One may suggest that the prognosis of carcinosarcoma might be determined by the sarcoma component of the tumor. Therefore the generally accepted therapies of soft tissue sarcomas should be adopted for the follow-up treatment of patients with pulmonary carcinosarcoma.

Between 1975 and 1993, lung resections were performed in 1735 patients because of malignancies, with an early postoperative mortality of 7.2% (125 patients). Early postoperatively acute cardiorespiratory failure was experienced by 32 patients (1.85%), of whom 26 died despite immediate resuscitation measures. In 20/26 patients autopsy was performed revealing central pulmonary embolism as the cause of death in 19 of them. In one patient a rupture of the free posterior left ventricular wall following transmural myocardial infarction was found. Two patients who could be resuscitated successfully were operated on with extracorporeal circulation after pulmonary angiography had been performed to confirm the diagnosis; however they died 2 days later of right heart failure. Of the survivors three cases had myocardial infarctions, one patient had arrhythmias of unknown etiology. Immediate embolectomy with the use of extracorporeal circulation was performed in two patients, only on the ground of suspected pulmonary embolism and without further diagnostic measures. Both patients survived. Of the 23 cases, with proven pulmonary embolism 17 were still under postoperative prophylaxis with heparin. Six patients were already fully mobilized. We conclude that massive pulmonary embolism is a frequent early postoperative fatal complication after lung resections, which cannot be safely prevented by postoperative heparinization. The only successful life-saving measure in the case of central pulmonary embolism is immediate pulmonary embolectomy, if necessary without further diagnostic measures.

No abstract

Between 1975 and June 1992, pneumonectomy was performed in 594 patients, of whom 33 (5.6%) developed bronchopleural fistulae postoperatively. Until 1989 25 cases were reoperated: 5 patients were treated by thoracoplasty primarily, 20 by repair of the stump with sutures and by covering the stump with pericardial tissue or intercostal muscle, of whom 10 suffered from empyema. In 5/20 patients (25%) chronic fistulae developed making further interventions necessary. Since 1989 seven patients with bronchial stump fistulae have been reoperated with a delay of less than 12 h after diagnosis. Surgery consisted of reclosure of the stump with sutures in five patients. In addition, every patient was treated with the intrathoracic transposition of a petiolated ipsilateral pectoral muscle graft, which was the only treatment in two patients. Neither recurrence of the bronchopleural fistula nor empyema was seen in this group of patients (0%). We conclude that bronchial stump fistulae in patients after pneumonectomy can be treated successfully by the use of pectoral muscle flaps either combined with a closure of the leak using sutures or as the only measure. The method proved to be simple, safe and without major impairment of the patient. In combination with early reintervention, postpneumonectomy empyema including a disfiguring thoracoplasty can thereby often be avoided.

Mitral valve replacement (MVR) is still associated with a relatively high mortality. To investigate the influence of chordal preservation in MVR on left ventricular size and function, we studied a series of 82 patients who underwent MVR either with (group A n = 50) or without (group B n = 32) preservation of the subvalvular structures and compared the two groups. Echocardiography was performed preoperatively, and 7 days and 3 months postoperatively. Echocardiographic investigations included left atrial and ventricular diameters, right ventricular diameters and left ventricular length. Preoperatively there were no difference between the two groups of patients. Intraoperative and postoperative management was similar in the groups. Three months postoperatively echocardiographic examinations demonstrated that chordal preservation in MVR resulted in smaller left ventricular systolic and diastolic diameters (LVESD: gr. A 43.4 +/- 7.8 mm vs gr. B 48.8 +/- 9.2 mm P < 0.05, LVEDD: 57.3 +/- 7.8 mm vs 62.9 +/- 10.5 mm P < 0.05) and a significantly decreased left ventricular length (87.1 +/- 4.2 mm in gr. A vs 97.5 +/- 5.7 mm in gr. B P < 0.05). In addition, left ventricular ejection fraction in group A was significantly improved compared to group B (54.2 +/- 11.2% vs 48.1 +/- 12.4%, P < 0.05). We conclude that chordal preservation in MVR improves left ventricular function and reduces left ventricular diameters and volumes compared to resection of the mitral subvalvular appartus and that these beneficial effects can be maintained in the postoperative course.

