We included a total of 51 high-risk patients with severe aortic valve stenosis. Patients were allocated to transapical aortic valve implantation (n = 21) or minimally invasive aortic valve replacement via a partial upper sternotomy (n = 30), in a nonrandomized fashion. Patient age, preoperative comorbidities, and perioperative risk, expressed as logistic EuroSCORE (38% ± 14% vs 35% ± 9%), were matched between the 2 groups.

Early morbidity and mortality were comparable between groups, but transapical aortic valve implantation was associated with shorter operative time (P = .004), ventilation time (P < .001), intensive care unit stay (P < .001), and hospital stay (P < .001). Thirty-day mortality was 14% (n = 3) in the transcatheter group versus 10% (n = 3) in the surgical group. After a mean follow-up of 12 ± 4 months (100% complete), there were a total of 5 (24%) deaths in the transapical group versus 5 (17%) deaths in the open surgery group. There was 1 intraoperative death in the transapical group versus none in the surgery group. In the transapical group, there were 2 re-explorations for bleeding, 2 intraoperative conversions, 1 case of prosthesis migration, and 2 impairments of coronary arteries. The surgery group included 1 re-exploration, 1 stroke, 1 pacemaker implantation for complete atrioventricular block, and 3 cases of atrial fibrillation.

Current data suggest a faster postoperative recovery after transapical aortic valve implantation, with early and late morbidity and mortality comparable with those of minimally invasive aortic valve replacement via partial upper sternotomy.

Between June 2007 and February 2009, 203 high-risk patients (EuroSCORE, 22% ± 14%; mean age, 81 ± 7 years) underwent transcatheter aortic valve implantation via a transapical (n = 50) or transfemoral (n = 153) access. The transapical implantation technique was chosen only in patients who had no access through diseased femoral arteries.

Thirty-day survival was 88.8% after transfemoral versus 91.7% after transapical implantation (P = .918). The transapical group had a significantly higher preoperative brain natriuretic peptide value and a significantly higher incidence of peripheral vessel, cerebrovascular, and coronary heart disease. Death within 30 days was valve related in 25% (transapical) and 31% (transfemoral), cardiac in 25% and 13%, and noncardiac in 50% and 56%, respectively (no significant difference). Complications specific to the access site (peripheral vessel injury or apex complications) occurred in both groups, whereas neurologic events did not occur in the transapical group (P = .041).

Our patient and access site selection process, with the transfemoral technique considered the access site of first choice, results in comparable survival and morbidity for either transfemoral or transapical transcatheter aortic valve implantation. Both techniques are associated with certain access site–specific complications that require highly qualified management. The neurologic risk profile of the patients should be included in the decision-making process before transcatheter aortic valve implantation, inasmuch as neurologic events may be reduced with the transapical access.

Retrospective review was performed for all cases of proximal aortic surgery between January 2004 and May 2007. Of these 271 patients, 105 had emergency and 166 had elective operation. Selection bias was controlled using propensity scoring methods. Multivariable logistic regression analysis was used to model adverse outcomes as a function of selective antegrade cerebral perfusion, emergency status, and their interaction, adjusted for the propensity score. Adjusted odds ratios were formulated with 95% confidence intervals.

Operative mortality occurred in 12.1% (33/271) of patients: 8.8% (18/205) in patients with selective antegrade cerebral perfusion versus 22.7% (15/66) in those with deep hypothermic circulatory arrest alone (P = .003). Temporary neurologic dysfunction occurred in 5.9% (15/255) of patients: 4.5% (9/198) in selective antegrade cerebral perfusion versus 10.5% (6/57) in deep hypothermic circulatory arrest alone (P = .09). Stroke occurred in 4.3% (11/255) of patients with no difference between groups. In the elective setting, selective antegrade cerebral perfusion was associated with a significant decrease in operative mortality compared with deep hypothermic circulatory arrest alone. Overall, selective antegrade cerebral perfusion was associated with shorter intensive care unit and ventilator times and fewer renal and pulmonary complications. Significant multivariable predictors of operative mortality were emergency status, previous coronary surgery, and cardiopulmonary bypass time.

Use of selective antegrade cerebral perfusion confers a survival advantage during proximal aortic surgery that is most apparent in the elective setting. Improved resource utilization and fewer pulmonary and renal complications were observed in patients with selective antegrade cerebral perfusion.

Seventeen sheep had radiopaque markers implanted; 16 around the annulus and 2 on middle anterior and posterior leaflet edges. Four-dimensional marker coordinates were acquired with biplanar videofluoroscopy at 60 Hz. Hinge angle was quantified between fibrous and muscular annular planes, with 0° defined at end diastole, to characterize its contribution to alterations in mitral septal–lateral dimension and 2-dimensional total annular area throughout the cardiac cycle.

During isovolumic contraction (pre-ejection), hinge angle abruptly increased, reaching maximum (steepest saddle shape, change 18° ± 13°) at peak left ventricular pressure. During ejection, hinge angle did not change; it then decreased during early filling (change 2° ± 2°). Septal–lateral dimension and total area paralleled hinge angle dynamics and leaflet distance (anterior to posterior marker). Pre-ejection septal–lateral reduction was 13% ± 7% (3.3 ± 1.5 mm) from 9% muscular dimension fall and 18° ± 13° hinge angle increase.

Pre-ejection increase in hinge angle contributes substantially to septal–lateral and total area reduction, facilitating leaflet coaptation. Semirigid annuloplasty rings or partial bands may preserve hinge motion, but possible recurrent annular dilatation could result in recurrent mitral regurgitation. Long-term clinical studies are required to determine who might benefit most from preserving intrinsic hinge motion without compromising repair durability.

The confidential dataset of the Office of Statewide Health Planning and Development patient discharge database was queried for 1997 to 2006. A risk model was developed using International Classification of Diseases, Ninth Revision, Clinical Modification procedures and diagnostic codes from the combined pool of isolated coronary artery bypass graft and percutaneous coronary intervention procedures performed during 2005 and 2006. In-hospital mortality was corrected for "same-day" transfers to another health care institution. Early failure rate was defined as in-hospital mortality rate plus reintervention for another percutaneous coronary intervention or cardiac surgery procedure within 90 days.

Coronary artery bypass graft volume decreased from 28,495 (1997) to 15,520 (2006), whereas percutaneous coronary intervention volume increased from 38,098 to 53,703. Risk-adjusted mortality rate decreased from 4.7% to 2.1% for coronary artery bypass graft procedures and from 3.4% to 1.9% for percutaneous coronary intervention. Expected mortality rate increased for both procedures. Early failure rate decreased from 13.1% to 8.0% for percutaneous coronary intervention and from 6.5% to 5.4% for coronary artery bypass graft. For the years 2004 and 2005, the risk of recurrent myocardial infarction or need for coronary artery bypass graft during the first postoperative year was 12% for percutaneous coronary intervention and 6% for coronary artery bypass grafts.

This study shows that as volume shifted from coronary artery bypass grafts to percutaneous coronary intervention, expected mortality increased for both procedures. Risk-adjusted mortality rate decreased for both procedures, more so for coronary artery bypass grafts, so that corrected in-hospital mortality rates essentially equalized at approximately 2.0% in 2006. The post-procedural risk of reintervention, death, or myocardial infarction within the first year was twice as high for percutaneous coronary intervention as for coronary artery bypass grafts.

From March 1998 to July 2008, 12 patients (10 male and 2 female patients; mean age, 37.8 ± 11.6 years) affected by Marfan syndrome underwent endovascular treatment for dissection of the descending aorta after previous open aortic root/arch surgery. Stent graft procedures were performed urgently in 5 patients and electively in 7 patients.

Neither in-hospital deaths nor perioperative paraplegia or stroke occurred. Follow-up (median, 31 months; range, 3–57 months) was 100% complete. One patient needed surgical conversion for persistent type I endoleak, leading to false lumen expansion 3 months after endovascular repair. Extension of the dissection occurred in 2 patients 1 month and 2 years after the procedure, respectively. No late death or aortic rupture was observed.

Endovascular repair of the dissected descending thoracic aorta can be performed in patients with Marfan syndrome with a low risk of death or major complications. In case of staged procedures, stent graft treatment can be considered a possible alternative to open reoperation. Long-term durability remains to be determined.

We performed analyses of 12,415 primary isolated coronary artery bypass grafting operations performed during 1970–2003, with follow-up of 5-year mortality up to December 2006.

The prevalence of diabetes mellitus continuously increased up to 25% among patients undergoing coronary artery bypass grafting in 2003. The 1892 patients with type 2 diabetes mellitus were older, more often female, and more frequently had cardiovascular risk factors, acute coronary syndrome, 3-vessel disease, and severely reduced left ventricular function than patients without diabetes mellitus. Early mortality was 3.4% in patients with diabetes mellitus versus 1.8% in patients without diabetes mellitus. The multivariable adjusted odds ratio was 2.0, and the 95% confidence interval was 1.4 to 2.7. Early adjusted mortality was significantly lower in patients operated on during 2000–2003 than those operated on during 1970–1989 in patients with diabetes mellitus (odds ratio, 0.3; 95% confidence interval, 0.1–0.9) and without diabetes mellitus (odds ratio, 0.4; 95% confidence interval, 0.2–0.7). Mortality until 5 years was 14.6% in patients with diabetes mellitus versus 8.3% in patients without diabetes mellitus (hazard ratio, 1.8; 95% confidence interval, 1.5–2.0). Five-year mortality was reduced by 40% in patients operated on during 2000–2003 compared with that seen in those operated on during 1970–1989 in patients with and without diabetes mellitus.

Diabetes mellitus was associated with an almost 2-fold increased risk of early and 5-year mortality. Early and late mortality were substantially reduced in patients with and without diabetes mellitus operated on more recently, but the mortality disadvantage associated with diabetes mellitus was not eliminated.

Echocardiograms demonstrating severe cardiomyopathy (ejection fraction ≤30%) were retrospectively examined for left ventricular false tendons. The ejection fraction, cause of left ventricular systolic dysfunction, left ventricular diastolic dimensions, severity of mitral regurgitation, mitral annular diameter, mitral valve coaptation depth, mitral valve coaptation area, and orientation of false tendon were evaluated. The patients with false tendons were compared with a control group with cardiomyopathy without false tendons.

A cohort of patients (n = 82) with severe left ventricular systolic dysfunction (mean ejection fraction, 21%) and false tendons were compared with a control group with similar left ventricular dysfunction and no false tendons (n = 121; mean ejection fraction, 20%; P = .10). The patients with false tendons had similar left ventricular diastolic internal dimensions compared with the control group (5.99 and 6.18 cm, respectively; P = .086). Yet patients with false tendons had a very low incidence of severe functional mitral regurgitation compared with the control group (4.9% vs 27%, P < .001). Patients with false tendons had significantly smaller mitral annular diameters (3.57 vs 4.03 cm, P < .001), shorter mitral valve coaptation depths (0.89 vs 1.24 cm, P < .001), and reduced coaptation areas (1.61 vs 2.52 cm², P < .001) than the control group. The reduction of mitral regurgitation was more significant for patient with transverse midcavity false tendons.

Patients with false tendons and cardiomyopathy have less severe mitral regurgitation. The mechanism for the reduction in functional mitral regurgitation might be less mitral valve deformation, specifically lower coaptation depth and coaptation area when a false tendon is present.

We reviewed 20 patients with an acute traumatic thoracic aorta lesion treated with a thoracic endograft between August 1997 and July 2007. All patients had multi-trauma resulting from high-velocity accidents or accidents with great impact. The diagnosis of aortic injury was made on a clinical basis and conventional imaging, confirmed by computed tomographic angiography. The following parameters were studied: age, sex, type and site of the lesion, type of endovascular graft, endovascular operation time, length of stay in the intensive care unit, length of stay in the hospital, immediate and perioperative complications, and mortality. Follow-up data were recorded, consisting of clinical visits, computed tomographic angiography, and plain chest radiographs at regular intervals (3, 6, and 12 months and every subsequent year). The mean follow-up was 58 months.

All endovascular procedures were technically successful, and the mean operating time for the endovascular procedure was 74 minutes (range, 55–130 minutes). We recorded an external iliac lesion during the procedure as an unique immediate complication, and it was corrected by an iliofemoral bypass. The only perioperative death (perioperative mortality rate of 5%) was unrelated to the aortic rupture or stent placement. There was no intervention-related mortality during the follow-up. Postoperative data showed no severe endovascular graft- or procedure-related morbidity. We recorded 2 cases of stent fracture, diagnosed by chest radiograph and computed tomographic angiography, without clinical impact or signs of endoleak.

The short- and mid-term results of immediate endovascular repair of traumatic aortic injuries are promising, especially when compared with open surgical treatment, indicating that endovascular therapy is preferable in patients with multi-trauma and traumatic ruptures of the thoracic aorta. Nevertheless, long-term follow-up data are necessary to assess the overall durability of this procedure, considering the young age of these patients. The long-term follow-up results will determine whether endovascular treatment should replace open surgery as first-line therapy in thoracic aortic injuries.

Mortality risk was estimated for 148 types of operative procedures using data from 77,294 operations entered into the European Association for Cardiothoracic Surgery (EACTS) Congenital Heart Surgery Database (33,360 operations) and the Society of Thoracic Surgeons (STS) Congenital Heart Surgery Database (43,934 patients) between 2002 and 2007. Procedure-specific mortality rate estimates were calculated using a Bayesian model that adjusted for small denominators. Each procedure was assigned a numeric score (the STS–EACTS Congenital Heart Surgery Mortality Score [2009]) ranging from 0.1 to 5.0 based on the estimated mortality rate. Procedures were also sorted by increasing risk and grouped into 5 categories (the STS–EACTS Congenital Heart Surgery Mortality Categories [2009]) that were chosen to be optimal with respect to minimizing within-category variation and maximizing between-category variation. Model performance was subsequently assessed in an independent validation sample (n = 27,700) and compared with 2 existing methods: Risk Adjustment for Congenital Heart Surgery (RACHS-1) categories and Aristotle Basis Complexity scores.

Estimated mortality rates ranged across procedure types from 0.3% (atrial septal defect repair with patch) to 29.8% (truncus plus interrupted aortic arch repair). The proposed STS–EACTS score and STS–EACTS categories demonstrated good discrimination for predicting mortality in the validation sample (C-index = 0.784 and 0.773, respectively). For procedures with more than 40 occurrences, the Pearson correlation coefficient between a procedure's STS–EACTS score and its actual mortality rate in the validation sample was 0.80. In the subset of procedures for which RACHS-1 and Aristotle Basic Complexity scores are defined, discrimination was highest for the STS–EACTS score (C-index = 0.787), followed by STS–EACTS categories (C-index = 0.778), RACHS-1 categories (C-index = 0.745), and Aristotle Basic Complexity scores (C-index = 0.687). When patient covariates were added to each model, the C-index improved: STS–EACTS score (C-index = 0.816), STS–EACTS categories (C-index = 0.812), RACHS-1 categories (C-index = 0.802), and Aristotle Basic Complexity scores (C-index = 0.795).

The proposed risk scores and categories have a high degree of discrimination for predicting mortality and represent an improvement over existing consensus-based methods. Risk models incorporating these measures may be used to compare mortality outcomes across institutions with differing case mixes.

