Before creation of an anterolateral left ventricular infarction by ligation of diagonal arteries, 16 sonomicrometry transducers were placed in the left ventricular free wall of 8 sheep to assess regional deformation in the infarct, adjacent, and normally perfused remote myocardial regions over 8 weeks' duration. Hemodynamic, echocardiographic and sonomicrometric data were collected before infarction and then 30 minutes and 2, 6, and 8 weeks after infarction. At the end of the study, regional myocardial tissues were collected for apoptotic signaling proteins.

At terminal study, an increase in left ventricular end-diastolic pressure of 8.1 ± 0.1 mm Hg, a decrease in ejection fraction from 54.19% ± 5.68% to 30.55% ± 2.72%, and an end-diastolic volume increase of 46.08 ± 5.02 mL as compared with the preinfarct values were observed. The fractional contraction at terminal study correlated with the relative abundance of apoptotic protein expressions: cytochrome c (r ² = 0.02, P < .05), mitochondrial Bax (r ² = 0.27, P < .05), caspase-3 (r ² = 0.31, P < .05), and poly (adenosine diphosphate–ribose) polymerase (r ² = 0.30, P < .05). These myocardial apoptotic activities also correlated with remodeling strain: cytochrome c (r ² = 0.02, P < .05), mitochondrial Bax (r ² = 0.28, P < .05), caspase-3 (r ² = 0.43, P < .05), and poly (adenosine diphosphate–ribose) polymerase (r ² = 0.37, P < .05).

Increase in regional remodeling strain led to an increase in myocardial apoptosis and regional contractile dysfunction in heart failure.

Patients undergoing primary elective coronary artery bypass grafting (n = 14) were randomized into 2 equal groups to receive saline infusion during cardiopulmonary bypass (control group) or high-dose aprotinin. Experimental skin blisters (in duplicate) were induced on the forearm by means of topical application of the vesicant cantharidin, and blister fluid was sampled at 5 hours postoperatively. Inflammatory leukocyte subsets in blister fluid were analyzed by means of flow cytometry by using expression of CD11b and CD62L as a phenotypic marker of activation.

In the control group of patients, cardiopulmonary bypass surgery triggered a 381% increase in leukocyte extravasation into the skin compared with reference blisters carried out before surgical intervention, with neutrophil (P = .014), monocyte (P = .014), and eosinophil (P = .009) levels all statistically significantly increased. In the aprotinin group there was no statistically significant increase during cardiopulmonary bypass surgery in any inflammatory leukocyte subset. The activation phenotype of extravascular leukocytes was not significantly altered between surgical groups.

This study introduces the cantharidin blister technique as a powerful new research tool for analyzing the inflammatory effect of cardiopulmonary bypass in vivo. It has provided detailed molecular insight into the extravascular leukocyte population during cardiopulmonary bypass. Although aprotinin blocked cardiopulmonary bypass–dependent extravasation of leukocytes, there was no change in their CD11b/CD62L activation status. The cantharidin skin test thus represents a novel research tool for evaluating future anti-inflammatory interventions in cardiothoracic surgery.

Eight pigs underwent median sternotomy, left internal thoracic artery harvesting, followed by topical negative pressure treatment. Magnetic resonance imaging was used to quantify both tissue fluid and/or blood content (T2-weighted short tau inversion recovery [T2-STIR]) and internal thoracic artery blood flow (flow quantification).

Before application of topical negative pressure, the T2-STIR signal intensity ratio was lower for the left than for the right hemisternum (left, 1.3; right, 2.6), indicating lower levels of tissue fluid content on the left, devascularized side. On application of topical negative pressure, the T2-STIR signal intensity ratio increased immediately for both the sternal bone and the pectoral muscle (left hemisternum after 4 minutes of topical negative pressure: 2.3), leveled off after 4 minutes, and remained unchanged for the ensuing 40 minutes, suggesting movement of fluid and/or blood into the tissue of the wound edge. Topical negative pressure did not affect blood flow in the right internal thoracic artery.

T2-STIR measurements show that topical negative pressure increases sternotomy wound edge tissue fluid and/or blood content. Topical negative pressure creates a pressure gradient that presumably draws fluid from the surrounding tissue to the sternal wound edge and into the vacuum source. This "endogenous drainage" may be one possible mechanism by which osteitis is resolved by topical negative pressure in poststernotomy mediastinitis.

