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The purpose is to describe our experience with endovascular treatment of type B aortic dissections. Five patients were treated for complications following type B dissections like, false channel aneurysm formation, rupture and arterial obstruction. They were treated in general anaesthesia using a 'homemade' endoprosthesis or a commercially available endoprosthesis (Excluder) deployed during fluoroscopy. The patients have been followed at regular intervals with a median observation time of 18 months (range 12--36). One patient needed a secondary intervention due to dislodgement of the proximal stentgraft with haemorrhage into both the false and the true lumen. Otherwise there have been no early or late mortality or major complications in this series. Even if our experience with endovascular treatment of type B dissections is rather limited, the results so far are promising. Open surgery in many of these cases is complicated with high morbidity and mortality rate and the endovascular technique offers great advantages. A longer follow-up period is necessary to define the place of endovascular treatment.

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This investigation was performed to study the reasons for receiving disability pension after aortocoronary bypass surgery. During the period March 1983 to November 1985, 250 patients underwent aortocoronary bypass surgery. At a mean follow-up of 4.9 years (range 3.6-6.7) after the operation, 31 patients were dead. Of the 219 survivors, all except four underwent a follow-up examination including an exercise test. The mean physical work capacity had increased from 92.2 W preoperatively to 119.3 W at follow-up (p < 0.001). At follow-up, however, 72 patients had received disability pension. The percentage of positive ECG-tests were equal among those who were working and those who had received disability pension. We suggest that, among those who had received disability pension, about 50% were in sufficient physical condition to manage their previous jobs or another type of job. Reasons other than physical working capacity played an important part as criteria for receiving disability pension.

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Silent ischaemia, defined as ST-depression > or = 1 mm without chest pain, was found on exercise testing in 22 (10.7%) of 206 patients who underwent aortocoronary bypass surgery in the period from March 1983 to November 1985. Exercise testing was performed 4.9 (range 3.6-6.7) years after operation on an electrically braked bicycle. Sixteen of the 22 patients were free from chest pain, while the remaining six had slight to moderate angina pectoris on exercise. Coronary angiography was performed in 21 patients with silent ischaemia; one of the 22 patients died before this investigation. Some 13 patients had one or more occluded grafts, one a new stenosis in a native vessel and five incomplete myocardial revascularization. For the remaining two patients, no aetiology for the ischaemia was found, and revascularization appeared to be complete. Before surgery, 13 patients had three-vessel disease, six two-vessel disease and three one-vessel disease. At follow-up, two patients had three-vessel disease, ten two-vessel disease and seven one-vessel disease. The value of identifying patients with silent ischaemia after aortocoronary bypass surgery with regard to life expectancy and quality is controversial. Subsets of patients, namely, those with main-stem stenosis and three-vessel disease, may benefit from secondary operation. Identification of these patients may therefore be of clinical importance.

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A prospective, randomised, double-blind study was performed to compare the effects of propranolol and placebo on sudden cardiac death in a high-risk group of patients who survived acute myocardial infarction. Altogether 4929 patients with definite acute myocardial infarction were screened for inclusion: 574 (11.6%) died before randomisation, and 3795 (77%) were excluded. Five hundred and sixty patients aged 35 to 70 years were stratified into two risk groups and randomly assigned treatment with propranolol 40 mg four times a day or placebo. Treatment started four to six days after the infarction. By one year there had been 11 sudden deaths in the propranolol group and 23 in the placebo group (p less than 0.038, two-tailed test analysed according to the "intention-to-treat" principle). Altogether there were 25 deaths in the propranolol group and 37 in the placebo group (P less than 0.12), with 16 and 21 non-fatal reinfarctions respectively. A quarter of the patients were withdrawn from each group. Withdrawal because of heart failure during the first two weeks of treatment was significantly more common among propranolol-treated patients than among the controls, but thereafter the withdrawal rate was the same. The significant reduction in sudden death was comparable with that after alprenolol, practolol, and timolol, which suggests that the mechanism of prevention is beta-blockade rather than any other pharmacological property of the individual drugs.