Between 2003 and 2007, 7 patients underwent a unifocal bilateral bidirectional cavopulmonary anastomosis, and 5 patients underwent a hepatoazygos venous connection associated with a previous (n = 4) or concomitant (n = 1) Kawashima operation. Computational fluid dynamics simulations allowed investigation of 2 sets of comparative models: (1) bifocal versus unifocal bilateral bidirectional cavopulmonary anastomosis and (2) classic hepatic vein–pulmonary artery channel versus hepatoazygos direct anastomosis for Fontan completion after or combined with the Kawashima operation.

There was 1 hospital death in the unifocal bilateral bidirectional cavopulmonary anastomosis group. At a mean follow-up of 15.6 ± 7.40 months after a unifocal bilateral bidirectional cavopulmonary anastomosis and of 38.7 ± 13.2 months after direct hepatoazygos venous connection, respectively, all 11 survivors are in New York Heart Association class I with functional anastomoses. Computational assessment of bifocal bilateral bidirectional cavopulmonary anastomosis demonstrated weak perfusion between caval veins against symmetric and steady bilateral flow fields in the unifocal arrangement. In the classic post-Kawashima Fontan completion model, the hepatic venous flow to the pulmonary artery was held back by means of preponderant opposite flow, whereas in the direct hepatoazygos venous connection model, the hepatic venous flow merged smoothly into the azygos vein. Power-loss calculation showed no significant difference between bifocal and unifocal bilateral bidirectional cavopulmonary anastomosis topology, whereas the hepatoazygos connection clearly had better energy preservation than the classical connection.

This limited clinical and computational fluid dynamics assessment suggests the efficacy of this new rationale to reduce the additional thrombotic risks produced by systemic venous anomalies in single-ventricle patients.

We studied 40 patients with pulmonary atresia with intact ventricular septum who underwent initial right ventricular decompression for planned staged repair. The initial Z-value of the tricuspid valve diameter (Zt1) was obtained from the echocardiography-derived normal value. The late Z-value (Zt2) was measured before definitive repair or the last available Z-value, if definitive repair was not yet reached. The factors associated with the changes of Z-values (Zt2 – Zt1) were analyzed.

The mean initial tricuspid Z-value (Zt1) was –6.2 ± 3.5. After treatment (Zt2), the mean Z-value was –6.0 ± 3.4 (n = 34). Overall, the tricuspid Z-values did not change. Individually, the change in Z-value (Zt2 – Zt1) was larger than +2 in 11 (32%) patients and smaller than –2 in 6 (18%) patients. Increases in Z-value (Zt2 – Zt1) were significantly associated with right ventricular pressure/left ventricular pressure ratio measured after initial palliation (r = –0.54; P = .001) and the initial tricuspid valve Z-value (Zt1) (r = –0.40; P = .02).

Disproportional growth of the tricuspid valve can occur, especially in patients with small tricuspid valves and lower right ventricular pressures after decompression. The findings support the possibility of neonates with small tricuspid valves undergoing biventricular repair after right ventricular decompression surgery.

Between 1975 and 2006, 21 patients underwent correction of atrioventricular septal defect with double-orifice left atrioventricular valve. Clinical data were obtained by means of retrospectively reviewing inpatient and outpatient medical records. To evaluate the influence of double-orifice left atrioventricular valve on mortality and the need for reoperation, a comparison was made with 291 consecutive patients who, during the same period, underwent correction of atrioventricular septal defect without double-orifice left atrioventricular valve.

None of the 21 patients with double-orifice left atrioventricular valve had undergone a previous operation. The accessory orifice was managed with different techniques depending on the severity of the regurgitation. There was no in-hospital mortality, and there were 3 late deaths. Seven patients required 12 reoperations, 7 for left atrioventricular valve insufficiency. Double-orifice left atrioventricular valve had no influence on mortality but was a significant predictor for reoperation compared with repair of atrioventricular septal defect without double-orifice left atrioventricular valve. At the latest follow-up, all 18 survivors were in New York Heart Association functional class I without medication. Only 1 patient showed residual mild left atrioventricular valve insufficiency.

Atrioventricular septal defect with double-orifice left atrioventricular valve can be repaired with low mortality. However, double-orifice left atrioventricular valve is a predictor for reoperation. The accessory orifice is often competent and should then be left untouched. If regurgitation of the accessory orifice is present, this is best managed with suture or patch closure.

A retrospective single center cohort study was performed. Categorical variables were analyzed with the ² test. Preoperative variables were analyzed with logistic and linear regression analysis to determine whether they were associated with adverse outcomes.

Analysis was performed on 280 patients, of whom 124 were female and 156 were male. Seventy-one patients were neonates (≤30 days) at the time of the operation. Ninety patients had an absolute lymphocyte count of less than 3000 cells/µL before the operation. Regression models showed that RACHS-1 categories 5 and 6, age, and preoperative lymphopenia were significantly associated with postoperative mortality (P < .0006). Within RACHS-1 groups, lymphopenia remained a significant predictor of mortality for patients in RACHS categories 3 and 4. Lymphopenia and age were associated with longer length of stay and length of mechanical ventilation within RACHS categories 1 to 4 (P < .05). Preoperative lymphopenia was the only predictor of use of postoperative nitric oxide (P < .05).

Preoperative lymphopenia is a predictor of adverse postoperative outcomes in children with congenital heart disease who undergo a corrective or palliative procedure with cardiopulmonary bypass during the first 2 years of life.

We retrospectively reviewed the records of 56 consecutive patients who underwent pulmonary resections for multidrug-resistant tuberculosis between January 2000 and June 2007. There were 42 males and 14 females (mean age, 46 years; range, 22-64 years). Isolates were resistant to a mean of 5.6 drugs (range, 2-10 drugs). Multi-drug regimens employing 3 to 7 drugs (mean, 4.6 drugs) were initiated in all patients. Indications for surgery were a high risk of relapse for 37 patients, persistent positive sputum for 18, and 1 with associated empyema.

The 56 patients underwent 61 pulmonary resections (3 completion pneumonectomies, 19 pneumonectomies, 33 lobectomies, and 6 segmentectomies). Bronchial stumps were reinforced with muscle flaps in 54 resections. Operative mortality and morbidity rates were 0% and 16%, respectively. All patients attained postoperative sputum-negative status. Relapse occurred in 5 patients; 3 were converted by a second resection, and 1 responded to augmentation of chemotherapy. Late death occurred for 2 patients without evidence of relapse. Among 54 survivors, 53 (98%) were considered cured.

Surgical treatment that complements medical treatment has proved safe and efficacious for patients with multidrug-resistant tuberculosis. In an era with extensively drug-resistant tuberculosis, an aggressive treatment approach to multidrug-resistant tuberculosis continues to be justified until a panacea for this refractory disease is available.

Between 1989 and 2008, we performed pulmonary artery reconstruction in 105 patients with non–small cell lung cancer (tangential resections not included). Twenty-seven patients received induction therapy. We performed 47 pulmonary artery sleeve resections, 55 reconstructions by pericardial patch (with 3 left pneumonectomies under cardiopulmonary bypass), and 3 by pericardial conduit. In 65 patients, a bronchial sleeve resection was associated; in 6 cases superior vena caval reconstruction was also required. Fifteen patients had stage IB disease, 37 stage II, 31 IIIA, and 22 IIIB. Sixty-one patients had epidermoid carcinoma, and 38 adenocarcinoma. Mean follow-up was 46 ± 40 months.

The procedure–related complications were 1 pulmonary artery thrombosis requiring completion pneumonectomy and 1 massive hemoptysis leading to death (operative mortality, 0.95%); 28 patients had other complications, with the most frequent prolonged air leakage. Overall 5-year survival was 44%. Five- and 10-year survivals for stages I and II versus stage III were, respectively, 60% versus 28% and 25% versus 12%. Five-year survivals were 52.6% for N0 and N1 nodal involvement versus 20% for N2; 10-year survivals were 28% versus 3%. Multivariate analysis yielded induction therapy, N2 status, adenocarcinoma, and isolated pulmonary artery reconstruction as negative prognostic factors.

Pulmonary artery reconstruction is safe, with excellent long-term survival. Our results support this technique as an effective option for patients with lung cancer.

Between 1995 and 2007, 26 patients underwent a 3-cm cut elongation gastroplasty with a transverse widening of the fundus followed by a 3-cm total (n = 24) or partial (n = 2) fundoplication. Indications for the operation were symptomatic massive hiatal hernias (n = 4), hiatal hernias with Barrett's esophagus (n = 8), or correction of previously failed antireflux fundoplications (n = 14). Barrett's esophagus was documented in 19 of the 26 patients. Pre- and postoperative assessment included symptoms, barium swallow, endoscopy, manometry, and 24-hour pH monitoring.

There was no postoperative mortality. Complications were recorded in 6 patients. Median follow-up was 105 months. Reflux symptoms present in all patients before the operation were found in 5 patients postoperatively (P < .001). Radiologic assessment documented an intact fundoplication in all patients. Lower esophageal sphincter gradient increased from a mean of 7.5 to 15 mm Hg (P = .003). Acid exposure (17% preoperatively) decreased significantly to 1% postoperatively (P < .001). Endoscopically, mucosal damage quantification decreased (3.1 preoperatively to 1.5 postoperatively; P < .001). All mucosal breaks healed but the columnar-lined metaplasia persisted.

This modified elongation gastroplasty provided a reliable repair for massive hernias, shortened Barrett's esophagus, and reoperations. The lower esophageal sphincter gradient was restored and remained stable. Reflux exposure was reduced, and acute mucosal damage disappeared. Columnar-lined metaplasia remained unchanged.

Seventy-eight patients with non–small cell lung cancer who were potential candidates for surgical resection and admitted to the thoracic surgery unit of our hospital from March 2006 to June 2008 joined this prospective study. Positron emission tomographic–computed tomographic scanning was performed as part of the prospective studies used to diagnose or stage the tumors. All 78 patients underwent tissue sampling of mediastinal lymph nodes to compare these with imaging results. The diagnostic efficacy of the computed tomographic and positron emission tomographic–computed tomographic scans compared with histopathologic findings were calculated with sensitivity, specificity, positive and negative predictive values, and accuracy.

Final histology was available on 397 lymph node stations (N1, N2, and N3) sampled from 78 patients during mediastinoscopy or surgical intervention. Sensitivity, specificity, and positive and negative predictive values of mediastinal lymph node involvement in patients undergoing thoracic computed tomographic scanning were 45.4%, 80.5%, 27.7%, and 90%, respectively. The accuracy of computed tomographic scanning was 75.6%. The sensitivity, specificity, and positive and negative predictive values of mediastinal lymph node involvement in patients undergoing positron emission tomographic–computed tomographic scanning were 81.8%, 89.5%, 56.2%, and 96.7%, respectively.

There is a need for mediastinoscopy in positron emission tomographic–computed tomographic scanning–positive mediastinal lymph nodes, but it might not be necessary for positron emission tomographic–computed tomographic scanning–negative lymph nodes.

From November 1991 to December 2007, in our department, 1306 patients with non–small cell lung cancer, judged operable at conventional staging, underwent videothoracoscopy before the operation. Thoracoscopy revealed inoperability in 58 (4.4%) patients, mostly owing to pleural dissemination (2.5%) or mediastinal infiltration (1.7%). In the remaining 1248 (95.6%), thoracoscopy did not reveal inoperability. Of these, 449 (34.4%) underwent thoracoscopic resection. The other 799 (61.2%) underwent thoracotomy: 767 underwent resection, but 32 (2.5%) had an exploratory thoracotomy. Thoracoscopy had suggested unresectability in 7 (0.5%) patients, had been incompletely carried out in 4 (0.3%), and was unfeasible in 21 (1.6%) owing to insurmountable technical reasons. In our previous series from 1980 to 1991 the exploratory thoracotomy rate had been 11.6%. In the present series, after the introduction of routine thoracoscopy in the staging process, the exploratory thoracotomy rate was 2.5%. Thoracoscopy was reliable in excluding unresectability (negative predictive value 0.97). The global percentage of correct staging was significantly better (P < .0001) by thoracoscopy (73.3%) than by computed tomography (48.7%). Considering T descriptor, video-assisted thoracic surgery correctly matched with final pathologic staging in 96.2% of patients.

Routine preliminary videothoracoscopy ensured assessment of tumor resectability and feasibility of the resection through thoracoscopy and limited unnecessary thoracotomies.

Cardioplegic arrest and subsequent reperfusion inevitably expose the heart to iatrogenic ischemia/reperfusion injury. We previously reported that iatrogenic ischemia/reperfusion injury caused myocyte induction of urocortin, an endogenous cardioprotective peptide.

Two sequential biopsies were obtained from the right atrium of 25 patients undergoing coronary artery bypass grafting at the start of grafting (internal control) and 10 minutes after release of the aortic clamp.

In hearts exposed to iatrogenic ischemia/reperfusion injury, induction of urocortin was documented at both the mRNA (255% of basic levels; P < .05) and the protein (4-fold increase; P < .01) levels. Iatrogenic ischemia/reperfusion injury also induced a selective increase of protein kinase C mRNA (225% of internal control; P < .05) and a 2-fold overexpression of total protein kinase C (P < .05), which paralleled a 2.9-fold increase in protein kinase C phosphorylation (P < .01). Mitochondrial translocation of activated protein kinase C was observed only in postcardioplegic samples, using both subcellular fractionation (P < .05) and immunostaining techniques (P < .05). Enhanced protein kinase C/mitochondria colocalization was selectively observed in viable myocytes, showing concurrently positive staining for urocortin (P < .05). Finally, co immunoprecipitation experiments documented an iatrogenic ischemia/reperfusion injury-enhanced physical interaction of phosphorylated protein kinase C with the 6.1 inwardly rectifying potassium channel subunit of the K_ATP channels (P < .05).

After iatrogenic ischemia/reperfusion injury, urocortin expression in viable cells selectively colocalized with enhanced phosphorylation and mitochondrial relocation of protein kinase C, suggesting a cardioprotective role for endogenous urocortin. The physical interaction of activated protein kinase C with 6.1 inwardly rectifying potassium channel, enhanced by cardioplegic arrest, may represent a conjectural mechanism of urocortin-mediated cardioprotection.

Fifteen New Zealand rabbits, irrespective of gender, weighing 2.5 to 3.0 kg, were randomly divided into 3 groups: (A), the experimental group (n = 5), tracheal allotransplantation after 4 weeks of vitrified cryopreservation; (B), the negative control group (n = 5), fresh tracheal autotransplantation; and (C), the positive control group (n = 5), fresh tracheal segments implanted as allografts. The patency of implanted grafts, lymphocytic infiltrate, cartilage scores, and ink perfusion to evaluate revascularization were used to investigate the impact of vitrified cryopreservation on the antigenicity of tracheal grafts and vascular regeneration.

Rabbits in groups A and B all had uneventful postoperative courses with patent lumens and structural integrity, with obvious vascular regeneration and less lymphocytic infiltrate. Although in excellent condition, animals were sacrificed after a short-term follow-up of 4 weeks for further examination as scheduled. In group C, massive lymphocytic infiltrate and inflammatory cells without noticeable revascularization were observed, and rabbits died within 2 weeks after surgery for airway stenosis or severe obstruction.

