From 1989 to 2008, 216 patients entered a pathway aiming for complete repair by unifocalizing major aortopulmonary arteries to a right ventricle-pulmonary artery conduit with ventricular septal defect closure. Where ventricular septation was not possible, definitive repair was considered to include pulmonary artery reconstruction and a right ventricle-pulmonary artery conduit or systemic shunt. Native pulmonary artery morphology was classified into confluent intrapericardial (n = 139), confluent intrapulmonary (n = 51), and nonconfluent intrapulmonary (n = 26).

A total of 203 patients (85%) had definitive repair at a median age of 2.0 years. There was no statistically significant difference in survival after complete repair among the 3 morphologic pulmonary artery groups (P = .18). A total of 132 patients (56%) had complete repair with ventricular septal defect closure, as a single procedure in 111 patients and a staged procedure in 21 patients. Focalization of major aortopulmonary collateral arteries with proven long-term patency with the right ventricle was associated with a survival benefit compared with 14 patients in whom unifocalization was not possible and who had only systemic shunts. Overall survival was 89% at 3 years after definitive repair. During follow-up, 190 patients required 196 catheter reinterventions and 60 surgical reinterventions.

By using a strategy of unifocalization, intrapericardial pulmonary artery reconstruction, and right ventricle-pulmonary artery conduit, excellent long-term survival can be achieved in this group of patients even in the absence of native intrapericardial pulmonary arteries.

All patients with borderline left heart structures and endocardial fibroelastosis who underwent a primary left ventricular rehabilitation procedure were retrospectively analyzed to determine operative mortality, reintervention rates, and hemodynamic status. Left heart dimensions and hemodynamics were recorded from preoperative and postoperative echocardiogram and cardiac catheterization. Postoperative left atrial pressure was obtained from the intracardiac line early after left ventricular rehabilitation. Preoperative and postoperative values were compared by paired t test.

Between 1999 and 2008, 9 patients with endocardial fibroelastosis and borderline left heart disease underwent left ventricular rehabilitation at a median age of 5.6 months (range, 1–38 months). There was no operative mortality, and at a median follow-up of 25 months (6 months to 10 years) there was 1 death from noncardiac causes and 2 patients required reoperations. Significant increases in ejection fraction and left ventricular end-diastolic volume were observed, whereas left atrial pressure and right ventricular/left ventricular pressure ratios decreased postoperatively.

In patients with borderline left hearts, primary left ventricular rehabilitation with endocardial fibroelastosis resection and mitral and aortic valvuloplasty results in improved left ventricular systolic and diastolic performance and decreased right ventricular pressures. This approach may provide an alternative to single-ventricle management in this difficult patient group.

We examined 56 autopsy specimens and reviewed another series of 12 consecutive patients with the malformation. Truncal origin was categorized as 1 of the following 5 types: exclusive origin from either the right or left ventricle, predominant origin from either ventricle, or balanced origin. We measured the size of ventricular septal defect ("width" and "depth") in specimens for any correlation with truncal origin.

Balanced origin was seen in approximately one half of cases in both autopsy and clinical series. Predominantly or exclusively right ventricular origin was more prevalent than left ventricular origin in autopsy series (40% vs 9%, respectively), but such predilection was not observed in clinical series (both 25%). The more the truncal valve was committed to the right ventricle, the smaller was the "width" of the ventricular septal defect (predominant and exclusive vs balanced origin; both P < .0001), with similar tendency in the "depth." In 1 heart with extreme right ventricular origin, the defect was slit-like.

Origin of the truncal valve demonstrated a morphologic spectrum and correlated with the size of ventricular septal defect that was the main or even sole exit from the left ventricle in hearts with right ventricular origin. Truncal origin, therefore, requires recognition to optimize surgery.

