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The Society of Thoracic Surgeons (STS) established the National Database (NDB) for Cardiac Surgery in 1989. Since then it has grown to be the largest database of its kind in medicine. The NDB has been one of the pioneers in the analysis and reporting of risk-adjusted outcomes in cardiothoracic surgery.This report explains the numerous changes in the NDB and its structure that have occurred over the past 2 years. It highlights the benefits of these changes, both to the individual member participants and to the STS overall. Additionally, the vision changes to the NDB and reporting structure are identified. The individuals who have participated in this effort since 1989 are acknowledged, and the STS owes an enormous debt of gratitude to each of them.Because of their collective efforts, the goal to establish the STS NDB as a "gold standard" worldwide for process and outcomes analysis related to cardiothoracic surgery is becoming a reality.

The Society of Thoracic Surgeons National Database Committee is committed to risk stratification and assessment as integral elements in the practice of cardiac operations. The National Cardiac Surgery Database was created to analyze data from subscribing institutions across the country. We analyzed the database for valve replacement procedures with and without coronary artery bypass grafting to determine trends in risk stratification.The database contains complete records of 86,580 patients who had valve replacement procedures at the participating institutions between 1986 and 1995, inclusive. The 1995 harvest of data was conducted in late 1996 and available for evaluation in 1997. These records were used to conduct an in-depth analysis of risk factors associated with valve replacement and to provide prediction of operative death by using regression analysis. Regression models were made for six subgroups.Adverse patient risk factors, including diabetes, hypertension and reoperation, but not ventricular function, increased over time. There were trends with regard to increasing age of the various population subsets. The types of prostheses used remained similar over time, with more mechanical prostheses than bioprostheses used for both aortic and mitral valve replacement. There was a trend toward increased use of bioprostheses in aortic replacements and decreased use in mitral replacements between 1991 and 1995 than between 1986 and 1990. The mortality rate was determined by patient subset for primary operation and reoperation and by urgency status. The modeling showed that the predicted and observed mortality correlated for all age groups and within patient subsets.Risk modeling is a valuable tool for predicting the probability of operative death in any individual patient. This large, multiinstitutional database is capable of determining modern operative risk and should provide standards for acceptable care. The study illustrates the importance of risk stratification for early death both for the patient and the surgeon.

Health-related quality of life has not been evaluated as a predictor of mortality following coronary artery bypass graft (CABG) surgery. Evaluation of health status as a mortality predictor may be useful for preoperative risk stratification.To determine whether the Physical and Mental Component Summary scores from the preoperative Short-Form 36 (SF-36) health status survey predict mortality following CABG surgery after adjustment for known clinical risk variables.Prospective cohort study conducted between September 1992 and December 1996.Fourteen Veterans Affairs hospitals.Of the 3956 patients undergoing CABG surgery only and who were enrolled in the Processes, Structures, and Outcomes of Care in Cardiac Surgery study, the 2480 who completed a preoperative SF-36.All-cause mortality within 180 days after surgery.A total of 117 deaths (4.7%) occurred within 180 days of CABG surgery. The Physical Component Summary of the preoperative SF-36 was a statistically significant risk factor for 6-month mortality after adjustment for known clinical risk factors for mortality following CABG surgery. In multivariate analysis, a 10-point lower SF-36 Physical Component Summary score had an odds ratio (OR) of 1.39 (95% confidence interval [CI], 1.11-1.77; P=.006) for predicting mortality. The SF-36 Mental Component Summary score was not associated with 6-month mortality in multivariate analyses (OR, 1.09; 95% CI, 0.92-1.29; P=.31).The Physical Component Summary score from the preoperative SF-36 is an independent risk factor for mortality following CABG surgery. The baseline Mental Component Summary score does not appear to be predictive of mortality. Preoperative patient self-report of the physical component of health status may be helpful for risk stratification and clinical decision making for patients undergoing CABG surgery.

