Between November 14, 2005, and December 18, 2006, a total of 53 thoracic endograft procedures were performed at our institution. Of these, 13 (25%) involved either open aortic arch or abdominal debranching to create proximal or distal landing zones for endovascular repair. Patients undergoing arch debranching (n = 7) had aneurysms involving the transverse arch with less than 2 cm of proximal landing zone distal to the innominate artery, necessitating stent graft coverage of both the innominate and left common carotid arteries. Patients undergoing complete abdominal debranching (n = 6) had either thoracoabdominal aortic aneurysms (extent II, n = 1; extent V, n = 3) or visceral button false aneurysms after prior open thoracoabdominal aortic aneurysm repair (n = 2). In all cases, endovascular aneurysm exclusion was performed at the same operation.

Mean patient age was 63 ± 11 years (range 46-83 years); all patients had significant comorbidities, including prior open aortic surgery in 8 (62%). There were no perioperative (30 day) deaths and no permanent neurologic deficits, either cerebrovascular accident or paraparesis/paraplegia. At a mean follow-up of 7.5 ± 6.0 months, there has been no late mortality and all debranching bypass grafts remain patent without need for further intervention. Computed tomographic scans demonstrate no type I or III endoleaks, and all aneurysms are thrombosed with stable (n = 4) or decreasing aortic dimensions (n = 9).

"Hybrid" aortic debranching using custom fabricated Dacron branch grafts with a single inflow source combined with endovascular aneurysm exclusion appears to be a safe alternative to conventional open repair for thoracoabdominal and arch aneurysms and avoids the need for cardiopulmonary bypass and aortic crossclamping. This technique may be ideally suited to patients with significant comorbidity or prior open aortic surgery. Longer term follow-up is needed to determine the durability of this approach.

A total of 9408 patients undergoing coronary artery bypass grafting, 8461 on pump and 947 off pump, operated on between 1995 and 2004 were included in the study. Adjusted hazard function for long-term mortality was estimated with Poisson regression analysis in a model that included variables reflecting completeness of revascularization, operative method (on/off pump), and background risk factors for death.

Mean follow-up after surgical intervention for survivors was 5.0 ± 2.8 years (range, 0.5–10.5 years), with a total follow-up of 45,076 patient years. Leaving 1 diseased vascular segment without a bypass graft in 2- or 3-vessel disease did not increase the hazard ratio for death in comparison with complete revascularization (hazard ratio, 1.05; 95% confidence interval, 0.87–1.27; P = .60). In contrast, leaving 2 vascular segments without a bypass graft in 3-vessel disease was associated with an increased hazard ratio for death (hazard ratio, 1.82; 95% confidence interval, 1.15–2.85; P = .01). Incomplete revascularization was more common in the off-pump group (P < .001) in our study. If adjusting for incomplete revascularization, there was no significant influence of the use of on/off-pump techniques on the hazard ratio for death (hazard ratio, 1.08; 95% confidence interval, 0.82–1.40; P = .57).

Incomplete revascularization of patients with 3-vessel disease is an independent risk factor for increased long-term mortality after coronary artery bypass grafting. In contrast, the use of on- or off-pump techniques had no significant effect on survival after adjusting for incomplete revascularization.

The graft comprised an interior of knitted polyglycolic acid compounded with collagen to supply a scaffold for tissue growth and an exterior of woven poly-l-lactic acid for reinforcement. All components were biocompatible and biodegradable, with excellent cellular affinity. The grafts, measuring 10 mm in internal diameter and 30 mm in length, were implanted into porcine aortas, and their utility was evaluated to 12 months after grafting.

All explants were patent throughout the observation period, with no sign of thrombus formation or aneurysmal change. Presence in the neomedia of endothelialization with proper integrity and parallel accumulation of functioning smooth muscle cells, which responded to vasoreactive agents, was confirmed in an early phase after implantation. Sufficient collagen synthesis and lack of elastin were quantitatively demonstrated. Dynamic assessment and long-term results of the in vivo study indicated adequate durability of the implants.

The graft showed morphologic evidence of good in situ cellularization, satisfactory durability to withstand arterial pressure for 12 postoperative months, and the potential to acquire physiologic vasomotor responsiveness. These results suggest that our tissue-engineered vascular graft shows promise as an arterial conduit prosthesis.