Immature Yorkshire piglets were assigned to one of four study groups: (1) deep hypothermic circulatory arrest at 18°C, (2) deep hypothermic circulatory arrest at 18°C with selective cerebral perfusion, (3) moderate hypothermic circulatory arrest at 25°C with selective cerebral perfusion, or (4) age-matched control animals without surgery. Animals undergoing cardiopulmonary bypass were cooled to their assigned group temperature and exposed to 1 hour of hypothermic circulatory arrest. After arrest, animals were rewarmed, weaned off bypass, and allowed to recover for 4 hours. Cerebrospinal fluid collected from surgical animals after the recovery period was compared with cerebrospinal fluid from controls by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry. Protein spectra were analyzed for differences between groups by Mann–Whitney U test and false discovery rate analysis.

Baseline and postbypass physiologic parameters were similar in all surgical groups. A total of 194 protein peaks were detected. Compared with controls, groups 1, 2, and 3 had 64, 100, and 13 peaks that were significantly different, respectively (P < .05). Three of these peaks were present in all three groups. Cerebrospinal fluid protein profiles in animals undergoing cardiopulmonary bypass with moderate hypothermic circulatory arrest (group 3) were more similar to controls than either of the groups subjected to deep hypothermia.

The mass spectra of cerebrospinal fluid proteins are altered in piglets exposed to cardiopulmonary bypass and hypothermic circulatory arrest. Moderate hypothermic circulatory arresst (25°C) with selective cerebral perfusion compared with deep hypothermic circulatory arrest (18°C) is associated with fewer changes in cerebrospinal fluid proteins, when compared with nonbypass controls.

We reviewed outcomes of major lung resection in The Society of Thoracic Surgeons General Thoracic Surgery Database from 2002 to 2008 to determine the relationship of diffusing capacity (expressed as percent of predicted) to postoperative pulmonary complications stratified by chronic obstructive pulmonary disease status.

Percent of predicted diffusing capacity was measured in 7891 (57%) patients. There were 3905 women and 3986 men with a mean age of 66.3 ± 10.6 years who underwent lobectomy (6904; 87.5%), bilobectomy (463; 5.9%), and pneumonectomy (524; 6.6%). Chronic obstructive pulmonary disease was identified in 2711 (34.4%) patients. Pulmonary complications occurred in 13%, and the operative mortality was 1.9%. Percent of predicted diffusing capacity was strongly associated with the development of pulmonary complications (odds ratio, 1.12 per 10-point decrease; P < .0001). Decreasing percent of predicted diffusing capacity was incrementally related to an increased incidence of pulmonary complications regardless of chronic obstructive pulmonary disease status. There was no apparent interaction between percent of predicted diffusing capacity and chronic obstructive pulmonary disease status in the predictive model.

Percent of predicted diffusing capacity predicts pulmonary complications after lung resection in patients without chronic obstructive pulmonary disease. We recommend measurement of diffusing capacity in lung resection candidates, regardless of chronic obstructive pulmonary disease, as an important element in the accurate assessment of operative risk.

One hundred forty-four patients with pulmonary adenocarcinoma underwent surgery in our institute from 2000 to 2008. We used immunohistochemical analysis and real-time reverse-transcriptase polymerase chain reaction to determine the expression of DYRK2 and compared this with the clinicopathologic factors and survival.

We found no correlation between DYRK2 expression by immunohistochemical and clinicopathologic factors; however, a negative nodal status and negative lymphatic invasion were significantly associated with DYRK2 expression by reverse-transcriptase polymerase chain reaction. Five-year disease-free survival in the DYRK2-positive group (75.4%) was significantly different from that in the negative group (55.4%; P = .03) by immunohistochemical analysis. The 5-year overall survival of 89.2% in the DYRK2-positive group was better than the 66.3% survival of the DYRK2-negative group (P = .01). Quantitative real-time reverse-transcriptase polymerase chain reaction analyses showed a significant difference between positive and negative expressions for disease-free survival (P = .003) and overall survival (P = .007). In multivariate Cox regression analysis, negative DYRK2 protein and messenger RNA expression showed a worse prognostic value of survival (hazard ratio [HR] = 4.7, 95% confidence intervals [CI] = 1.5–14.5, P=.007; HR = 2.5, 95% CI = 1.1–6.1, P = .04, respectively). When we analyzed adenocarcinoma cases except for bronchioloalveolar carcinoma, we found a close correlation between DYRK2 expression by immunohistochemical analysis and nodal status (P = .03). Furthermore, disease-free survivals between positive and negative groups of DYRK2 expression by immunohistochemistry (P = .03) and reverse-transcriptase polymerase chain reaction (P = .02) without bronchioloalveolar carcinoma were significantly different. Overall survivals in both groups showed significant differences by immunohistochemistry (P = .02) but not by reverse-transcriptase polymerase chain reaction (P = .08).