More than 600,000 coronary artery bypass graft (CABG) procedures are done annually in the United States. Some data indicate that 10 to 20% of patients who are undergoing a CABG procedure have a serum creatinine of more than 1.5 mg/dl. There are few data on the impact of a mild increase in serum creatinine concentration on CABG outcome.We analyzed a Veterans Affairs database obtained prospectively from 1992 through 1996 at 14 of 43 centers performing heart surgery. We compared the outcome after CABG in patients with a baseline serum creatinine of less than 1.5 mg/dl (median 1.1 mg/dl, N = 3271) to patients with a baseline serum creatinine of 1.5 to 3.0 mg/dl (median 1.7, N = 631).Univariate analysis revealed that patients with a serum creatinine of 1.5 to 3.0 mg/dl had a higher 30-day mortality (7% vs. 3%, P0.001) requirement for prolonged mechanical ventilation (15% vs. 8%, P = 0.001), stroke (7% vs. 2%, P0.001), renal failure requiring dialysis at discharge (3% vs. 1%, P0.001), and bleeding complications (8% vs. 3%, P0.001) than patients with a baseline serum creatinine of less than 1.5 mg/dl. Multiple logistic regression analyses found that patients with a baseline serum creatinine of less than 1.5 mg/dl had significantly lower (P0.02) 30-day mortality and postoperative bleeding and ventilatory complications than patients with a serum creatinine of 1.5 to 3.0 mg/dl when controlling for all other variables.These results demonstrate that mild renal failure is an independent risk factor for adverse outcome after CABG.

Traumatic injury to the heart is no longer a death sentence. Efficient urban transport systems and surgeons who are expert in trauma care combine to achieve meaningful survival rates after both penetrating and blunt violations of the heart. Almost all cases of injury to the heart can be repaired without cardiopulmonary bypass and, therefore, are within the purview of the thoracic surgical trauma specialist.

New volume requirements for coronary artery bypass grafting are being imposed on cardiac surgeons by hospitals, managed care groups, and others. The rationale for this is unclear. The available literature as well as additional sources relating volume and outcomes in cardiac surgery were extensively reviewed and reexamined. There are no data to conclusively indicate that outcomes of cardiac operations are related to a specific minimum number of cases performed annually by a cardiac surgeon. Each cardiothoracic surgeon should participate in a national database that permits comparison of his or her outcomes on a risk-adjusted basis with other surgeons. Until conclusive data become available that link volume to outcome, volume should not be used as a criterion for credentialing of cardiac surgeons by hospitals, managed care groups, or others. Instead, each surgeon should be evaluated on his or her individual results.

Our data suggest that CMVIG in combination with ganciclovir effectively reduces the incidence, and delays the onset of CMV infections in seropositive lung transplant recipients. In addition, its use may be associated with less severe CMV infection and a lower incidence of bacterial or fungal opportunistic infection. Although the number of patients in the study is small, high-titer CMVIG may be more effective than standard titer immunoglobulin in the prevention of CMV disease in lung transplant recipients. Several questions remain in addition to these: What is the optimal dosage and duration of treatment with CMVIG for prophylaxis of CMV infection and disease in lung transplant recipients; Is this strategy cost-effective; Will it reduce the incidence of obliterative bronchiolitis following lung transplantation and enhance allograft survival? A prospective, random-assignment trial is warranted to answer these questions.

For the determination of the risk factors associated with the development of and death caused by prosthetic valve endocarditis, data were reviewed from 66 patients who were prospectively entered into the Veterans Affairs Cooperative Study on Valvular Heart Disease and in whom prosthetic valve endocarditis subsequently developed. Data were recorded at 13 medical centers between October 1977 and September 1982 in patients randomized to receive a mechanical valve (Bjork-Shiley spherical disc, n = 510 patients) or a bioprosthetic valve (Hancock porcine heterograft, n = 522 patients). The average rate of prosthetic valve endocarditis development was 0.8% per year over an average follow-up period of 7.7 years. Of the 66 patients in whom prosthetic valve endocarditis developed (5.8%), 15 cases occurred within 2 months of operation (early) and 51 occurred after operation (late). The most significant preoperative predictor of prosthetic valve endocarditis was active endocarditis at the time of operation (7.4% versus 0.9%) (p = 0.001). Early prosthetic valve endocarditis occurred more frequently in patients who underwent operation for multivalvular disease (p = 0.023). Significantly related perioperative variables were coma, prolonged mechanical ventilation, deep postoperative wound infection, postoperative jaundice, ventricular tachycardia, ventricular fibrillation, and replacement of more than one valve (p0.05). Multivariate predictors were hypoxia (p = 0.001), preoperative endocarditis (p = 0.003), preoperative valve lesion (p = 0.020), and resident surgeon (p = 0.05). Significant preoperative variables predictive of late prosthetic valve endocarditis were mitral stenosis and mixed mitral stenosis-regurgitation. The only multivariate predictor of late prosthetic valve endocarditis was superficial wound infection (p = 0.004). Of deaths attributable to prosthetic valve endocarditis, 41% occurred in patients treated with antibiotics alone, 48% occurred in patients treated with surgical intervention and antibiotics, and death resulted in both patients who received no treatment. No difference was found in the risk of early or late postoperative prosthetic valve endocarditis developing in patients receiving the mechanical valve versus those receiving the bioprosthetic valve.