Stress cardiac tomography was performed in 362 patients 5 years after coronary artery bypass grafting. Cardiac death and myocardial infarction were considered as events. Cox proportional hazards analysis was used to identify predictors of events and parametric survival analysis to predict time to events.

During a median follow-up of 27 months, 22 cardiac events occurred (6.1% cumulative event rate). At multivariable Cox analysis, ischemia at cardiac tomography (hazards ratio 3.7, 95% confidence interval 1.5–9.1; P = .004), and diabetes (hazards ratio 3.6, 95% confidence interval 1.5–8.5; P = .006) resulted in independent predictors of events. Event-free survival was 96% in patients with normal cardiac tomography, 86% in those with abnormal tomography without ischemia, and 70% in those with (log–rank 10.6, P for trend = .008). The parametric survival model revealed that the cardiac risk was greater for all time intervals and accelerated more over time in patients with ischemia than in those without (² 21.4, P < .0001). Patients without diabetes and normal cardiac tomography remained below a defined risk level (5%) for the entire follow-up period.

Stress cardiac tomography performed 5 years after coronary artery bypass grafting is useful to characterize the risk of cardiac events and its temporal variation. Parametric survival model estimates the predicted time to risk and the level of risk at specific time intervals after coronary artery bypass grafting.

From 2001 until 2006, the Shelhigh NR-2000C stentless valved conduit was implanted in 115 patients for various aortic root pathologies. The conduit consists of a bovine pericardial straight graft with an incorporated porcine stentless valve. Aortic root repair was performed during standard cardiopulmonary bypass and mild hypothermia in the majority of patients. Deep hypothermic circulatory arrest combined with selective antegrade cerebral perfusion was used when the repair extended into the arch.

Seven patients with uncomplicated early outcome presented with unexpected sudden disastrous findings at the level of the aortic root, although 1-year follow-up computed tomographic scans were normal. Four of these patients underwent emergency operations because of desintegration of the graft, along with rupture of the aortic root. Retrospectively, the main findings were persistent fever or subfebrility over months and a halo-like enhancement on computed tomographic scans. Extensive microbiologic examinations were performed without finding a causative organism.

The use of the Shelhigh aortic stentless conduit can no longer be advocated, and meticulous follow-up of patients in whom this device has been implanted has to be recommended.

Myocardial infarction was induced by ligating the left anterior descending artery. The rats developed left ventricular aneurysms and underwent left ventricular restoration by the plication of the left ventricular aneurysm 4 weeks after the ligation. Thereafter, the rats were randomized into a left ventricular restoration (vehicle) group and left ventricular restoration with spironolactone (100 mg/kg/d, by mouth) group.

Echocardiography revealed that in the left ventricular restoration with spironolactone group, late cardiac redilation was significantly attenuated (left ventricular end-diastolic area: 0.51 ± 0.03 cm² vs 0.63 ± 0.03 cm², P < .05) and late left ventricular function was preserved (fractional area change: 48.8% ± 3.0% vs 35.8% ± 2.4%, P < .01). Hemodynamically, rats in the left ventricular restoration with spironolactone group exhibited improved systolic function (maximal end-systolic pressure-volume relationship: 0.38 ± 0.03 mm Hg/µL vs 0.11 ± 0.04 mm Hg/µL, P < .01) and diastolic function (: 18.5 ± 1.5 sec vs 23.1 ± 1.4 sec, P < .05) than those in the LVR group. Histologically, interstitial fibrosis in the remote area was significantly reduced (5.6% ± 1.3% vs 12% ± 1.0%, P < .01), and fibrosis around the pledgets (near area) was also attenuated in the left ventricular restoration with spironolactone group. The myocardial messenger ribonucleic acid expressions of transforming growth factor-β1 and brain natriuretic peptide measured using the real-time polymerase chain reaction were lower in the left ventricular restoration with spironolactone group (transforming growth factor-β1: 0.13 ± 0.02 vs 0.28 ± 0.02, P < .01; brain natriuretic peptide: 0.99 ± 0.14 vs 1.54 ± 0.18, P < .05). The systemic blood pressure and heart rate did not differ between the 2 groups.

Spironolactone reduced the gene expression of transforming growth factor-β1 and brain natriuretic peptide and alleviated not only cardiac redilation but also the deterioration of left ventricular function late after left ventricular restoration without inducing hypotension, a major side effect of angiotensin-converting enzyme inhibitors or angiotensin receptor blocker. Spironolactone is a promising therapeutic option for alleviating remodeling after left ventricular restoration.

