventricular aneurysms were excluded. Patients were divided into two groups: group 1 (n = 15) underwent ventricular reconstruction with the beating heart technique, whereas group 2 (n = 38) underwent restoration with the aorta cross-clamped. Clinical and hemodynamic data were collected from medical records and computerized databases and compared between the two groups., Results: Fifty-three patients underwent endoventricular circular patch plasty. All patients had enlarged ventricles (echocardiogram demonstrating unidimensional end-diastolic diameter >/= 6.0 cm) and echocardiographic evidence of severe left ventricular dysfunction (mean ejection fraction: group 1 = 21.4%; group 2 = 23.4%). No operative mortalities occurred in either group and all patients were discharged home alive (mean postoperative hospital stay 8.3 days [6 to 22 days]). All patients had improvement in left ventricular function with mean postoperative left ventricular ejection fraction of 36.9% (25% to 52%) in group 1 versus 38.1% (31% to 50%) in group 2, p = 0.081. Ventricular arrhythmias occurred in 5 of 15 group 1 patients and in 9 of 38 group 2 patients. Two patients in the entire cohort (1 patient in group 1, and 1 patient in group 2) had at least one readmission within 12 months with evidence of heart failure. The group 1 patient went on to successful transplant 11 months later, whereas the group 2 patient died 10 months later., Conclusions: These results demonstrate that the Dor technique of ventricular restoration significantly improves left ventricular function and the beating heart approach provides no additional advantage over continuous aortic cross clamping.

Background: Thoracic aortic aneurysm after patch repair of aortic coarctation is a potentially lethal complication. We hypothesized that transverse arch hypoplasia in association with patch repair of aortic coarctation predisposes aneurysm formation., Methods: A retrospective analysis was performed on all patients undergoing isolated aortic coarctation repair at the University of Virginia Health Systems between 1970 and 1995. Of 244 repairs, 38 patients underwent patch repair. These 38 patients were divided into two groups. The aneurysm group (n = 15) had aortic aneurysms develop at the repair site, which required aneurysmectomy. The nonaneurysm group (n = 23) did not have any aneurysms develop. Univariate analysis and Fisher's exact text were used to identify factors that independently predict aneurysm formation., Results: Univariate analysis demonstrated aortic arch hypoplasia associated with patch repair independently predicts future aneurysm formation (p < 0.01). Patients who had an aneurysm develop also had a similar incidence of bicuspid aortic valves, mild restenosis, and late hypertension compared with patients in the nonaneurysm group., Conclusions: Aneurysm formation after patch repair of aortic coarctation develops into a subgroup of patients. Aortic arch hypoplasia associated with coarctation independently predicts future aneurysm formation.

Background: Thoracic outlet syndrome (TOS) is a clinical diagnosis encountered by both thoracic and vascular surgeons. The goal of surgical therapy involves relieving compression of the neurovascular structures at the superior thoracic aperture. The traditional approach to thoracic outlet decompression has been transaxillary; however more centers are moving toward a more tailored approach through a supraclavicular incision., Methods: The medical records of 67 patients who underwent surgical decompression between 1993 and 2001 for TOS were retrospectively reviewed. Patient demographics and early outcome were assessed through clinic follow-up., Results: Seventy-two thoracic outlet decompressions were performed on 67 patients with the diagnosis of TOS. Five patients underwent bilateral thoracic outlet decompression. All operations in this time period were safely accomplished through a supraclavicular approach. The syndromes associated with thoracic outlet compression were neurogenic (n = 59), venous (n = 10), and arterial (n = 3). Forty-six of 72 (63.9%) operations resulted in complete resolution of symptoms, 17 cases (23.6%) had partial resolution, and 9 patients (12.5%) had no resolution. There were no deaths and morbidity was minimal with 6 complications (8.3%)., Conclusions: The supraclavicular approach is a safe and effective technique in managing all forms of thoracic outlet compression.

Background: This study investigates the efficacy of pinacidil, an adenosine triphosphate-sensitive potassium (KATP) channel opening agent, added to custadiol solution on myocardial protection during deep hypothermia and prolonged global ischemia on isolated rat hearts., Methods: After 20 minutes of stabilization, 24 rats were divided into two groups. In group I (n=12), hearts were arrested with cold (4 degrees C) custadiol solution containing 50 micromol/L of pinacidil and subsequently dipped into the same solution for 120 minutes at 4 degrees C. Group I hearts were perfused with low-flow pinacidil-custadiol (PC) solution during the ischemic period. Group II (n=12) hearts, after the stabilization period, were arrested with cold custadiol solution only, then subsequently dipped and perfused with the same solution for 120 minutes at 4 degrees C. All hearts were reperfused with Krebb's-Henseleit solution at 37 degrees C for 60 minutes. Hemodynamic parameters (peak systolic pressure, end diastolic pressure, maximum rate of increase of left ventricular pressure [+dP/dt], ischemic contracture, and coronary sinus flow) were recorded at the end of the stabilization period and at 10-minute intervals during the reperfusion period. Biochemical data (creatine kinase [CK-MB] washout and troponin I [cTnI] levels) were compared between the two groups., Results: There was no significant difference in any hemodynamic or biochemical parameters between the two groups during the stabilization period. The peak systolic pressure, +dP/dt, ischemic contraction amplitude, and coronary flow values were significantly higher in group I ( P<0.05) compared with group II during reperfusion. End diastolic pressures as well as CK-MB and cTnI levels were lower in the pinacidil-treated group, which is consistent with improved functional recovery during the reperfusion period., Conclusion: The addition of pinacidil to the preservation solution, custadiol, improves myocardial recovery after deep hypothermia and prolongs ischemia.

Background: Pulmonary hypertension with associated right ventricular dysfunction may complicate the postoperative cardiac patient despite maximum pharmacologic and ventilatory support. The purpose of this study was to retrospectively review our experience with inhaled nitric oxide (INO) in adult postoperative cardiac patients with pulmonary hypertension., Methods: We retrospectively reviewed the medical records of 17 adult cardiac patients treated with INO postoperatively between November 1998 and February 2000. The INO was used to manage pulmonary hypertension postoperatively in patients who had undergone coronary artery bypass graft (CABG) (n = 13), valve operation (n = 3), and combined CABG/aortic valve replacement (n = 1). Hemodynamic and respiratory measurements before INO and again 6 hours after administration were examined. Student's t test was used to analyze the data., Results: Inhaled nitric oxide (20 ppm to 30 ppm) was administered for a median duration of 30.2 hours. The group, as a whole, demonstrated a significant decrease in both mean pulmonary artery pressure and right ventricular stroke work index. In addition, a significant increase in posttherapeutic cardiac index and Pao2/Fio2 ratio was observed. The vasodilatory effects of nitric oxide were specific to the pulmonary circulation as no significant change in mean arterial pressure was noted. Overall mortality was 6%., Conclusions: Inhaled nitric oxide effectively and selectively lowered right ventricular afterload and right ventricular work in critically ill adult cardiac patients with acute pulmonary hypertension.

Tissue adhesives are common adjuncts in surgical practice. Fibrin sealants are the most prevalent adhesives today. Recently, new adhesives have been approved for use in the United States, including cyanoacrylates, albumin-based compounds, collagen-based compounds, glutaraldehyde glues, and hydrogels. This review summarizes all the available tissue adhesives, focusing on their current and prospective indications in the clinical forum.