The antigenicity of tracheal allografts was significantly decreased by using the vitrified cryopreservation method, which would be a novel alternative method to store donor trachea to make tracheal banking possible.

A computational fluid dynamics model was developed to simulate systolic flow through a geometric mesh of the aortic root and transcatheter aortic valves. Hemodynamic measurements were made at discrete moments during ejection. Unsteady control volume analysis was used for calculations of force on the mesh.

Results of the simulation indicate that a total force of 0.602 N acts on the transcatheter aortic valves during systole, 99% of which is in the direction of axial flow. The largest contributor to force was the dynamic pressure gradient through the transcatheter aortic valves. This antegrade force is approximately 10 times smaller than the retrograde force (6.01 N) on the closed valve during diastole.

Our model simulated systolic flow through a transcatheter aortic valve and demonstrated migration into the left ventricle to be of greater concern than antegrade ejection.

United Network for Organ Sharing provided deidentified patient-level data. The study population included 8780 adult recipients (age > 12 years) having lung transplantation from January 1, 1999, to December 31, 2006. Multivariate logistic regression (backward, P > .10) was performed. Using the odds ratio for each identified variable, an RSS was devised. The RSS included only pretransplant recipient variables and excluded donor variables.

The strongest negative predictors of 1-year survival included extracorporeal membrane oxygenation, decreased estimated glomerular filtration rate, total bilirubin >2.0 mg/dL, recipient age, hospitalization at time of transplant, O₂ dependence, cardiac index <2, steroid dependence, donor:recipient weight ratio <0.7, all non–cystic fibrosis/chronic obstructive pulmonary disease etiologies, and female donor–to–male recipient. Threshold analysis identified 4 discrete groups: low risk, moderate, elevated risk, and high risk. The 1-year actuarial survival was 80.4% for the entire group, compared with 56.8% in the high-risk group (RSS > 7.2, n = 490; 6%).

Pretransplant recipient variables significantly influence both early and late survival following lung transplantation. Some patients face a higher than average risk of mortality during their first year posttransplant, which challenges the goals of equitable organ allocation. RSS may improve organ allocation strategies by avoiding the potential negative impact of performing transplantation in extremely high-risk candidates.

The prosthesis consists of a polypropylene mesh tube reinforced with a polypropylene spiral and atelocollagen layer. The cervical tracheas of 18 beagle dogs were replaced with the prosthesis. The collagen layer was soaked with peripheral blood in 6 of the dogs, with bone marrow aspirate in another 6, and with autologous multipotential bone marrow–derived cells (mesenchymal stem cells) in another 6. The dogs were humanely killed at 1 to 12 months after the operation.

All 18 dogs survived the postoperative period. Bronchoscopically, 3 of 4 dogs in the peripheral blood group showed stenosis, whereas no stenosis was evident in all 8 of the dogs in the bone marrow and mesenchymal stem cell groups 6 months after the operation. Faster epithelialization and fewer complications, such as mesh exposure and luminal stenosis, were observed in these two groups than in the peripheral blood group. Histologically, the cells from autologous bone marrow were found to proliferate into the tracheal tissue during the first month. Cilial movement in these two groups was faster than that in the peripheral blood group and recovered to 80% to 90% of the normal level.

Bone marrow aspirate and mesenchymal stem cells enhance the regeneration of the tracheal mucosa on this prosthesis. This in situ tissue engineering approach may facilitate tracheal reconstruction in the clinical setting.

We reviewed 240 patients with pulmonary aspergilloma who were diagnosed between 1990 and 2006. Of these, 135 patients underwent surgical procedure (group A) and 105 patients were managed with conservative treatment (group B).

Forty complications (29.6%) and 6 operative mortalities (4.4%) developed in group A. During the follow-up period, there were 5 recurrences (3.9%) after surgical procedure. The overall 10-year survival rates of group A and group B were 84.8% and 56.7% (P < .001). In multivariate analysis, age, sex, and surgical treatment were favorable prognostic factors. Symptoms of hemoptysis and blood-tinged sputum were not significant prognostic factor even in univariate analysis.

Our results indicate that (1) early morbidity and mortality rates of surgical treatment for pulmonary aspergilloma are acceptable, and (2) surgical treatment is helpful not only to reduce symptoms but also to prolong the survival of patients with pulmonary aspergilloma. Although more studies are needed, our data support the conclusion that surgical resection should be considered for all patients with pulmonary aspergilloma who have acceptable pulmonary reserve.

All the data of patients presenting with congenital adenomatoid malformations histologically diagnosed and operated on between 1998 and 2005 at our institution were retrospectively reviewed. Patients were divided into 2 groups: group A comprised asymptomatic infants, and group B comprised symptomatic infants. Major outcomes considered were the length of ventilation, pleural drainage, and hospital stay. Postoperative morbidity and mortality were also evaluated. Asymptomatic patients were further stratified for age at the time of the operation to evaluate whether age at surgical intervention affects the outcome. The Fisher's exact and Mann–Whitney tests were used as appropriate.

Fifty-seven patients were consecutively treated. Thirty-five patients were given diagnoses of asymptomatic lesions and were enrolled into group A, whereas 22 patients presenting with symptoms were entered into group B. The lengths of ventilation, pleural drainage, and hospital stay were significantly longer in patients with symptomatic congenital adenomatoid malformations. Moreover, symptomatic patients presented with a higher postoperative complication rate. The age-based stratification of asymptomatic children did not show any difference on either postoperative mortality or major outcome considered.

Children with congenital adenomatoid malformations operated on when asymptomatic present a better short-term outcome than symptomatic children. In addition, age at the time of the operation does not negatively affect the outcome. Our findings support early surgical treatment for asymptomatic congenital adenomatoid malformation.

Case histories of all patients (n = 133) undergoing esophageal resection from 1979 to 2007 with pT1 adenocarcinoma of the esophagus were reviewed. Univariate and multivariate analyses of esophageal tumor length and other standard prognostic factors were performed.

Patients with early-stage pT1 esophageal adenocarcinoma with tumors less than 3 cm demonstrate decreased long-term survival (3 years: >3 cm = 46% vs 93%; P < .001) and higher risk of lymph node involvement (lymph node positive: >3 cm = 47% vs 10%; P < .001). Multivariable analysis shows that esophageal tumor length (>3 cm) is an independent risk factor for survival in patients with pT1 early-stage esophageal cancer (hazard ratio: 4.8, 95% confidence intervals: 1.4–16.5; P < .001) even when controlled for submucosal involvement, lymph node involvement, and lymphatic/vascular invasion status. In combination with submucosal involvement, esophageal tumor length (>3 cm) identifies a high-risk population of pT1 esophageal adenocarcinoma (3 years: group 1 [0 risk factors] = 100%, group 2 [1 risk factor] = 87%, and group 3 [2 risk factors] = 33%; P < .001).

This study demonstrates that esophageal tumor length (>3 cm) is a risk factor for long-term survival and lymph node involvement in early-stage pT1 esophageal adenocarcinoma. Esophageal tumor length (>3 cm) in combination with submucosal involvement may help to identify a high-risk group of patients with pT1 esophageal adenocarcinoma.

An intraoperative ultrasonographic procedure was prospectively performed on 44 patients harboring ground-glass opacities of less than 20 mm in diameter to localize these lesions and to achieve adequate margins. We also examined whether there were any complications resulting from the intraoperative ultrasonogram, such as lung injury, heart injury, or arrhythmia. We excluded patients with both asthma and chronic obstructive pulmonary disease from this study inasmuch as the intraoperative ultrasonographic procedure is more difficult to interpret when residual air is present in the lung.

A total of 53 ground-glass opacities were successfully identified by intraoperative ultrasonography without any complications. Of the 20 mixed ground-glass opacities that we examined, 15 were found on palpation. However, only 4 (12.1%) of the 33 pure ground-glass opacities could be palpated. In all instances in which complete collapse of the lung was achieved (30/53 of these cases), high-quality echo images were obtained. Additionally, a strong correlation was found between the resection margins measured by ultrasonogram and the margins determined by histologic examination in the resected lung specimens (r ² = 0.954, P < .001).

Intraoperative ultrasonography can both safely and effectively localize pulmonary ground-glass opacities in a completely deflated lung. This procedure is also useful for the evaluation of surgical margins in a resected lung. Hence, ultrasonography may assist surgeons to perform minimally invasive lung resections with clear surgical margins during the treatment of solitary lung ground-glass opacity.

We performed a retrospective review of all patients undergoing induction therapy before lung resection for non–small cell lung cancer and malignant pleural mesothelioma at the University Health Network between January 1996 and December 2007.

Venous thromboembolism developed in 23 (12.3%) of 186 patients undergoing induction therapy. The venous thromboembolism was diagnosed during induction therapy in 11 patients. The proportion of pulmonary embolism was higher during induction therapy (9/11 patients), whereas deep venous thromboses were observed predominantly postoperatively (7/12 patients) (P = .02). The risk of postoperative complications or death was not increased in patients undergoing surgery despite a preoperative diagnosis of venous thromboembolism. However, the risk of postoperative pulmonary embolism was higher in patients undergoing surgery without insertion of an inferior vena cava filter (1/2 patients vs 0/7 after insertion of an inferior vena cava filter, P = .047). The overall survival was similar between patients with or without venous thromboembolism complications.

This study demonstrates that venous thromboembolism events in patients undergoing multimodality therapy for lung malignancies is high and deserves careful consideration. Patients with a venous thromboembolism diagnosis during induction therapy may potentially benefit from a temporary inferior vena cava filter before surgery to limit the risk of recurrent pulmonary embolism. A preoperative diagnosis of venous thromboembolism, however, does not affect early and late outcomes after surgery and should not be viewed as a negative prognostic marker.

The study population included 277 patients who underwent primary resection (192) or induction chemotherapy followed by surgery (85) for preoperatively diagnosed, potentially resectable N2 non–small cell lung cancer. N2 descriptors were prospectively recorded. Kaplan–Meier curves were used to evaluate survival, and statistical significance of differences between curves was assessed by log-rank test. Cox regression was used for multivariate analyses.

Preoperative significant prognostic factors were number of mediastinal node levels involved (P < .001), symptom severity (P = .013), clinical T (P = .041), and induction chemotherapy (P = .001). Three groups with different prognoses were based on individual prognostic score. The group that did best had a median survival of 29.6 months. Postoperative predictors of survival were pathologic T (P = .003), tumor residue (P = .034), and number of mediastinal nodes involved (P < .001). Of 3 groups with different prognoses, the most favorable had a median survival as long as 42 months.

This study provides a practical tool that uses significant prognostic factors to predict which patients with preoperatively diagnosed N2 non–small cell lung cancer have better prognoses. Because patients with the favorable prognostic factors showed good long-term survival and excellent local disease control, surgery should still play an important role in the multimodality treatment of these patients.

From 1988 to 2006, 103 consecutive patients with Marfan syndrome (mean age, 37 ± 12 years) and aortic root aneurysm had aortic valve–sparing operations. Emergency surgery was performed in 11 patients: 8 for acute type A aortic dissection and 3 for unexplained persistent chest pain. Fourteen patients also had mitral valve surgery. The technique of aortic valve reimplantation was used in 77 patients, and aortic root remodeling was used in 26 patients. Patients were followed prospectively and underwent annual echocardiographic studies. The mean follow-up was 7.3 ± 4.2 years and 100% complete.

There was 1 operative death and 5 late deaths. Four of the 6 deaths were due to complications of aortic dissections. The patients' survival at 15 years was 87.2% compared with 95.6% for the general population of Ontario matched for age and sex. Seven patients had important aortic insufficiency: 4 mild to moderate, 2 moderate, and 1 moderate to severe. Freedom from greater than mild aortic insufficiency at 15 years was 79.2%. Three patients, all after aortic root remodeling, had aortic valve replacement, 2 for aortic insufficiency and 1 for endocarditis. At the most recent follow-up, 97 patients were alive: 86 were in functional class I, and 11 were in functional class II.

Aortic valve–sparing operations provided excellent clinical outcomes in this series of patients with Marfan syndrome. Postoperatively, complications of aortic dissections were the leading cause of death.

A meta-analysis was performed on all published studies of retrograde endovascular stent graft placement encompassing 3 or more patients with type B aortic dissection. Thirty-nine studies, involving a total of 1304 patients from January 2001 to December 2007, were included.

The average patient age was 52 years. Procedural success was reported in 99.2% ± 0.1% of patients. Major complications were reported in 3.4% ± 0.1% patients, with the most severe neurologic complications in 0.6%. Periprocedural stroke was encountered more frequently than paraplegia (0.2% vs 0%). The overall 30-day mortality was 2.6% ± 0.1%. In addition, 1.5% ± 0.1% of patients died over a mean follow-up period of 27.1 ± 17.5 months. Life-table analysis yielded overall survival rates of 96.9% at 30 days, 96.7% at 6 months, 96.4% at 1 year, 95.6% at 2 years, and 95.2% at 5 years.

Although therapy with traditional medicines still remains the first line of treatment for type B aortic dissection, endovascular stent graft placement has shown its advantages, with a success rate of 99% or greater in a select cohort. The technical survival rate, major complications, and acute and midterm survival rates in the Chinese-language literature appeared to favorably compare with that seen in published literature. This analysis is the first to provide an overview of the currently available literature on endovascular stent graft placement in type B aortic dissection in China.

A retrospective cohort study was performed of patients (n = 10,863) undergoing primary coronary artery bypass grafting surgery with cardiopulmonary bypass between January 1995 and June 2005. Patients with preoperative renal insufficiency (n = 1385) and patients with preoperative normal renal function (n = 9478) were further classified as obese (body mass index, ≥30 kg/m²) or nonobese (body mass index, 18.5–29.9 kg/m²). Multivariate, stepwise logistic regression was performed, controlling for demographic factors, medications, and perioperative risk factors to determine whether obesity is independently associated with an increased risk of adverse postoperative outcomes after coronary artery bypass grafting surgery in patients with or without renal insufficiency.

Obese patients with preoperative renal insufficiency had higher rates of postoperative myocardial infarction (5.9% vs 3.4%) and low cardiac output syndrome (24.5% vs 18.6%) and increased hospital stay (14.9 ± 13.7 vs 13.2 ± 13.0 days) than nonobese patients with preoperative renal insufficiency (all outcomes, P < .05). Multivariate analysis revealed that obese patients with preoperative renal insufficiency were independently associated with an increased risk of postoperative myocardial infarction (odds ratio, 1.82; 95% confidence interval, 1.07–3.07; P < .05) and low cardiac output syndrome (odds ratio, 1.53; 95% confidence interval, 1.15–2.03; P < .01) and increased hospital stay (P < .05). In contrast, obese patients with normal preoperative renal function were independently associated only with an increased risk of postoperative sternal wound infection (odds ratio, 2.55; 95% confidence interval, 1.40–4.67; P < .01) and leg wound infection (odds ratio, 2.27; 95% confidence interval, 1.71–3.02; P < .01).