These data showed that DYRK2 expression is associated with a favorable prognosis.

Recurrence patterns, time to recurrence, and median survival were examined in 267 patients who had esophagectomy after neoadjuvant chemoradiation therapy at Johns Hopkins over 19 years.

Of 267 patients, 82 (30.7%) showed complete response to neoadjuvant therapy, with 108 (40.4%) and 77 (28.8%) showing partial response or no response, respectively. Recurrence developed in 84 patients (patients with complete response 18/82, 21.4%; patients with partial response 39/108, 36.1%; patients with no response 27/77, 35.1%; P = .055, respectively). Most patients had recurrences at distant sites (65/84;77.4%) regardless of pathologic response, and subsequent survival was brief (median 8.37 months). Median disease-free survival was short (10 months) and did not differ based on recurrence site for patients with partial response or no response, but was longer for patients with complete response with distant recurrence, whose median disease-free survival was 27.3 months (P = .008). By multivariate analysis, no other factor except for pathologic response to neoadjuvant therapy was associated with disease recurrence or death. Patients with partial response or no response were 1.97 and 2.23 times more likely to have recurrence than patients with complete response (P = .024 and P = .012, respectively).

Most esophageal cancer recurrences after neoadjuvant therapy and surgery are distant, and survival time after recurrence is short regardless of pathologic response. Fewer patients achieving complete response had recurrences, and distant recurrences in these patients manifest later than in patients showing partial response and those showing no response. Only pathologic response is significantly associated with disease recurrence, suggesting that tumor biology and chemosensitivity are critical in long-term patient outcome.

A total of 225 consecutive anatomic segmentectomies were performed for stage IA (n = 138) or IB (n = 87) non–small-cell lung cancer from 2002 to 2007. Primary outcome variables included hospital course, complications, mortality, recurrence, and survival. Statistical comparisons were performed utilizing the t test and Fisher exact test. The probability of overall and recurrence-free survival was estimated with the Kaplan-Meier method, with significance being estimated by the log-rank test.

Mean age (69.9 years) and gender distribution were similar between the video-assisted thoracic surgery and open groups. Average tumor size was 2.3 cm (2.1 cm video-assisted thoracic surgery; 2.4 cm open). Mean follow-up was 16.2 (video-assisted thoracic surgery) and 28.2 (open) months. There were 2 perioperative deaths (2/225; 0.9%), both in the open group. Video-assisted thoracic surgery segmentectomy was associated with decreased length of stay (5 vs 7 days, P < .001) and pulmonary complications (15.4% vs 29.8%, P = .012) compared with open segmentectomy. Overall mortality, complications, local and systemic recurrence, and survival were similar between video-assisted thoracic surgery and open segmentectomy groups.

Video-assisted thoracic surgery segmentectomy can be performed with acceptable morbidity, mortality, recurrence, and survival. The video-assisted thoracic surgery approach affords a shorter length of stay and fewer postoperative pulmonary complications compared with open techniques. The potential benefits and limitations of segmentectomy will need to be further evaluated by prospective, randomized trials.

Patients having cardiogenic shock owing to acute coronary syndrome and ST-segment elevation myocardial infarction who required hemodynamic support with intra-aortic balloon counterpulsation were retrospectively retrieved from the clinical information system in a tertiary medical center in Taiwan. A propensity score–based matching process was applied to find equalized groups with documented involvement of more than 2 coronary vessels who received percutaneous coronary intervention only (PCI only group) and who underwent subsequent coronary artery bypass graft surgery after percutaneous coronary intervention (PCI+CABG group). A logistic regression model was used to find the factors associated with 30-day mortality.