This report examines and compares the causes of late non-surgical death in 146 of 690 (21%) patients undergoing isolated aortic valve replacement (AVR) and in 79 of 273 (29%) patients undergoing mitral valve replacement (MVR) over a five year follow up period. The distribution of valve related, cardiac but not valve-related and non-cardiac deaths was 43%, 23% and 34% respectively for AVR and 65%, 29% and 6% respectively for MVR; the difference between these distributions was statistically significant. The specific causes of valve related deaths included bleeding (11% vs. 5% for MVR vs. AVR), systemic embolization (6% vs. 4% for MVR vs. AVR), endocarditis (14% vs. 8% for MVR vs. AVR), valve regurgitation (8% vs. 5% for MVR vs. AVR) and valve obstruction (3% vs. 5% for MVR vs. AVR). Sudden death (less than one hour from the onset of acute symptoms) accounted for 23% of deaths for MVR and 16% for AVR. The deaths due to congestive heart failure with normal prosthetic valve function were 13% and 8% for MVR and AVR respectively. Non-cardiac causes accounted for only 6% of MVR deaths but 34% of AVR deaths (p0.001). There was no significant difference in the late mortality between mechanical and bioprosthetic valves in the aortic position (24% vs. 22%), but the cumulative rate of late deaths was higher in patients with the Björk-Shiley than with the Hancock valve in the mitral position (41% vs. 25%, p0.02). In conclusion, about one quarter of patients surviving either aortic or mitral valve replacement died within five years.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary vascular resistance is significantly increased in the transplanted lung. We hypothesized that the ischemic or reperfusion injuries incurred by the transplanted lung may produce pulmonary vasomotor dysfunction, which in turn may produce increased pulmonary vascular resistance. In a dog model of autologous lung transplantation, the purpose of this study was to examine the following mechanisms of pulmonary vasomotor control and to relate each of them to cold ischemia and to reperfusion: (1) endothelium-dependent cyclic guanosine monophosphate-mediated vasorelaxation (response to acetylcholine 10(-6) mol/L), (2) endothelium-independent cyclic guanosine monophosphate-mediated vasorelaxation (response to sodium nitroprusside 10(-6) mol/L), and beta-adrenergic cyclic adenosine monophosphate-mediated vasorelaxation (response to isoproterenol 10(-6) mol/L). Autologous right lung transplantation was performed in five dogs. At each of three times, two third-order pulmonary arteries were dissected from each transplanted lung and studied: control (immediately after harvest), cold ischemia (3 hours in 4 degrees C saline solution), and cold ischemia plus reperfusion (1 hour after lung reimplantation). The vasorelaxing effects of acetylcholine, sodium nitroprusside, and isoproterenol were studied in isolated pulmonary arterial rings, suspended on fine wire tensiometers in individual organ chambers. Statistical analysis was by analysis of variance. Results demonstrated significant dysfunction of beta-adrenergic cyclic adenosine monophosphate-mediated relaxation after cold ischemia alone, and this dysfunction was exacerbated by reperfusion. Endothelium-dependent cyclic guanosine monophosphate-mediated relaxation was not impaired by cold ischemia alone but was significantly impaired by reperfusion. Endothelium-independent cyclic guanosine monophosphate-mediated relaxation was not impaired by cold ischemia or reperfusion. We conclude that cold ischemia and reperfusion each produce different patterns of pulmonary vasomotor dysfunction. Cumulatively, such dysfunction may contribute to increased pulmonary vascular resistance in the transplanted lung.

A synopsis of both blunt and penetrating thoracic trauma, this article outlines an approach to management for injuries to the lung, heart, esophagus, tracheobronchial tree, diaphragm, and major thoracic vessels. Also outlined are the management of rib fractures, scapula fractures, sternal fractures, and, in particular, flail chest with associated pulmonary contusion.