Obesity is an independent risk factor for increased cardiovascular morbidity and prolonged hospital stay in patients with preoperative renal insufficiency undergoing primary coronary artery bypass grafting surgery.

Sixty-one patients affected by thoracic aortic aneurysms were treated between January 2000 and March 2008. The study cohort contained 54 men, with a mean age of 63.6 ± 17.9 years. The follow-up imaging protocol included chest radiographs and triple-phase computed tomographic angiography performed at 1, 4, and 12 postoperative months and annually thereafter.

Median follow-up was 32.4 months (range: 1–96 months). Endoleaks were detected in 9 (14.7%) patients, of which 7 were type 1. Five endoleaks were detected at 30 postoperative days, and the other 4 developed with a mean delay of 12 months. Endovascular or hybrid interventions were used to treat the endoleaks. Secondary technical success rate was 100%. Multivariate analysis demonstrated that the diameter of the aneurysmal aorta (odds ratio 1.75, 95% confidence interval 1.07–2.86) and the coverage of the left subclavian artery (odds ratio 12.05, 95% confidence interval 1.28–113.30) were independently associated with endoleak development. The percentages of patients in whom reinterventions were unnecessary were 94.6% ± 3.0%, 88.3% ± 4.5%, and 85.4% ± 5.2%, at 1, 2, and 5 years, respectively. The actuarial survival estimates at 1, 2, and 5 years were 85.2% ± 4.6%, 78.1% ± 5.4%, and 70.6% ± 6.4%, respectively.

The diameter of the aneurysmal aorta and the position of the landing zone are independent predictors of endoleak occurrence after thoracic stent-graft procedures. A careful follow-up program should be considered in patients in whom these indices are unfavorable, because most of the endoleaks may be successfully and promptly treated by additional endovascular procedures.

We studied 511 patients who underwent isolated mitral valve repair for degenerative disease with a 63-mm posterior band used for annuloplasty. Operations were performed between 1994 and 2001, and average follow-up was 4.8 ± 3.1 years. Echocardiographic data were reviewed, with specific focus on the relationship between patient size and residual mitral regurgitation and gradient.

Mean age at the time of operation was 59.3 ± 13.5 years, and 72% were male. Body mass index was 25.8 ± 4.1 kg/m², and body surface area was 1.97 ± 0.24 m². Preoperative mean ejection fraction was 64% ± 7%, and 96% of patients had severe mitral regurgitation on preoperative echocardiography. The 30-day mortality was 0.8%. At hospital discharge, the mean gradient was 4.7 ± 3.1 mm Hg. Body surface area, body mass index, and weight were not associated with postoperative gradients or residual regurgitation at discharge. At last follow-up, 89% of patients had no or mild regurgitation, and the mean ejection fraction was 58% ± 9%. At 5 years, survival was 95% and cumulative risk of reoperation was 3%.

A standard-sized (unmeasured) posterior annuloplasty band provided excellent intermediate results with good durability. There were neither excess gradients in larger patients nor excess regurgitation in smaller patients. Measured annuloplasty is unnecessary for most adults undergoing mitral valve repair.

Eighty-nine patients (mean age, 45.67 ± 10.18 years; range, 21–68 years) with chronic type A dissection underwent total arch replacement combined with stented elephant trunk implantation between April 2003 and March 2007. Careful assessment of the visceral arteries and location of entry and re-entry was done before surgery. Postoperative patency of the visceral arteries and diameter of the aortic artery and the residual false lumen were evaluated by computed tomography.

One (1.12%) hospital death and 2 (2.25%) late deaths occurred at a mean follow-up of 28.5 months (range, 8–52 months). Visceral malperfusion was not observed. Two patients had spinal cord injury and recovered during follow-up. One patient had a transient neurologic deficit and recovered completely before discharge. One patient underwent thoracoabdominal aortic replacement for aneurysmal dilatation of the residual descending aorta 3 months after the operation. Thrombus obliteration of the false lumen at the distal edge of the stented elephant trunk and at the diaphragmatic level was 94.2% (81/86) and 61.6% (53/86), respectively.

Satisfactory results with low morbidity and mortality were obtained. No visceral malperfusion and a low risk of postoperative spinal cord injury favor this technique in patients with chronic type A dissection.

We designed a case–control study in two groups of patients who underwent cardiac surgery just before and after aprotinin was suspended in China. The aprotinin group (n = 1699) was defined as operations performed from June 19, 2007, to December 18, 2007, when aprotinin was used in all the patients. The control group (n = 2225) was defined as operations performed from December 19, 2007, to June 18, 2008, when aprotinin was not used. We compared early postoperative outcomes between the two groups.

The aprotinin group had less postoperative blood loss, transfusion requirement, and reoperation for bleeding. Application of aprotinin did not increase the risk of in-hospital mortality (0.5% vs 1.0%; P = .08) and other major adverse outcome events, including renal, cardiac, neurologic, and pulmonary complications. The aprotinin group had a shorter mechanical ventilation time (P = .04), a lower rate of delayed mechanical ventilation time (P = .04), and a higher arterial oxygen tension/inspired oxygen fraction ratio in arterial blood gas analysis (P < .001). Multivariable logistic regression analysis confirmed findings from univariate analysis. After propensity adjustment for the baseline characteristics, we obtained similar results.

Use of aprotinin in cardiac surgery could reduce blood loss and transfusion requirement significantly and showed a protective effect on the lungs, but it did not increase the risk of mortality or major complications.

Preoperative risk associated with cardiac surgery can be ascertained through a variety of risk prediction models, none of which is specific to the Australian population. Recently, it was shown that the widely used EuroSCORE model validated poorly for an Australian cohort. Hence, a valid model is required to appropriately guide surgeons and patients in assessing preoperative risk.

Data from the Australasian Society of Cardiac and Thoracic Surgeons database project was used. All patients undergoing isolated coronary artery bypass grafting between July 2001 and June 2005 were included for analysis. The data were divided into creation and validation sets. The data in the creation set was used to develop the model and then the model was validated in the validation set. Preoperative variables with a P value of less than .25 in ² analysis were entered into multiple logistic regression analysis to develop a preoperative predictive model. Bootstrap and backward elimination methods were used to identify variables that are truly independent predictors of mortality, and 6 candidate models were identified. The Akaike Information Criteria (AIC) and prediction mean square error were used to select the final model (AusSCORE) from this group of candidate models. The AusSCORE model was then validated by average receiver operating characteristic, the P value for the Hosmer–Lemeshow goodness-of-fit test, and prediction mean square error obtained from n-fold validation.

Over the 4-year period, 11,823 patients underwent cardiac surgery, of whom 65.9% (7709) had isolated coronary bypass procedures. The 30-day mortality rate for this group was 1.74% (134/7709). Factors selected as independent predictors in the preoperative isolated coronary bypass AusSCORE model were as follows: age, New York Heart Association class, ejection fraction estimate, urgency of procedure, previous cardiac surgery, hypercholesterolemia (lipid-lowering treatment), peripheral vascular disease, and cardiogenic shock. The average area under the receiver operating characteristic was 0.834, the P value for the Hosmer–Lemeshow ² test statistic was 0.2415, and the prediction mean square error was 0.01869.

We have developed a preoperative 30-day mortality risk prediction model for isolated coronary artery bypass grafting for the Australian cohort.

This is a retrospective review of all 278 neonates with the diagnosis of tetralogy of Fallot and truncus arteriosus undergoing right ventricular outflow tract reconstruction at a single center between 1990 and 2007. Diagnostic variants included tetralogy of Fallot/pulmonary stenosis (n = 83), tetralogy of Fallot/pulmonary atresia (n = 81), and tetralogy of Fallot with absent pulmonary valve (n = 17). Truncus arteriosus was present in 97 patients. Patients were analyzed on the basis of diagnosis and the method of right ventricular outflow tract reconstruction: aortic homograft, pulmonary homograft, transannular patch, transannular patch with monocusp pulmonary valve, and nontransannular patch. Freedom from reoperation/reintervention was determined by using the log-rank test.

The mean age at right ventricular outflow tract reconstruction was 11.8 ± 8 days, and hospital survival was 95.0% for the tetralogy of Fallot group and 90.7% for the truncus arteriosus group. Overall freedom from reoperation and reintervention was 76.2% ± 14.8% in the nontransannular patch group and 59.5% ± 6.8% in the transannular patch group; both were significantly greater than seen in patients receiving either aortic (0%) or pulmonary (6.7% ± 4.2%) homografts (P < .05). There was no difference between aortic and pulmonary homografts. Among patients with tetralogy of Fallot/pulmonary stenosis, there was no difference in 10-year freedom from reoperation/reintervention between the transannular (70.8% ± 7.4%) and nontransannular patch methods (76.2% ± 14.8%, P = .53). At 10 years, the diagnosis of tetralogy of Fallot/pulmonary stenosis was associated with a greater freedom from reoperation/reintervention (68% ± 6.8%) when compared with tetralogy of Fallot/pulmonary atresia (5.3% ± 4.3%, P = .0001), tetralogy of Fallot/absent pulmonary valve (0%, P = .00315), or truncus arteriosus (4.2% ± 2.8%, P = .0001). Eight patients (4 with tetralogy of Fallot/pulmonary stenosis, 3 with tetralogy of Fallot/pulmonary atresia, and 1 with tetralogy of Fallot/absent valve) underwent placement of a transannular patch with monocusp valve. Among this group, freedom from reoperation/reintervention is 41.7% ± 20.5% at 2.5 years. Monocusp function, as determined by means of echocardiographic analysis obtained at 11.4 ± 11.7 months (range, 0.3–31 months) showed an average monocusp gradient of 23.5 ± 26.1 mm Hg, and 3 (37.5%) patients had more than moderate pulmonary regurgitation.

The durability of neonatal right ventricular outflow tract reconstruction is diagnosis and method dependent. Anatomy allowing right ventricular outflow tract patching (either transannular or nontransannular) provides a durability advantage compared with that seen with a homograft. There was no difference in performance between aortic and pulmonary homografts, and the monocusp valve has limited durability and effectiveness in neonatal right ventricular outflow tract surgery. The long-term outcomes of transannular and nontransannular patching techniques for neonatal repair of tetralogy of Fallot/pulmonary stenosis are similar.

The proposed algorithm would identify "high-risk" subjects on the basis of risk factors on medical history, echocardiography, and noninvasive angiography. The efficacy of this algorithm in screening for subjects deemed to be inoperable after catheterization was evaluated retrospectively in 151 children. For this analysis, results of conventional angiography (assumed to be equivalent to noninvasive angiography) were used.

According to the algorithm, 95 (63%) of 151 subjects had no risk factors ("low risk") whereas 56 (37%) of 151 had 1 risk factor or more ("high risk"). Nine (6%) of 151 subjects were found to be inoperable after catheterization and all 9 were correctly classified as high risk by the algorithm. In the 135 of 151 subjects who underwent a Fontan operation, the algorithm predicted an adverse postoperative outcome with a sensitivity of 51% and specificity of 78%. However, this prediction was not improved by including elevated pulmonary artery pressure or ventricular filling pressure as additional risk factors.

The proposed algorithm effectively screened for subjects who were deemed unsuitable for a Fontan procedure. In addition, omitting preoperative invasive hemodynamic assessment did not impair prediction of adverse postoperative outcomes. Prospective evaluation of such a noninvasive diagnostic strategy before the Fontan operation is warranted.

Children who underwent neonatal cardiac surgery for interrupted aortic arch at 6 weeks old or younger between 1996 and 2006 had a multidisciplinary neurodevelopmental assessment at 18 to 24 months old (mental and psychomotor developmental indices as mean ± SD and delay [score <70]). Survivor outcomes were compared by univariate and multivariate analyses and compared between children with and without chromosomal abnormality.

Outcomes were available for all 26 survivors (mortality, 3.7%). Mental and psychomotor developmental indices were 75.8 ± 17.1 and 72.3 ± 16.9, respectively, with significantly lower scores for children with chromosomal abnormalities, which accounted for 29% of the variance in developmental indices. For the remaining 17 children without chromosomal abnormalities, mental and psychomotor developmental indices were 82.7 ± 14.5 and 79.1 ± 14.3, respectively, with deep hypothermic circulatory arrest time and Apgar score at 5 minutes contributing 46% of the variance in mental developmental index.

The neurodevelopmental indices of children who have undergone neonatal cardiac surgery for interrupted aortic arch are below normative values; those of children with chromosomal abnormalities are even lower. For children without a chromosomal abnormality, longer deep hypothermic circulatory arrest times and low Apgar scores predict lower mental developmental indices at 18 to 24 months of age.

Between August 1996 and December 2004, all patients who underwent a sex-differentiated surgical approach were included. Hospital results were compared with those of a group undergoing full sternotomy (control subjects). Patients' clinical conditions and satisfaction at follow-up were evaluated.

Three hundred eight patients underwent the sex-differentiated surgical approach: (1) minithoracotomy in 147 (47.7%) and (2) ministernotomy in 161 (52.3%). Thirty patients had a full sternotomy for atrial septal defect closure. The most common diagnosis was an atrial septal defect (231 [75%] patients). None of the patients required an extension of the surgical access. There were neither major complications nor hospital deaths. All patients were discharged home without residual defects. Median follow-up time was 71.5 months (range, 48.2–85.7 months). There were no late deaths. No scoliosis, asymmetric breast development, or lactation problems were reported in the minithoracotomy group. Twenty-five (17%) of 147 patients with minithoracotomies complained of a trivial, persistent (<6 months), sensitive skin deficit in the mammary area, most often localized at the inferomedial quadrant. The vast majority of patients (296 [96%] 308 patients) were in New York Heart Association class I, and 282 (91.5%) of 308 patients were satisfied with the cosmetic result of the operation.

The sex-differentiated surgical approach for simple congenital heart disease is a safe procedure, providing both excellent functional and cosmetic results. Anterolateral minithoracotomy is a valid and highly appreciated procedure in female patients.

Between 1994 and 2008, of 121 consecutive patients having Fontan conversion and arrhythmia surgeries, 120 patients underwent pacemaker implantation at the time of Fontan conversion (mean age 22.9 ± 8.1 years). Prior pacemakers were in place in 32/120 (26.7%) patients. Between 1994 and 1998, single-chamber atrial antitachycardia pacemakers were implanted (n = 12); atrial rate-responsive pacemakers (n = 31) were implanted between 1998 and 2002. Dual-chamber rate-responsive pacemakers (n = 16) were used between 2002 and 2003, and subsequently dual-chamber antitachycardia pacemakers (n = 61) have become the pacemaker of choice. Leads have evolved from transatrial endocardial leads to epicardial unipolar and subsequently bipolar leads.

Among 87 patients with adequate follow-up, all are currently atrially paced at a minimum lower rate ≥70 beats per minute. Single-chamber atrial pacemakers were implanted in 43 (antitachycardia in 12), and dual-chamber pacemakers in 77 (antitachycardia in 61); multisite ventricular leads were placed in 7 patients. Far-field R-wave sensing in 78.6% of unipolar atrial leads led to use of epicardial bipolar leads. Late atrioventricular block (24%) led to routine implantation of dual-chamber pacemakers. Antitachycardia pacing was utilized in 7%. One patient required acute lead revision and 4 required late upgrade to dual-chamber pacemakers. There was no pacemaker-related infection. Twenty patients required generator change, and the mean device longevity was 7.53 years.