The propensity analysis identified 44 patients in the PCI only group (35 men, 65 ± 2 years, and 9 women, 75 ± 4 years) and the other 44 patients in the PCI+CABG group (31 men, 67 ± 2 years, and 13 women, 71 ± 2 years) who had comparable baseline characteristics. The 30-day mortality, 40.9% in the PCI only group and 20.5% in the PCI+CABG group, was positively associated with percutaneous coronary intervention only (odds ratio, 3.33; 95% confidence intervals, 1.14–10.0; P = .03), increased age (odds ratio, 1.06 for each year; 95% confidence intervals, 1.01–1.12; P = .01) and a need to use extracorporeal membrane oxygenation (odds ratio, 9.64; 95% confidence intervals, 2.19–42.4; P < .001).

This study has shown the survival benefit of surgical intervention in high-risk patients with acute coronary syndrome or ST-segment elevation myocardial infarction who had cardiogenic shock after percutaneous coronary intervention.

From February 2005 to October 2007, the prospectively collected data of 18 consecutive patients undergoing hybrid repair were analyzed. Median age was 73 years; Crawford–Safi extent included 2 type I, 8 type II, 7 type III, and 1 type V thoracoabdominal aortic aneurysms; 13 were atherosclerotic and 5 were postdissecting aneurysms. Previous open or endovascular aortic surgery had been performed in 11 (61.1%) patients. Society for Vascular Surgery/North American Chapter of the International Society for Cardiovascular Surgery preoperative risk stratification identified mild-to-severe hypertension and pulmonary and cardiac status in 88.9%, 67.7%, and 88.9% of the patients, respectively.

Fifty-four visceral vessels were bypassed in 18 patients. As an adequate inflow site, the common iliac artery was identified in 15 (83.3%) patients, the infrarenal native aorta was identified in 1 (5.6%) patient, and a previous tube graft was identified in 2 (11.1%) patients. Median operating time was 360 minutes (range, 210–600 minutes), and median blood loss was 3200 mL (range, 1000–18,000 mL). Aneurysm exclusion was achieved in 17 patients. Thirty-day mortality was 16.7% (n = 3/18). Complications included paraplegia (n = 1) and acute myocardial infarction (n = 2). Median follow-up was 23 months (range, 8–42 months), with visceral graft patency at follow-up or death of 98.1% (n = 53/54). One early and 1 late type Ia endoleak (11.8%, n = 2/17), no type III endoleaks, and 5 type II endoleaks were detected, none necessitating adjuvant procedures.

The visceral hybrid repair is a feasible and relatively safe procedure for extensive thoracoabdominal aortic aneurysms. Even considering the significantly high mortality and morbidity rates, it might represent a viable alternative in a cohort of patients historically deemed at high risk for traditional surgical intervention.

One hundred ninety-two asymptomatic patients (mean age, 63 ± 13 years) with severe degenerative mitral regurgitation diagnosed by 2-dimensional echocardiography between 1990 and 2001 were prospectively followed for a median of 8.5 years.

Overall, cardiovascular, and event-free survival was evaluated in 2 groups of patients: a "conservative approach" group (n = 67) and an "early surgery" group (n = 125). Outcomes were also analyzed among patients with atrial fibrillation, pulmonary hypertension, or both, as well as in patients free of any mitral regurgitation complications. In the whole population, 10-year overall survival was significantly lower with the conservative approach than early surgery (50% ± 7% vs 86% ± 4%, log-rank < 0.0001). Similar results were obtained in the subgroups with atrial fibrillation and/or pulmonary hypertension. The 10-year propensity-matched score-adjusted hazards ratio for overall mortality, cardiac mortality, and cardiovascular events for the conservative treatment were 5.21, 4.83, and 4.40, respectively.

Our results show that the outcome of asymptomatic patients with severe degenerative mitral regurgitation is better with an early surgical approach rather than a more conservative treatment strategy.

Between 1979 and 2003, 195 consecutive patients underwent repair for acute ascending aortic dissection within 2 weeks of the onset of symptoms. Mean follow-up was 7.0 ± 5.9 years (range, 0–26 years) and was 100% complete.

