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Adventitial cystic disease is an uncommon vascular anomaly known to occur in peripheral vessels but mediastinal appearances are extremely rare. Herein, we report the case of an adventitial cyst occurring in the right brachiocephalic vein which might have been associated with ovarian hyperstimulation syndrome.

We describe a modification to the aortic cusp extension technique that eliminates aortic regurgitation in pediatric small bicuspid valves. This simple and reproducible cusp extension technique secures coaptation and commissure suspension of the reconstructed aortic valve and may act as a bridge option for forthcoming reoperations.

We report a case of a newborn infant who experienced circulatory collapse caused by a calcified lesion occluding the main pulmonary artery (PA). The baby was full-term at birth at a normal birth weight. Cyanosis was noted immediately after birth. Echocardiography revealed a main PA occlusion caused by a calcified lesion. Bradycardia and circulatory failure occurred at postnatal day 4, and an urgent surgical resection was successfully performed. Idiopathic calcification causing both PA obstruction and circulatory collapse is rare. Our report indicates that PA calcification can cause hemodynamic instability requiring early surgical intervention.

BACKGROUND: A malpositioned heart with apicocaval juxtaposition may complicate the management of patients with functional single ventricles when total cavopulmonary connection is performed. We reviewed our experience with extracardiac total cavopulmonary connection in patients with apicocaval juxtaposition with a special focus on route selection and outcomes. METHODS: Of 68 patients who underwent extracardiac total cavopulmonary connection at our hospitals, 10 patients with apicocaval juxtaposition were included in this study. The mean follow-up was 40 ± 28 months. Patient demographics were compared with data on patients without apicocaval juxtaposition. RESULTS: The age at operation was 8 ± 7 years. We carefully chose conduit routes to create satisfactory fluid dynamics. The conduit was placed between the inferior vena cava and the ipsilateral pulmonary artery in 2 patients, and the conduit crossed midline in 8 patients. The mean postoperative pulmonary artery pressure was 13 ± 2 mm Hg. The surgical and postoperative data were not significantly different when compared with the patients without apicocaval juxtaposition. There were no conduit-related early or late complications except for 1 patient who had poor ventricular function. CONCLUSIONS: Extracardiac total cavopulmonary connection in apicocaval juxtaposition can be carried out with favorable midterm outcomes. The route between the inferior vena cava and the contralateral pulmonary artery should be the primary choice when the relevant pulmonary artery is in good shape. Care must be taken in regard to critical conduit oppression by the ventricle in cases with large ventricular volume or poor ventricular function.

Neutrophil is a major focus in efforts to ameliorate the systemic inflammatory response associated with cardiopulmonary bypass. Neutrophil elastase is a powerful proteolytic enzyme, and plays a pivotal role in the development of the inflammatory response. This study assesses the inhibitory effects of sivelestat, a highly specific neutrophil elastase inhibitor, on elastase levels, cytokine production, and the functional changes of neutrophils in a simulated extracorporeal circulation model.Simulated recirculation was established by recirculating heparinized (3.75 U/mL) human blood for 120 minutes in an oxygenator and a roller pump circuit with and without 100 micromol/L of sivelestat (n = 7 for each group). Neutrophil elastase and interleukin-8 were measured with an enzyme immunoassay. Neutrophil deformability was evaluated by simulated microcapillaries. The neutrophil F-actin and the expression of CD11b and L-selectin were measured by flow cytometry.Sivelestat reduced both neutrophil elastase levels (p = 0.0006) and interleukin-8 production (p0.0001) at 120 minutes of recirculation. Sivelestat also significantly preserved neutrophil deformability (p = 0.017) and reduced F-actin expression (p = 0.0037). The drug did not modulate the changes of CD11b or L-selectin.This study suggests that specific elastase inhibition with sivelestat could be a feasible therapeutic strategy for patients undergoing cardiopulmonary bypass to attenuate neutrophil-derived inflammatory response and organ injuries.

Background High-frequency QRS potentials are sensitive to myocardial ischemia. The aim of this study was to evaluate the usefulness of high-frequency QRS potentials as a marker of myocardial dysfunction after cardiac surgery. Methods Seventy patients undergoing coronary artery bypass grafting or heart valve surgery were involved. High-frequency QRS potentials were measured by signal-averaged electrocardiogram, and calculated as the root-mean-square voltage of the total QRS duration (RMST). The postoperative RMST was expressed as a percentage of the preoperative RMST. The mean RMST at 1 to 2 hours after removing the aortic cross-clamp was compared with the cardiac index, inotropic agents, and aortic cross-clamping time. The occurrence of ventricular tachycardia within 24 hours and the RMST at 2 postoperative days were also evaluated. Patients were divided into quartile groups from highest to lowest at postoperative RMST (groups 1, 2, 3, and 4, respectively, from maximum to minimum). Results In postoperative states, cardiac index significantly decreased in accordance with the RMST decrease in a stepwise manner, although there were no differences in cardiac index among the four groups preoperatively. Inotropic agents and aortic cross-clamping time increased as RMST decreased. A high rate of ventricular tachycardia within 24 hours and delayed RMST recovery at 2 postoperative days were seen in group 4. The curve of sensitivity and specificity showed that severe reduction (threshold, 35%) of RMST indicated low-output syndrome. Conclusions The severe reduction of filtered high-frequency QRS potentials was related to myocardial dysfunction. Measurement of filtered high-frequency QRS potentials could become a useful, noninvasive, real-time monitor of myocardial dysfunction after surgery.