Poly-(D,L-lactic-co-glycolic acid) (PLGA) microspheres loaded with the antineoplastic agent paclitaxel were prepared and tested for antitumor efficacy in an in vitro cell proliferation assay for tumor inhibition and induction of apoptosis. The in vivo prevention of Lewis lung carcinoma cell establishment and growth in subcutaneous tissues of mice was also assessed by comparing 4 treatment groups: Lewis lung carcinoma cells alone, Lewis lung carcinoma cells combined with 100 x 10⁶ unloaded (carrier alone) PLGA microspheres, and Lewis lung carcinoma cells combined with 50 x 10⁶ or 100 x 10⁶ paclitaxel-loaded PLGA microspheres. After the coinjection of Lewis lung carcinoma cells with or without microspheres, in vivo tumor growth was monitored, and tumor weight was recorded on death.

Paclitaxel-loaded PLGA microspheres were found to effectively prevent growth of tumor cells in culture through the induction of apoptosis. Similarly, paclitaxel-loaded PLGA microspheres significantly inhibited tumor growth in vivo at both the 50 x 10⁶ and 100 x 10⁶ microsphere dose (0.497 ± 0.183 and 0.187 ± 0.083 g total tumor weight, respectively) compared with 2.91 ± 0.411 g for Lewis lung carcinoma cells with unloaded microspheres and 3.37 ± 0.433 g for untreated tumor (P < .001). Toxicity was not clinically apparent in any animal treated with paclitaxel-loaded PLGA microspheres.

Paclitaxel-loaded PLGA microspheres induce tumor apoptosis and inhibit the establishment and growth of lung cancer cells both in vitro and in vivo without obvious systemic toxicity. By using models consistent with localized microscopic tumor burdens, these results suggest that local delivery of paclitaxel through a microsphere system might lead to an effective future method of decreasing local tumor recurrence in non–small cell lung cancer when applied to the surgical margins at risk for microscopic tumor foci. Such an approach might be particularly efficacious after wedge resection in the setting of poor pulmonary reserve or significant comorbidity, where local recurrence rates are increased and acceptable alternative treatment options are limited.

We retrospectively reviewed the charts of all patients with renal cell carcinoma whose histologic specimens were evaluated at our institution from January 1, 2000, through December 31, 2006. Using Kaplan–Meier estimates, we compared the survival of patients who underwent resection of asynchronous mediastinal lymph node metastases with that of patients with stage IV disease.

During the 7-year study period, of the 386 patients with renal cell carcinoma who were evaluated at our institution, 9 underwent resection of asynchronous mediastinal lymph node metastases. After primary tumor resection and before diagnosis of asynchronous mediastinal lymph node metastases, all patients completed chemotherapy, cytokine therapy, or tumor vaccination; 3 underwent radiotherapy. The median age at resection of mediastinal lymph nodes was 57.7 years (range, 39.7–81.2). The median time from primary tumor resection to mediastinal lymph node resection was 2.8 years (range, 0.5–23.3). In all, 4 patients underwent resection of metastases via thoracotomy and 5, via thoracoscopy. The median number of mediastinal lymph nodes pathologically evaluated was 7 (range, 2–28); the median number of positive mediastinal lymph nodes per patient was 1.5 (range, 1–3). We found no surgical complications. The median survival after resection of metastases (3.2 years) was significantly longer (P = .021) than for other patients with stage IV disease at our institution (1.1 years).

Resection of renal cell carcinoma mediastinal lymph node metastases is safe, appears to extend survival, and should be considered an important component of treating patients with renal cell carcinoma who have asynchronous mediastinal lymph node metastases.

Immunohistochemistry was performed on paraffin-embedded tissue specimens from 68 resected esophageal squamous cell carcinoma tumor specimens to detect the expression of β-catenin and p53. The correlation between the results of immunoexpression and the clinicopathologic parameters and patient survival was processed statistically.

