[Invasion of the pulmonary artery by an undifferentiated carcinoma]. / Obstruction tumorale de l'artère pulmonaire par un carcinome indifférencié

INTRODUCTION: The diagnosis of chronic obstruction of the pulmonary artery is difficult. We present the case of a woman with an invasive, undifferentiated carcinoma of the pulmonary artery. CASE REPORT: A 61 year old woman complained of increasing dyspnoea. This was evaluated by computed tomography which showed a defect in the main pulmonary artery. There was no clinical or radiological improvement following anticoagulant treatment for two months. A repeat CT scan showed a persisting intravascular defect and the diagnoses considered included post-embolic pulmonary arterial hypertension and angiosarcoma. A surgical biopsy was performed and pericardial and aortic tumour nodules were found during the operation. The pathological examination revealed undifferentiated carcinoma. Further investigations failed to reveal the primary site. CONCLUSION: Invasion of the pulmonary artery by angiosarcoma or other tumour is part of the differential diagnosis of chronic thromboembolic disease. The diagnosis rests on histology obtained by an intravascular or surgical procedure. Complete surgical excision may be possible in angiosarcoma but it was impossible in our patient. The patient died despite two courses of chemotherapy and targeted therapy with erlotinib.

[Long-term results of tricuspid prostheses]. / Devenir au long cours des prothèses en position tricuspide.

The results of a series of 38 patients with a tricuspid valve prostheses (:76% Starr-Edwards ball valves) associated with correction of one or two left heart valvular lesions are presented. 24 patients underwent clinical and haemodynamic assessment on average 4,2 years after surgery. The conclusions were that signs of systemic venous hypertension were mainly related to residual right ventricular failure despite normal valve function and secondarily to the poor hemodynamic profile of these prostheses and their paradoxical motion. Using these results: 18% early mortality; 24% late mortality; 24% late thrombosis amongst survivors and 52% residual right ventricular failure; and 47,5% of excellent results. The clinical and haemodynamic profiles of the patients were analysed to determine the surgical indications. Apart from the correction of associated left heart valve lesions, it seems that the prognosis in tricuspid valve repair depends on the duration of tricuspid regurgitation and the severity of right ventricular myocardial disease. In elderly patients with chronic tricuspid regurgitation and severe right ventricular failure, long-term analysis showed 87,5% poor results, whilst in younger patients with a shorter history of tricuspid regurgitation and less severe right ventricular failure, there was 77,7% excellent long-term results. Semi circular annuloplasty is widely indicated in mild or severe functional tricuspid regurgitation. Tricuspid valve replacement, a much more serious operation, remains essential in chronic organic lesions and in some cases of massive functional tricuspid regurgitation. A regards the choice of prosthesis, the authors suggest the Hancock bioprosthesis as a logical choice in cases of severe right ventricular failure as they are less prone to thrombosis than mechanical prostheses and have good haemodynamic profiles. The evolution of the right ventricular failure even after correction of tricuspid regurgitation underlines the importance of preventative therapy by early correction of left heart lesions.

[Late thromboses on tricuspid valve prostheses. Apropos of 6 cases]. / Thromboses tardives sur prothèses tricuspidiennes. A propos de 6 cas.