Patients were aged 62 ± 15 years on average and were mostly male (66%) and hypertensive (69%). Risk of death early and late after the operation decreased over the study period, with hospital mortality decreasing from 21% to 4% when comparing the first and most recent quartiles (P = .007, ² test for trend). At 1, 5, 10, and 20 years postoperatively, survival was 84%, 69%, 55%, and 30%, respectively, and freedom from cardiovascular death was 86%, 80%, 71%, and 51%, respectively. Additional independent risk factors for death were older age (P < .001), renal dysfunction (P < .003), syncope (P = .007), and peripheral vascular disease (P = .006). During the study period, echocardiographic and computed tomographic diagnostic imaging replaced routine aortic angiographic analysis, and operative techniques involved more frequent use of open distal anastomoses, retrograde cerebral perfusion, earlier restoration of antegrade perfusion, and a conservative approach to aortic arch repair. Freedom from reoperation on the aorta or aortic valve was 93% and 84% at 5 and 10 years, respectively.

Early and late survival after repair of acute ascending aortic dissection has improved progressively over 25 years in association with noticeable changes in preoperative and intraoperative management. Aortic reoperations were infrequent during follow-up.

Between April 2003 and June 2007, 107 patients (17 women, 90 men; mean age, 45 ± 11 years; range, 17–78 years) with acute type A dissection underwent total arch replacement combined with stented elephant trunk implantation under hypothermic cardiopulmonary bypass and selective cerebral perfusion. Computed tomography was performed to evaluate the residual false lumen in the descending aorta during follow-up.

Thirty-day mortality was 3.74% (4/107 patients), and in-hospital mortality was 4.67% (5/107 patients). Spinal cord injury was observed in 3 patients (1 patient with left lower-extremity paraparesis and 2 patients with paraplegia). Cerebral infarction was observed in 3 patients, ventilator support exceeding 5 days was required in 9 patients, and rebleeding was observed in 4 patients. During a mean follow-up of 35 ± 14 months, 3 patients died and 3 patients were lost to follow-up. On postoperative computed tomography, complete thrombus formation was observed around the stented elephant trunk in 95% of patients (95/100) and at the diaphragmatic level in 69% of patients (69/100).

Low morbidity and mortality were achieved using total arch replacement combined with stented elephant trunk implantation. These encouraging surgical results and postoperative outcomes favor this more aggressive procedure for acute type A dissection.

A total of 276 patients (174 men; mean age 59.5 ± 13.4 years) underwent surgery for acute type A dissection between October 1994 and January 2008. Preoperative malperfusion syndromes were diagnosed in 93 (33.7%) patients (group I) and involved coronary circulation in 41 (15%) patients, central nervous system in 39 (14%) patients, limb ischemia in 32 (11.6%) patients, and mesenteric circulation in 8 (3%) patients. Postoperative results were compared between patients with preoperative malperfusion and those without this complication (group II, n = 183).

In-hospital mortality was 29.0% in group I versus 13.6% in group II (P = .002). The postoperative intensive care unit stay was longer (11.4 ± 9.7 vs 7.7 ± 6.9 days; P = .04) in the malperfusion group. A total of 6 (75%) patients with mesenteric malperfusion died. Long-term follow-up (range, 1–122 months postoperatively) was available in 100% of survivors. One-year and 5-year overall survivals were 49.8% ± 11.8% and 41.8% ± 12.6% in group I versus 70.4% ± 7.6% and 56% ± 10.4% in group II (P = .005). Cox regression analysis identified preoperative malperfusion as a significant risk factor for long-term mortality after surgery for type A dissection (hazard ratio, 1.7; 95% confidence intervals, 1.2–3.1).

Preoperative malperfusion is a significant risk factor influencing perioperative and long-term survival after surgery for acute type A dissection. Percutaneous interventional procedures and delayed surgery should be considered in patients with clinically apparent mesenteric malperfusion because of the dismal prognosis of immediate surgical therapy.