Reduced membranous β-catenin expression was noted in 43 (63.2%) of 68 tumor specimens. Increased expression of p53 was observed in 43 (63.2%) of 68 specimens. Reduced membranous β-catenin protein expression was associated with the presence of distant metastasis (P = .006). Patients with reduced membranous β-catenin expression had a worse prognosis than patients with normal membranous β-catenin expression (P = .005). Patients with combined increased p53 and reduced membranous β-catenin protein expression had the worst prognosis (P = .012). In a multivariate survival analysis, reduced membranous β-catenin expression and nodal involvement were independent prognostic factors (P = .004 and .019, respectively).

Immunohistochemical analysis revealed that reduced membranous β-catenin protein expression was associated with the presence of distant metastasis and a poor prognosis in patients with esophageal squamous cell carcinoma. Combined increased p53 and reduced membranous β-catenin protein expression indicated a very poor prognosis in patients with esophageal squamous cell carcinoma. Further investigation is needed to understand the roles of β-catenin and p53 in the tumorigenesis and metastasis of esophageal squamous cell carcinoma.

Patients with advanced non–small cell lung cancer who had received neoadjuvant chemotherapy in the context of a prospective phase II trial were analyzed for the p53 genotype of their tumors. Response to induction therapy was then correlated to the p53 genotype as assessed by complete direct DNA sequencing. Patients had received 3 cycles of cisplatin and etoposide, and 1 cycle of simultaneous radiochemotherapy. All 3 treatment components mediate their cytotoxic effect through induction of apoptosis, which is suggested to require an intact p53 gene. In addition, the results from a previously published hypothesis-finding study are updated to demonstrate the consistency of clinical results and summarize currently available clinical evidence.

In the phase II trial, 35 patients underwent resection after induction chemotherapy, allowing a pathohistologic response assessment. The presence of a mutant p53 genotype was highly indicative of resistance to induction chemotherapy (P < .002). The sensitivity of a mutant p53 genotype to identify nonresponders was 94% (71.3–99.9 confidence interval). A normal p53 gene was significantly associated with radical resection (P < .004) and survival advantage (P = .02).

This is the second clinical evaluation demonstrating a significant relation between p53 genotype and response to induction therapy in non–small cell lung cancer. We conclude that the p53 genotype should be evaluated as a predictive marker for response to induction therapy in prospective randomized protocols.

Fifty-eight patients with acute aortic dissection, whose average age was 83.2 years, were divided into 2 groups: Group I comprised 30 patients who underwent emergency surgery, and group II comprised 28 patients who were treated conservatively. We compared the 2 groups in terms of mortality and morbidity.

In group I, postoperative hospital mortality was 13.3% (4 patients). In group II, 17 patients (60.7%) died in the hospital. In group I, although emergency aortic replacement was successfully completed, 5 patients became bedridden after surgery and 2 patients died of pneumonia or stroke in the early stages of institutional care. Thirteen patients in group I died of malignancies, abdominal aortic rupture, traffic accident, heart failure, or late-stage senility in later phase. There was no difference in actuarial survivals at 5 years, which were 48.5% in group I and 35.4% in group II.

Emergency surgery for octogenarians with acute aortic dissection showed acceptable mortality. However, families had to take responsibility for patients who experienced unconsciousness, had dementia, or became bedridden. It is important to have consensus between the family and surgeons about emergency surgical treatment for octogenarians.

The data of 8555 patients who had undergone coronary bypass operations in the years between 1996 and 2004 were analyzed. Depending on their diagnosis on admission and their fasting plasma glucose levels, these patients were classified as having "no diabetes" (fasting plasma glucose level < 126 mg/dL), "undiagnosed diabetes" (glucose level ≥ 126 mg/dL), "oral therapy diabetes," or "insulin-treated diabetes." The 3 diabetic groups were compared with the nondiabetic group in terms of the preoperative and postoperative characteristics.

The reintubation rate among patients with undiagnosed diabetes (4.6%) and among those with insulin-treated diabetes (4.5%) was significantly higher than that of nondiabetic patients (1.8%; P < .01). The proportion of patients who required respiration for periods longer than 1 day was also significantly higher among patients with undiagnosed diabetes (9.9%) and those with insulin-treated diabetes (8.6%) than among the nondiabetic patients (4.8%; P < .01). The regression models show that unidentified diabetes and insulin-treated diabetes constitute independent risk factors for perioperative pulmonary complications.