Thirty-one single lung transplantations were performed between March 17, 1988, and November 1, 1990. Postoperative infection, especially with cytomegalovirus, has been the major cause of morbidity and mortality. Eighteen of the 31 patients were receiving prednisone before transplantation. Every patient was prepared preoperatively with oral cyclosporine 5 mg/kg and azathioprine (Imuran) 2 mg/kg. Every patient received methylprednisolone for 3 days postoperatively, followed by prednisone 1.0 mg/kg/day, oral cyclosporine, and azathioprine. Ten patients additionally had cytolytic therapy with OKT3 and 12 with antilymphocyte globulin. Nine patients had no cytolytic therapy. Cytolytic therapy was chronologic, not randomized. Postoperative infection occurred in 20 patients, 13 of whom had cytomegalovirus infection. Preoperative use of prednisone did not correlate with postoperative infection, cytomegalovirus, or death. Postoperative infection occurred in 17 of 22 patients with cytolytic therapy compared with three of nine without cytolytic therapy (p = 0.035). Cytomegalovirus infection occurred in 13 of 22 with cytolytic therapy and in none of the nine without cytolytic agents (p = 0.003). Therefore preoperative prednisone does not appear to be a contraindication to single lung transplantation. Cytolytic therapy with either OKT3 or antilymphocyte globulin increases the prevalence of postoperative infection with cytomegalovirus and should not be used in patients undergoing lung transplantation.

Twenty-two patients have undergone 23 single lung transplants between March 1980 and April 1990 at the University of Texas Health Science Center at San Antonio. The actuarial survival rate is 77.27% at 12 months and 72.73% at 24 months. There have been no instances of bronchial dehiscence or stenosis, even though 13 of the patients were on a program of preoperative prednisone, every patient had high-dose perioperative methylprednisolone, and omental wraps were not used on any bronchial anastomosis. Of particular interest is the fact that three patients had primary pulmonary hypertension, three had secondary pulmonary hypertension, and 10 patients had chronic obstructive pulmonary disease, due in five cases to an alpha 1-antitrypsin deficiency. Each of these entities was previously thought to contraindicate single lung transplantation. Donor selection was based on an oxygen tension/inspired oxygen concentration ratio greater than 300, donor/recipient chest circumference within 3 inches, clear chest x-ray film, negative sputum Gram stain, and less than 6-hour estimated ischemic time. Harvest technique included donor prostaglandin E1 500 micrograms, topical slush, and pulmonoplegia with cold Euro-Collins solution. The heart and lung were separated in situ rather than the heart lung block being removed. A telescoping bronchial anastomosis was performed with 4-0 Prolene (not absorbable) sutures. We conclude that single lung transplantation has evolved into a simple operation, necessitating meticulous preoperative and postoperative care, which can be performed on a wide spectrum of critically ill patients with an acceptable mortality rate.

As part of a prospective program to use risk-adjusted outcome (operative mortality and morbidity) as a measure of quality of care, we have analyzed perioperative complication data in 10,634 patients representing 73% of all patients undergoing cardiac surgery requiring cardiopulmonary bypass at Veterans Administration medical centers between April 1, 1987, and March 31, 1989. One or more complications occurred in 15% of patients undergoing coronary artery bypass grafting, and in 24% of patients undergoing valve and other cardiac surgery. Patients experiencing one or more complications had an eightfold to 10-fold increase in operative mortality compared with patients with no perioperative complications. The most frequent complication was requirement for mechanical ventilation for at least 48 hours occurring in 8% of patients undergoing coronary artery bypass and in 15% of patients undergoing valve and other cardiac surgery; 24-25% of these patients died within 30 days of surgery or as a direct result of a surgical complication. Previous heart surgery was a strong predictor of development of one or more complications in both groups of patients, being associated with an adjusted relative risk of 1.6-2.0. Other important predictors in both surgical groups were surgical priority, older age, peripheral vascular disease, and higher serum creatinine. Although a number of preoperative risk factors could be identified for the development of renal failure, low cardiac output, and requirement for prolonged mechanical support, few risk factors could be identified for the development of mediastinitis and reoperation for bleeding. This observation suggests that mediastinitis and reoperation for bleeding are more likely the result of technical factors rather than patient-related risk factors.

Pulmonary fibrosis was induced in eight baboons with bleomycin; five untreated animals were controls. After 45-65 U/kg of bleomycin, lung volumes and diffusing capacity were reduced, and static lung pressure-volume curves were shifted to the right. Right middle lobes were resected at this time in five bleomycin-treated and two control animals. Compared to controls, right middle lobes from bleomycintreated animals had increased weight and contained increased amounts of total protein, collagen, elastin, and DNA; synthesis of collagen and noncollagen protein were also elevated. Occasional alveolar septae were edematous and infiltrated by mononuclear inflammatory cells; a slight increase in collagen was demonstrable histologically. Four of six treated animals died with extensive diffuse interstitial fibrosis after 95 U/kg of bleomycin. Biochemical analyses revealed significantly elevated lobar contents of dry weight, protein, elastin, and collagen. Two animals survived 95 U/kg of bleomycin and were terminated 6 mo after treatment. In these animals, physiologic studies were indicative of restrictive lung disease, but lung histology was nearly normal. Lung weight, total protein, and DNA had returned to control values, but collagen and elastin were increased in amount and concentration. Bleomycin induces an intense inflammatory response in the lung. During this inflammation, connective tissue proliferation occurs in concert with proliferation of other tissue components. Cessation of bleomycin treatment is followed by resolution of inflammation manifested by decreases in tissue mass, cellular content, and nonconnective tissue protein. Collagen and elastin deposited during inflammation are less successfully removed during resolution, leading to a stage characterized by increased concentrations of these proteins. A similar sequence of tissue alterations may occur in idiopathic diffuse interstitial fibrosis of man in response to various lung injuries.