We prospectively enrolled 282 cardiac surgery patients undergoing cardiopulmonary bypass and assigned a RIFLE and Acute Kidney Injury Network class to each patient. The incidence of acute kidney injury and in-hospital mortality across classes was compared by using the ² test, and their prognostic value was compared by using the area under the curve receiver-operating characteristic for in-hospital mortality.

According to the RIFLE (45.8%) or Acute Kidney Injury Network (44.7%) classification, a similar proportion of patients had acute kidney injury. There was large agreement between classifications according to patients graded as having nonacute kidney injury; however, there was some disagreement across classes for staging the severity of acute kidney injury. The area under the curve for in-hospital mortality was similar for all classifications: 0.91 for the RIFLE classification (95% confidence interval, 0.82–0.99) and 0.94 for the Acute Kidney Injury Network classification (95% confidence interval, 0.81–0.97; P = .6 for area under the curve comparison).

In patients undergoing cardiac surgery, modifications of the RIFLE classification for acute kidney injury do not materially improve the clinical usefulness of the definition. Other factors, such as the applicability of the acute kidney injury definition and classification system to be applied, need to be considered.

Data were obtained from the University HealthSystem Consortium database. We conducted a retrospective analysis of data of 15,067 adults who had coronary artery bypass grafting between 2003 and 2006 and received perioperative aspirin alone or in combination with clopidogrel, with the latter administered within 2 days after coronary artery bypass grafting. Logistic regression was used to analyze in-hospital mortality, 30-day readmission, ischemic or thrombotic events, and bleeding events, with propensity score adjustment for clopidogrel treatment.

Combined aspirin and clopidogrel were used in 3268 patients (22%). Compared with aspirin alone, aspirin plus clopidogrel was associated with reductions of in-hospital mortality (0.95% vs 1.78%; adjusted odds ratio: 0.50; 95% confidence interval: 0.25, 0.99) and bleeding events (4.19% vs 5.17%; adjusted odds ratio: 0.70; 95% confidence interval: 0.51, 0.97). Ischemic or thrombotic events were not significantly different (1.29% vs 1.53%; adjusted odds ratio, 0.99; 95% confidence interval: 0.59, 1.64). The relative effect of combined treatment did not differ between on-pump and off-pump coronary artery bypass grafting.

Early postoperative clopidogrel combined with aspirin may be safe and beneficial compared with perioperative aspirin treatment alone, in both on-pump and off-pump coronary artery bypass grafting. However, a possibility of selection bias calls for randomized controlled trials to confirm our findings.

Eighteen adult dogs were randomized equally into 3 groups. Leukocyte-depleting filters were used for 10 minutes in the LD-S group, throughout cardiopulmonary bypass in the LD-T group, and not used in the control group. Neutrophil counts, elastase, and interleukin-8 concentrations in plasma, myeloperoxidase and interleukin-8 concentrations in pulmonary tissue, and pulmonary vascular resistance and oxygen index were determined to evaluate the inflammatory response and damage to pulmonary function.

Although the neutrophil count and pulmonary parenchymal myeloperoxidase contents were significantly lower in both LD-S and LD-T groups than that in the control group, lower pulmonary parenchymal interleukin-8 level, lower pulmonary vascular resistance (113 ± 33 dyne · s/cm⁵), higher oxygen index (366 ± 82.3 mm Hg), and thinner alveolus wall thickness were seen only in the LD-S group, and the pulmonary parenchymal interleukin-8 levels were also lower in the LD-S group after cardiopulmonary bypass. The plasma elastase and interleukin-8 levels were significantly lower in the LD-S group, but they were significantly higher in the LD-T group compared with the control group after cardiopulmonary bypass.

Short-term rather than prolonged leukocyte depletion during cardiopulmonary bypass appears to be more efficacious in protecting pulmonary function via attenuation of the extracorporeal circulation–induced inflammatory response.

Abdominal aortas from C57B6 mice (n = 79) were perfused with elastase or saline (control) and harvested at 1, 3, 7, or 14 days. Aortas were analyzed by means of quantitative polymerase chain reaction and immunohistochemistry for smooth muscle cell marker genes, including SM22A, smooth muscle -actin, and matrix metalloproteinases 2 and 9. In complimentary experiments human aneurysms (n = 10) and control aorta (n = 10) were harvested at the time of surgical intervention and analyzed.

