We have demonstrated a high prevalence of sleep apnoea, which persisted after 2 months of medical treatment, in patients referred for acute left ventricular failure. Central sleep apnoea can be considered a marker of the severity of congestive heart failure.

A 58 year old woman on long term treatment with chloroquine for systemic lupus erythematosus presented with cardiac conduction disorders and heart failure with hypertrophic cardiomyopathy, which was confirmed by histology to be related to chloroquine toxicity. The heart failure improved on stopping chloroquine treatment. (Heart 1999;81:221-223) Keywords: chloroquine; cardiomyopathy; arrhythmias A 58 year old female domestic worker was admitted to the department of general medicine because of diVuse abdominal pain and breathlessness on exertion. She also had fatigue and was found on examination to have right sided pleural and peritoneal eVusions. These were confirmed by echography. History included pulmonary tuberculosis at the age of 18 and a diagnosis of disseminated lupus erythematosus (SLE) at the age of 20 with weakness, fever, lymphadenopathy, and a rash, which preceded nephropathy. She had been treated with corticosteroids for 15 years ; with azathioprine and cyclophosphamide for seven years ; with the antimalarial drugs hydroxychloquine for 25 years to a cumulative dose of 4380 g and then chloroquine for two years to a cumulative dose of 657 g; and with phenylbutazone for polyarthritis for four years . On examination, she was generally unwell with a weight loss of 13 kg over two years. On admission, she weighed 46 kg (height 159 cm). She had no fever, blood pressure was 120/80 mm Hg, and heart rate 74 beats/min. There was a short pericardial rub and signs of heart failure without any cardiac murmur.Biochemical examination showed no indication of active SLE-C reactive protein was 7 mg/l (normal < 12). Erythrocyte sedimentation rate was 2 mm in the first hour and her blood count was normal. Autoantibodies including antinuclear, anti-DNA, and rheumatoid factor were negative. There was proteinuria at 0.015 g/l and creatinine clearance was 0.78 ml/s. Creatine kinase was 219 UI/l (normal < 131) with a normal MB fraction. Aspartate aminotransferase was 54 U/l (normal < 36), alanine aminotransferase 52 U/l (normal < 36), and alkaline phosphatase 49 UI/l (normal < 76). Abdominal echography showed only moderate ascites, and chest radiography showed cardiomegaly with an increased cardiothoracic ratio of 50% compared with 39% one year earlier. There was also a small right sided pleural eVusion. ECG showed complete right bundle branch block with a long PR interval. Previously there had been complete left bundle branch block. The patient was admitted and His bundle ECG showed a His conduction velocity of 70 ms without any other conduction anomaly. A DDD type pacemaker was implanted for security.Transthoracic echocardiography (fig 1) suggested a diagnosis of biventricular cardiac hypertrophy with a left ventricular diameter of 37 mm and left wall thickness of 15 mm, giving a relative wall thickness of 0.81 and a left ventricular mass index of 170 g/m 2 . Left ventricular ejection fraction was 45% and the Appleton profile on the mitral valve Doppler was a restrictive type 3. The right atrium was dilated and ...

BP abnormalities should be considered as markers of an elevated risk in diabetic subjects but cannot be considered at present as predictive of the appearance of micro-albuminuria or other abnormalities. ABPM is thus of interest in type I or type II diabetes both in the initial assessment and in the follow-up and adaptation of treatment. PHARMACO-THERAPEUTIC USES: The introduction of ABPM has truly changed the means and possibilities of approach to the study of the effects of anti-hypertensive medications, with new possibilities of analysis such as trough-peak ratio smoothness index, etc.

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Summary:Thrombolysis may favorably affect the clinical outcome of mobile right atrial thrombus following puimonary embolism (PE). We report the case of three patients with mobile right atrial thrombus following PE, in whom fibrinolysis was performed. Atrial mass disappeared on the control echocardiogram, but control ventilation perfusion scan showed new perfusion defects in all patients. Thrombolysis seems successful for the treatment of patients with mobile right atrial thrombus following PE; however, recurrent PE may be induced by fibrinolysis. This may affect the benefit of such therapy and should be taken into account when using this therapeutic treatment.

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A 62-year-old man had an acute episode of hypertension 72 h after fine needle aspiration biopsy of an intrahepatic nodule. The patient had been operated 3 years previously for a right adrenal phaeochromocytoma with no evidence of metastases at that time. Thus, a relapse of the tumour was postulated and confirmed by raised levels of urinary metanephrines. The extent of the metastases precluded surgical intervention and thus localised embolisation was proposed and permitted a clinical Keywords: phaeochromocytoma; metastases; fine needle aspiration biopsy; embolisation A 62-year-old man was hospitalised 72 h after a fine needle aspiration biopsy of a hepatic nodule with headache, sweats, palpitations and vertigo. He was found to have a very high blood pressure (200/100 mm Hg). Three years previously, he had had several hypertensive crises with blood pressure rising to 240/140 mm Hg, with similar symptoms. The diagnosis of a right sided adrenal phaeochromocytoma was established by urinary metanephrine levels (87 mol/24 h, normal Ͻ4.2) and by abdominal CT scan which showed a heterogeneous right adrenal mass (80 × 70 mm) (Figure 1). There was no evidence of spread of the tumour to other sites. After the introduction of treatment with labetolol at 200 mg/day the patient underwent total resection of the right adrenal tumour. Histological examination confirmed an adrenal phaeochromocytoma of 181 grams with areas of haemorrhagic necrosis and no evidence of extension beyond the capsule. The post-operative period was uneventful and the patient was asymptomatic without any treatment. Follow-up was limited to an annual abdominal ultrasound examination and nothing abnormal was found until the discovery 3 years after the original intervention of two nodules in the segment VI of the liver. It was following a fine needle aspiration biopsy of one of these nodules that the patient was hospitalised in our unit for a hypertensive crisis. The histological and cytological examination of the samples showed only normal liver tissue. The diagnosis of metastasis from a phaeochromocytoma was postulated and confirmed by the levels of urinary metanephrines (23 mol/24 h). A CT scan of the abdomen (Figure 2) demonstrated three hepatic lesions in segments VI and VII, the largest being 50 × 40 mm. Thoracic CT scan was normal and total body scan by metaiodobenzylguanidine (MIBG) showed uptake not only in the liver but also in the