The eighteenth survivor of correction of an anomalous left pulmonary artery arising from the right pulmonary artery is reported. This is the first case in which postoperative angiography demonstrated patency of the left pulmonary artery. The onset of symptoms in infancy, predominance of expiratory rather than inspiratory stridor, anterior indentation of the esophagus, and lethal progression of symptoms during the first year of life are peculiar to this anomaly. Operation through a left thoracotomy is advocated, with division of the proximal left pulmonary artery and implantation into the main pulmonary artery posterior to the phrenic nerve. Previously reported cases are collectively reviewed.

This study was performed to determine if systemic temperature affects the rate of cooling and rewarming of the myocardium between infusions of cold potassium cardioplegic solution and if it alters the degree of myocardial protection. Twenty-one dogs underwent cardiopulmonary bypass and 3 hours of ischemic arrest produced by infusing 0 degrees to 4 degrees C potassium cardioplegic solution every 20 minutes. The animals were perfused at different systemic temperatures--Group A, 23 degrees C; Group B, 30 degrees, C; and Group C, 37 degrees C. Myocardial temperature decreased to 11 degrees C in Groups A and B as compared with 13 degrees C in Group C immediately after infusion of the potassium cardioplegic solution (p0.0007). Myocardial temperature increased to 19 degrees, 21 degrees, and 26 degrees C in Groups A, B, and C (p0.000005) 20 minutes after infusion. Myocardial adenosine triphosphate (ATP) concentration significantly decreased, from 6.69 to 3.56 mumoles/gm (p0.0003) in Group B and from 4.99 to 2.80 (p0.005) in Group C at the end of 3 hours of cardioplegic arrest. Myocardial glycogen levels also significantly decreased, from 1.156 to 446 mg% (p0.003) in Group B and from 811 to 439 mg% (p0.04) in Group C. Myocardial ATP and glycogen did not decrease significantly in Group A during the period of arrest. Myocardial lactate values increased more in Groups B and C during the arrest period than in Group A. 12.6 versus 6.5 mumoles/gm (p0.03). Moderate systemic hypothermia, therefore, appears to enhance the myocardial protection of potassium cardioplegia.

The case histories of 2 patients with atrial rupture from blunt chest trauma are presented, one of whom is the tenth survivor. Based on a review of these cases and the literature, important factors in the diagnosis and treatment of this easily repairable anatomic lesion are discussed. The importance of rapid recognition and early operation are emphasized.

Ventricular fibrillation is frequently induced during cardiac surgery to quiet the operative field. The reported effects of fibrillation on the myocardium vary considerably. In an attempt to better define these effects, we subjected 28 dogs to one hour of total normothermic bypass. Myocardial blood flow, lactate, adenosine triphosphate (ATP), oxygen consumption, and left ventricular fibrillation was induced in 5 dogs and continuous electrical fibrillation in 7 dogs. These groups were compared to two respective control groups with beating hearts of 8 animals each. Coronary sinus flow, total coronary blood flow, left ventricular flow, myocardial oxygen consumption, and myocardial tissue lactate increased significantly in the fibrillating hearts. Left ventricular dp/dt decreased with fibrillation, but not significantly. It is concluded that the metabolic demands of ventricular fibrillation exceed the increase in coronary blood flow, when compared to demands of the beating heart, and that decreased left ventricular performance may result.

Air embolism following penetrating lung trauma has been reported infrequently and its existence is questioned. A death resulting from air embolism following a high-velocity gunshot wound is presented. Appropriate treatment and preventive measures are discussed.