Six out of 24 patients with tricuspid valve prostheses, operated between 1968 and 1978, followed-up from 1 to 10 years (average 4,2 years) developed thrombosis. This complication occurred between 15 and 59 months after operation (average 37 months). All patients were female with ages ranging from 18 to 44 years (average 38 years). Starr-Edwards prostheses were used in all cases. Five of these patients were on anticoagulants therapy, which was well within therapeutic limits in 3 patients. In contrast to thrombosis of mitral or aortic valve prostheses, the presenting symptoms were slowly progressive and discreet in 4 patients; in 1 case, the thrombosis was diagnosed on routine follow-up examination. The slow clinical presentation allows time for useful complementary investigations, catheterisation and angiocardiography being the most reliable methods of confirming this difficult diagnosis: these investigations were carried out in 2 patients, and in both cases, very high right atrial pressure with diastolic gradients between the right atrium and right ventricle of over 10 mm Hg were recorded. Cineangiography showed tricuspid regurgitation in both cases with reflux in the vena cavae and very dilated right atria, stagnation of contrast and poor right ventricular filling. Five patients were reoperated with two postoperative deaths. Particular anatomical appearances were observed at operation or autopsy with fibrin and platelet deposits at different levels of the prosthesis (sewing ring and/or struts) interfering and even blocking the function of the ball or disc. Organized thrombus on the cage was only observed in one patient. In this case, the struts on the prosthesis were set in the right ventricular cavity. Thrombosis of tricuspid valve prostheses is generally a slowly progressive complication and may be diagnosed in time by regular follow-up, so that reoperation may be considered without unnecessary delay.

[Action of aminophylline on the strength of contraction of the diaphragm in patients with chronic obstructive respiratory insufficiency]. / Action de l'aminophylline sur la force de contraction du diaphragme des malades atteints d'une insuffisance respiratoire obstructive chronique.

The effect of a sustained-release aminophylline preparation on diaphragmatic contractility was investigated in patients with stable chronic obstructive lung disease (FEV1 = 22.6% of predicted value). Ten such patients were tested before (control) and after a week's course of oral aminophylline. Diaphragmatic contractility was evaluated by measuring the transdiaphragmatic pressure generated at residual functional capacity by bilateral electrical stimulation of the phrenic nerves. The nerves were stimulated supramaximally at 1 Hz, using needle electrodes. Plasma aminophylline levels (12.5 +/- 0.9 mg/l) were within therapeutic range in all patients. After treatment with aminophylline, for each stimulation the transdiaphragmatic pressure increased significantly from 14 +/- 1.3 to 17 +/- 1.3 cm H2O (+21%; P less than 0.005). These results confirm that aminophylline increases the force of contraction of the diaphragmatic fibres electively tested by the technique used. Long-term treatment with theophylline in therapeutic doses may be of interest in such patients, as it might improve their diaphragmatic contractility and result in better control of both respiratory muscle fatigue and episodes of acute respiratory failure.

The future ain't what it used to be.

Base salaries for all health care managers will rise an average of 4.0 to 4.5 percent from 1993 to 1994--less than in previous years. Why the slowdown?

Effects of digoxin on diaphragmatic strength generation in patients with chronic obstructive pulmonary disease during acute respiratory failure.

We studied the effects of digoxin, a compound that has an inotropic effect on the myocardium, on diaphragmatic function in 8 patients with chronic obstructive pulmonary disease. All the patients were in acute respiratory failure and were artificially ventilated. Diaphragmatic strength was assessed by measuring the transdiaphragmatic pressure generated at functional residual capacity during bilateral supramaximal electrical stimulation of the phrenic nerves. The latter were stimulated before and at 45 and 90 min after administration of digoxin (0.02 mg/kg infused for 10 min). In all the patients, cardiac output was measured by the thermodilution technique using a Swan-Ganz catheter placed in the pulmonary artery. Arterial blood gases and pH were maintained within normal range by mechanical ventilation. In all the patients, digoxin plasma levels reached the therapeutic range (mean values, 2.82 +/- 0.17 and 2.90 +/- 0.20 nmol/L at 45 and 90 min, respectively) after digoxin administration. Diaphragmatic strength improves significantly after digoxin administration, the transdiaphragmatic pressure for an identical phrenic stimulation increasing by 19.5% (p less than 0.001) on the average. This increase was noted 45 and 90 min after digoxin administration. We conclude that digoxin has a potent effect on diaphragmatic strength generation that may be beneficial in patients with chronic obstructive pulmonary disease during acute respiratory failure. Furthermore, this inotropic positive effect of digoxin on the diaphragm, as previously observed for the myocardium, emphasizes the similarities between these 2 contractile tissues.