To determine the relationships among complement activation, pulmonary leukosequestration, and oxygen free radical generation, we prospectively studied 15 patients undergoing cardiopulmonary bypass for myocardial revascularization. Plasma levels of C3a, C4a, and hydrogen peroxide (a marker of oxygen free radical generation) were measured before, during, and after extracorporeal circulation. The results confirm that cardiopulmonary bypass activates complement via the alternate (C3a) pathway. This first phase of complement activation was accompanied by an increase in plasma H202 (from 80 + 8 to 155 + 13 ,ctM/ml; p < .001) and by pulmonary sequestration of polymorphonuclear leukocytes. Protamine administration after cardiopulmonary bypass further activated complement via the classical (C4a) pathway but was not accompanied by a change in plasma hydrogen peroxide. We hypothesize that both complement activation and excess oxygen free radical generation contribute to the pathophysiology of extracorporeal circulation. Circulation 74(suppl III), III-130, 1986. THE COMPLEMENT SYSTEM can be activated by one of two pathways. Activation of the classical pathway by antigen-antibody reaction involves the first complement component, C1, which subsequently interacts with C4 and C2 and then activates C3 and the remainder of the components through C9. Thus, with activation of the classical pathway, there are elevated levels of the anaphylatoxins C4a and C3a. With complement activation via the alternate pathway, interaction of properdin with other serum factors directly activates C3 and the remainder of the complement cascade. Thus, with activation of the alternate pathway, there would be normal levels of C4a but elevated levels of C3a. The altemate pathway of complement activation is stimulated by a variety of interactions, including the contact of blood with the constituents of cardiopulmonary bypass and hemodialysis circuits.'-8 In these situations, C5a-aggregated granulocytes accumulate in the pulmonary vasculature. It has been hypothesized that these activated neutrophils liberate excessive quantities of oxygen free radicals, including the superoxide anion, hydrogen peroxide, and hydroxyl radiFrom the Sections of Thoracic and Cardiovascular Surgery and Clinical Chemistry. Mayo Clinic and Mayo Foundation, Rochester. MN. Address for correspondence: Hartzell V. Schaff, M. D. Mayo Clinic, 200 First St. SW, Rochester. MN 55905. Ill130 cal; when liberated in excessive quantities, these oxygen radicals may contribute to endothelial damage in the lung manifested by increased capillary permeability.9-12 Previous studies have clearly documented the occurrence of complement activation during and after extracorporeal circulation.1-3^ x The present study was designed to correlate changes in complement activation and pulmonary leukosequestration with serum hydrogen peroxide, a marker of oxygen free radical generation. Materials and methods Fifteen patients undergoing cardiopulmonary bypass for myocardial revascularization were entered into this study. All patients had good left ventricular function and no associated pulmonary disease or history of hypersensitivity reactions. No patient received corticosteroids before or during cardiopulmonary bypass. Extracorporeal circulation was conducted in the usual fashion with a Sarnes roller pump, a Bentley Bos-10 bubble oxygenator, a cardiotomy reservoir, and a Pall arterial filter. Crystalloid solution was used to prime the extracorporeal circuit unless patients had preoperative anemia (hemoglobin < 10 g/dl), in which case whole blood was added. Before cannulation, patients received heparin at a dose of 350 units/kg body weight. After cardiopulmonary bypass, protamine (1.3 mg/100 units heparin) was administered over 5 min to neutralize heparin. Administration of protamine occurred at a mean interval of 5 min after discontinuation of bypass.

BACKGROUND. Primary malignant fibrous histiocytoma (MFH) of the lung is a rare clinical entity. Only 23 reports of 49 cases have been reported in the literature. Surgery was the primary mode of therapy, with high rates of local and distant recurrence reported. The role of radiation therapy and chemotherapy has never been clearly defined.METHODS. The records of the Mayo Clinic in Scottsdale and Rochester from 1970 to 1990 were reviewed for cases of primary pulmonary MFH. A review of the literature was also undertaken.RESULTS. Four cases from the Mayo records and 49 cases from a review of the literature were identified. Eight patients were alive at 5 years from diagnosis; all had been treated with surgery as the primary modality. No definite relationship between histologic subtype of MFH and survival could be identified and no definite role of radiation therapy or chemotherapy could be defined.CONCLUSIONS. MFH of the lung should be treated by surgical resection if technically feasible. The role of adjuvant therapy remains undefined. (C) 1996 American Cancer Society.