Ascending aortic segments were obtained from patients with thoracic aortic dissection (n = 8) and age-matched normal donors (n = 6). The differentially expressed proteins of their media tissues were analyzed by 2-dimensional electrophoresis and mass spectrometry, and verified by Western blotting. Oxidative stress was measured by functional assays in a larger sample size (15 patients and 10 controls).

Image analysis of the protein profiles from 2-dimensional gels revealed 126 differentially expressed proteins, of which 26 were identified by mass spectrometry. Among them, extracellular superoxide dismutase, an enzyme involved in oxidative stress, was selected for further studies. Western blotting showed that extracellular superoxide dismutase expression was more than 50% lower in patient samples than in controls (P < .001). Superoxide dismutase activity was consistently decreased (P < .001) and lipid peroxidation was increased (P = .019) in patient media homogenates compared with that in controls.

Our results indicate that protein expression profiles in the aortic media from thoracic aortic dissection differ significantly from that of controls, which may provide important insights into the disease mechanisms. This study also suggests that increased oxidative stress may play an important role in the disease.

From March 15, 2006, through November 19, 2007, 129 patients underwent mitral valve surgery for pure myxomatous disease, and 124 valves (96.1%) were repaired. The Myxo-ETlogix ring was used in 100 cases and the Physio ring (Edwards) in 24. The Myxo-ETlogix design includes a 3-dimensional shape to reduce systolic anterior motion and a larger orifice to accommodate elongated leaflets and decrease need for sliding plasty. Direct mitral valve measurements were made. Sizing was based on A2 height, and choice of ring type was based on unresected leaflet heights.

There was no operative mortality or lasting perioperative morbidity. The Myxo-ETlogix group had taller A2, P1, P2, and P3 leaflet segments than the Physio group (P ≤ .003). Only 1 sliding plasty was performed for asymmetry in the Myxo-ETlogix group. Predischarge and follow-up echocardiograms (n = 338 in 124 patients) disclosed transient nonobstructive chordal systolic anterior motion in 3 echocardiograms in 3 patients. No patients had 2+ or greater mitral regurgitation. At discharge, 5.7% had 1+ mitral regurgitation; this proportion was 17.3% at last follow-up (mean 6.1 ± 4.4 months).

In initial experience with the Myxo-ETlogix ring, nonobstructive systolic anterior motion has been rare and obstructive systolic anterior motion not observed. Ongoing prospective echocardiographic and clinical studies will elucidate the role of this etiology-specific ring.

These combined procedures were performed in 123 patients with a mean age of 51 ± 16 years; 67% were men. The aortic root pathology was an aneurysm in 76 patients and other disorders in 47 patients. The mitral valve pathology was degenerative disease in 62 patients and other diseases in 61 patients. Sixty-four patients (52%) underwent previous cardiac surgery. The aortic valve was preserved in 21 patients, and the mitral valve was preserved in 67 patients; the remaining patients underwent valve replacement. In addition, 57 patients underwent other procedures. The mean follow-up was 4.9 ± 4.3 years and complete.

The operative mortality rate was 6.5% (8 patients), and late mortality was 9.7% (12 patients). Reexploration of the mediastinum for bleeding (15%) and implantation of permanent pacemaker (18%) were the most common postoperative complications. Urgent surgery and functional class IV were predictors of operative mortality by univariate analysis. Survival at 1, 5, and 10 years was 90.9% ± 2.6%, 86.1% ± 3.3%, and 79.3 ± 4.9%, respectively. Six patients required reoperation. Freedom from reoperation at 1, 5, and 10 years was 100%, 96.4% ± 2.5%, and 85.7% ± 6.4%, respectively. At the latest follow-up, 98 patients were alive and free from reoperation; 92 patients were in functional classes 1 and 2, and 88 patients were free from any cardiac or valve-related complication.

Aortic root replacement combined with mitral valve surgery is a complex operation associated with high morbidity, but the operative mortality is reasonably low and the long-term outcomes are gratifying.

We performed a retrospective chart review of 224 patients (aged 1 month to 18 years, median 20 months) undergoing surgery for congenital heart defects requiring cardiopulmonary bypass. Patients mechanically ventilated preoperatively were excluded. A stepwise logistic regression model was used to test for the independent influence of various perioperative factors on extubation in the operating room.