Patients with undiagnosed and insulin-treated diabetes have a higher risk of having pulmonary complications in the perioperative course of coronary bypass operations than do nondiabetic patients. These results may be explained if one considers the lung as another target organ of the diabetic disease.

The 75-patient study population (between 2004 and 2006) with severe heart failure included 35 patients undergoing surgical ventricular restoration (mean age, 62.6 ± 8.7 years), sometimes together with coronary artery bypass grafting or mitral surgery, and 40 cardiac transplant recipients (mean age, 55.6 ± 7.7 years). Preoperative and 6-month postoperative function (peak Vo ₂, the anaerobic threshold, and the slope of minute ventilation/carbon dioxide uptake), cardiac catheterization parameters (left and right), and hospital and early outcomes were evaluated.

The 2 groups had comparable baseline functional impairment and experienced similar hospital stay and early outcomes. They also showed similar improvements in left ventricular volume indexes and hemodynamic parameters and sustained significant improvements of median Vo ₂, anaerobic threshold, and minute ventilation/carbon dioxide uptake values.

Both surgical strategies resulted in a significant and comparable improvement of functional capacity at the 6-month evaluation. These early studies must be repeated to determine the long-term benefits of surgical ventricular restoration because maximal Vo ₂ and ventilatory efficiency lose their prognostic survival role after transplantation.

From 1964 to 2005, 323 patients had cardiac surgery for resection of primary cardiac tumors; 53 (16%) patients had primary ventricular tumors. We randomly sampled 53 characteristics of ventricular tumors.

Patients with ventricular tumors were younger than those with atrial tumors (34.8 vs 54.6 years; P < .0001). New York Heart Association functional status was similar at presentation, although patients with atrial tumors had increased risk of atrial fibrillation (P < .05), thromboembolic events (P = .04), and mitral stenosis (P = .008) at the time of presentation. Patients with ventricular tumors had an increased incidence of myocardial invasion (14% vs 2%; P = .02) and had significantly longer cardiopulmonary bypass (80 vs 65 minutes; P < .05) and crossclamp (52 vs 39 minutes; P = .03) times. Operative mortality was 4% and 0% in the ventricular and atrial groups, respectively (P = not significant). Follow-up was obtained in 89% of patients at a mean follow-up time of 7.21 years. A Kaplan–Meier survival plot demonstrated no difference in survival characteristics of both groups. At follow-up, 81% and 74% of ventricular and atrial tumors, respectively, were minimally symptomatic (New York Heart Association class I/II; P = .13). Patients with atrial and ventricular tumors had a 6% and 0% tumor recurrence rate, respectively (P = .12).

Surgical resection for ventricular tumors is effective and results in excellent long-term outcome. Early surgical treatment should be strongly considered in patients with primary ventricular tumors.

In a randomized single-center trial, 331 patients underwent total arterial revascularization using single or bilateral internal thoracic and radial arteries versus conventional revascularization using the left internal thoracic artery and saphenous vein grafts. We report the results from 3 months' follow-up.

The mean age of patients was 59 ± 8 years, and 39 were women (12%). The median EuroSCORE was 2 (interquartile range 1–4). The arterial group comprised 161 patients, and the conventional group comprised 170 patients. The mean number of bypasses in the arterial group was 2.9 ± 0.9 versus 3.2 ± 0.9 in the conventional group (P = .004). Three months' follow-up for the arterial versus conventional groups showed the following: deaths: 1 (0.6%) versus 0; stroke: 3 (1.9%) versus 3 (1.8%); myocardial infarction: 6 (3.7%) versus 4 (2.4%); sternal wound reoperation: 4 (2.5%) versus 0 (P = .054); arm and leg wound complications requiring hospitalization: 3 (1.9%) versus 6 (3.5%) (P = .50), respectively.

These results confirm previous reports that total arterial revascularization can be performed with low in-hospital morbidity and mortality. Further, in the 3 postoperative months, total arterial revascularization did not lead to more complications or admissions than conventional surgery. Arterial grafting was performed with significantly fewer bypasses, but no differences in anginal status were seen after 3 months. A tendency toward more sternal complications after arterial grafting was observed, but clinical outcomes were comparable to conventional grafting.