Customized pacemaker therapy can optimize management of patients following Fontan conversion. Device longevity is excellent. Based on our experience with 120 Fontan conversions, we recommend placement of a dual-chamber antitachycardia pacemaker with bipolar steroid-eluting epicardial leads in all patients at the time of the conversion.

We retrospectively reviewed 24 cardiac magnetic resonance studies of patients (mean age, 3.1 ± 1.0 years) referred before the Fontan operation. Cardiac magnetic resonance measured the cross-sectional area and flow to each branch pulmonary artery. Post-Fontan hospital course data were acquired from the medical record.

Prolonged length of stay after the Fontan operation is observed among patients with one branch that is less than 25% of the total cross-sectional area (18.0 ± 5.5 vs 8.2 ± 3.8 days, P = .01) or with less than 40% flow to one branch (12.5 ± 6.9 vs 7.6 ± 1.5 days, P = .04). There is moderate correlation between the total branch pulmonary area and length of stay (r = –0.75).

Cardiac magnetic resonance noninvasively assesses the branch pulmonary area size and flow before the Fontan operation. These data predict which patients are more likely to experience a prolonged hospital course.

All consecutive patients still mechanically ventilated on day 3 after cardiac surgery were included in a prospective observational cohort. Patients' preoperative, intraoperative, and postoperative data were recorded. Logistic regression analysis was used to identify factors associated with successful weaning from mechanical ventilation by postoperative day 10.

Among 2620 patients who underwent cardiac surgery, 163 were still receiving ventilatory assistance on day 3. By day 10, 50 (31%) patients had been successfully weaned, 78 (48%) were still receiving mechanical ventilation, and 35 (21%) had died. Multivariable regression analysis retained 6 day-3 factors associated with successful weaning (odds ratio): urine output 500 mL/24 hours or greater (16.47), Glasgow coma score of 15 (9.75), arterial bicarbonates 20 mmol/L or greater (6.09), platelet count 100 g/L or greater (3.18), patients without inotropic support with epinephrine/norepinephrine (2.84), and absence of lung injury (2.40). The area under the receiver operating characteristics curve for the simple score based on this model's β-coefficients was 0.84 (95% confidence intervals, 0.78–0.91). Depending on the threshold chosen for this scoring system, only 3% to 17% of the patients would have received a needless intervention.

A simple score based on postoperative day-3 physiologic parameters might help intensivists early identify patients with a strong likelihood of success in rapid weaning from mechanical ventilation and therefore prevent needless procedures aimed at reducing duration of mechanical ventilation and related complications.

Patients undergoing isolated coronary artery bypass grafting between January 2000 and December 2007 (n = 8500) were studied. Preoperative demographic data and risk factors and outcome data (mortality data) were prospectively collected in a database. Preoperative C-reactive protein levels were retrieved from the laboratory data.

In 5669 of 8500 cases, the preoperative C-reactive protein level could be retrieved. Seventy-five patients were unavailable for follow-up. A preoperative C-reactive protein level greater than 10 mg/L was an independent risk factor for early mortality, whereas a level greater than 5 mg/L was a risk factor for late mortality. Other risk factors were age, sex, chronic obstructive pulmonary disease, diabetes, left ventricular ejection fraction less than 35%, peripheral vascular disease, and previous cardiac surgery. We found a higher mean C-reactive protein value in patients with a left ventricular ejection fraction less than 35% (18.5 ± 33 mg/L) than in those with an ejection fraction greater than 35% (P < .0001).

Preoperative C-reactive protein levels can be used in risk stratification in coronary artery bypass grafting surgery. A C-reactive protein level greater than 10 mg/L is a risk factor for early mortality, whereas a level greater than 5 mg/L is a risk factor for late mortality.

This prospective, randomized, clinical trial included 94 patients undergoing high-risk cardiac surgery comparing a 5-day course of continuous nesiritide (at a dose of 0.01 µg · kg^–1 · min^–1 started before surgery) versus placebo. The primary end point was dialysis and/or all-cause mortality within 21 days; secondary end points were incidence of acute kidney injury, renal function, and length of stay.

Nesiritide did not reduce the primary end point of incidence of dialysis and/or all-cause mortality through day 21 (6.6% vs 6.1%; P = .914). Fewer patients receiving nesiritide had acute kidney injury (defined as an absolute increase in serum creatinine ≥ 0.3 mg/dL from baseline or a percentage increase in serum creatinine ≥ 50% from baseline within 48 hours) compared with controls (2.2% vs 22.4%; P = .004), and mean serum creatinine was lower in the immediate postoperative period in the nesiritide group (1.18 ± 0.41 mg/dL vs 1.45 ± 0.74 mg/dL; P = .028). However, no difference in length of stay was noted (nesiritide 20.73 ± 3.05 days vs control 21.26 ± 4.03 days; P = .917).

These results do not demonstrate a benefit for prophylactic use of nesiritide on the incidence of dialysis and/or death in patients undergoing high-risk cardiac surgery. Although nesiritide may provide some renal protection in the immediate postoperative period, no effect on length of stay was observed.

This single-center prospective study investigated 1214 consecutive patients undergoing coronary artery bypass grafting between January 2004 and June 2007, collecting 100 variables per patient. In 1047 patients (median age 64 years, 18.8% female, 38.9% diabetic, 31.9% urgent/emergency, 15.3% with low preoperative left ventricular ejection fraction) who underwent on-pump procedures and received no preoperative transfusion, the prevalence of preoperative anemia (according to World Health Organization definition) and its unadjusted and adjusted relationships with in-hospital death, cardiac morbidity, and acute kidney injury (AKI–RIFLE [Risk, Injury, Failure, Loss, End-stage kidney disease] criteria) were obtained.

The prevalence of preoperative anemia was 28%. In-hospital death averaged 3.9%, cardiac morbidity 7.3%, and acute kidney injury 4%. Unadjusted odds ratios (Ors) for in-hospital death, cardiac morbidity, and acute kidney injury were 3.8 (95% confidence interval [CI] 2.0–7.3), 1.7 (95% CI 1.1–2.8), and 4.0 (95% CI 2.1–7.6), respectively. Adjusting for anemia in confounders proved an independent predictor of acute kidney injury (OR 2.06; 95% CI 1.14–3.70), whereas the cardiac morbidity and in-hospital mortality were independently predicted by kidney function. No dose–response relationship emerged between anemia severity and acute kidney injury.

Preoperative anemia is independently associated with acute kidney injury after coronary artery bypass grafting. Further studies are warranted to determine whether preoperative low hemoglobin concentration is a marker of severity of illness or a modifiable risk factor.

Early and late mortality were determined retrospectively among consecutive patients having isolated coronary bypass at a single Dutch institution between January 1998 and December 2007. Patients were stratified into 4 groups according to preoperative renal function. Expected survival was gauged using a general Dutch population group that was obtained from the database of the Dutch Central Bureau for Statistics; for each of our renal function groups, a general population group was assembled by matching for age, gender, and year of operation.

After excluding 122 patients lost to follow-up, 10,626 patients were studied; in 10,359, preoperative creatinine clearance could be calculated. Multivariate logistic regression and Cox regression analysis identified renal dysfunction as a predictor for early and late mortality. When long-term survival of patient groups was compared with expected survival, only patients with a creatinine clearance less than 30 mL · min^–1 showed a worse outcome. Patients with a creatinine clearance between 60 and 90 mL · min^–1 had a long-term survival exceeding the expected survival.

Severity of renal dysfunction was related to poor survival. When compared with expected survival, however, patients having coronary bypass had a worse outcome only when severe preoperative renal dysfunction was present.

The mid left anterior descending coronary artery in 14 Yorkshire swine was acutely occluded for 60 minutes, followed by reperfusion for 120 minutes. Controls (n = 7) received placebo, and treatment animals (n = 7) received sulfide 10 minutes before and throughout reperfusion. Hemodynamic and functional measurements were obtained. Evans blue and triphenyl tetrazolium chloride staining identified the area at risk and infarction. Coronary microvascular reactivity was assessed. Tissue was assayed for myeloperoxidase activity and proinflammatory cytokines.

Pre-ischemia/reperfusion hemodynamics were similar between groups, whereas post-ischemia/reperfusion mean arterial pressure was reduced by 28.7 ± 5.0 mm Hg in controls versus 6.7 ± 6.2 mm Hg in treatment animals (P = .03). Positive first derivative of left ventricular pressure over time was reduced by 1325 ± 455 mm Hg/s in controls versys 416 ± 207 mm Hg/s in treatment animals (P = .002). Segmental shortening in the area at risk was better in treatment animals. Infarct size (percent of area at risk) in controls was 41.0% ± 7.8% versus 21.2% ± 2.5% in the treated group (P = .036). Tissue levels of interleukin 6, interleukin 8, tumor necrosis factor-alpha, and myeloperoxidase activity decreased in the treatment group. Treated animals demonstrated improved microvascular reactivity.

Therapeutic sulfide provides protection in response to ischemia/reperfusion injury, improving myocardial function, reducing infarct size, and improving coronary microvascular reactivity, potentially through its anti-inflammatory properties. Exogenous sulfide may have therapeutic utility in clinical settings in which ischemia/reperfusion injury is encountered.

Myoblast sheets were constructed in dishes that release confluent cells from the dish surface via temperature reduction. Sixty infarcted Lewis rats underwent implantation of myoblast sheets on the infarcted area. There were 4 groups (n = 15 in each group): S1: one layer, S3: three layers, S5: five layers, and a sham group. We examined cardiac function by echocardiography and catheterization, mRNA expression by real time reverse-transcriptase polymerase chain reaction, and histology.

The ejection fraction and end-systolic pressure–volume relationship in the S5 and S3 groups were significantly improved. End-diastolic area was significantly reduced in the S5 group. The mRNAs for hepatocyte growth factor, vascular endothelial growth factor, and stromal cell–derived factor-1 were all up-regulated in dose-dependent fashion. On histologic examination, fibrosis was most decreased in S5, and vascular density was increased. Cellular hypertrophy was attenuated in both the S5 and S3 groups. Elastic fibers were massively up-regulated in the infarction and implanted sheets in the S5 and S3 groups, with expression of the elastin gene.

Implantation of three- and five-layered myoblast sheets yields favorable results, with better improvement of cardiac function, induction of angiogenesis, more elastic fibers, and less fibrosis. Thus, layered myoblast sheets, in optimal numbers, may attenuate adverse cardiac remodeling of the infarcted heart.

Twenty two sheep were included. All animals underwent myocardial infarction by ligation of 2 coronary artery branches (distal left anterior descending artery and D2). After 4 weeks, autologous cultured myoblasts were injected in the infarcted areas with or without pacemaker implantation. Atrial synchronized biventricular pacing was performed using epicardial electrodes. Echocardiography was performed at 4 weeks (baseline) and 12 weeks after infarction.

Echocardiography showed a significant improvement in ejection fraction and limitation of left ventricular dilatation in cell therapy with cardiac resynchronization therapy as compared with the other groups. Viable cells were identified in the infarcted areas. Differentiation of myoblasts into myotubes and enhanced expression of slow myosin heavy chain was observed in the electrostimulated group. Transplantation of cells with cardiac resynchronization therapy caused an increase in diastolic wall thickening in the infarcted zone relative to cells-only group and cardiac resynchronization therapy–only group.

Biventricular pacing seems to induce synchronous contraction of transplanted myoblasts and the host myocardium, thus improving ventricular function. Electrostimulation was related with enhanced expression of slow myosin and the organization of myoblasts in myotubes, which are better adapted at performing cardiac work. Patients with heart failure presenting myocardial infarct scars and indication for cardiac resynchronization therapy might benefit from simultaneous cardiac pacing and cell therapy.

With institutional review board approval, 50 rats were randomly assigned to one of 3 groups: rats of the cardiopulmonary bypass group were subjected to 75 minutes of normothermic cardiopulmonary bypass. Sham-operated animals underwent identical preparation but were not connected to cardiopulmonary bypass, whereas rats of the control group were neither anesthetized nor cannulated. Ten rats per group survived 4 hours after cardiopulmonary bypass or the sham operation for immediate postoperative determination of tumor necrosis factor –expressing cells (immunohistochemistry) and cerebral tumor necrosis factor mRNA levels (polymerase chain reaction). The remaining animals survived 10 days for neurocognitive assessment by using the modified hole-board test and for analysis of cerebral tumor necrosis factor activation in the late postoperative period.

Expression of tumor necrosis factor mRNA was increased 4 hours after cardiopulmonary bypass and the sham operation, with higher expression in the cardiopulmonary bypass group (² [2] = 25.08, P < .001). Both experimental groups demonstrated larger numbers of tumor necrosis factor –positive cells in the early and late postoperative periods (F [1] = 13.08, P ≤ .001) and an impaired neurocognitive performance on the first postoperative days compared with that seen in the control group (F [2, 24] = 4.26, P = .02).

Cerebral tumor necrosis factor activation in both experimental groups during the early postoperative period was accompanied by transient neurocognitive impairment. Therefore cardiopulmonary bypass alone demonstrated no effect on cerebral inflammation and neurocognitive outcome.

Interstitial cells were isolated from normal and stenotic human aortic valve leaflets, and cellular bone morphogenic protein 2 levels were analyzed by means of immunoblotting. Cultured interstitial cells from normal aortic valves were stimulated with bone morphogenic protein 2 to determine its effect on cellular Runx2 and osteopontin levels.

Interstitial cells from stenotic aortic valves express greater levels of bone morphogenic protein 2 than cells from normal valves. Stimulation of human aortic valve interstitial cells with bone morphogenic protein 2 induced marked increases in Runx2 and osteopontin levels at 48 hours. The changes in Runx2 and osteopontin levels were preceded by phosphorylation of Smad1 and extracellular signal-regulated kinase 1/2 but not p38 mitogen-activated protein kinase. Silencing Smad1 reduced Runx2 and osteopontin levels, whereas inhibition of extracellular signal-regulated kinase 1/2 reduced osteopontin expression without an influence on Runx2 expression.

Interstitial cells of stenotic human aortic valves are characterized by increased bone morphogenic protein 2 levels. A short period of exposure of human aortic valve interstitial cells to bone morphogenic protein 2 induces the expression of Runx2 and osteopontin. The extracellular signal-regulated kinase 1/2 pathway modulates bone morphogenic protein 2–induced osteopontin expression, and the Smad1 pathway plays a role in regulating the expression of both Runx2 and osteopontin induced by bone morphogenic protein 2.

Between 2002 and 2006, 153 patients underwent Norwood stage I reconstruction with a right ventricle–pulmonary artery conduit (125 in the right-sided group and 28 in the left-sided group). The previous 150 consecutive classic Norwood procedures (1997–2002) were used as a control group. Outcomes from stages I and II were analyzed, including ventricular function and pulmonary artery morphology.