Overall, 79% of patients were extubated in the operating room. Younger age and longer cardiopulmonary bypass time were the strongest predictors for not extubating. Each step down to a younger age group (<2, 2–4, 4–6, 6–12, >12 months) reduced the chance of extubation in the operating room by 56%. Cardiopulmonary bypass time for more than 150 minutes was associated with an 11.8-fold increased risk of not being extubated.

Male gender and high inotrope requirement after cardiopulmonary bypass were also significantly associated with fewer children being extubated.

Extubation in the operating room after surgery for congenital heart disease was successful in the majority of patients. The strongest independent risk factors for failure of this strategy included younger age and longer cardiopulmonary bypass time.

A nested case–control study was conducted of 368 patients who underwent stage 1 reconstruction at a single center between January 1998 and April 2005.

Among the 313 (85%) hospital survivors, there were 33 (10.5%) interstage deaths. Cases more frequently presented with intact or restrictive atrial septum (9 [27%] vs 4 [4%]; P < .001), were older at the time of surgery (5 [2–40] vs 3 [1–42] days; P = .005), had more postoperative arrhythmias (12 [36%] vs 15 [15%]; P = .01), and a higher incidence of airway or respiratory complications (12 [36%] vs 19 [19%]; P = .04). By multivariate analysis, only intact atrial septum (odds ratio 7.6; 95% confidence intervals 1.9–29.6; P = .003) and age at operation greater than 7 days (odds ratio 3.8; 95% confidence intervals 1.3–11.2; P = .017) were predictors of interstage death.

The presence of intact atrial septum and older age at the time of surgery are associated with a higher risk of interstage death. In addition, postoperative arrhythmia and airway complications are associated with a higher risk of interstage death in univariate analysis. The results of this study provide a focus for interstage monitoring and risk stratification of these high-risk infants, which may improve overall survival.

The National Heart, Lung, and Blood Institute Pediatric Heart Network conducted a cross-sectional analysis of patients who had undergone a Fontan procedure at the 7 network centers. Analysis was based on 521 patients with an electrocardiogram (n = 509) and/or bicycle exercise test (n = 404). The Child Health Questionnaire parent report and the oxygen consumption at the anaerobic threshold were used as markers of functional outcome.

Various Fontan procedures had been performed: intracardiac lateral tunnel (59%), atriopulmonary connection (14%), extracardiac later tunnel (13%), and extracardiac conduit (11%). Prior volume unloading surgery was performed in 389 patients: bidirectional Glenn (70%) and hemi-Fontan (26%). A history of atrial tachycardia was noted in 9.6% of patients and 13.1% of patients had a pacemaker. Lower resting heart rate and higher peak heart rate were each weakly associated with better functional status, as defined by higher anaerobic threshold (R = –0.18, P = .004, and R = 0.16, P = .007, respectively) and higher Child Health scores for physical functioning (R = –0.18, P < .001, and R = 0.17, P = .002, respectively). Higher anaerobic threshold was also independently associated with younger age and an abnormal P-axis. Resting bradycardia was not associated with anaerobic threshold or Child Health scores.

In pediatric patients (6–18 years) after the Fontan procedure, a lower resting heart rate and a higher peak heart rate are each independently associated with better physical function as measured by anaerobic threshold and Child Health scores. However, these correlations are weak, suggesting that other, nonrhythm and nonrate, factors may have a greater impact on the functional outcome of pediatric patients after the Fontan operation.

Between 1996 and 2006, 200 patients had the extracardiac conduit Fontan operation. The median age at operation was 3.4 years. Most patients (89.5%) underwent a bidirectional cavopulmonary shunt. Fenestration was required in 85 patients. Overall, the 10-year survival was 92.4% ± 2.1%. Multivariate analysis identified severe infection during the early postoperative period and a high pulmonary arterial pressure during the preoperative period as independent risk factors for patient mortality. The Kaplan–Meier estimate for freedom from reoperation was 82.4% ± 4.1% at 10 years. Arrhythmia occurred in 32 patients after the Fontan operation; freedom from arrhythmia was 85.1% ± 4.4% at 10 years. The risk factors for arrhythmia were the heterotaxy syndrome, follow-up duration, and age at Fontan operation. Freedom from thromboembolism at 10 years was 92.9% ± 1.9%. Among all of the patients, 95.2% were classified in New York Heart Association class I.