Prospectively collected long-term follow-up data from 469 consecutive patients who underwent aortic valve replacement between 1995 and 1998 were reviewed. The indexed effective orifice area was derived from the reference normal values of effective orifice area divided by the patient's body surface area. Outcome was stratified according to the severity of prosthesis–patient mismatch: moderate mismatch was defined as 0.65 to 0.85 cm²/m² and severe mismatch as less than 0.65 cm²/m². The Cox proportional-hazards model with propensity score adjustment was used to adjust for the observed differences in baseline characteristics between the mismatch groups.

The degree of prosthesis–patient mismatch was minimal in 57% of patients, moderate in 39%, and severe in 4%. Predictors of clinically significant mismatch included small aortic valve sizes (19 and 21 mm), obesity, age greater than 65 years, and class III or IV heart failure. During a median follow-up period of approximately 7.9 years, overall survival was 77% in patients with minimal mismatch, 63% in those with moderate mismatch, and only 47% in those with severe mismatch (P < .001). Moderate or severe mismatch was a significant predictor of poorer survival (hazard ratio, 1.6; 95% confidence interval, 1.4–2.3; P < .01), even after adjustment for all significant clinical predictors (ie, propensity score; hazard ratio, 1.2; 95% confidence interval, 1.0–1.5; P = .05).

In a large aortic valve surgery population, prosthesis–patient mismatch occurred in 43% of patients, and those with significant mismatch had worse long-term outcomes than those with minimal mismatch.

After anterolateral minithoracotomy, the aortic valve isolation chamber system was inserted into the descending aorta and pushed forward transluminally into the aortic position to generate a separate operation space between the subvalvular and the proximal ascending aortic area. After deployment and sealing of the chamber, stable function with a continuous chamber lavage of 1.58 L/min saline solution was established (8/10 cases). The endoscopically guided laser fiber was delivered via the right carotid artery. After fixation of a leaflet by a forceps catheter, the native leaflets were resected each by a thulium:YAG laser with 20-W power rating. Macropathology and micropathology of surrounding anatomic structures were analyzed.

The duration of transluminal positioning and deployment of the aortic valve isolation chamber took 7.3 ± 5.8 minutes. Fluoroscopy confirmed sealed chambers. The resection was completed in all leaflets and took, on average, 6.0 ± 3.5 minutes per leaflet. The aortic wall was moderately injured in 4 of 10 cases and the aortic annulus in two cases with one aortic wall perforation. The surrounding tissue, the coronary ostia, the mitral valve, and the left ventricular outflow tract remained unaffected.

This study demonstrates the feasibility of endovascular resection of human aortic valves in situ. This is a subsequent step toward complete percutaneous replacement (resection and implantation) of human aortic valves.

A total of 437 consecutive patients were analyzed who underwent mitral valve reconstruction with annuloplasty using the Colvin–Galloway Future band at the German Heart Center in Munich between 2001 and 2005. A total of 237 patients (54.2%) underwent isolated mitral valve repair, and 200 patients (45.8%) underwent a combined procedure. The follow-up is 97% complete (mean follow-up of 405 survivors 2.1 ± 1.1 years).

Overall 30-day mortality was 2.7%. Twenty patients (4.6%) died later after an average of 1.1 ± 1.1 years. Actuarial survival at 4 years after isolated mitral valve reconstruction and combined procedures was 91% ± 4% and 87% ± 2.5%, respectively (P < .001). Twelve patients (2.7%) required a mitral valve reoperation after an average of 4.5 ± 4.3 months. Five of these reoperations were required for band dehiscence, and 1 reoperation was required for band fracture. Freedom from reoperation at 4 years was 97% ± 0.9%. At the latest follow-up, 93.5% of the patients showed trivial or mild mitral valve regurgitation, and 86.4% of the patients showed New York Heart Association functional class I or II.

Mitral valve annuloplasty with the Colvin–Galloway Future band can be performed with a low early and late mortality and an excellent functional outcome. The low incidence of reoperation demonstrates that the Colvin–Galloway Future band is a safe and effective device. The importance of secure anchoring of the device in the mitral annulus has to be emphasized to prevent band dehiscence.