The 30-day survival was 88% (110/125) in the right-sided group, 75% (21/28) in the left-sided group, and 70% (105/150) in the control group (P < .001, right-sided vs control groups). The conduit length was 35 ± 9 mm in the right-sided group and 26 ± 8 mm in the left-sided group (P = .001). Survival at 6 months demonstrated a significant survival benefit in the right-sided right ventricle–pulmonary artery conduit group over the control group (P = .009, log-rank test). There was no difference in ventricular function between the groups and no regional dyskinesia associated with the right ventricle–pulmonary artery conduit. Despite larger branch pulmonary artery size in the right ventricle–pulmonary artery conduit groups (compared with the control group), central pulmonary artery stenoses were common (62% in the right conduit and 80% in the left conduit). Bypass and ischemic times at stage II were 49 ± 10 and 23 ± 13 minutes in the right-sided group compared with 61.5 ± 9.5 and 31 ± 14 minutes in the left-sided group (P < .001 and P = .03, respectively). The 30-day mortality after the stage II procedure was 1.3% (1/76) in the right-sided group, 0% (0/18) in the left-sided group, and 3.3% (3/90) in the control group.

The right-sided conduit is a safe technique and has improved 30-day and overall post–stage II survival compared with that seen with the classic Norwood procedure. The right ventricle–pulmonary artery conduit is associated with central pulmonary artery stenosis but good development of the branch pulmonary arteries and preservation of ventricular function. The right-sided conduit significantly reduces cardiopulmonary bypass times at stage II.

Microarray expression analyses were performed with left ventricular tissue from 10- and 90-day-old rats exposed to hypoxia (inspired oxygen fraction 0.12) for the first 10 days after birth then subsequently reared in ambient air and with tissue from age-matched rats reared entirely in ambient air. Changes in expression of selected genes were confirmed with real-time reverse transcriptase polymerase chain reaction. Left ventricular cardiomyocytes were isolated from adult animals in both groups, and cellular morphology and viability were compared.

Microarray analyses revealed significant changes in 1945 and 422 genes in neonates and adults, respectively. Changes in genes associated with adaptive vascular remodeling and energy homeostasis, as well as regulation of apoptosis, were confirmed by real-time reverse transcriptase polymerase chain reaction. The viability of cardiomyocytes isolated from hypoxic animals was significantly lower than in those from control animals (36.7% ± 13.3% vs 85.0% ± 2.9%, P = .024).

Neonatal hypoxia is associated with significant changes in left ventricular gene expression in both neonatal and adult rats. This may have physiologic implications for the adult myocardium.

From 1996 to 2006, 167 neonates and infants younger than 90 days with simple coarctation underwent repair. Median patient age was 16 days (range, 1–85 days). Median patient weight was 3.4 kg (range, 0.8–6.0 kg), with 29 patients weighing less than 2.5 kg. All 167 patients included in the study underwent repair through a left thoracotomy.

There was 1 early death (1/167, 0.6%). Median follow-up of 4.8 years (range, 0–11.8 years) demonstrated 2 late deaths unrelated to recurrent coarctation. Eighteen patients underwent intervention for recurrent arch obstruction a median of 0.48 years postoperatively (range, 0.14–9.8 years). All were treated with balloon angioplasty and have required no additional intervention. Actuarial freedom from reintervention was 90% at 1 year and 89% at 5 years for infants weighing more than 2.5 kg and 89% at 1 year and 86% at 5 years (P = .31) for infants weighing less than 2.5 kg. There was no difference between survival or reintervention for neonates 30 days of age or younger compared with infants 31 to 90 days of age. Use of polypropylene sutures and female sex did correlate with increased reintervention.

Low weight does not affect survival or reintervention rates after coarctation repair in neonates and infants less than 3 months of age. Balloon angioplasty is an effective treatment for recurrent obstruction after coarctation repair in infancy. In the current era, timing of the operation should be based on clinical status.

This was a retrospective study of consecutive adult patients undergoing surgical intervention between 1995 and 2006. A multivariate logistic regression model was used to identify determinants of prolonged hospitalization.

One hundred sixteen patients (mean age, 36 ± 11 years) underwent 118 pulmonary valve replacements. Most (95%) operations included additional procedures, such as pulmonary artery/outflow tract reconstruction or tricuspid valve annuloplasty. The early postoperative mortality (<30 days) was 2.5%. The majority of the patients (60%) had no postoperative complications. The postoperative adverse events included postoperative arrhythmias (19%), respiratory complications (13%), reoperation during admission (13%), renal dysfunction (13%), and myocardial infarction (3%). Postoperative adverse events were associated with prolonged hospitalization (14 ± 12 vs 7 ± 3 days, P = .001). In the multivariate analysis age at reoperation of greater than 45 years (odds ratio, 6.1; 95% confidence interval, 1.6–23.6; P = .009), the number of previous sternotomies (odds ratio, 3.8; 95% confidence interval, 1.4–10; P = .007), and the need for urgent surgical intervention (odds ratio, 5.7; 95% confidence interval, 1.1–27.8; P = .03) were predictors of prolonged hospitalization.

Pulmonary valve replacement in adults with repaired tetralogy of Fallot has a low mortality risk. The most common early postoperative complications are arrhythmias and respiratory and renal complications. Although most early postoperative complications do not result in long-term sequelae, they are associated with prolonged hospitalization. Patients undergoing urgent interventions, older patients, and those with multiple previous sternotomies are at the highest risk for prolonged hospitalization.

Aminoterminal pro–brain natriuretic peptide plasma levels of 78 patients after the bidirectional Glenn operation with a median age of 3.2 years and a median follow-up time of 3 years were measured by using an automated enzyme immunoassay. The severity of heart failure was quantified by using the New York University Pediatric Heart Failure Index.

The 97.5th percentile of aminoterminal pro–brain natriuretic peptide level in patients without congestive heart failure was 339 pg/mL. Aminoterminal pro–brain natriuretic peptide levels strongly correlated with the New York University Pediatric Heart Failure Index score (P < .001). In patients with congestive heart failure (31/78), the aminoterminal pro–brain natriuretic peptide levels were significantly higher (median, 670 pg/mL) than in patients without congestive heart failure (median, 171 pg/mL). In 41 patients who underwent the Fontan operation, the time to removal of chest tubes and the length of hospital stay positively correlated with the preoperative value of aminoterminal pro–brain natriuretic peptide.

In children with a bidirectional Glenn anastomosis without signs of heart failure, aminoterminal pro–brain natriuretic peptide levels were within the normal range and correlated with the severity of congestive heart failure. Further studies are needed to determine whether aminoterminal pro–brain natriuretic peptide levels can aide clinicians in the early detection of congestive heart failure in this patient group.

This retrospective study reviews the outcome of 787 patients (median age 6.3 months) who underwent primary (598) or staged (189) repair of a conotruncal defect between 1992 and 2007.

Proven genetic syndrome was diagnosed in 211 patients (26.8%), including del22q11 (91 patients), trisomy 21 (29 patients), VACTERL (18 patients), and other syndromes (73 patients). Primary repair was accomplished in 80.9% of nonsyndromic patients and 74.4% of syndromic patients (P = .18) Fifteen-year cumulative survival was 84.3% ± 2.3% in nonsyndromic patients and 73.2% ± 4.2% in syndromic patients (P < .001). Primary and staged repair allowed similar 15-year survival (81.4% ± 4.5% vs 79.1% ± 5.1%, P = .8). Freedom from noncardiac cause of death was significantly lower in syndromic patients (P = .0056). Fifteen-year Kaplan–Meier survival was 87.6% ± 3.9% for del22q11, 95.8% ± 4.1% for trisomy 21, 56.8% ± 6.3% for VACTERL, and 62.3% ± 12.7% for patients with other syndromes (P = .022). Total intensive care unit stay was 10.8 ± 4.9 days in syndromic patients and 5.1 ± 1.7 days in nonsyndromic patients (P < .001). Freedom from reintervention 15 years after repair was 79.6% ± 4.9% in nonsyndromic patients and 62.4% ± 7.4% in syndromic patients (P = .007).

Del22q11 and trisomy 21 do not represent risk factors for mortality after repair of conotruncal anomalies, whereas other syndromes adversely affect the surgical outcome for predominant noncardiac attrition. Higher morbidity and lower mid-term freedom from reintervention can be predicted in syndromic patients.

In 11 patients, aged from 0.8 to 27 years, all with complex congenitally malformed hearts, an unequivocal decision regarding the optimum surgical strategy had not been reached when using standard diagnostic tools. Therefore, we constructed 3-dimensional virtual computer and printed cast models of the heart on the basis of high-resolution whole-heart or cine magnetic resonance imaging or computed tomography. Anatomic descriptions were compared with intraoperative findings when surgery was performed.

Independently of age-related factors, images acquired in all patients using magnetic resonance imaging and computed tomography proved to be of sufficient quality for producing the models without major differences in the postprocessing and revealing the anatomy in an unequivocal 3-dimensional context. Examination of the models provided invaluable additional information that supported the surgical decision-making. The anatomy as shown in the models was confirmed during surgery. Biventricular corrective surgery was achieved in 5 patients, palliative surgery was achieved in 3 patients, and lack of suitable surgical options was confirmed in the remaining 3 patients.

Realistic 3-dimensional modeling of the heart provides a new means for the assessment of complex intracardiac anatomy. We expect this method to change current diagnostic approaches and facilitate preoperative planning.

Retrospective review was conducted on a video-assisted thoracoscopic surgical database including all patients who underwent video-assisted thoracoscopic surgical sympathectomy for palmar hyperhidrosis.

Video-assisted sympathectomy was performed in 282 patients for palmar hyperhidrosis from May 2002 through July 2005; in all, 179 patients (64%) underwent division at T2 level only and 103 at levels T2, T3, and T4. The groups were similar in age and sex distribution. The rate of compensatory hyperhidrosis was significantly less in the T2 group (23 patients, 13%) than in the T2 through T4 group (35 patients, 34%)(P = .011). The most common site of compensatory hyperhidrosis in both groups was the lower back. Patients with compensatory hyperhidrosis were older (median 31 years vs 23 years, P = .037), had body mass index greater than 28 (P = .048), and underwent multiple level sympathectomy (P = .004).

Compensatory hyperhidrosis continues to occur after sympathectomy for palmar hyperhidrosis; however, a significant reduction in incidence can be achieved by dividing the sympathetic chain at a single level (T2). Patients who are older and/or have increased body mass index should be warned of their increased risk of compensatory hyperhidrosis after sympathectomy.

Twelve-centimeter tracheal segments were harvested from Yorkshire boars. Half of each segment was subjected to a detergent–enzymatic method (containing sodium deoxycholate/DNase lavations) of decellularization for as many cycles as needed, and the other half was stored in phosphate-buffered saline at 4°C as a control. Bioengineered and control tracheas were then implanted in major histocompatibility complex–unmatched pigs (allograft) or mice (xenograft) heterotopically for 30 days. Structural and functional analysis and immunostaining were performed after each detergent–enzymatic method cycle and transplantation.

Compared with control tracheas, bioengineered matrices displayed no major histocompatibility complex class I and II antigens after 17 detergent–enzymatic method cycles, without significant (P > .05) differences in their strain ability (rupture force, 56.1 ± 3.3 vs 55.5 ± 2.4 N; tissue deformation at 203% ± 13% vs 200% ± 8% or 12.2 ± 0.8 vs 12 ± 0.5 cm; and applied maximum force, 173.4 ± 3.2 vs 171.5 ± 4.6 N). Thirty days after implantation, significantly (P < .01) smaller inflammatory reactions (392 vs 15 macrophages/mm² and 874 vs 167 T lymphocytes/mm²) and P-selectin expressions (1/6 vs 6/6) were observed in both the xenograft and allograft models with bioengineered matrices compared with those seen with control tracheas. There was no development of anti-pig leukocyte antigen antibodies or increase in both IgM and IgG content in mice implanted with bioengineered tracheas.

Bioengineered tracheal matrices displayed similar structural and mechanical characteristics to native tracheas and excite no immune response to 30 days when implanted as allografts or xenografts. This method holds great promise for the future of tissue-engineered airway replacement.

Records of all patients who underwent resection for adenocarcinoma of the distal esophagus or gastroesophageal junction from 1987 to 2007 were retrospectively reviewed. Based on the endoscopic location of the epicenter of the tumor in relation to the gastroesophageal junction, tumors were categorized in 301 patients as being of the distal esophagus and in 208 as being of the gastroesophageal junction.

There were no significant differences in age, sex, or body mass index between patients with adenocarcinoma of the distal esophagus or gastroesophageal junction. Patients with adenocarcinoma of the distal esophagus were more likely to have reflux symptoms (75% vs 53%, P < .0001) and peritumoral intestinal metaplasia (73% vs 51%, P < .0001) and be in a surveillance program (54% vs 9%, P = .0005) compared with patients with adenocarcinoma of the gastroesophageal junction. However, the prevalence and location of nodal metastases was similar, and in node-positive patients mediastinal node involvement was present in more than 40% of the patients in each group (distal esophageal adenocarcinoma, 47%; gastroesophageal junction adenocarcinoma, 41%). Survival was similar (5 years: distal esophageal adenocarcinoma, 45%; gastroesophageal junction adenocarcinoma, 38%; P = .14), as was the prevalence and type of recurrence.

The prevalence and distribution of lymph node metastases in patients with adenocarcinoma of the distal esophagus and gastroesophageal junction were similar, and after esophagectomy, there was no difference in overall survival or recurrence. Efforts to differentiate between these tumors are unnecessary, and both are effectively treated with esophagectomy.

Consecutive patients with small (≤5 mm) bronchopleural fistulae in proximal airways were included in the study. After measurement of bronchopleural fistula size through a flexible videobronchoscopy, a standard bronchoscopic cytology brush covered with silver nitrate was passed through the working channel of the scope and was rubbed against the fistula's orifice producing blanching and edema on the mucosa. This procedure was repeated until closure of the fistula's orifice (treatment success) or absence of any tissue response after 2 bronchoscopic sessions (treatment failure).

Of 16 patients referred, 5 were excluded from treatment because of large (>5 mm) fistulae. Among the 11 treated patients (median fistula diameter 3 mm, range 2–5 mm), treatment failure was observed in 2 patients in whom treatment was attempted early (15 days postsurgery). In the remaining 9 patients, treatment success was achieved (81.8% success rate) after a median of 2.5 (range 1–10) applications of silver nitrate. After 11 (0.5–24) months of follow-up, no relapse was observed among successfully treated fistulae.

The local application of silver nitrate through a flexible bronchoscopic brush produced a burn and healing process on the mucosa of small bronchopleural fistulae of the central airways, leading to effective and lasting treatment in most cases.

In 40 patients with an adenocarcinoma of the distal esophagus or gastroesophageal junction, blue dye was injected around the tumor intraoperatively. Sentinel nodes (blue-stained) and nonsentinel nodes were identified and dissected during transhiatal esophagectomy. In sentinel nodes negative for tumor cells on routine hematoxylin-eosin examination, multilevel sectioning and immunohistochemical staining were performed to search for micrometastases.