Reoperation on prosthetic heart valves is increasingly under consideration for both clinical and prophylactic indications. To determine the correlates of hospital events, including in-hospital mortality, new persisting neurologic deficit, and length of postoperative stay, a three-institution study of 2246 consecutive prosthetic valve reoperations performed on 1984 patients between 1963 and 1992 was undertaken. The combined experience ranged from high-risk patients coming moribund to the operating room to an important number of well individuals undergoing prophylactic reoperations on potentially failing valves. The risk-unadjusted hospital mortality was 10.8%, neurologic deficit at hospital discharge 1.1%, and length of stay 10 days (median). Multivariably determined correlates of outcome included age at reoperation, degree, severity, and acuity of impairment of cardiac function, extensiveness of valvular heart disease, coexisting morbid conditions, number of previous heart operations, and concomitant procedures. The risk-adjusted hospital mortality for the first elective reoperation in a good-risk patient was 1.3% (90% confidence limits 0.3% to 4.4%), neurologic deficit 0.3% (90% confidence limits 0.02% to 1.8%), and length of postoperative stay 7 days (90% confidence limits 4 to 13), emphasizing the wide variance in outcome events. Equations were developed to permit wide application of the results of the study for quantitatively estimating the risk of outcome events based on individual preoperative patient characteristics. These estimates should be useful for informed patient consent, considerations of prophylactic valve replacement, and cost and resource use.

Bronchial carcinoid tumors are rare neuroendocrine neoplasms that arise from the Kulchitsky cells of the bronchial epithelium. These tumors can manifest as central carcinoid tumors, pulmonary carcinoid tumorlets, or peripheral carcinoid tumors. Occasionally, the peripheral carcinoid tumors produce corticotropin and result in Cushing's syndrome. Herein we report the first case of Cushing's syndrome associated with a peripheral pulmonary carcinoid tumor that was excised by video-assisted thoracoscopy. After excision, the patient had complete remission. Video-assisted thoracoscopy may be ideal for resecting a peripheral pulmonary carcinoid, especially in patients with debilitation but no evidence of metastasis.

Cardiac valve replacement with use of only the Björk-Shiley prosthesis was performed in 1253 patients between January 1973 and December 1982. There were 828 patients having aortic valve replacement, 280 patients having mitral valve replacement, and 145 patients having double valve replacement with aortic and mitral valve prostheses. Patient outcome was stratified according to multiple variables, including valve position and valve model (spherical versus convexo-concave discs). No valve failure due to strut fracture was identified in 26 high-risk patients (mitral valve replacement with greater than or equal to 29 mm implanted in patients less than or equal to 50 years of age) followed up for a mean of 10 years postoperatively. Fifteen patients had late thrombosis of their Björk-Shiley prosthesis (0.28 per 100 patient-years), but there was no significant difference in risk of valve thrombosis comparing the spherical and convexo-concave discs (0.27 per 100 patient-years versus 0.27 per 100 patient-years). One hundred two patients had 128 thromboembolic episodes; rates of thromboembolism after aortic valve replacement, mitral valve replacement, and double valve replacement were 2.1, 4.3, and 4.6 per 100 patient-years, respectively. Percentages of patients free from thromboemboli after aortic valve replacement, mitral valve replacement, and double valve replacement were 93 % ± 1%, 86% ± 2%, and 89% ± 3% at 5 years postoperatively and 87% ± 2%, 79% ± 5%, and 77% ± 8% 10 years postoperatively. There was no significant difference in the rates of thromboemboli for spherical and convexo-concave discs for all patients and for each of the subgroups. Ten-year actuarial survival estimates for patients dismissed alive from the hospital after aortic valve replacement, mitral valve replacement, and double valve replacement with the Björk-Shiley valve were 65% ± 4%, 63% ± 5%, and 55% ± 8%, respectively. Overall event-free survival (freedom from death, thromboembolism, anticoagulant-related bleeding, endocarditis, and reoperation) was similar for the three patient groups. Performance of the Björk-Shiley valve as judged by late patient follow-up is similar to other mechanical valves, and modifications in disc design do not appear to have reduced the threat of late valve thrombosis and thromboemboli. Evidence does not support elective explantation of this prosthesis.

Nearly 30 years have elapsed since Dr Starr's publication introducing the Starr-Edwards valve. Despite reputed difficulties with a ball-and-cage prosthesis, Starr's dedication in developing this concept has resulted in a valve that today continues to be a benchmark of longevity and function.