Nine sheep underwent myocardial infarction and aneurysm repair with a linear repair (13.4 ± 2.3 weeks postmyocardial infarction). Satisfactory magnetic resonance imaging examinations were obtained in 6 sheep (6.6 ± 0.5 weeks postrepair). Finite element models were constructed from in vivo magnetic resonance imaging-based cardiac geometry and postmortem measurement of myofiber helix angles using diffusion tensor magnetic resonance imaging. Material properties were iteratively determined by comparing the finite element model output with systolic tagged magnetic resonance imaging strain measurements.

At the mid-wall, fiber stress in the border zone decreased by 39% (sham = 32.5 ± 2.5 kPa, repair = 19.7 ± 3.6 kPa, P = .001) to the level of remote regions after repair. In the septum, however, border zone fiber stress remained high (sham = 31.3 ± 5.4 kPa, repair = 23.8 ± 5.8 kPa, P = .29). Cross-fiber stress at the mid-wall decreased by 41% (sham = 13.0 ± 1.5 kPa, repair = 7.7 ± 2.1 kPa, P = .01), but cross-fiber stress in the un-excluded septal infarct was 75% higher in the border zone than remote regions (remote = 5.9 ± 1.9 kPa, border zone = 10.3 ± 3.6 kPa, P < .01). However, end-diastolic fiber and cross-fiber stress were not reduced in the remote myocardium after plication.

With the exception of the retained septal infarct, end-systolic stress is reduced in all areas of the left ventricle after infarct plication. Consequently, we expect the primary positive effect of infarct plication to be in the infarct border zone. However, the amount of stress reduction necessary to halt or reverse nonischemic infarct extension in the infarct border zone and eccentric hypertrophy in the remote myocardium is unknown.

A total of 153 patients underwent 184 thoracic endovascular aortic repairs between 1998 and 2005. Prospectively collected data were entered into statistical software. Univariate and multivariate analyses were performed.

The underlying pathologies included descending thoracic aortic aneurysm (n = 91), acute type B aortic dissection (n = 25), chronic type B aortic dissection (n = 42), aortic transection (n = 12), and penetrating aortic ulcer (n = 14). Thoracic endovascular aortic repair was technically successful in all but 3 patients. Another 3 patients required an open repair within the first month. Early and late mortality rates were 9.8% (n = 18) and 19% (n = 35) in a 16-month average period of follow-up, respectively. Type I procedural endoleak was the only significant predictor of early death in the multivariate model (P = .0036; odds ratio: 8.4; 95% confidence interval: 1.6–43.9). Multivariate Cox regression revealed chronic obstructive pulmonary disease (P = .024; odds ratio: 3.8; 95% confidence interval: 1.2–12.1), postoperative myocardial infarction (P = .0053; odds ratio: 9.7; 95% confidence interval: 2.0–48.4), and acute renal failure (P = .0006; odds ratio: 22.8; 95% confidence interval: 3.8–137.6) to be independent risk factors for late mortality.

Procedural type I endoleak is an independent risk factor of early mortality after thoracic endovascular aortic repair. Chronic obstructive pulmonary disease, postoperative myocardial infarction, and acute renal failure are predictors of late death in the multivariate analysis.

Fifty patients were randomly assigned to on-pump or off-pump coronary artery bypass grafting. All cardiac biomarkers were measured in serial venous blood samples drawn before heparinization in both groups and after aortic unclamping at 1, 2, 4, 8, 24, 48, and 72 hours in the on-pump group. In the off-pump group samples were taken after the last distal anastomosis and at same time intervals as in the on-pump group.

The total amount of heart-type fatty acid–binding protein, cardiac troponin I, and high-sensitivity C-reactive protein released was significantly higher in the on-pump group than in the off-pump group. Receiver operating characteristic curve analysis of cardiac biomarkers indicated cardiac troponin I and heart-type fatty acid–binding protein as the superior diagnostic discriminators of myocardial injury, with an optimal cutoff value of greater than 0.92 ng/mL (area under the curve, 0.95 [95% CI, 0.88–1.00]; sensitivity, 92%; specificity, 92%; likelihood ratio [+], 11.50) and greater than 6.8 ng/mL (area under the curve, 0.94 [95% CI, 0.88–1.00]; sensitivity, 88%; specificity, 88%; likelihood ratio [+], 7.33), respectively. Logistic regression analysis revealed that patients with increased cardiac troponin I levels of greater than 0.92 ng/mL and heart-type fatty acid–binding protein levels of greater than 6.8 ng/mL were at 132.25 (95% confidence interval, 17.14–1020.49) times and 53.77 (95% confidence interval, 9.76–296.12) times higher risk of myocardial injury after on-pump coronary artery bypass grafting.