By 14 days, aortic diameter was larger after elastase perfusion compared with control diameter (100% ± 9.6% vs 59.5% ± 18.9%, P = .0002). At 7 days, elastase-perfused mice had a 78% and 85% reduction in SM22 and smooth muscle -actin expression, respectively, compared with that seen in control animals well before aneurysms were present, and these values remained repressed at 14 days. Immunohistochemistry confirmed less SM22 and smooth muscle -actin in experimental aneurysms at 14 days in concert with increased matrix metalloproteinase 2 and 9 expression at 7 and 14 days. Similarly, human aneurysms had less SM22 and smooth muscle -actin and increased matrix metalloproteinase 2 and 9 staining, compared with control values, as determined by means of quantitative polymerase chain reaction.

Aneurysms demonstrate smooth muscle cell phenotypic modulation characterized by downregulation of smooth muscle cell marker genes and upregulation of matrix metalloproteinases. These events in experimental models occur before aneurysm formation. Targeting smooth muscle cells to a reparative phenotype might provide a novel therapy in the treatment of aortic aneurysms.

Bone marrow cells and the right atrial appendage were obtained from patients undergoing elective cardiac surgery. Myocardial slices were subjected to 90 minutes of simulated ischemia/120 minutes of reoxygenation at 37°C following various protocols. Tissue injury was assessed by creatine kinase released into the media during the reoxygenation period, and myocardial necrosis and apoptosis were determined by propidium iodide and terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling (percent of aerobic control).

Autologous unfractionated bone marrow cells significantly reduced myocardial injury. Maximal protection was obtained with 5 x 10⁶ autologous cells (~1.5 x 10⁵ cells/mg wet myocardium) that caused a reduction in creatine kinase release and cell death by necrosis and apoptosis of 70% to 80%. Allogenic bone marrow cells were as protective as the autologous cells and their effect was unaffected by prior frozen storage or culturing. Similar myocardial protection was also attained when bone marrow cells were present only before or during ischemia, or during reoxygenation, a benefit that was comparable with that of ischemic preconditioning. Conditioned media by the bone marrow cells was sufficient to induce protection, which was abolished by the selective insulin-like growth factor-1 receptor blocker PQ401.

Bone marrow cells possess potent myocardial protective properties that are triggered by a secreted factor or factors and mediated by insulin-like growth factor-1 receptor. These results have important clinical implications for the therapeutic use of bone marrow cells in ischemic heart disease and for the design of future clinical studies.

In experiment 1 (RIPC group), 3 cycles of limb remote ischemic preconditioning within different episodes (2, 3, or 5 minutes) were induced before spinal cord ischemia in rats (N = 5, n = 8). In experiment 2, animals were pretreated intravenously by the vehicles, cannabinoid 1 (AM251, 1 mg/kg) or cannaboid 2 (AM630, 1 mg/kg) receptor antagonist 15 minutes before remote ischemic preconditioning, or else they were subjected to a sham operation. Thirty minutes after the pretreatment, spinal cord ischemia was induced (N = 8, n = 8). In experiment 3, the arachidonylethanolamide and 2-arachidonoylglycerol contents in the spinal cord after remote ischemic preconditioning and spinal cord ischemia were detected in rats (N = 2, n = 12). Spinal cord ischemia was induced by 12 minutes of thoracic aorta occlusion in rats. Neurologic function was assessed 24 and 48 hours after reperfusion. Histopathologic examination was performed and the number of normal neurons in anterior spinal cord were counted.

In experiment 1, 3 cycles of limb remote ischemic preconditioning (3 minutes of ischemia/3 minutes of reperfusion) induced ischemic tolerance on the spinal cords of the rats. The RIPC group showed a significant reduction in motor deficit index (P < .01) as well as an increase in the number of normal neurons (P < .01). In experiment 2, the cannabinoid 1 receptor antagonist AM251 pretreatment abolished the protective effects of remote preconditioning. In experiment 3, arachidonylethanolamide content in spinal cord was elevated by remote ischemic preconditioning in rats.