An alternative pulmonary valve-sparing technique for primary repair of tetralogy of Fallot is presented. Reconstruction of the right ventricular outflow tract was accomplished by augmentation of the anterior facing pulmonary cusp, the pulmonary annulus, and the main pulmonary artery using a single autologous pericardial patch. This valve-sparing technique preserves the coaptation and suspension mechanisms of the native pulmonary cusp and therefore may minimize pulmonary insufficiency in the long term.

Background A bone marrow (BM) response induced by cardiopulmonary bypass (CPB) as a systemic inflammatory reaction has previously been postulated but not clarified. Newly released polymorphonuclear leukocytes (PMNs) and monocytes from the BM are known to be immature, indicating their greater potential to damage tissue. The present study aimed to examine the kinetics of BM–derived leukocytes associated with CPB in a nonhuman primate model. Methods Normothermic CPB was performed in cynomolgus monkeys for 2 hours through a median sternotomy. Leukocyte precursors were labeled in the BM of the monkeys in vivo by an intravenous injection of 5-bromo-2'-deoxyuridine (BrdU), and their release into the circulation and recruitment to the lungs after operation with or without CPB (control group) were monitored over time by flow cytometry. Results In normal-state monkeys, the calculated transit time of BrdU-labeled PMNs (PMN BrdU ) through the BM was 143.6 ± 4.5 hours and that of monocytes was 100.9 ± 7.6 hours. CPB caused a rapid release of PMNs and monocytes from the BM, shortened their transit through the BM to 92.0 ± 4.1 and 60.3 ± 2.9 hours, respectively, and further induced their increased appearance in the alveolar spaces, with a significant increase in both interleukin (IL)-6 and IL-8 levels in the bronchoalveolar lavage fluid (BALF) 24 hours after CPB. Conclusions CPB accelerated the release of PMNs and monocytes from the BM and their recruitment to the lungs in our monkey model, indicating that this model is relevant for monitoring the kinetics of BM-derived leukocytes in humans.

Background While β-blockers can be effective in controlling tachyarrhythmias after pediatric cardiac surgery, a negative inotropic influence sometimes complicates their use. Landiolol hydrochloride is a novel, ultra-short-acting β-blocker recently developed in Japan. The drug has higher β1:β2 selectivity ratio and a less negative inotropic effect. This study retrospectively evaluates the efficacy and safety of landiolol in the management of tachyarrhythmias after pediatric cardiac surgery. Methods A retrospective analysis was performed on 312 consecutive patients undergoing surgery for congenital heart disease. Twelve patients were treated with landiolol for critical tachyarrhythmia. The mean age of patients was 28.7 ± 10.6 months. Five junctional ectopic tachycardia, 2 atrial flutters, 1 paroxysmal supraventricular tachycardia, 1 atrial fibrillation, 1 atrioventricular reciprocating tachycardia with Wolff-Parkinson-White syndrome and 2 excessive sinus tachycardia were treated. Results The mean loading and maintenance doses were 11.3 ± 4.0 and 6.8 ± 0.9 μg/kg per minute, respectively. Rate control was achieved in all patients. Landiolol reduced the heart rate from 169.7 ± 11.4 to 127.7 ± 7.5 beats per minute (p < 0.05) while blood pressure did not significantly change. Tachyarrhythmias were converted to sinus rhythm in 70.0% of the cases and the average time needed to achieve heart rate reduction was 2.3 ± 0.5 hours. Conclusions Landiolol was efficacious in treating tachyarrhythmia in pediatric cardiac surgery. The desired negative chronotropic effect was achieved without significant hemodynamic compromise. The ultra-short half-life of landiolol provided rapid dose manipulation. This study suggests that landiolol is a promising option for the management of postoperative tachyarrhythmias in pediatric patients.

We present a case of innominate artery rupture after descending necrotizing mediastinitis (DNM) on day 36 of cervicomediastinal drainage. The patient recovered after aortosubclavian arterial bypass grafting followed by resection of the eroded artery. Because mechanical pressure caused by drains in addition to the inflammatory process can cause major vessel erosion, prolonged transcervical tube drainage for treating descending necrotizing mediastinitis should be avoided even if the drains applied are soft and thin.