Off-pump coronary artery bypass grafting provides better myocardial protection than on-pump coronary artery bypass grafting. Cardiac troponin I and heart-type fatty acid–binding protein, but not high-sensitivity C-reactive protein, served as superior diagnostic discriminators of perioperative myocardial damage after on-pump coronary artery bypass grafting.

Patient records were reviewed, and all patients were mailed a medical questionnaire or contacted by means of telephone. Patients who had pulmonary atresia with an intact ventricular septum, complex conotruncal abnormalities, and atrioventricular discordance with ventriculoarterial discordance were excluded.

From April 1, 1972, to January 1, 2006, 539 patients with Ebstein anomaly had 604 cardiac operations. The mean age at the time of the initial operation at our institution was 24 years (range, 8 days–79 years). Three hundred seventeen of the patients were female. One hundred forty-three (26.5%) patients had a prior invasive cardiac procedure before coming to Mayo Clinic. At the time of the first operation at Mayo Clinic, 182 patients had tricuspid valve repair, and 337 had tricuspid valve replacement. The 30-day mortality was 5.9% for the entire cohort (2.7% after 2001). Late survival was 84.7% at 10 years and 71.2% at 20 years. In a multivariate analysis of overall mortality for the patients' first operation at Mayo Clinic, increased hematocrit values, pulmonary valve stenosis, tricuspid valve replacement, absence of ablation of an accessory pathway, miscellaneous arrhythmia procedure, branch pulmonary artery enlargement, need for mechanical support postoperatively, emergency chest opening in the intensive care unit, and absence of sinus rhythm at dismissal were all predictive of mortality. When only preoperative characteristics were included, increased hematocrit values, mitral valve regurgitation requiring surgical intervention, prior cardiac procedure, and moderate-to-severe to severe reduction in right ventricular systolic function were associated with mortality. Preoperative sinus rhythm and an accessory pathway were associated with survival. Patients rated their health as excellent or good (New York Heart Association class I or II) in 83% of surveys returned.

Ebstein anomaly can be surgically treated with low perioperative mortality. Both tricuspid valve repair and tricuspid valve replacement are associated with good long-term survival. Risk factors for poorer outcome included right, and/or left ventricular systolic dysfunction; increased hemoglobin/hematocrit values; male sex; right ventricular outflow tract obstruction; or hypoplastic pulmonary arteries.

A retrospective study of all patients undergoing the double-switch procedure from 1991 through 2004 was performed. Patients were divided into 2 groups: those not requiring morphologic left ventricle training (n = 33) and those completing morphologic left ventricle training by means of pulmonary artery banding (n = 11).

The time spent with the morphologic left ventricle conditioned at systemic pressures was longer for the group not requiring morphologic left ventricle training (median, 730 days; interquartile range, 399–1234 vs median, 436 days; interquartile range, 411–646; P = .19). The overall mortality (not requiring morphologic left ventricle training, 12.1%; requiring morphologic left ventricle training, 9.1%; P = 1) and rate of death/transplantation, development of moderate-to-severe morphologic left ventricle dysfunction, or both (not requiring morphologic left ventricle training, 21.2%; requiring morphologic left ventricle training, 45.5%; P = .14) were similar between groups. Actuarial freedom from death/transplantation with good morphologic left ventricular function was superior for patients whose morphologic left ventricle did not require training (P = .04). The follow-up was not different between groups (not requiring training: median, 1435 days [interquartile range, 285–2570 days]; requiring morphologic left ventricle training: median, 568 days [interquartile range, 399–1465 days]; P = .14). On multivariate analysis, the completion of morphologic left ventricle training predicted death/transplantation, development of moderate-to-severe morphologic left ventricle dysfunction, or both (P = .02).

The early results of the double-switch procedure in patients whose morphologic left ventricle required training compare favorably with those of patients whose morphologic left ventricle required no training. There is an increased risk of deterioration of morphologic left ventricle function over time in patients whose morphologic left ventricle requires training, and these patients need to be followed up regularly to detect this.