These results indicated that endogenous cannabinoids, through acting on cannabinoid 1 receptors, were involved in the neuroprotective phenomenon on spinal cords of limb remote ischemic preconditioning.

Heart transplant and lung transplant recipients were randomized to nitric oxide or prostacyclin as initial treatment, followed by a crossover to the other agent after 6 hours. Pulmonary vasodilators were initiated in the operating room for pulmonary hypertension, refractory hypoxemia, or right ventricular dysfunction. Nitric oxide was administered at 20 ppm, and prostacyclin was administered at 20,000 ng/mL. Hemodynamic and oxygenation parameters were recorded before and after initiation of pulmonary vasodilator therapy. At 6 hours, the hemodynamic and oxygenation parameters were recorded again, just before discontinuing the initial agent. Crossover baseline parameters were measured 30 minutes after the initial agent had been stopped. The crossover agent was then started, and the hemodynamic and oxygenation parameters were measured again 30 minutes later.

Heart transplant and lung transplant recipients (n = 25) were randomized by initial treatment (nitric oxide, n = 14; prostacyclin, n = 11). Nitric oxide and prostacyclin both reduced pulmonary artery pressure and central venous pressure, and improved cardiac index and mixed venous oxygen saturation on initiation of therapy. More importantly, at the 6-hour crossover trial, there were no significant differences between nitric oxide and prostacyclin in the reduction of pulmonary artery pressures or central venous pressure, or in improvement in cardiac index or mixed venous oxygen saturation. Nitric oxide and prostacyclin did not affect the oxygenation index or systemic blood pressure. There were no complications associated with nitric oxide or prostacyclin.

In heart transplant and lung transplant recipients, nitric oxide and prostacyclin similarly reduce pulmonary artery pressures and central venous pressure, and improve cardiac index and mixed venous oxygen saturation. Inhaled prostacyclin may offer an alternative to nitric oxide in the treatment of pulmonary hypertension in thoracic transplantation.

The United Network for Organ Sharing provided de-identified patient-level data. The study population included 10,668 orthotopic heart transplant recipients aged 18 years old or older and undergoing transplantation between January 1, 2001, and December 31, 2006. Follow-up data were provided through August 3, 2008, with a mean follow-up time of 3.17 ± 2.15 years (range, 0–8.11 years). The primary outcome was actuarial posttransplant graft survival. Other outcomes of interest included infection, stroke, and dialysis during the transplant hospitalization; primary graft failure at 30 days; transplant hospitalization length of stay; and long-term complications including diabetes mellitus, transplant coronary artery disease, and chronic dialysis. Multivariable Cox proportional hazards regression (backward, P < .15) was used to determine the relationship between groups and overall graft survival, and multivariable logistic regression analysis (backward, P < .15) was used to determine the relationship between groups and secondary outcome measures.

In multivariable Cox regression analysis, when compared with the nonbridged group, risk-adjusted greater than 90-day graft survival was diminished among the EXTRA group (hazard ratio = 3.54, 2.28–5.51, P < .001), but not the INTRA group (1.04, 0.719–1.51, P = .834) or the PARA group (1.06, 0.642–1.76, P = .809). There were no significant differences in risk-adjusted graft survival across the 4 groups during the 90-days to 1-year or 1- to 5-year intervals. However, at more than 5 years, risk-adjusted graft survival in the INTRA group (0.389, 0.205–0.738, P = .004) was better than in the nonbridged group. The EXTRA, PARA, and INTRA groups all experienced increased risks of infection. The EXTRA group had increased risks of dialysis, stroke, and primary graft failure at 30 days, whereas neither the PARA nor the INTRA group differed from the nonbridged group. Long-term complications did not differ by group.

The use of implantable left ventricular assist devices as bridges to transplantation, including both intracorporeal and paracorporeal devices, is not associated with diminished posttransplant survival. However, 90-day survival was diminished in recipients bridged with extracorporeal devices.

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.