Search

Objective: The 2 main causes of death after thromboendarterectomy for chronic pulmonary thromboembolism are incomplete repermeabilization responsible for persistent pulmonary hypertension and acute high-permeability pulmonary edema. We wish to establish an experimental model of chronic pulmonary thromboembolism to replicate the conditions encountered during and after pulmonary thromboendarterectomy. Methods: Multiple-curled coils and tissue adhesive were embolized in 6 piglets to induce complete obstruction of the left pulmonary artery, documented by angiography. After 5 weeks, the main pulmonary artery was repermeabilized by thromboendarterectomy during circulatory arrest. The left lung was reperfused ex vivo with autologous blood at constant flow, and patency of the pulmonary artery was evaluated on a barium angiogram. The endarterectomy-reperfusion procedure was also done in 6 nonembolized piglets that served as the controls. The severity of lung injury induced by 60 minutes of reperfusion was assessed on the basis of measurements of the lung filtration coefficient and of lung myeloperoxidase activity. Results : Marked hypertrophy of the bronchial circulation was seen in the chronic pulmonary thromboembolism group. Thromboendarterectomy removed the organized obstructing thrombus that was incorporated into the arterial wall and restored patency of the pulmonary artery. Acute lung inflammation and high-permeability edema occurred after reperfusion, as indicated by a 1.5-fold increases in both lung filtration coefficient and lung myeloperoxidase values in the chronic pulmonary thromboembolism group; these 2 variables being correlated. Conclusions : Our model replicated the perioperative conditions of pulmonary thromboendarterectomy, suggesting that it may prove useful for improving the repermeabilization technique and for investigating the mechanisms and prevention of reperfusion injury. (J Thorac Cardiovasc Surg 1999;117:787-93)

Background: The occurrence of a progressive pulmonary venous obstruction after the repair of the total anomalous pulmonary venous connection is a severe complication. Objectives: The objectives of this study were to retrospectively review the patients with this condition and to report our experience with a new surgical technique with a sutureless in situ pericardium repair. Methods: Of 178 patients who underwent correction of total anomalous pulmonary venous connection, 16 patients (9%) experienced the development of a progressive pulmonary venous obstruction in a median interval of 4 months (5 weeks–12 years). Three patients had isolated anastomotic stenosis, 4 patients had isolated pulmonary venous ostial stenosis, and 9 patients had both. Pulmonary venous obstruction was bilateral in 7 patients. The surgical procedures used at reoperation included 8 patch enlargements, 5 ostial endarterectomies, 1 intraoperative stenting, and 7 sutureless in situ pericardium repairs. Results: There were 4 deaths after reoperation (4 of 15 patients; 27%). The only significant mortality risk factor was the bilateral location of the pulmonary venous obstruction ( P = .045). In patients with isolated anastomotic stenosis or with only 1 pulmonary venous ostial stenosis (n = 5), there was no death, except the patient presenting with a single ventricle. In patients with 2 or more pulmonary venous ostial stenoses (n = 10), there were 3 deaths; 5 of the 7 survivors were successfully treated with the in situ pericardial technique, with normalized pulmonary artery pressure at a mean follow-up of 26 months. Conclusion: Progressive pulmonary venous stenosis after repair of total anomalous pulmonary venous connection remains a severe complication when bilateral. The sutureless in situ pericardial repair offers a satisfactory solution, particularly on the right side. (J Thorac Cardiovasc Surg 1999;117: 679-87)