The sentinel node procedure was technically successful in 39 of 40 patients (98%). The median number of sentinel nodes identified was 4. Sentinel nodes were present in more than 1 nodal station in 8 patients (21%). In 6 patients in whom the sentinel node was negative for metastasis, nonsentinel nodes were positive for tumor cells (false-negative rate 6/39 = 15%). Micrometastases and isolated tumor cells were detected in 7 of 19 patients (37%) with sentinel nodes, but this finding did not affect the false-negative rate.

Detection of sentinel nodes is technically feasible during esophagectomy for cancer. However, given the relatively high false-negative rate of 15% and the high frequency of sentinel nodes in more than 1 nodal station, the clinical relevance of the sentinel node concept (through application of the blue dye technique) in the current treatment of patients with an adenocarcinoma of the distal esophagus or gastroesophageal junction seems limited.

This was an experimental animal study, and target segments were established preoperatively. Six adult beagle dogs underwent thoracotomy. After the corresponding pulmonary artery of the target segment had been ligated, indocyanine green was administered intravenously during infrared thoracoscopy. The lung was separated into 2 areas, white and blue, according to the blood flow on the monitor. We marked the visceral pleura with electrocautery along the transition zone showing a change in color from blue to white. The experimental lung was removed and subjected to pathologic and radiologic analysis.

After injection of indocyanine green, infrared thoracoscopy showed that the area of normal perfusion changed to blue, whereas the area at which perfusion was absent remained white. The transition zone between colors was distinct, and the blue stain remained visible during the marking procedure. Three-dimensional computed tomographic analysis indicated that the marking separated the target segmental bronchus from the adjacent one. Detailed macroscopic and microscopic study confirmed that the marking corresponded to the intersegmental line.

By using infrared thoracoscopy with indocyanine green, it is possible to detect the intersegmental line without inflating the lung.

From October 1994 to April 2008, 70 patients were selected for extrapleural pneumonectomy. Univariate analysis was performed using the Kaplan–Meier method and compared using the log-rank test. Multivariate analysis with entering and removing limits of P less than .10 and P greater than .05, respectively, was used. The prognostic factors included age, gender, side of disease, asbestos exposure, histology, positron emission tomography, date of surgery, neoadjuvant chemotherapy, completeness of cytoreduction, lymph node involvement, perioperative morbidity, adjuvant radiotherapy, and pemetrexed-based chemotherapy.

The mean age of patients was 55 years (standard deviation = 10). Fifty-eight patients had epithelial tumors. Six patients received neoadjuvant chemotherapy, 28 patients received adjuvant radiotherapy, and 16 patients received postoperative pemetrexed-based chemotherapy. Forty-four patients had no lymph node involvement. The perioperative morbidity and mortality were 37% and 5.7%, respectively. Complications included hemothorax (n = 7), atrial fibrillation (n = 6), empyema (n = 4), bronchopulmonary fistula (n = 3), right-sided heart failure (n = 2), pneumonia (n = 1), constrictive pericarditis (n = 1), acute pulmonary edema (n = 1), small bowel herniation (n = 1), and disseminated intravascular coagulopathy (n = 1). The median survival was 20 months, with a 3-year survival of 30%. Asbestos exposure, negative lymph node involvement, and receipt of adjuvant radiation or postoperative pemetrexed-based chemotherapy were associated with improved survival on both univariate and multivariate analyses.

The present study supports the use of extrapleural pneumonectomy-based multimodal therapy in carefully selected patients with malignant pleural mesothelioma.

A retrospective analysis of 28 patients undergoing endovascular interventions for acute type B aortic dissection was performed. Kaplan–Meier survival analysis was used for statistical computation.

Indications for emergency endografting were rupture in 4 (14%) patients, severe lower body malperfusion in 8 (29%) patients, visceral/renal malperfusion in 7 (25%) patients, persistent chest pain despite proper anti-impulsive therapy in 5 (18%) patients, uncontrollable hypertension in 1 (4%) patient, and acute dilatation of false lumen with impending rupture in 3 (11%) patients. Three (11%) patients died early. Three patients died during follow-up of non–aorta-related causes. Overall survival was 82% and 78% at 1 and 5 years' follow-up, respectively. The aorta-related mortality was 10% for the entire follow-up period. Complete thrombosis of the false lumen in the thoracic aorta was achieved in 22 (85%) members of the surviving cohort, and partial thrombosis was achieved in the remainder. The rate of treatment failure according to Stanford criteria was 18% at 5 years. Mean follow-up was 36 months, and follow-up was complete in 28 (100%) patients.

Thoracic aortic endografting for complicated acute type B aortic dissection can be performed with a relatively low postoperative morbidity and mortality in experienced hands. The endovascular approach to life-threatening complications of acute type B aortic dissection appears to have a favorable outcome in midterm follow-up.

A total of 157 patients who underwent valve replacement for pure aortic stenosis were reviewed. Late mortality, morbidity, left ventricular mass regression, transprosthetic gradient at rest and after exercise, exercise capacity, and occurrence of arrhythmias were evaluated.

Prosthesis–patient mismatch, defined as an indexed effective orifice area of 0.75 cm²/m² or more, occurred in 96 (61.1%) patients and had no significant impact on early and late mortality. The only independent predictor of mortality was age greater than 65 years. At follow-up, multivariate analysis of prosthetic gradient at rest of 35 mm Hg end exercise capacity or more revealed that both these evidences were associated with high left ventricular mass (P < .001), female gender (P < .001), and follow-up time (P < .001). Arrhythmias occurred during exercise in 34.1% of patients (40/117). Multivariate analysis of occurrence of arrhythmias revealed that they were associated with high mean transprosthetic gradients: values of 50 mm Hg or more during exercise had 95% sensitivity and 72% specificity for predicting arrhythmias.

Prosthesis–patient mismatch failed to demonstrate any significant impact on early and late mortality and morbidity and in left ventricular mass regression. High transprosthetic gradients influence exercise capacity and occurrence of arrhythmias.

Ninety-eight patients with lone aortic insufficiency (≥3+ with a preoperative mean gradient <30 mm Hg) were followed over 7.7 ± 4.3 years (maximum, 17.5 years) with clinical and echocardiographic assessments. They were compared with 707 patients who had aortic valve replacement for aortic stenosis or mixed disease. Prosthesis–patient mismatch was defined as an in vivo indexed effective orifice area of 0.85 cm²/m² or less.

Compared with patients with aortic stenosis/mixed disease, patients with aortic insufficiency had approximately half the incidence of prosthesis–patient mismatch (P = .003). Patients with prosthesis–patient mismatch had significantly higher transprosthesis gradients postoperatively. An independent detrimental effect of prosthesis–patient mismatch on survival was observed in patients with aortic stenosis/mixed disease who had preoperative left ventricular dysfunction (hazard ratio, 2.3; P = .03) but not in patients with aortic insufficiency, irrespective of left ventricular function (hazard ratio, 0.7; P = .7). In patients with aortic stenosis/mixed disease with left ventricular dysfunction, prosthesis–patient mismatch predicted heart failure symptoms by 3 years after aortic valve replacement (odds ratio, 6.0; P = .002), but there was no such effect in patients with aortic insufficiency (P = .8). Indexed left ventricular mass regression occurred to a greater extent in patients with aortic insufficiency than in patients with aortic stenosis/mixed disease (by an additional 29 ± 5 g/m², P < .001), and there was a trend for prosthesis–patient mismatch to impair regression in patients with aortic insufficiency (by 30 ± 17 g/m², P = .1).

The incidence and significance of prosthesis–patient mismatch differs in patients with aortic insufficiency compared with those with aortic stenosis or mixed disease. In patients with aortic insufficiency, prosthesis–patient mismatch is seen less frequently and has no significant effect on survival and freedom from heart failure but might have a negative effect on left ventricular mass regression.

Eleven weeks after coronary ligation, 24 dogs received intramyocardial injections of mononuclear cells (227.106 ± 32.106 cells), mesenchymal stem cells (232.106 ± 40.106 cells), or placebo (n = 8 per group). Cardiac performance and remodeling were assessed up to 16 weeks' follow-up.

At echocardiographic analysis, the wall motion score index showed a sustained improvement after mononuclear cell transfer (from 1.8 ± 0.1 to 1.5 ± 0.07) and a moderate late improvement after mesenchymal stem cell transfer (from 1.9 ± 0.08 to 1.7 ± 0.1). After mononuclear cell transfer, end-systolic elastance increased (from 2.23 ± 0.25 to 4.42 ± 0.55 mm Hg/mL), infarct size decreased (from 13% ± 0.67% to 10% ± 1.17%), N-terminal B-type natriuretic propeptide level decreased (from 608 ± 146 to 353 ± 118 pmol/L), and relative wall area and arterial density increased. Vascular endothelial growth factor receptor 2 expression was upregulated in the border zone. No change in cardiac contractility or histologic parameters was noted in the mesenchymal stem cell group.

In a canine model of chronic myocardial infarction, bone marrow mononuclear cell transfer is superior to mesenchymal stem cell transfer in improvement of cardiac contractility and regional systolic function and reduction in infarct size and plasma N-terminal B-type natriuretic propeptide level. Functional improvement is associated with a favorable angiogenic environment and neovascularization.

Hospital outcome and serial clinical and echocardiographic (preoperative, discharge, 6 months, end of follow-up) follow-up assessments were recorded for 82 consecutive patients with ischemic cardiomyopathy with chronic mitral regurgitation having coronary artery bypass grafting + mitral restrictive annuloplasty (2 sizes ring downsizing). Recurrent ischemic cardiomyopathy with chronic mitral regurgitation was defined by grade ≥ 2 at echocardiography.

Hospital mortality was 4.9%; 17.7 ± 1.7 (standard error) months (range 1–55) survival was 95.5% ± 2.5%. Two-year Kaplan-Meier freedom from reintervention was 94.2% ± 4.2%; from rerevascularization, 87.5% ± 11.7%; from congestive heart failure, 83.8% ± 5.7%; from ischemic cardiomyopathy with chronic mitral regurgitation grade ≥ 2, 46.5% ± 11.2%. Recurrence of ischemic cardiomyopathy with chronic mitral regurgitation gave lower 2-year Kaplan-Meier freedom from death (P = .03) and lower 2-year freedom from congestive heart failure (P = .0001), reintervention (P = .034), and tricuspid insufficiency (P = .0001). Ischemic cardiomyopathy with chronic mitral regurgitation recurrence correlated with worsened New York Heart Association class (P = .0001), left ventricular ejection fraction (P = .024), pulmonary arterial pressures (P = .0001), left ventricular end-diastolic diameter (P = .004), left ventricular end-systolic diameter (P = .014), indexed left ventricular mass (P = .008), and coaptation depth (P = .0001). Independent predictors for recurrent ischemic cardiomyopathy with chronic mitral regurgitation were previous anterior + posterior myocardial infarction (odds ratio 3.70; confidence interval 2.93–5.41; P = .001), preoperative left ventricular end-diastolic diameter ≥ 70 mm (odds ratio 3.91; confidence interval 2.65–5.22; P = .001), and coaptation depth at discharge ≥ 0.5 cm (odds ratio 11.9; confidence interval 5.91–21.34; P = .0001). Preoperative left ventricular end-diastolic diameter ≥ 70 mm correlated with higher congestive heart failure (P = .002), recurrent ischemic cardiomyopathy with chronic mitral regurgitation (P = .0001), worsened New York Heart Association class (P = .0001), and higher diuretics (P = .0001). Coaptation depth < 0.5 cm at discharge accounted for better survival (P = .010), lower incidence of congestive heart failure (P = .0001), lower need for diuretics (P = .0001), and improved New York Heart Association class (P = .0001).

Failure of mitral restrictive annuloplasty is responsible for follow-up mortality and congestive heart failure and correlates with absence of cardiac reverse remodeling. Prognosis of patients having mitral restrictive annuloplasty for ischemic cardiomyopathy with chronic mitral regurgitation is good, as long as a low postoperative coaptation depth is achieved. Patients with significant left ventricular dilation should be considered for different surgical strategies.

Between 2000 and 2003, 285 consecutive patients with coronary artery disease and moderately impaired left ventricular function (ejection fraction 30%–40%) were surgically treated with coronary artery bypass grafting alone (group 1, n = 165) or open left ventricular remodeling in addition to revascularization (group 2, n = 120). Preoperatively, the New York Heart Association class, left ventricular ejection fraction, and end-diastolic diameter were comparable. Early and midterm outcomes, hemodynamic performance, and quality of life assessed by Minnesota Quality of Life Questionnaire were evaluated during a mean follow-up period of 70 months.

Group 2 patients demonstrated significantly longer ventilation times, higher blood loss, and need for blood transfusion but had significantly lower operative mortality (4.5% compared with 8.5% in group 1). Seven-year follow-up demonstrated survival of 74.3% ± 8.1% in group 1 versus 84.2% ± 5.4% in group 2 (P < .05). Follow-up examinations revealed greater improvement of functional class in group 1 with mean 1.7 ± 0.7 versus 2.03 ± 0.8 in group 2 (P < .05). Cardiac-related hospital readmissions were comparable (3.8% vs 4.1%, P = .73).

Patients with ischemic cardiomyopathy, in whom surgical ventricular remodeling was possible and performed, experienced more perioperative complications but had superior early and midterm outcome regarding survival, functional class, and quality of life.

Intraoperative transit-time measurements and postoperative angiographic findings were obtained for 111 patients undergoing coronary artery bypass grafting with gastroepiploic artery and bilateral internal thoracic arteries: mean, maximum, and minimum flows; pulsatility index; insufficiency rate; and differentiated index of early diastolic flow.

Favored target for gastroepiploic artery was posterior descending artery (106 patients, 95%). Patency rates were 91.0% for gastroepiploic artery, 98.2% for left internal thoracic artery, and 97.5% for right internal thoracic artery. There were four flow profiles of gastroepiploic arteries: A (systolic protruded), B (trapezoidal), C (sine waved), and D (diastolic-dominant biphasic). Functional gastroepiploic arteries showed A in 16 cases, B in 6, C in 31, and D in 48, with prevalence according to severity of stenosis in target coronary artery. Two occluded gastroepiploic arteries showed type A, and reverse or competitive flows were types A in 1, B in 1, C in 4, and D in 2. Relative to functional internal thoracic arteries, functional gastroepiploic arteries showed significantly lower minimum flow, higher insufficiency rate, and lower differentiated index of early diastolic flow.

Intraoperative transit-time flow profiles of patent in situ gastroepiploic arterial grafts were classified into four types, closely associated with disease severity of target coronary artery. Patent in situ gastroepiploic arterial grafts show more regurgitant flow and lower differentiated index of early diastolic flow than in situ internal thoracic arterial grafts.

The vascular ring connector is a titanic ring used as a stent in the vascular graft to achieve a quick, blood-sealed, and sutureless anastomosis. From November 2007 to December 2008, 19 consecutive patients (age range 36–77 years; 16 male and 3 female) with aortic dissection underwent open surgery. All patients received aortic reconstruction with vascular grafts (including 5 cases of arch replacement). The combined procedures were 5 Bentall and 4 coronary artery bypass graft operations.

There were no significant blood leaks from the anastomotic sites. The time required for each anastomosis was 1 to 2 minutes. All patients were discharged uneventfully and are still doing well after a follow-up period of 1 to 12 months.