The results of this study showed that during 10 years of follow-up, the overall survival and the functional status of the survivors after an extracardiac Fontan procedure were satisfactory. We might infer that fenestration provided benefit inasmuch as the high-risk Fontan patients fenestrated had similar outcomes to those not fenestrated, who were presumably low risk. The incidence of late death, reoperation, obstruction of the cavopulmonary pathway, arrhythmias, and thromboembolism was low.

DNA was isolated from 165 children with single-ventricle congenital heart disease born between January 1980 and December 2006. The endothelin-1 G5665T single nucleotide polymorphism genotype was determined by using real-time polymerase chain reaction. Kaplan–Meier survival curves were generated with a combined end point of death or transplantation. The Cox proportional hazard method was used to evaluate potential covariates.

The endothelin-1 G5665T genotype was significantly associated with transplant-free survival for the group as a whole (P = .002), with the greatest effect in children with hypoplastic left heart syndrome (n = 64, P = .0002) as opposed to patients with other types of single-ventricle anatomy (n = 101, P = .1). Cox proportional hazard modeling revealed 3 independent predictors of poor outcome: endothelin G5665T genotype (T/T genotype, P = .001), prematurity (gestational age <37 weeks, P = .02), and era of surgical intervention (1990s vs other decades, P = .02).

Long-term survival of single-ventricle patients is dependent on many factors. These data suggest that genetic variability involving vascular resistance modifiers, such as endothelin-1, might play an important role, particularly in patients with hypoplastic left heart syndrome. Future studies should include evaluation of the relationship between endothelin genotype and plasma endothelin levels and possibly therapeutic trials of endothelin blockers in high-risk patients.

Respiratory mass spectrometry was used to continuously measure systemic oxygen consumption (VO₂) in 22 infants for 72 hours postoperatively. Arterial, superior vena caval and pulmonary venous blood gases were measured at 2 to 4 hour intervals to calculate CO. The comprehensive Aristotle score was collected.

Hospital mortality was 4.5%. The comprehensive Aristotle score ranged from 14.5 to 23.5 and negatively correlated with CO (P = 0.027). Among the patient-adjusted factors, myocardial dysfunction (n = 10), mechanical ventilation to treat cardiorespiratory failure (n = 9) and atrioventricular valve regurgitation (n = 4) (P = 0.01) negatively correlated with CO (P = 0.06 to 0.07). Aortic atresia (n = 9) was associated with a lower CO (P = 0.01) for the first 24 hours which linearly increased overtime (P = 0.0001). No correlation was found between CO and other factors (P > 0.3 for all).

Comprehensive Aristotle score significantly negatively correlates with CO after the Norwood procedure. A preoperative estimation of the comprehensive Aristotle score, particularly in association with myocardial dysfunction, mechanical ventilation to treat cardiorespiratory failure, atrioventricular valve regurgitation and aortic atresia may help to anticipate a high postoperative morbidity with low cardiac output syndrome.

We observed 25 consecutive patients who underwent elective coronary artery bypass grafting with cardiopulmonary bypass. The sublingual microcirculation was investigated using side-stream dark-field imaging. Side-stream dark-field imaging was performed before (baseline), during, and after surgery. Microvascular blood flow was estimated with a semiquantitative microvascular flow index in small, medium, and large microvessels. Changes in microvascular flow were tested with Wilcoxon signed rank test.

Median microvascular flow index of medium blood vessels decreased after starting cardiopulmonary bypass relative to that after anesthetic induction (2.6, interquartile range 1.6–3.0, vs 3.0, interquartile range 2.8–3.0, P = .02). There was a trend toward decreased microvascular flow index of small and large vessels relative to baseline (P = .08 and P = .05, respectively). Decreases in microvascular flow index occurred irrespective of changes in systemic blood pressure. After each patient's return to the intensive care unit, microvascular flow index increased and normalized in all microvessels.

For the first time, sublingual microvascular blood flow alterations have been observed during cardiopulmonary bypass–assisted coronary artery bypass grafting.

Perioperative saphenous endothelial cell monolayers were pretreated and then stimulated with perioperative inflammatory mediators. Endothelial production of interleukin 6, interleukin 8, and adhesion molecules necessary for neutrophil tissue penetration, were examined, together with inflammatory endothelial coagulant responses. Pretreatment effects on isolated blood neutrophil inflammatory responses were similarly noted. Mechanistic insight was obtained through assessment of the temporal response of nuclear factor-kB and its association with heat shock protein 72(HSP72) expression.