Objectives: The purpose of this study was to analyze the mechanisms associated with lung injury after cardiopulmonary bypass and to propose strategies of prevention. Methods: Thirty-two neonatal piglets underwent 90 minutes of hypothermic cardiopulmonary bypass without aortic crossclamping. Five experimental groups were defined: group I had standard cardiopulmonary bypass (control), group II received continuous low-flow lung perfusion during cardiopulmonary bypass, group III treatment was similar to that of group I with maintenance of ventilation, group IV received pneumoplegia, and group V received nitric oxide ventilation (30 ppm) after cardiopulmonary bypass. Data drawn from hemodynamic and gas exchange values and muscular and pulmonary tissular levels of adenosine triphosphate (in micromoles per gram) and myeloperoxidase (in international units per 100 mg) were used for comparisons before and 30 and 60 minutes after cardiopulmonary bypass. Pulmonary and systemic vascular endothelial functions were assessed in vitro after cardiopulmonary bypass on isolated rings of pulmonary and iliac arteries. Results: Pulmonary vascular resistance index, cardiac index, and oxygen tension were better preserved in groups II, IV, and V. All groups disclosed a significant decrease in lung adenosine triphosphate levels and an increase in myeloperoxidase activity whereas these levels stayed within pre–cardiopulmonary bypass ranges in muscular beds. Endothelium-dependent relaxation was preserved in systemic arteries but was strongly affected in pulmonary arteries after cardiopulmonary bypass. None of the methods that aimed to protect the pulmonary vascular bed demonstrated any preservation of pulmonary endothelial function. Conclusion: Cardiopulmonary bypass results in ischemia-reperfusion injury of the pulmonary vascular bed. Lung protection by continuous perfusion, pneumoplegia, or nitric oxide ventilation can prevent hemodynamic alterations after cardiopulmonary bypass but failed to prevent any of the biochemical disturbances. (J Thorac Cardiovasc Surg 1997;114:1061-9)

Objective: The aim of the study was to analyze the long-term results of subaortic stenosis relief and the risk factors associated with recurrence and reoperation. Methods: One hundred sixty patients with subaortic stenosis underwent biventricular repair. Before the operation the mean left ventricle–aorta gradient was 80 ± 35 mm Hg, 57 patients had aortic regurgitation, and 34 were in New York Heart Association functional class III or IV. Median age at repair was 10 years. For discrete subaortic stenosis (n = 120), 39 patients underwent isolated membranectomy, 67 underwent membranectomy with associated septal myotomy, and 14 underwent septal myectomy. Tunnel subaortic stenosis (n = 34) was treated by myotomy in 10 cases, myectomy in 12, septoplasty in 7, Konno procedure in 3, and apical conduit in 2. Aortic valve replacement was performed in 6 cases, mitral valve replacement in 2 cases, and mitral valvuloplasty in 4 cases. Results: There were 5 early (3.1%) and 4 late (4.4%) deaths. Within 3.6 ± 3.3 years a recurrent gradient greater than 30 mm Hg was found in 42 patients (27%), 20 of whom had 26 reoperations. According to multivariable Cox regression analysis survival was influenced by hypoplastic aortic anulus ( P = .01) and mitral stenosis ( P = .048); recurrence and reoperation were influenced by coarctation and immediate postoperative left ventricular outflow tract gradients. At a median follow-up of 13.3 years, mean left ventricle–aorta gradient was 20 ± 13 mm Hg. Relief of the subaortic stenosis improved the degree of aortic regurgitation in 86% of patients with preoperative aortic regurgitation. Actuarial survival and freedom from reoperation rates at 15 years were 94% ± 1.3% and 85% ± 6%, respectively. Conclusion: Although surgical treatment provides good results, recurrence and reoperation are significantly influenced by previous coarctation repair and by the quality of initial relief of subaortic stenosis. (J Thorac Cardiovasc Surg 1999;117:669-78)

Three groups of unusual forms of tracheobronchial compression caused by vascular anomalies are presented. Three patients had an encircling right aortic arch with a left-sided descending aorta and ligamentum arteriosum (group 1), two patients had airway compression caused by a pincer effect between a malposed and enlarged ascending aorta and the descending aorta (group 2), and three patients had airway compression after an arterial switch operation for transposition of the great arteries (group 3). Symptoms developed in all patients before the age of 4 months, and six of them had multiple failed attempts at extubation before the surgical intervention directed at relieving the airway compression. Fiberoptic endoscopy was used in all patients as a first-line diagnostic tool and was 100% accurate in establishing the diagnosis. The operations performed were aortic uncrossing in group 1, dissection and aortopexy of the right or left main bronchus in group 2, and dissection of the left main bronchus and lysis of adhesions in group 3. In group 1 there was one early death, resulting from aspiration, and one late death 4 years later, resulting from an unrelated cause. In this group, bronchomalacia was noted after the operation and resolved gradually in the year after the intervention. In group 2, one patient died of an aortobronchial fistula after placement of a bronchial stent. Group 3 patients had good postoperative results. Two of them are completely symptom-free and one has residual bronchomalacia and may need placement of a bronchial stent. (J Thorac Cardiovasc Surg 1996;112:415-23)