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Systolic pressure in the pulmonary artery was estimated from the interval between pulmonary valve closure and tricuspid valve opening, and the heart rate using a nomogram previously described. The timing of valve movements was recorded by Doppler ultrasound. The estimated pressure correlated well with that obtained at catheterisation in 45 of 48 patients with pulmonary hypertension. Instantaneous variations in pressure and changes with treatment and during exercise could be measured. The method was easy to apply in all age groups, and was found useful both in detecting pulmonary hypertension and in the follow-up of patients. It may help to determine the optimal time for surgery or the effect of treatment.

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The peak pressure drop across the aortic valve in aortic stenosis has been measured by Doppler ultrasound. Maximum velocity in the Doppler signal from the aortic jet was recorded using a maximum frequency estimator. With an angle close to zero between ultrasound beam and maximal velocity in the jet, peak pressure drop can be calculated from the maximal velocity measured; a larger angle will underestimate maximal velocity and pressure drop. In 57 of 63 patients with aortic stenosis, the aortic jet could be reached by the ultrasound beam and, in 37 of these, peak pressure drop by ultrasound was compared with that obtained at catheterisation. In patients less than 50 years of age the aortic jet was easy to find, the measurement was reproducible, and underestimation of the pressure drop obtained at catheterisation was within 25 per cent in 17 of 18 patients. In patients over 50 years Doppler signals from the aortic jet were more difficult to obtain, and pressure drop was significantly underestimated in one-third, but time of maximum velocity in systole could indicate whether moderate or severe aortic stenosis was present.

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The mean pressure drop across the mitral valve and atrioventricular pressure half-time were measured noninvasively by Doppler ultrasound in 40 normal subjects, in 17 patients with mitral regurgitation, 32 patients with mitral stenosis and 12 with combined stenosis and regurgitation. In normal subjects pressure half-times were 20--60 msec, in patients with isolated mitral regurgitation 35--80 msec and in patients with mitral stenosis 90--383 msec. There was no significant change in pressure half-time with exercise or on repeat examinations, indicating relative independence of mitral flow. In 25 patients with mitral stenosis and seven with combined stenosis and regurgitation, pressure half-time was related to mitral valve area calculated from catheterization data. Increasing pressure half-times occurred with decreasing mitral valve area, and this relationship was not influenced by additional mitral regurgitation. Noninvasive measurement of pressure half-time together with mean pressure drop was useful for evaluating patients with mitral valve disease.

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A noninvasive method is described for measuring the pressure drop across the mitral valve in mitral stensois by Doppler ultrasound. A maximum frequency estimator was used to record maximum velocity in the Doppler signal from the mitral jet. Provided the angle between the ultrasound beam and the maximum velocity is close to zero the pressure drop can be calculated directly. Good correlation was found between Doppler measurements and simultaneous pressure recordings during heart catheterisation in 10 patients. No false negative or false positive diagnoses of mitral stenosis were made among 55 patients (35 patients with mitral stenosis and 20 patients with other valve lesions). The measurements were easy to perform in most patients and the method seems well suited both to diagnose and to follow patients with mitral stenosis.

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The effect of bumetanide, a new potent diuretic, was studied in twelve patients with severe chronic renal failure (GFR 2.7 - 10.7 ml/min). Bumetanide 8 mg i.v. caused increased excretion of water and sodium in all patients. In some patients sodium excretion was greater than 50% of filtered load indicating an effect on proximal tubules. Bumetanide 2 mg i.v. was significantly less effective than 8 mg and a greater diuretic effect was produced by bumetanide 16 mg. In a comparative study bumetanide 8 mg was less potent than furosemide 250 mg, a finding in contrast to the potency rate ratio of 1/40 in other conditions. Side effects consisted of mild to moderate muscle pain and stiffness, especially localized in the neck, shoulders and calves. These side effects occurred only in patients with a GFR less than 5.3 ml/min. They were noted in all patients receiving 16 mg and in 3 out of 12 patients who took bumetanide 8 mg. There was no relationship between the occurrence of side effects and plasma bumetanide levels, electrolyte levels or the renal excretion of bumetanide and electrolytes.

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