Four-hour pretreatment markedly reduced inflammatory endothelial release of interleukin 8 (2587 ± 82 pg/mL control vs 208 ± 3 pg/mL -3 pretreated, P < .01) and endothelial expression of intercellular adhesion molecule 1 (196.1 ± 2.0 vs 71.9 ± 0.6 mean channel fluorescence, P < .01) in response to endotoxin and tumor necrosis factor a. Neutrophil activation (CD11b and respiratory burst) was maintained, but pretreated neutrophils had shorter survival. Endothelial inflammatory stimulation produced rapid increase in nuclear activity of nuclear factor-kB, which was attenuated by 43% with -3 pretreatment (P < .01). This coincided with 3-fold increase (P = .03) in protective HSP72 expression with pretreatment.

Acute pre-treatment with a clinically acceptable -3 infusion attenuates perioperative endothelial-neutrophil activation through transcription-level interaction.

Rats transfected intratracheally with β-galactosidase vector, atrial natriuretic peptide vector, or mock vector were investigated for the evaluation of β-galactosidase expression, atrial natriuretic peptide mRNA expression, and inflammatory cell infiltration. Rats were divided into 5 treatment groups (n = 73): normoxic rats treated intratracheally with mock vector or atrial natriuretic peptide gene and chronic hypoxic rats treated similarly with mock vector, atrial natriuretic peptide, or a reporter gene, β-galactosidase. Pulmonary hypertension and transfected gene expression were evaluated.

β-Galactosidase gene transfer induced its intense enzymatic activity in bronchial and alveolar epithelial cells but not in other organs in normoxic rats. Transfected lungs were not associated with inflammatory cell infiltration. Atrial natriuretic peptide gene transfection inhibited pulmonary hypertension, which is associated with its mRNA expression in the lungs. Indices of right ventricular hypertrophy and pulmonary vascular diseases induced by chronic hypoxia were significantly but incompletely ameliorated.

HVJ-envelope vector is an efficient, relatively safe, and ready-to-use gene delivery system for pulmonary vascular diseases. Atrial natriuretic peptide gene transfer to lungs by using this vector could be a promising therapeutic approach against pulmonary hypertension.

Sixteen calves were implanted with devices giving differing degrees of pulsatile circulation: 6 had a continuous flow left ventricular assist device (LVAD); 6 had a continuous flow right ventricular assist device (RVAD); and 4 had a pulsatile total artificial heart (TAH). Six other calves were histologic and immunohistochemical controls. In the LVAD group, the pulsatility index was significantly lower (0.28 ± 0.07 LVAD vs 0.56 ± 0.08 RVAD, vs 0.53 ± 0.10 TAH; P < 0.01), and we observed severe periarteritis in all cases in the LVAD group. The number of angiotensin II type 1 receptor–positive cells and angiotensin converting enzyme–positive cells in periarterial areas was significantly higher in the LVAD group (angiotensin II type 1 receptor: 350 ± 139 LVAD vs 8 ± 6 RVAD, vs 3 ± 2 TAH, vs 3 ± 2 control; P < .001; angiotensin-converting enzyme: 325 ± 59 LVAD vs 6 ± 4 RVAD, vs 6 ± 5 TAH, vs 3 ± 1 control; P < .001).

The reduced pulsatility produced by a continuous flow LVAD implantation induced severe periarteritis in the kidneys. The local renin–angiotensin system was up-regulated in the inflammatory cells only in the continuous flow LVAD group.

Aortic transplantation was performed with inbred rats, and aortic allografts, isografts, and control grafts were obtained for the following analyses. The extent of inflammatory-related and indoleamine 2,3-dioxygenase gene expression was measured by means of quantitative reverse transcriptase–polymerase chain reaction, and tryptophan metabolite production in the graft was measured by means of liquid chromatographic/tandem mass spectrometric analysis. The bacteriostatic effect of each graft and tryptophan metabolites was determined by using the methicillin-resistant Staphylococcus aureus proliferation assay.

The inflammatory response, including interferon , tumor necrosis factor , and indoleamine 2,3-dioxygenase gene expression, was significant in the allografts but minimal in the isografts and control grafts. Methicillin-resistant S aureus proliferation was remarkably suppressed when cultured with the allografts but not with the control grafts. Among tryptophan metabolites, the bacteriostatic effect against methicillin-resistant S aureus was remarkable with 3-hydroxykynurenine, with a minimum inhibitory concentration of 32 mg/L. The 3-hydroxykynurenine level in the allografts was 9-fold greater than that in the control grafts.

