BACKGROUND Many secondary abnormalities in chronic heart failure (CHF) may reflect physical deconditioning. There has been no prospective, controlled study of the effects of physical training on hemodynamics and autonomic function in CHF. METHODS AND RESULTS In a controlled crossover trial of 8 weeks of exercise training, 17 men with stable moderate to severe CHF (age, 61.8 +/- 1.5 years; left ventricular ejection fraction, 19.6 +/- 2.3%), increased exercise tolerance (13.9 +/- 1.0 to 16.5 +/- 1.0 minutes, p less than 0.001), and peak oxygen uptake (13.2 +/- 0.9 to 15.6 +/- 1.0 ml/kg/min, p less than 0.01) significantly compared with controls. Training increased cardiac output at submaximal (5.9-6.7 l/min, p less than 0.05) and peak exercise (6.3-7.1 l/min, p less than 0.05), with a significant reduction in systemic vascular resistance. Training reduced minute ventilation and the slope relating minute ventilation to carbon dioxide production (-10.5%, p less than 0.05). Sympathovagal balance was altered by physical training when assessed by three methods: 1) RR variability (+19.2%, p less than 0.05); 2) autoregressive power spectral analysis of the resting ECG divided into low-frequency (-21.2%, p less than 0.01) and high-frequency (+51.3%, p less than 0.05) components; and 3) whole-body radiolabeled norepinephrine spillover (-16%, p less than 0.05). These measurements all showed a significant shift away from sympathetic toward enhanced vagal activity after training. CONCLUSIONS Carefully selected patients with moderate to severe CHF can achieve significant, worthwhile improvements with exercise training. Physical deconditioning may be partly responsible for some of the associated abnormalities and exercise limitation of CHF, including abnormalities in autonomic balance.

Since their introduction several years ago, the 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase inhibitors-the statins-have been widely used for hyperlipidemia and for the primary/secondary prevention of cardiovascular diseases. They have been shown to be safe as well as efficacious in a number of different clinical trials; however, studies have suggested that they can interact with other co-administered therapies. More recently, the thienopyridines have been successfully integrated with the conventional medical treatment of coronary disease as they showed effectiveness in reducing platelet activity both in stable and unstable settings. They also improve the outcome of patients treated with percutaneous coronary intervention. The potential interaction of statins and thienopyridines is a matter of concern. Despite some preclinical data suggesting an interaction between statins metabolized by the liver cytochrome P3A4-such as atorvastatin, lovastatin and simvastatin-and clopidogrel, there is no compelling clinical evidence to stop their co-administration.

Sarcomas as a group are the second most common type of primary tumour of the heart.' Angiosarcoma is, however, an unusual form of tumour within this group and is rarely diagnosed during life.2 It is almost exclusively a tumour of the right atrium and pericardium, patients presenting with symptoms of right heart inflow obstruction and pericardial disease.3 We present here a case of primary angiosarcoma of the heart causing obstruction of the mitral valve. Two dimensional echocardiography suggested the presence of a left atrial myxoma. Resection was attempted. The histological diagnosis was made from tissue obtained at surgery. Case reportA 48 year old unemployed farm worker presented to his local hospital with ill health of several weeks' duration, weight loss, anorexia, and vomiting. Initial examination showed wasting and hepatomegaly and investigations showed anaemia (haemoglobin 11 g/dl) and an erythrocyte sedimentation rate of 120 mm in one hour. Further investigation was advised but the patient declined it. One month later he returned after an episode of central chest pain and severe dyspnoea. In the intervening month he had noticed increasing breathlessness. On examination there were signs of biventricular failure, a pericardial rub, and an apical diastolic murmur. Ultrasound examination showed a mass in the left atrium.The patient was transferred to the regional cardiac unit, where examination showed an ill, thin man with peripheral oedema. His pulse was 110 beats/min and regular, his blood pressure 110/90 mm Hg. The central venous pressure was raised and the left ventricular impulse tapping. There was a loud pericardial rub and a loud mitral diastolic murmur. The liver was enlarged 6 cm below the costal margin. The electrocardiogram showed sinus rhythm with evidence of left atrial hypertrophy. The QRS complexes were of small amplitude and there were widespread nonspecific ST segment and T wave changes. There were bilateral pleural effusions on the chest radiograph. The ascending aorta appeared prominent. appeared to be indented by the "effusion" in ventricular systole. The echo free space extended anterior to the right ventricular outflow tract but no other abnormality of the great vessels was seen. A diagnosis of left atrial myxoma and pericardial effusion was made. The latter seemed remarkable, but in the presence of severe biventricular cardiac failure, pleural effusions, and hypoalbuminaemia this was attributed to his general condition. The patient was referred for resection of the tumour.At operation, no pericardial effusion was found but the pericardial cavity was full of blood clot. There were extensive pericardial adhesions. There was a large extracardiac tumour occupying the space between the superior vena cava and the aorta. The tumour was distorting and eroding the right atrium but there was no tumour in the right heart cavities. The right atrium and pulmonary artery were enlarged. A large endothelialised tumour was found occupying the entire left atrial cavity, almost totally obstructing the ...

SUMMARY Ninety patients undergoing coronary bypass surgery were studied prospectively by bedside and subsequent ambulatory electrocardiographic monitoring to investigate the incidence, possible causes, and prevention of atrial fibrillation. Patients with good left ventricular function were divided randomly into a control group or groups treated with digoxin or propranolol. In the control group the incidence of atrial fibrillation was 27% and of significant ventricular extrasystoles 3%. Propranolol reduced the incidence of atrial fibrillation (14-8%), whereas digoxin had no effect and increased the incidence of ventricular extrasystoles. Age, sex, severity of symptoms, cardiomegaly, heart failure, previous myocardial infarction, and number of grafts did not affect the result. The operative myocardial ischaemic time was related to the occurrence of atrial fibrillation. There was also a significant relation between atrial fibrillation and bundle branch block. Atrial fibrillation is common after coronary artery grafting; it may be due to diffuse myocardial ischaemia or hypothermic injury. The incidence may be reduced by beta blockade.