To evaluate cytokine balance related to cardiopulmonary bypass, we prospectively investigated 11 infants undergoing cardiac operations for congenital heart disease. Proinflammatory cytokines (tumor necrosis factor-α and interleukin-8) and the antiinflammatory cytokine interleukin-10 were measured at multiple time points before, during, and after bypass. Tumor necrosis factor-α and interleukin-8 values were within normal range before the operation. These values increased significantly during bypass, reaching their peaks after protamine administration (tumor necrosis factor-α, 133.6 ± 124.9 pg/ml; mean ± standard deviation; p < 0.005) and 2 hours after termination of the procedure (interleukin-8, 92.1 ± 44.1 pg/ml; p < 0.01). Tumor necrosis factor-α and interleukin-8 equaled normal prebypass values from the first postoperative day on. Interleukin-10 levels were within normal range before the operation and were already significantly increased 10 minutes after initiation of bypass (interleukin-10, 39.4 ± 34.3 pg/ml; p < 0.05). These levels remained elevated throughout the procedure but returned to normal after protamine administration. A second significant release of interleukin-10 occurred from the early postoperative period on, reaching its peak 24 hours after termination of cardiopulmonary bypass (interleukin-10, 351.6 ± 304.0 pg/ml; p < 0.01). Interleukin-10 values were normal on the second postoperative day in all patients. Interleukin-10 kinetics showed an inverse pattern compared with tumor necrosis factor-α and interleukin-8. This difference suggests an interplay between proinflammatory and antiinflammatory cytokines released during and after cardiopulmonary bypass. Interleukin-10 levels measured 4 and 24 hours after bypass strongly correlated with the degree of hypothermia during bypass (Spearman's correlation coefficient, -0.77 [ p < 0.01] and -0.89 [ p < 0.0005], respectively); these levels did not correlate with duration of bypass and aortic crossclamping, however. This result suggests that besides immunologically mediated production of interleukin-10, hypothermia itself could modulate interleukin-10 production. In conclusion, this study demonstrates interleukin-10 production, in addition to interleukin-8 and tumor necrosis factor-α synthesis, in response to cardiopulmonary bypass in infants. Interleukin-10 could play a protective role by down-regulating proinflammatory cytokine release during and after cardiopulmonary bypass. (J THORAC CARDIOVASC SURG 1996;111:545-53)

Out of 180 patients who underwent biventricular repair of double-outlet right ventricle between 1980 and 1995, 9 (5%) required reoperation because of subaortic stenosis. Two other patients who initially underwent operation elsewhere underwent reoperation at our institution because of subaortic stenosis. The median age at biventricular repair was 4 months. Repair consisted of tunnel construction from the left ventricle to the aorta in nine patients; the remaining two patients received an arterial switch operation with ventricular septal defect closure. Subaortic stenosis developed with time: the mean postoperative left ventricle–to–aorta gradient after repair was 10 ± 19 mm Hg (range, 0 to 50 mm Hg) and became 84 ± 27 mm Hg (range, 40 to 124 mm Hg) in a mean delay of 45 ± 66 months (range, 1 to 213 months). At reoperation, the obstruction was caused by the protrusion of the inferior rim of the ventricular septal defect into the left ventricular outflow tract associated with subaortic hypertrophied muscle and membrane. The 11 patients underwent 15 reoperations. Surgical technique consisted of an extended septoplasty in 6 reoperations. In this technique an incision was made in the septal patch and was extended into the muscle toward the apex until a large opening of the left ventricular outflow pathway was obtained. A new patch was then secured to streamline the left ventricular outflow tract. None of the patients who underwent extended septoplasty had to undergo reoperation. There were no early or late deaths. At 115 ± 85 months after biventricular repair, all patients were in New York Heart Association functional class I or II and the mean postoperative left ventricle–to–aorta gradient was 20 ± 24 mm Hg (range, 0 to 60 mm Hg). We conclude that after biventricular repair of double-outlet right ventricle, the subaortic region is at risk for the development of stenosis. Surgical treatment adapted to the anatomy of the obstruction can offer good early and midterm results. It seems that an aggressive approach by an extended septoplasty avoids multiple reoperations. (J Thorac Cardiovasc Surg 1996;112:1570-80)