The vascular ring connector may improve the early surgical results of aortic dissection by reducing both the time for anastomosis and the risk of bleeding and may be an alternative technique for aortic reconstruction. Its usefulness in the routine treatment of aortic dissection warrants further evaluation.

A meta-analysis was performed of randomized controlled trials and observational trials reporting the impact of preoperative statin therapy on the incidence of any type and new-onset atrial fibrillation after cardiac surgery. Unadjusted and adjusted treatment effects (odds ratio, 95% confidence intervals) were pooled using a random-effects model, and publication bias was assessed.

Thirteen studies were identified (3 randomized controlled trials, 10 observational trials) that reported the incidence of postoperative atrial fibrillation in 17,643 patients having cardiac surgery with (n = 10,304; 58%) or without (n = 7339; 42%) preoperative statin use. New-onset atrial fibrillation was reported in a total of 7855 patients. Postoperative incidence rates for any or new-onset atrial fibrillation were 24.6% and 29.9%, respectively. Preoperative statin use resulted in a 22% and 34% unadjusted odds reduction for any atrial fibrillation (odds ratio, 0.78; 95% confidence interval, 0.67–0.90) or new-onset atrial fibrillation (odds ratio, 0.66; 95% confidence interval, 0.51–0.84) after surgery (P < .001). Relevant publication bias and an unequal distribution of confounding variables favoring patients treated with statins were identified. Nevertheless, the beneficial actions of statins on atrial fibrillation persisted after pooled analysis of risk-adjusted treatment effects from randomized controlled trials and observational trials (any atrial fibrillation—odds ratio, 0.64; 95% confidence interval, 0.48–0.87; new-onset atrial fibrillation—odds ratio, 0.66; 95% confidence intervals, 0.48–0.89; P < .01).

Our meta-analysis provides evidence that preoperative statin therapy is associated with a reduction in the incidence of atrial fibrillation after cardiac surgery.

We retrospectively analyzed data collected prospectively in the Quality Assurance Database at the Heart Center of the Klinikum Augsburg, Germany. All relevant perioperative data for resources consumption were analyzed and compared in patients with and without excessive postoperative hemorrhage in cardiac surgery. Multivariate regression analysis identified the incremental costs of postoperative hemorrhage while adjusting for potential confounding.

A total of 1118 patients had cardiac surgery between January and December 2006. Six percent were identified with excessive postoperative hemorrhage. The risk of experiencing a postoperative complication (including death) (P < .0001), returning to operating room for reexploration (P < .0001), staying in intensive care unit for longer than 72 hours (P < .0001), receiving ventilation for longer than 24 hours (P < .0001), and receiving any kind of postoperative blood transfusion (P < .0001) was significantly higher in patients with excessive postoperative hemorrhage. Twenty-two percent of patients with excessive postoperative hemorrhage died compared with 6% of the patients without excessive postoperative hemorrhage (P < .0001). When adjusting for potential confounding factors, the incremental costs of excessive postoperative hemorrhage was \#8364;6251 (95% confidence interval, 4594–7909).

The average hospital costs related to excessive postoperative hemorrhage in cardiac surgery in Germany are substantial and associated with a significant risk of postoperative complications and death. Clinical interventions that can effectively prevent or address excessive postoperative hemorrhage in cardiac surgery are likely to have substantial cost-effectiveness potential.

In a retrospective group (group A, n = 12) of patients undergoing elective thoracoabdominal aortic aneurysm surgery, clinically relevant diffuse bleeding after weaning from cardiopulmonary bypass was treated with allogeneic blood products (platelet concentrates, followed by fresh frozen plasma) according to a predetermined algorithm.

In a prospective group (group F, n = 6) a first therapy step with fibrinogen concentrate was added to the algorithm. The dose of fibrinogen concentrate was estimated by using thromboelastometric data (ROTEM FIBTEM). Before each step of hemostatic therapy, blood loss in the range of 60 to 250 g per 5 minutes was confirmed.

In group F, administration of 7.8 ± 2.7 g of fibrinogen concentrate established hemostasis, completely avoiding intraoperative transfusion of fresh frozen plasma and platelet concentrates. Transfusion of blood products after cardiopulmonary bypass and during the 24 hours after surgical intervention was markedly lower in group F than in group A (2.5 vs 16.4 units; 4/6 patients in group F required no transfusion of blood products), as was 24-hour drainage volume (449 vs 1092 mL). Fibrinogen plasma levels, standard coagulation parameters, and hemoglobin and hematocrit values were comparable between the 2 groups on the first postoperative day.

FIBTEM-guided post–cardiopulmonary bypass administration of fibrinogen concentrate resulted in improved intraoperative management of coagulopathic bleeding in thoracoabdominal aortic aneurysm operations and reduced transfusion and 24-hour drainage volume.

In a randomized clinical trial, 156 patients undergoing off-pump coronary artery bypass grafting were assigned to receive either 1 liter of hetastarch or 1 liter of albumin as part of intraoperative volume replacement. Sample recruitment was halted in a review per protocol by the study's Data Safety Monitoring Committee. We assessed the rate of postoperative bleeding by monitoring the number of units of blood products transfused in the first 24 postoperative hours in the intensive care unit and the hourly chest tube drainage in the first 12 postoperative hours.

Intraoperative administration of 1 liter of hetastarch was associated with statistically significant increases in 3 measures: transfusion requirements on postoperative day 1 (red blood cells, 1.14 vs 0.40 units, P = .017; fresh-frozen plasma, 0.57 vs 0.15, P = .009; platelets, 0.35 vs 0.10, P = .013); the overall likelihood of receiving transfusion on postoperative day 1 (46.2% vs 25.6%, P = .012); and the volume of chest tube drainage in the first 12 hours postoperatively (732.0 vs 563.6 mL, P < .001).

In patients undergoing off-pump coronary artery bypass, the intraoperative administration of hetastarch increases the postoperative transfusion requirement and the volume of blood drained postoperatively.

Six pigs had median sternotomy followed by negative pressure wound therapy at –75, –125, and –175 mm Hg. Real-time magnetic resonance imaging movies (10 images/s) were acquired in a midventricular transverse plane or a midsagittal plane during the application of negative pressure wound therapy.

Similar finding were observed at all different negative pressures studied. Negative pressure wound therapy caused the heart to be displaced toward the thoracic wall, and in some cases, the right ventricular free wall bulged into the space between the sternal edges, and the sharp edges of the sternum jutted into and deformed the anterior surface of the right ventricular free wall. These events were not affected by the interposition of 4 layers of paraffin gauze dressing but were hindered by the placement of a rigid barrier between the anterior portion of the heart and the inside of the thoracic wall.

The results show altered position of the heart in relation to the sternum during negative pressure wound therapy. This may explain 2 potentially hazardous events associated with negative pressure wound therapy, namely, risk for heart rupture and reduced cardiac output. Inserting a rigid barrier over the heart may be a protective measure that is clinically practicable.

Expansible rings were composed of an elastomer core covered by polyester fabric. After in vitro analysis of their mechanical properties, the rings were implanted in 6 sheep at both the level of the annular base and sinotubular junction (double subvalvular and supravalvular external aortic annuloplasty). Root dynamics were assessed by using intracardiac ultrasonography before surgical intervention and at 6 months. Histologic, scanning electron microscopic, and mechanical studies were then performed on explanted samples.

The expansible ring produced a significant reduction of the aortic annular base and sinotubular junction diameters. Coaptation height was increased from 2.5 ± 0.7 mm to 6.2 ± 1.1 mm (P < .001). Mechanical testing on 6-month explanted samples revealed no significant differences in elastic modulus. Dynamics of the root were well preserved. Histomorphologic studies showed incorporation of the material without degradation.

Expansible aortic ring implantation produces a significant annuloplasty that increases coaptation height while preserving the dynamics of the aortic root. The effectiveness of the device in treating aortic insufficiency is currently being evaluated in the prospective Conservative Aortic Valve surgery for aortic Insufficiency and Aneurysm of the Aortic Root trial comparing conservative aortic valve surgery versus mechanical valve replacement.

Heart tissue of 19 patients with bacterial endocarditis and 10 controls without bacterial endocarditis was analyzed by immunohistochemistry. The effect of human recombinant Deleted in Malignant Brain Tumors 1 on erythrocyte aggregation was measured using an automated red blood cell aggregometer MA1. Binding of human recombinant Deleted in Malignant Brain Tumors 1 to erythrocyte membranes, platelets, fibrin, and fibrinogen was analyzed by Western blotting and enzyme-linked immunosorbent assay.

Deleted in Malignant Brain Tumors 1 expression was up-regulated in affected heart valves with bacterial endocarditis and limited to the colonizing bacteria on the heart valves and granulocyte-depleted fibrin/fibrinogen formations, and around localized atheromatosis. Patients with aggressive bacteria showed higher DMBT1 levels than patients with less aggressive bacteria. Human recombinant Deleted in Malignant Brain Tumors 1 aggregates erythrocytes and binds to erythrocyte membranes, platelets, and fibrin/fibrinogen.

Deleted in Malignant Brain Tumors 1 up-regulation at sites of bacterial endocarditis, its association with platelets and fibrin/fibrinogen, and its ability to aggregate erythrocytes through binding to their membranes indicate a potential role in the development of vegetations and thrombosis.

Percutaneous pulmonary valve replacement was first performed in 6 sheep used a homemade valved stent. Two months after the initial procedure, the 6 sheep previously implanted with a valved stent underwent the same implantation procedure of a pulmonary valved stent. Hemodynamic assessment of the bioprosthetic pulmonary valve was obtained by echocardiography immediately post-implant and at 2 months follow-up.

All 6 sheep had successful transcatheter stent-mounted pulmonary valve replacement in the first experiment. After 2 months, reimplantation was successful in 5 sheep but failed in 1 sheep because the first valved stent was pushed to the bifurcation of the pulmonary artery by the delivery sheath. Echocardiography confirmed the stents were in the desired position during the follow-up. The remaining 5 sheep with normal valvular and cardiac functionality survived for 3 months after implantation.

Transcatheter stent-mounted bioprosthetic pulmonary valve reimplantation is feasible in an animal model and more convenient than open chest reimplantation.

A retrospective review identified 9 patients aged 4.1 to 45.6 years (median, 25.4 years) with pulmonary atresia and ventricular septal defect who underwent heart–lung transplantation. Four (44.4%) patients had previous heart operations: 3 of them had palliative procedures (systemic-to-pulmonary shunts), and 1 had multistage correction. A standard transplantation method was used, with the exception of 1 patient with heterotaxy syndrome who underwent a modified operation. Major aortopulmonary collateral arteries were controlled by using various techniques.

Follow-up ranged between 2 days and 12.6 years (median, 1.2 years). The hospital mortality rate was 22.2% (n = 2). In the late postoperative period, 3 patients died. The survival curve was similar to that of patients with other diagnoses undergoing heart–lung transplantation. The median length of intensive care unit stay was 58 days (range, 22–82 days), and the median length of hospital stay was 83 days (range, 35–136 days). The most common early complication was bleeding requiring re-exploration. In all cases the bleeding was proved to be from collateral vessels.

Heart–lung transplantation in patients with pulmonary atresia and ventricular septal defect requires carefully planned and meticulously performed surgical intervention. This management should be taken into consideration as a future option if the specific anatomy is uncorrectable in early childhood, and the palliative procedures should be avoided.

Experiments were performed by using an allomismatched rat heterotopic heart transplantation model. Recipients were treated with cyclosporine with or without pioglitazone and were divided into one of 4 groups: group I, no treatment; group II, low-dose cyclosporine (2 mg · kg^–1 · d^–1); group III, high-dose cyclosporine (5 mg · kg^–1 · d^–1); and group IV, low-dose cyclosporine with pioglitazone (3 mg · kg^–1 · d^–1).

Cyclosporine-treated rats showed significantly longer graft survival and less graft rejection but severe renal damage in a dose-dependent manner. Compared with group II, treatment with pioglitazone with low-dose cyclosporine (group IV) significantly suppressed graft infiltration of CD4/CD8 T lymphocytes and serum concentrations of interleukin 2 and interferon , leading to extended graft survival up to 60 days. These immunosuppressive effects in group IV were equivalent to those in group III. In addition, recipient kidneys in group IV had few apoptotic cells, possibly through upregulation of peroxisome proliferator–activated receptor and downregulation of transforming growth factor β1, and maintained stable renal functions, as evidenced by a normalization of blood urea nitrogen, creatinine, and creatinine clearance values. In vitro experiments also confirmed the renoprotective effects of pioglitazone on cyclosporine-induced toxicity.

Collectively, pioglitazone can reduce a dose of cyclosporine with sufficient immunosuppressive effects. Pioglitazone treatment with low-dose cyclosporine has synergistic protective effects for cardiac allografts and recipient kidneys, leading to improvement of graft survival with a minimal cyclosporine-induced nephrotoxicity.

Male Fisher 344 donor lungs were cold preserved in a low-potassium dextrose solution in the presence or absence of APT102 for 18 hours prior to transplantation into syngeneic male Fisher 344 recipients. Seven minutes after reperfusion, lung transplant recipients received either a bolus of APT102 or vehicle (saline solution). Four hours after reperfusion, APT102- and saline solution–treated groups were evaluated for lung graft function and inflammation.

APT102 significantly reduced lung graft extracellular pools of adenosine triphosphate and adenosine diphosphate, improved oxygenation, and protected against pulmonary edema. Apyrase treatment was associated with attenuated neutrophil graft sequestration and less evidence of tissue inflammation as assessed by myeloperoxidase activity, expression of proinflammatory mediators, and numbers of apoptotic endothelial cells.

Administration of a soluble recombinant apyrase promotes lung function and limits the tissue damage induced by prolonged cold storage, indicating that extracellular purigenic nucleotides play a key role in promoting ischemia–reperfusion injury following lung transplantation.

Human umbilical vein endothelial cells underwent simulated cold ischemia by replacing 37°C culture media with 4°C Perfadex (Vitrolife, Kungsbacka, Sweden) solution for 5 hours in 100% O₂. Culture dishes were allowed to warm to room temperature for 1 hour (implantation), and then Perfadex solution was replaced with 37°C culture media (reperfusion).

During cold ischemia, the human umbilical vein endothelial cell filamentous actin cytoskeleton quickly became rearranged, and gaps developed in the previously confluent monolayer occupying 20% of the surface area. Simulated reperfusion resulted in reorganization to a confluent monolayer. Development of gaps was not due to enhanced necrosis based on lactate dehydrogenase retention assay. Endothelial cytoskeletal rearrangement could account for early edema caused by ischemia–reperfusion injury with reperfusion. Mitogen-activated protein kinase and nuclear factor B activation occurred with simulated reperfusion despite normoxia. Levels of the proinflammatory cytokines interleukin 6 and interleukin 8 were significantly increased in media at the end of reperfusion.

Exposing human umbilical vein endothelial cells to simulated cold ischemia without hypoxia causes reversible cytoskeletal alterations, activation of inflammatory pathways, and elaboration of cytokines. Because this model accurately depicts events occurring during lung transplantation, it will be useful to explore mechanisms regulating lung cell response to this unique form of ischemia–reperfusion injury.