To determine a possible phase of hypercoagulability after the use of high-dose aprotinin, a prospective randomized double-blind study was performed. Twenty patients undergoing aortocoronary bypass surgery were investigated, a placebo group P (n = 10) was compared to an aprotinin group A (n = 10). Examining parameters of thrombin activation and fibrinolysis, we found during extracorporeal circulation--under continuous aprotinin infusion--a significant inhibition of thrombin activation and fibrinolysis in the aprotinin group (thrombin-antithrombin-III-complexes: 95 +/- 23 micrograms/l, d-dimers: 448 +/- 60 ng/ml, plasminogen activity: 33 +/- 3%, plasminogen activator inhibitor: 98 +/- 14 U/ml) compared to the placebo group (thrombin-antithrombin-III-complexes: 143 +/- 13 micrograms/l, d-dimers: 2755 +/- 430 ng/ml, plasminogen activity: 125 +/- 15%, plasminogen activator inhibitor: 10 +/- 4 U/ml). In contrast, after stopping the aprotinin infusion--from the end of extracorporeal circulation until the morning of the first postoperative day--strong thrombin activation took place in the aprotinin group (d-dimers increased from 472 +/- 90 to 1607 +/- 140 ng/ml), while in the placebo group a decrease could be registered. At this time, the fibrinolysis was still reduced in the aprotinin group (plasminogen activity: 48 +/- 6% vs 85 +/- 16% in the placebo group). In conclusion, interference with the thrombohemorrhagic balance induces hypercoagulability after the use of high-dose aprotinin, with elevated levels of thrombin-antithrombin-III-complexes, d-dimers, and plasminogen and a decreased level of plasminogen activator inhibitor. In our opinion, it is necessary to prevent this counter-regulation.(ABSTRACT TRUNCATED AT 250 WORDS)

In a prospective randomized double-blind study, the activated clotting time (ACT), heparin use, parameters of anticoagulation, and thrombin activation during extracorporeal circulation were studied in 20 patients who underwent aortocoronary bypass operations. The patients were divided into two groups: Group A was given a placebo, while Group B was given aprotinin according to the high-dosage Trasylol scheme. During ACT-controlled heparinization (ACT > 460 s) there was a significant heparin reduction in Group B (22,100 USP-E) in comparison to Group A (35,200 USP-E). Despite this lower quantity of total heparin, the ACT in Group B was significantly extended (Group B = 837 s, Group A = 492 s). The ACT did not correlate thereby with the heparin concentration or the total quantity of heparin in either group. In contrast to the control group, there was no increased thrombin generation in the aprotinin group. The thrombin-antithrombin III complexes (Group A = 143 micrograms/L, Group B = 102 micrograms/L) as well as the specific dimers (Group A = 2755 ng/ml, Group B = 448 ng/ml) were significantly lower under the use of aprotinin. The connection between the ACT, the heparin concentration, and the aprotinin concentration was further investigated in an ex-vivo model. The ACT samples were diluted with the aim of eliminating the influence of aprotinin. Under these conditions it was shown that for heparin concentrations between 2-4 U/ml there was a parallel shift of the ACT/heparinconcentration curve with the addition of aprotinin in a defined concentration range of 200-300 KIU.(ABSTRACT TRUNCATED AT 250 WORDS)

We report on a 31-year-old woman who underwent surgery for two metachronous cardiac myxomas - 7 and 9 years after excision of several cutaneous myxomas. Our observation is a further case of a syndrome-like complex of cardiac and cutaneous myxoma(s), pigmentation anomalies and endocrine disorders described only recently. As modern investigative methods and the development of cardiovascular surgery have brought about an essential improvement in diagnostics and prognosis of cardiac myxomas, the knowledge of this syndrome-like complex is of great therapeutic importance. Therefore, in our opinion, echocardiographic investigations are strongly recommended even in asymptomatic patients, once several cutaneous myxomas are diagnosed histologically.