Operative treatment of dissections of the ascending aorta differs from that for the descending aorta, not only because of the need for cardiopulmonary bypass, but also because of the frequent occurrence of aortic valve insufficiency. To determine the early and late results of operative repair, we have reviewed the case histories of 121 consecutive patients who underwent repair of ascending aortic dissections between 1962 and 1985. Ages ranged from 16 to 79 years (mean 56 ± 14 years); 54 patients had operation within 2 weeks of onset of symptoms (acute), and the remainder had later repair (chronic). Seventy patients (58%) had clinical evidence of aortic insufficiency at the time of admission. During repair of acute dissection, 10 patients (19%) had aortic valve resuspension and 15 patients (28%) had aortic valve replacement During repair of chronic dissection, eight patients (12%) had resuspension and 43 patients (64 %) had replacement Overall operative mortality was 22 %, significantly higher for patients with acute than for those with chronic dissections (39 % versus 9 %, p < 0.01). Operative risk was similar for patients who underwent repair of ascending aortic dissections without valve resuspension or replacement (31 %) versus those who had repair with aortic valve resuspension (17%) or replacement (17%). During a follow-up period ranging from 1 to 208 months, aortic regurgitation developed in only two patients who did not have aortic insufficiency at the time of repair. Late aortic regurgitation necessitating reoperation developed in one of the 15 survivors who had aortic valve resuspension. Eight patients undergoing aortic valve replacement had complications of their prostheses, including one periprosthetic leak and four mechanical failures. We conclude that resuspension or replacement of the aortic valve does not increase the risk of repair of ascending aortic dissections. Selective management of aortic insufficiency (with valve repair whenever possible) yields satisfactory long-term results.

Considerable contrasts are evident in this book. The approach in some chapters is so simplistic that the material seems geared for the lay population, whereas in other sections an engineering degree would be helpful for appreciating the mathematical models. Perhaps the authors intentionally use this broad and contrasting approach to create divergent appeal, but unfortunately a middle level is not achieved. I felt constant consternation because of the contrast from “spoon feeding” in one chapter to “an ivory tower approach” in the next. Nevertheless, a substantial amount of information is available in the book, and it certainly is of value for its historical compilation and excellent radiographic valve identification.

From January, 1974, to December, 1983, 75 patients with infections related to permanent pacemakers were successfully treated. Demographic characterization, mode of presentation, types of infecting organisms, potential predisposing factors, significance of a retained infected pacemaker lead, and various medical and surgical treatment methods were analyzed. Likely infecting organisms depended on the mode of presentation and the time of the infection. Dermatologic diseases accounted for a significant number of secondary infections. Removal of the entire infected pacing system was required for eradication of infection in 74 of 75 patients. In 31 patients, the infected system was removed at the same time that the new system was implanted. In 26 patients, a two-stage procedure was used that included a period of temporary pacing between explantation of the old system and implantation of the new. No difference in complications or incidence of reinfection was found between these two groups. Infections occurring within 2 weeks after operation accounted for 15 % of the cases. In these patients, Staphylococcus aureus was the most common organism. In patients with later infections, Staphylococcus epidermidis was the most common.

A prospective randomized trial involving 91 patients undergoing cardiopulmonary bypass compared the effects of bubble oxygenators (with and without methylprednisolone sodium succinate) and membrane oxygenators on complement activation and transpulmonary sequestration of leukocytes. Patients were divided as follows: Group I, 30 patients, bubble oxygenator; Group II, 31 patients, bubble oxygenator and methylprednisolone sodium succinate (30 mg/kg); Group III, 30 patients, membrane oxygenator. In Group I, C3a increased from 323 +/- 171 ng/ml during cardiopulmonary bypass to 1,564 +/- 785 ng/ml at 25 minutes after bypass (p less than 0.0001). A significant decrease in C3a was found in Groups II and III compared to Group I (p less than 0.0001). C5a did not change significantly during cardiopulmonary bypass in any group. Reestablishment of pulmonary circulation at the end of bypass produced significant transpulmonary leukocyte sequestration in Group I; the median cell difference was 1,700/microliter. Transpulmonary sequestration was significantly (p less than 0.0001) less in Group II (median cell difference = 200/microliter) and in Group III (median cell difference = 400/microliter) than in Group I. We conclude that cardiopulmonary bypass with a bubble oxygenator alone initiates significantly (p less than 0.0001) more C3a activation and leukocyte sequestration than when methylprednisolone sodium succinate (30 mg/kg) is given 20 minutes before the start of cardiopulmonary bypass with a bubble oxygenator or when a silicone membrane oxygenator is used.