The combination of coronary artery aneurysm and pulmonary artery fistula is extremely rare and its common cause is atherosclerosis. A 61- year-old woman presented with a giant coronary artery aneurysm with pulmonary artery fistula and intramyocardial calcifications of the left ventricle associated with progressive atherosclerosis due to chronic hemodialysis. The coronary artery aneurysm was resected under cardiopulmonary bypass because of hemodynamic instability due to restrictive cardiac dysfunction. The patient's restrictive cardiac dysfunction was improved after aneurysm resection. Surgical resection should be considered for giant coronary artery aneurysm with restrictive cardiac dysfunction.

We report a Kawashima procedure (total cavopulmonary shunt) successfully carried out for asplenia syndrome, pulmonary atresia, and major aortopulmonary collateral arteries. At the age of 8, the patient underwent staged bilateral unifocalizations using confluent central pulmonary arteries concomitant with bilateral modified Blalock-Taussig shunts. As the result of an interrupted inferior vena cava with azygous continuation, the patient required a Kawashima procedure with augmentation of the central pulmonary arteries for definitive palliation 1 year later. Cyanosis, respiratory distress, and ventricular function improved., Case report

Background Initial sequestration of activated neutrophils and platelet microaggregates in capillaries are responsible for the inflammatory response associated with cardiopulmonary bypass. The study assesses the inhibitory effects of nafamostat mesilate on neutrophil and platelet activation, and on the neutrophil deformability change and microaggregate formation during simulated extracorporeal circulation. Methods Fresh heparinized human blood was recirculated for 120 minutes in a membrane oxygenator and a roller pump with and without nafamostat (1.0 mg bolus plus 8.0 mg/h infusion; n=10 for each group). Neutrophil and platelet counts and platelet aggregation were measured. CD11b, L-selectin, and cytoplasmic F-actin of neutrophils were measured by flow cytometry. The microchannel transit time of whole blood was measured as a marker of neutrophil deformability and microaggregate formation. Neutrophil elastase and complement C4d were measured using enzyme immunoassay. Results Nafamostat preserved platelet counts and inhibited platelet aggregation. Nafamostat significantly reduced neutrophil elastase release at 120 minutes of recirculation, and F-actin expression at 30 and 60 minutes. The drug did not modulate the changes of CD11b, L-selectin, or C4d. Whole blood filterability was significantly preserved by nafamostat at 30 and 120 minutes. Conclusions Nafamostat preserves blood filterability during recirculation, possibly by suppression of F-actin expression and platelet activation. Nafamostat may reduce neutrophil sequestration and microaggregate formation in the microcirculation during cardiopulmonary bypass.

An infant with factor VII deficiency underwent palliative open heart surgery for pulmonary atresia with an intact ventricular septum. No references had been found on the management of this rare coagulation disorder in infantile cardiac surgery. We describe the peri- and postoperative management with a replacement therapy including a recombinant factor VIIa concentrate. We conclude that an appropriate replacement therapy is needed to control bleeding during open heart surgery with factor VII deficiency.

Background Among the serine proteases, neutrophil elastase is a powerful cytotoxic enzyme and plays a pivotal role in the inflammatory response associated with cardiopulmonary bypass. This study assesses the effects of the specific inhibition of neutrophil elastase by a novel, potent, low-molecular-weight neutrophil elastase inhibitor, ONO-6818. We hypothesized that ONO-6818 reduces inflammatory mediators and modulates adhesion molecules and the deformability of neutrophils during simulated extracorporeal circulation. Methods Simulated extracorporeal circulation was established by recirculating fresh heparinized (3.75 U/mL) human blood for 120 minutes in a membrane oxygenator and a roller pump with and without 1.0 μmol/L of ONO-6818 (n = 9 for control group, n=7 for ONO-6818 group). The neutrophil adhesion molecules, CD11b and L-selectin, and the cytoplasmic F-actin of neutrophils were measured by flow cytometry. Neutrophil deformability was evaluated using simulated silicon microcapillaries. Neutrophil elastase, interleukin 8, and C5b-9 were measured using enzyme immunoassay. Results Neutrophil elastase levels were significantly lower in the ONO-6818 group. ONO-6818 significantly reduced interleukin 8 and C5b-9 production. ONO-6818 did not modulate changes of CD11b and L-selectin during recirculation. Cytoplasmic F-actin content and changes of neutrophil deformability did not significantly differ between the groups. Conclusions Inhibition of neutrophil elastase activity with ONO-6818 reduces further interleukin 8 production and the formation of the complement membrane attack complex, and this results in a reduction of neutrophil elastase levels during simulated extracorporeal circulation. This study suggests that specific neutrophil elastase inhibition with ONO-6818 is a feasible therapeutic option to attenuate the exaggerated inflammatory response associated with cardiopulmonary bypass.