The bacteriostatic effect of the allografts was acquired by inducing indoleamine 2,3-dioxygenase, which resulted in local production of 3-hydroxykynurenine as an antimicrobial agent. This is the first report to document a mechanism of the allograft's infection-resistant property against methicillin-resistant S aureus growth.

We studied mitochondrial membrane potential, a surrogate for mitochondrial function, in human (n = 11) and rat hearts with physiologic (neonatal) and pathologic (pulmonary hypertension) right ventricular hypertrophy in vivo and in vitro. Mitochondrial membrane potential is higher in the normal left ventricle compared with the right ventricle but is highest in the hypertrophied right ventricle, both in myocardium and in isolated cardiomyocytes (P < .01). Mitochondrial membrane potential correlated positively with the degree of right ventricular hypertrophy in vivo and was recapitulated in phenylephrine-treated neonatal cardiomyocytes, an in vitro model of hypertrophy. The phenylephrine-induced mitochondrial hyperpolarization was reversed by VIVIT, an inhibitor of the nuclear factor of activated T lymphocytes, a transcription factor regulating the expression of several mitochondrial enzymes during cardiac development and hypertrophy. The clinically used drug dichloroacetate, known to increase the mitochondria-based glucose oxidation, reversed both the phenylephrine-induced mitochondrial hyperpolarization and nuclear factor of activated T lymphocytes (NFAT) activation. In Langendorff perfusions, dichloroacetate increased rat right ventricular inotropy in hypertrophied right ventricles (P < .01) but not in normal right ventricles, suggesting that mitochondrial hyperpolarization in right ventricular hypertrophy might be associated with its suboptimal performance.

The dynamic changes in mitochondrial membrane potential during right ventricular hypertrophy are chamber-specific, associated with activation of NFAT, and can be pharmacologically reversed leading to improved contractility. This mitochondrial remodeling might provide a framework for development of novel right ventricle–specific therapies.

Between July 1995 and October 2005, 75 consecutive patients with postpneumonectomy empyema were treated in Szczecin, Poland (n = 35), and Zurich, Switzerland (n = 40). The therapy consisted of repeated open surgical debridement of the pleural cavity after achievement of general anesthesia, a negative pressure wound therapy of the temporarily closed chest cavity filled with povidone-iodine–soaked towels, and continuous suction and systemic antimicrobial therapy. If present, bronchopleural fistulae were closed and reinforced either with a muscle flap or the omentum. Finally, the pleural space was filled with an antibiotic solution and definitively closed.

Of 75 patients (63 men; median age, 59 years; age range, 19–82 years), postpneumonectomy empyema was present on the right in 46 patients (32 with bronchopleural fistula) and in 29 patients (12 with bronchopleural fistula) on the left. Median time between pneumonectomy and postpneumonectomy empyema was 131 days (range, 7–7200 days). Bronchopleural fistulae have been closed and additionally reinforced by means of different methods (omentum, 18; muscle, 11; pericardial fat, 5; azygos vein, 1). The chest was definitively closed within 8 days in 94.6% of patients. The median hospitalization time was 18 days (range, 9–134 days). Postpneumonectomy empyema was successfully treated in 97.3% of patients, including 10 (13%) patients who needed a second treatment cycle. Three (4%) patients died within 90 days. The median follow-up time was 29.5 moths (range, 3–107 months).

Treatment of postpneumonectomy empyema with the accelerated treatment is effective and safe. Our results are superior compared with those in reported series using a (temporary) chest fenestration. Patients appreciate the physical integrity of the chest.

We performed a retrospective review of a prospective clinic and operative database between January 1998 and December 2006. All patients had calcified mediastinal lymph nodes, symptoms or complications from these nodes, or both.

There were 50 patients (23 men). Thirty-eight (76%) were symptomatic, which included hemoptysis in 11, persistent cough in 8, and recurrent pneumonia in 5, and all underwent rigid bronchoscopy. Thirty-four (89%) of the 38 symptomatic patients had stones eroding into the airway (broncholiths), and 2 had an airway esophageal fistula. The most common location of the broncholith was in the bronchus intermedius (n = 19). Endoscopic removal of the broncholith was performed in 29 patients and was successful in all. Elective thoracotomy with lymph node curettage, removal, or both was performed in 5 patients. These 5 patients had no significant morbidity and no operative mortality. Patients remained symptom free (median follow-up, 2.3 years; range, 8–42 months). Twelve asymptomatic patients with calcified lymph nodes were followed with serial computed tomographic scans and remain asymptomatic (median follow-up, 3.1 years).