Considerable controversy exists as to whether or not antibiotics should be administered "prophylactically" to patients with penetrating chest trauma. No prospective study of this problem has been reported. Therefore, 75 patients with isolated, penetrating chest injury were randomized prospectively in a double-blind study. Group A patients (38 patients) were given 300 mg. of clindamycin phosphate every 6 hours, beginning with admission and lasting until 1 day following chest tube removal or for 5 days, whichever was shorter. Group B patients (37 patients) were given a placebo on the same schedule. The patients' hospital course, fever, white blood count, culture data, and roentgenograms were recorded serially. Clindamycin-treated patients had a significantly lower incidence of radiographic pneumonia, less fever, and a lower incidence of positive pleural and wound cultures. They acquired empyema less frequently, required fewer operations, and had a shorter period of hospitalization. Antibiotics may be useful, therefore, as adjunctive therapy in the management of penetrating chest trauma.

During the 10-year period ending 1 March 1978, 100 consecutive patients with penetrating cardiac wounds entered the Bexar County Hospital with some sign of life. The early and late mortality rate, 11%, declined to 8% during the last 4 years. Noncardiac injuries were responsible for six of the eleven deaths. Complications occurred in 17. The most frequently injured chambers were the right ventricle (46) and left ventricle (30). Sixty-nine patients had stab wounds and 26 had gunshot wounds. Pericardiocentesis was falsely positive or negative in 12 of 47 patients. Two distinct syndromes were apparent, hemorrhagic shock and cardiac tamponade. Patients with shock had immediate thoracotomy. Patients with suspected tamponade had a subxiphoid pericardial window, under local or light general anesthesia, for diagnosis and decompression before endotracheal intubation and sternotomy. Most wounds were repaired by direct suture. Cardiopulmonary bypass and thoracotomy before arrival in the operating room were rarely indicated.

Ventricular fibrillation during normothermic cardiopulmonary bypass is deleterious to the myocardium. This study was undertaken to determine if moderate systemic hypothermia would protect the myocardium during ventricular fibrillation. Fourteen mongrel dogs were subjected to 1 hour, 15 minutes of total cardiopulmonary bypass. Ventricular fibrillation was induced by a continuous electrical alternating current applied at the beginning of bypass and lasting for 1 hour. Six animals were maintained at normothermia (Group I), and eight were cooled to 30 degrees C. for 1 hour (Group II). The hypothermic group (Group II) demonstrated lower myocardial oxygen consumption and metabolism, decreased coronary blood flow, and less myocardial lactate production during ventricular fibrillation than did Group I. It is concluded that hypothermia does offer some protection, although not complete, against the deleterious effects of ventricular fibrillation described previously.

Six venous cannulas (USCI No. 32, USCI No. 40, USCI No. 44, Sarns No. 40, Sarns two-stage cavoatrial, and Ferguson Argyle No. 40) were tested for efficiency of venous flow during cardiopulmonary bypass, with and without aortic cross-clamping. Each cannula was tested six times in dog models (twice in each of three dogs) and the data were averaged. The tip of the cavoatrial Sarns catheter was positioned as recommended. Two No. 32 USCI caval cannulas were placed either with or without caval snaring. The other cannulas were placed in the right atrium. Arterial flow was constant at 80 ml/kg/min, and aortic pressure averaged 84 mm Hg. Central venous pressure and the right ventricle excluded from the pulmonary artery so that blood which was not drained via the venous cannula was measured. Each single atrial cannula decompressed the right atrium (right atrial pressure 0 to 1 mm Hg) better than two caval cannulas (right atrial pressure 0 to 2 mm Hg). Caval snaring did not empty the right atrium (right atrial pressure 2 to 5 mm Hg) as well as any single cannula. The cavoatrial Sarns catheter did not empty the right atrium as well (right atrial pressure 2 to 4 mm Hg), but drained blood from the inferior vena cava (central venous pressure 0 mm Hg) better than other atrial cannulas (central venous pressure 1 to 5 mm Hg). All of the atrial cannulas performed equally well. The right ventricular vent flow varied between 63 and 70 ml/min with each of the atrial cannulas but rose to 85 ml/min with the cavoatrial Sarns catheter and 190 and 74 ml/min during caval cannulation with and without snaring, respectively. Aortic cross-clamping eliminated coronary sinus flow and decreased right ventricular vent flow. Therefore, a single atrial cannula is more efficient in draining blood from the right side of the heart than are two caval or a cavoatrial cannula. This advantage is negated by aortic cross-clamping.

The first two cases of intrapericardial diaphragmatic hernia following a subxiphoid epicardial pacemaker insertion are reported. Factors deemed responsible for this rare complication in one case were previous gastrectomy with a resulting paucity of omentum, and entrance into the peritoneal cavity during the pacemaker procedure.