Since January 1999, 72 patients weighing less than 20 kg underwent extracardiac conduit Fontan procedure with polytetrafluoroethylene conduits. The patients were divided into 2 groups: 36 patients weighing less than 10 kg in group S and 36 weighing more than 10 kg in group L. Mean weight, median age, and median follow-up period in groups S and L were 8.5 ± 1.1 and 14.0 ± 3.0 kg, 18.9 and 42.0 months, and 29.2 (1.7–79.7) and 42.1 (2.8–94.2) months, respectively. Postoperatively, most patients received peritoneal drainage catheters. We reviewed data precatheterization and postcatheterization and postoperative course.

Conduit sizes in groups S and L were 17.0 ± 1.3 and 17.9 ± 1.9 mm, respectively (P = .03). Five patients required fenestrations. There were 2 hospital deaths, 1 in each group, and 2 late deaths in group S. The postoperative course was identical in both groups, except for median length of stay in the intensive care unit and peritoneal drainage volume. Group S versus L: ventilator support, 11 versus 7 hours; pleural drainage, 9 days each; pleural drainage greater than 14 days, 6 versus 5 cases; peritoneal drainage, 8 versus 7 days; intensive care unit stay, 7 versus 4 days (P = .01), peritoneal drainage volume, 26.1 versus 14.1 mL · kg · d^–1 (P = .0007).

The early outcome of the extracardiac conduit Fontan procedure was satisfactory in patients weighing less than 10 kg. However, the required size of the conduit remains debatable.

A retrospective review of 56 patients who underwent surgical repair of ruptured sinus of Valsalva aneurysm between June 1990 and August 2006 was performed. Rupture of the right coronary sinus into the right ventricle was the most common anatomic type (39/56, 69.6%). Preoperative aortic regurgitation equal to or greater than grade II (n = 8, 17.9%) was managed by repair (aortic valvuloplasty, n = 5) or replacement (n = 3). Ruptured sinus of Valsalva aneurysm was repaired primarily (n = 7) or by patching (n = 10) through an aortotomy in 17 patients (transaortic group). In the remaining patients (n = 39), ruptured sinus of Valsalva aneurysm was repaired primarily from the chamber into which the corresponding aortic sinus ruptured, and the aneurysmal sac was reinforced with a supporting patch (non-transaortic group).

Median follow-up duration was 46 months (0.4–177 months). There were 2 late deaths. Excluding 3 patients with aortic valve replacement on aneurysm repair, 11 patients (11/53, 21%) had recurrent or new-onset significant aortic regurgitation (≥II/IV) during the follow-up period. By multivariable analysis, aortic valvuloplasty at initial operation was the only significant risk factor for postoperative aortic regurgitation (P < .001). After adjustment, the non-transaortic approach appeared to be associated with a lower risk of postoperative aortic regurgitation, with marginal significance (hazard ratio 0.28; P = .058). Five-year freedom from significant aortic regurgitation in the transaortic and non-transaortic groups was 68% ± 12% and 94% ± 4%, respectively.

Transaortic repair of ruptured sinus of Valsalva aneurysm may cause postoperative aortic regurgitation by progressive distortion of the aortic sinus geometry.

From January 1985 to February 2004, 100 status 2 patients were delisted for medical improvement (median on-list duration, 314 days). Return of heart failure, sudden cardiac death, and all-cause mortality were determined from follow-up (mean, 7.7 ± 3.9 years among survivors; 10% followed >12 years). Hazard function modeling, competing-risks analyses, simulation, and propensity matching to equivalent patients undergoing transplantation were used to analyze and compare outcomes and predict benefit of interventions.

Freedom from return of heart failure was 77% at 5 years. The most common mode of death was sudden cardiac death, with risk peaking at 2.5 years after delisting but remaining at 3.5% per year thereafter. Event-free survival at 1, 5, and 10 years was 94%, 55%, and 28%, respectively; simulation demonstrated that implantable cardioverter–defibrillators could have improved this to 45% at 10 years. Overall survival after delisting was better than that of matched status 2 patients who underwent transplantation, but was demonstrably worse after 30 months.

Status 2 patients, including those delisted, require vigilant surveillance and optimal medical management, implantable cardioverter–defibrillators, and a revised approach to transplantation timing, such that overall salvage is maximized while allocation of scarce organs is optimized.