Broncholiths that are not fixed to the airway can be safely removed with rigid and flexible bronchoscopic equipment. Thoracotomy with broncholithectomy is also safe and effective and is reserved for symptomatic lesions that cannot be removed bronchoscopically or for lesions that cause airway esophageal fistulas. Calcified nodes in asymptomatic patients are not an indication for intervention.

Between January 1997 and January 2007, we retrospectively reviewed 18 patients with descending necrotizing mediastinitis who were treated in the National Taiwan University Hospital. Diagnosis and Endo classification were confirmed by computed tomography of the neck and chest.

Eight women and 10 men were included in this study. The mean age was 57.8 ± 15.2 years. Cervical drainage was performed in the involved area in all patients. The methods for mediastinal drainage included transcervical (n = 10), video-assisted thoracic surgical drainage (n = 6), subxiphoid drainage (n = 1), and mediastinoscopy-assisted drainage (n = 1). We could not rescue 3 patients because of uncontrolled sepsis before surgery, for a mortality rate of 16.7%. Klebsiella pneumoniae uniquely represents the most common pathogen in diabetic patients (P = .01), leading to more complicated courses in older patients (P =.04) and requiring more surgical interventions (P =.05) than other pathogens.

Transcervical mediastinal drainage is first justified in patients with limited disease in the upper mediastinum. For those with involvement of the lower anterior mediastinum, an additional subxiphoid approach is suggested. Cervicotomy with video-assissted mediastinal drainage is an excellent combination for involvement of the posterior mediastinum and pleural space. Klebsiella pneumoniae uniquely represents the most important and threatening causative pathogen for diabetic patients with descending necrotizing mediastinitis.

Sera from 18 patients with esophageal adenocarcinoma and 14 with gastroesophageal reflux disease were added to microarrays designed to detect circulating autoantibodies to 51 tumor-associated antigens. Sera from the same patients were also added to a 53-plex assay for various cancer-related proteins. Cutoff values at 3 standard deviations above the mean expression of gastroesophageal reflux disease were used as a boundary for positivity.

Nine proteins and 11 autoantibodies were able to individually segregate at least 1 esophageal adenocarcinoma sample from gastroesophageal reflux disease by means of cutoff values. The most discriminative marker was Fas ligand in the protein array, which was associated with 83.3% sensitivity and 100% specificity. The best performing autoantibody, NY-ESO-1, detected 3 esophageal adenocarcinoma samples. When both of these markers were combined, a sensitivity of 88.9% and specificity of 100% were attained.

Cancer-related protein and autoantibody arrays provide a technically simple and rapid method of identifying potential biomarkers for the detection of esophageal adenocarcinoma in serum. Furthermore, combining these platforms improves the diagnostic power of either platform alone. Integrating technologies that detect the expression of multiple proteins and autoantibodies in serum may provide a noninvasive and accurate method of detecting early esophageal adenocarcinoma.

Fifty patients with locally advanced esophageal squamous cell carcinoma who received neoadjuvant therapy (chemotherapy 35, chemoradiotherapy 15) underwent positron emission tomography with fludeoxyglucose F 18 before surgical resection in evaluation of posttreatment maximum standardized uptake value, residual tumor size (maximum square area of longitudinal axis), histologic response, and postoperative survival.

After treatment, uptake was not noted in 21 patients (posttreatment maximum standardized uptake value <2.5, negative) but was detected in 29 (≥2.5, positive). Residual tumor size ranged from 0 to 54.0 mm² for negative results and 55.0 to 676.0 mm² for positive, clearly distinguishing histologic major response from nonresponse. The negative group demonstrated significantly higher 5-year cause-specific survival (67.7%) and lower hematogenous recurrence (4.8%) than the 36.5% and 37.0% values in the positive group, (P < .0042 and P = .0083, respectively). Univariate Cox regression analyses identified posttreatment maximum standardized uptake value (cutoff 2.5) as the only preoperative prognostic factor (P = .0071).

Posttreatment positron emission tomography with fludeoxyglucose F 18 reliably predicted histologic response and postoperative survival in advanced esophageal squamous cell carcinoma. This tool could potentially be used to tailor optimal treatment according to individual responses.