Recent reports of military thoracic injuries have advocated early thoracotomy and aggressive management of pulmonary injuries with resection as opposed to the more conservative and traditional treatment with chest tube thoracostomy. A retrospective study was therefore performed to determine the incidence of thoracotomy and lung resection in civilian injuries and to evaluate the effectiveness of treatment of these injuries. Between 1973 and 1985, in a series of 1,168 patients, there were 384 gunshot wounds and 784 stab wounds to the thorax. Two hundred eighty-three patients with a gunshot wound (74%) and 602 with a stab wound (77%) were treated with chest tubes alone. Sixty-eight patients (6% of the total) required operative repair of pulmonary hilar or parenchymal injury. Pulmonary resection was necessary in only 18 patients (nine with a gunshot wound and nine with a stab wound), and 10 patients had repair of hilar injuries (nine with a gunshot wound and one with a stab wound). Of patients requiring pulmonary resection, nine required wedge or segmental resection, six required lobectomy, and three patients required pneumonectomy. Mortality for all thoracic injuries was 2.3%: for those treated with chest tube alone, 0.7%; for pulmonary hilar injuries, 30%; for pulmonary parenchymal injuries, 8.6%; and for injuries necessitating lung resection, 28%. Most civilian lung injuries can be treated by tube thoracostomy alone. Although relatively few patients with primary pulmonary injury require thoracotomy, those that do are at significant risk and may require lung resection to control bleeding or hemoptysis or to remove destroyed or devitalized lung tissue.

Complement localization was examined by direct immunoperoxidase procedures on frozen sections of baboon myocardium obtained 24 hours after ligation of the left anterior descending coronary artery. There was extensive localization of C3, C4, and C5 in most infarcted myocardial fibers; however, in these infarcted areas of myocardium, complement components were not found in myocytes immediately adjacent to either the endocardium or epicardium. Although C3, C4, and C5 were all present within the same myocardial fibers as assessed in adjacent serial sections, the light microscopic distribution of these components was dissimilar, i.e., C3 and C5 were present in both a granular and a diffuse pattern within myocytes, whereas C4 was always localized in a diffuse pattern. Complement components C3 and C5, but not C4, were also localized in the walls of small muscular arteries in infarcted myocardium. No complement was observed in myocardial fibers or blood vessels in normal baboon myocardium. Electron microscopic evaluation of C3 localization within infarcted myocardium indicated that C3 was associated with contractile elements of myocytes, as well as with membranes of myocyte nuclei, mitochondria, and sarcoplasmic reticulum. Within vascular smooth muscular cells, C3 was associated with myofilaments and mitochondrial membranes. Thus, the results of this study provide new information regarding the cellular and subcellular distribution of complement components in infarcted baboon myocardium. If this localization of C3, C4, and C5 is a result of their in situ activation within the ischemic myocardium, a variety of complement-derived phlogistic products would be expected to have been produced and to have effected, in part, the subsequent inflammatory response.

We reviewed the records of 44 consecutive patients with advanced esophageal carcinoma treated at either a Veterans Administration or a city-country hospital. The patients, 38 men and six women, ranged in age from 27 to 72 years and had been referred for operative management. The average duration of dysphagia was 5 months. All patients underwent a one-stage esophagogastrectomy with esophagogastrostomy. The last 34 patients also had a modified fundoplication. Lesions at the gastroesophageal junction were approached via a low left thoracotomy and the others via a simultaneous right thoracotomy and laparotomy. All patients had preoperative enteral or parenteral hyperalimentation. Seven patients died within 30 days after operation (operative mortality 16%). Twenty-six patients lived from 3 to 28 months postoperatively (average 11.5 months). Eleven are alive at present (average 10 months). Postoperative complications were as follows: anastomotic leak, three patients (two died); respiratory failure, four (two died); stricture, three; myocardial infarction, two (two died); cholecystitis, one; and pulmonary embolus, one (patient died). Thirty-four patients had modified fundoplication, and an inconsequential anastomotic leak developed in one. In contrast, two of the 10 patients who did not have modified fundoplication died as a result of anastomotic leak. Preoperative hospital stay ranged from 10 to 28 days (average 18); postoperative stay ranged from 10 to 40 days (average 16). Except for the three patients in whom stricture developed, all patients (92%) had continuous relief of dysphagia. We conclude that one-stage esophagogastrectomy with esophagogastrostomy is applicable in most cases and is associated with both satisfactory long-term palliation and a reasonable period of hospitalization. The addition of a modified fundoplication results in a relatively low rate of anastomotic leak.