Although technically correct, the title of this book is misleading. In actuality, this text relates the application of noninvasive cardiologic techniques to the preoperative and postoperative evaluation of coronary artery surgical procedures. Inasmuch as these evaluations are generally done by cardiologists, this volume has little material for cardiac surgeons. Only two chapters are devoted to cardioplegia and myocardial protection, and unfortunately these are written as reviews rather than as attempts to provide direction. All of the chapters have excellent appended bibliographies, but few of the chapters contain meaningful substantive information.

Tricuspid valve insufficiency may contribute to a poor hemodynamic result after mitral valve replacement. To determine the role of surgical treatment, we have reviewed the records of 32 adult patients who underwent tricuspid valve repair or replacement 4 months to 14 years after mitral valve replacement. Mild tricuspid valve insufficiency at the time of mitral valve replacement was present in 21 patients (66%); 26 patients (81%) had New York Heart Association class IV disability. Tricuspid annuloplasty was performed in 16 patients, and the remainder received various prosthetic valves. Concomitant repair of mitral valve periprosthetic leak and/or replacement of the aortic valve was necessary in 18 patients (53%). Hospital mortality was 25%, and all early deaths were related to low cardiac output. Among hospital survivors there have been 14 late deaths for 3 and 5 year actuarial survival rates of 65% and 44%. Twelve of the 14 patients who died late and one of 10 patients who were alive at the end of the follow-up period had little or no functional improvement after tricuspid valve repair or replacement. The high early and late mortality and poor functional outcome for patients undergoing tricuspid valve surgery late after mitral valve replacement contrast with our good overall results in reoperation for prosthetic heart valves. It appears that serious tricuspid valve insufficiency after mitral valve replacement frequently signals right ventricular failure and dilatation; restoring valve competence is palliative. This experience encourages us to continue our policy of liberal indications for tricuspid valve annuloplasty at initial mitral valve replacement.

The long-term course (mean 15 years) of 336 patients with valvular incompetence who underwent Starr-Edwards ball valve implantation between 1962 and 1971 was reviewed. Eighteen patients (10%) with aortic valve replacement and 24 (16%) with mitral valve replacement died early postoperatively. Mortality remained high (31%) in the first 3 years after aortic valve replacement; it was highest (13%) in the first year after mitral valve replacement and then approached the normal rate. The most common mode of death was sudden death after aortic and cardiac failure after mitral valve replacement. At follow-up, 76% of survivors had improved symptomatically. Three instances of primary valve malfunction occurred. The probability of freedom from thromboembolism at 15 years postoperatively was 56% for aortic valve replacement and 52% for mitral valve replacement. The Starr-Edwards valve prosthesis is durable over prolonged follow-up period, but thromboembolism remains a persistent problem. Survival may be normal for patients surviving the early postoperative years.

Five hundred fifty-two patients underwent a total of 617 reoperations for repair or replacement of a prosthetic heart valve. Operative mortality for first reoperation (530 patients) was 5.9% for the aortic position and 19.6% for the mitral position. Overall operative mortality was 14% for second reoperation (69 patients) and 7% for third reoperation (14 patients). In addition to valve position, operative mortality for first reoperation appeared to be related to pre-reoperation functional class and urgency of operation. First reoperation for mitral valve patients in New York Heart Association (NYHA) Class II was 4.2%; for Class III. 9.3%; and for Class IV, 41%. In the aortic position, operative mortality was 2.4% for Class I, 1.6% for Class II, 6.3% for Class III, and 20.8% for Class IV. The mortality for elective mitral valve reoperation was 0%; for urgent operation, 20.3%; and for emergency procedures, 54.5%. Elective aortic valve reoperation carried a 1.4% mortality; urgent procedures, 8%; and emergency procedures, 37.5%. No significant differences in bleeding complications were noted between reoperations and initial valve replacement. The data appear to suggest that when significant valve dysfunction is first noted, reoperation should be undertaken to minimize operative risk.

Cardiac catheterizations and cardiac operations were evaluated in the population of Olmsted County, Minnesota, from 1973 through 1980, and trends in this region were compared with nationwide trends based on data from several sources. The rates of coronary arteriography and coronary-artery bypass operations in Olmsted county have increased over time, but overall, the rates of catheterization and operation appeared to be leveling off. For the country as a whole, the data appear to show similar trends, but there are wide differences among regions in the rates of operation and catheterization. In 1980 40 per cent of hospitals with cardiac-catheterization laboratories and 55 per cent of those with facilities for open-heart surgery were doing fewer than the suggested minimum numbers of these procedures necessary to achieve optimum results. The data support the view that further growth in the number of cardiac centers should be avoided. We believe there is a need for continued evaluation of the use of cardiac services if quality is to be protected and costs controlled.