Background The pharmacological inhibition of blood-foreign surface interactions is an attractive strategy for reducing the morbidity associated with cardiopulmonary bypass. We compared the inhibitory effects of nafamostat mesilate (a broad-spectrum synthetic protease inhibitor) and minimal-dose aprotinin on blood-surface interactions in clinical cardiopulmonary bypass. Methods Eighteen patients undergoing coronary surgery were divided into three groups: (1) the control group (heparin, 4 mg/kg; n=6), (2) the nafamostat mesilate group (heparin plus nafamostat, 0.2 mg/kg bolus followed by 2.0 mg/kg/h during cardiopulmonary bypass; n=6), and (3) the aprotinin group (heparin plus aprotinin, 2.0 × 10 4 KIU/kg; n=6). Platelet count, platelet aggregation, β-thromboglobulin, prothrombin fragment F1.2, thrombin-antithrombin complex, plasminogen activator inhibitor-1, α2-plasmin inhibitor-plasmin complex, D-dimer, neutrophil elastase, and interleukin-6 were measured before, during, and after bypass. Bleeding times and blood loss were recorded. Results There were no significant differences between groups in platelet count, β-thromboglobulin, plasminogen activator inhibitor-1, interleukin-6, bleeding times, or blood loss. Platelet aggregation was better preserved at 12 hours after surgery in the nafamostat and aprotinin groups than in the control group. Prothrombin fragment F1.2, thrombin-antithrombin complex and neutrophil elastase levels were significantly reduced by aprotinin, but not by nafamostat as compared with the control group. The α2-plasmin inhibitor-plasmin complex and D-dimer were significantly lower with either of the drugs. Aprotinin showed better control of D-dimer than did nafamostat. Conclusions Nafamostat mesilate fails to reduce thrombin formation and neutrophil elastase release, whereas minimal-dose aprotinin inhibits both. Neither nafamostat nor aprotinin inhibits platelet activation. Nafamostat reduces fibrinolysis during cardiopulmonary bypass, although its effect is not as potent as aprotinin.

Background Neutrophil sequestration and platelet microaggregates in organ capillaries have been implicated in the inflammatory response associated with cardiopulmonary bypass. We examined the filterability of neutrophils and platelet microaggregates through silicon microchannels during simulated extracorporeal circulation. We hypothesize that blood contact with artificial surfaces over time decreases the ability of neutrophils, platelets, and their aggregates to pass through microchannels. Methods Fresh human blood from donors (n = 9) was recirculated for 120 minutes in a simulated extracorporeal circuit. Blood samples were obtained from a donor at 0, 30, 60, and 120 minutes of recirculation. The microchannel transit time and the flow behavior of blood cells were evaluated by a silicon microchannel array flow analyzer. CD11b, L-selectin, and F-actin of neutrophils were measured by flow cytometry. Neutrophil and platelet counts and platelet aggregation to adenosine diphosphate were measured. Results The microchannel transit time was prolonged during recirculation, reaching 185.9% ± 25.6% of baseline at 120 minutes. The video microscope showed that neutrophils and platelet microaggregates plugged the microchannels. CD11b, L-selectin, and F-actin levels changed significantly by 120 minutes. Platelet counts decreased and platelet aggregability was attenuated. Conclusions Simulated extracorporeal circulation caused a progressive loss in the ability of neutrophils, platelets, and their aggregates to pass through the microchannels independent of neutrophil adhesion molecule expression.

Background . In the absence of papillary muscle rupture, the precise deformations that cause acute postinfarction mitral valve regurgitation are not understood and impair reparative efforts. Methods . In 6 Dorsett hybrid sheep, sonomicrometry transducers were placed around the mitral annulus (n = 6) and at the tips and bases of both papillary muscles (n = 4). Later, specific circumflex coronary arteries were occluded to infarct approximately 32% of the posterior left ventricle and produce acute 2 to 3+ mitral regurgitation. Before and after infarction, distance measurements between sonomicrometry transducers produced three-dimensional coordinates of each transducer every 5 ms. Results . After infarction, the annulus dilated asymmetrically orthogonal to the line of leaflet coaptation, but the annular area increased only 9.2% ± 6.3% ( p = 0.02). At end-systole, posterior papillary muscle length increased 2.3 ± 0.9 mm ( p = 0.005); the posterior papillary muscle tip moved closer to the annular plane and centroid, and the anterior papillary muscle tip moved away. Conclusions . Small deformations in mitral valvular spatial geometry after large posterior infarctions are sufficient to produce moderate to severe mitral regurgitation. The most important changes are asymmetric annular dilatation, prolapse of leaflet tissue tethered by the posterior papillary muscle, and restriction of leaflet tissue attached to the anterior papillary muscle.