A case is reported of a right aortic arch vascular ring composed of a right aortic arch with mirror image branches and a retroesophageal left aortic diverticulum with a left ductus arteriosus that appeared as a possible foreign body aspiration in an infant. This vascular ring caused partial occlusion of the left main bronchus with air trapping. A discussion of right aortic arch vascular rings and vascular anomalies that have caused unilateral lung hyperinflation is included in this report.

The human tumor clonogenic assay system has enabled human cancer cells to be grown in vitro and has the potential of providing chemosensitivity results in a manner much like bacterial antibiotic sensitivities. The in vitro growth of human lung cancer cells using this assay has not been previously reported. Over the past 2 years, 3,100 specimens have been plated by means of the two-layer agar technique as developed by Hamburger and Salmon, 302 of which were primary or metastatic lung tumors. Histologic, karyotypic, and nude mice studies confirmed that the colonies were composed of tumor cells. Growth rates (significant growth being greater than or equal to 5 colonies per plate) and plating efficiencies (the number of colonies grown per number of nucleated cells plated) were tabulated for each lung tumor cell type for primary, metastatic, and malignant pleural and pericardial fluids. The average overall growth rate was 199 of 302 (66%)--17 of 19 (90%) large cell carcinomas, 46 of 71 (65%) oat cell carcinomas, 57 of 91 (63%) adenocarcinomas, (* = p less than 0.05 when compared to large cell carcinomas) *40 of 68 (59%) squamous cell carcinomas, *and 39 of 53 (74%) of an undetermined cell type were grown. The average plating efficiency was 0.0236%. In primary tumors, large cell carcinomas had a plating efficiency of 0.0348%, adenocarcinoma 0.0247%, *oat cell 0.0224%, *and squamous cell 0.0113%.* It was concluded that lung tumor cells can be grown in vitro from 66% of lung tumor specimens. The highest growth rates and plating efficiencies were found in large cell carcinomas and the lowest rates in squamous cell carcinomas. This technique may provide a means of testing for the sensitivity of patients' lung tumor cells to various chemotherapeutic agents.

Corticosteroids frequently are used during cardiopulmonary bypass (CPB) to enhance total body perfusion and myocardial preservation. The mechanisms by which steroids might provide protection to the myocardium have not been clearly defined, however. Therefore this study was performed to measure the effects of methylprednisolone (M-P) on coronary flow and distribution, and on myocardial metabolism and contractility. Twenty-three dogs underwent 1 hour of total CPB, 80 cc/kg/minute at normothermia with beating hearts. Alternate animals received M-P, 30 mg/kg. Myocardial blood flow (microspheres technique), myocardial tissue lactate and adenosine triphosphate, lactate extraction, coronary sinus flow (CSF), and coronary vascular resistance (CVR) were measured before, during, and 60 minutes after bypass. LV dp/dt and cardiac output (CO) were measured before and after bypass. Total coronary flow was significantly higher in the M-P group after 10 and 30 minutes of bypass (93 vs 56 ml/100 gm/minute, p less than 0.05, and 96 vs 71 ml/100 gm/minute, p less than 0.05). Right ventricular flow was higher in the M-P group at 10 and 30 minutes of bypass (98 vs 66 ml/100 gm/minute, p less than 0.05, and 90 vs 78 ml/100 gm/minute). Left ventricular flow was higher in the M-P group at 10 minutes of bypass (79 vs 52 ml/100 gm/minute, p less than 0.08). Septal flow also was higher in the treated group at 10 minutes of bypass (64 vs 49 ml/100 gm/minute) and at 30 minutes of bypass (92 vs 67 ml/100 gm/minute, p less than 0.05). CVR after 10 minutes of bypass was lower in the steroid group (88 mm Hg/ml/100 gm/minute vs 1.39 in the control group, p less than 0.03). It is concluded that M-P increases coronary blood flow and decreases CVR in the empty beating heart during normothermic CPB without altering myocardial metabolism or contractility.20

A small infant with severe congenital aortic stenosis presents a difficult therapeutic problem. Both operative and nonoperative treatment are hazardous--especially when other cardiovascular anomalies are present. This report describes a simple, effective technique for dilating the stenotic aortic valve and simultaneously repairing certain associated defects. The procedure has been used successfully in 3 infants with a postoperative follow-up of 6 months to 4 years. There were no deaths, and the functional results have been excellent. This technique is presented as an alternative to the more hazardous approach to open valvotomy and/or stage correction of associated anomalies.