Five children with atrial isomerism developed intestinal obstruction caused by malrotation of the gut. Other than asplenia, the extracardiac anomalies in these syndromes are rarely regarded as important as the outcome after intestinal surgery is poor. As cardiac treatment improves, early investigation and intervention for intestinal symptoms becomes more important.

Drainage of the inferior vena cava directly into the left atrium is a rare but well recognised anomaly of systemic venous drainage. It has been reported in isolation and in association with other cardiac defects. We report a case of anomalous drainage of the inferior vena cava into the left atrium in association with total anomalous pulmonary venous drainage of the supracardiac type, a hitherto unreported combination.Case report A 7 month old boy presented with a three month history of intermittent cyanosis, breathlessness, and failure to thrive. A diagnosis of supracardiac total anomalous pulmonary venous drainage to the innominate vein was made at cardiac catheterisation and angiocardiography. The aortic saturation was 85% and the pulmonary artery pressure was 44/16 mm Hg. The ratio of the right to the left ventricular peak systolic pressure was 0-63.Corrective surgery was performed through a left anterolateral thoracotomy with trans-sternal extension. A 12cm common pulmonary venous channel was unobstructed throughout its course. The left atrium was larger than normally expected in this anomaly and there was a 12 mm secundum atrial septal defect. Cardiopulmonary bypass was established, a single systemic venous cannula being introduced through the right atrial appendage. Under circulatory arrest at 16°C, with both venae cavae snared, the left atrium was opened posteriorly. The atrial septal defect was closed by direct suture and the common pulmonary venous channel was anastomosed to the left atrium. The ascending pulmonary vein was ligated. Postoperative progress was uneventful and he was discharged home.Three months later his mother noticed cyanosis of the lips on exertion. At the age of 3 years, he was found to be centrally cyanosed with mild finger clubbing. Repeat cardiac catheterisation was performed via the right femoral vein. The catheter was manoeuvred easily from the inferior vena cava into the left atrium and with more difficulty into the superior vena cava. There was oximetric evidence of a significant right to left shunt, the left ventricular saturation being 89%. Through a median sternotomy cardiopulmonary bypass was established with bicaval cannulas. The inferior vena cava was cannulated directly as it could not be entered from the right atrium. The atrial appendages were morphologically normal. The azygos vein was not dilated. The right atrium was opened and the atrial septum was seen to be intact apart from a 2 mm defect within the previous repair. The coronary sinus was in the normal position, draining into the right atrium. The inferior vena caval orifice was not visible as it drained directly into the left atrium-to the left of the inferior portion of the interatrial septum. The atrial septum was excised and replaced by an oval patch of calf pericardium directing the inferior vena cava into the right atrium.The boy has made a satisfactory recovery and three months after operation is symptom free.

Mitral regurgitation due to avulsion of a papillary muscle is a rare complication of closed injury to the anterior chest wall. Rupture of the chordae tendinae producing mitral regurgitation is more commonly found."' Avulsion of the anterior papillary muscle has been reported as a finding at necropsy,56 but to our knowledge survival after such an injury has not been reported previously. We now report such a case. Case reportA 28-year-old man was admitted to a district general hospital~w ith dyspnoea after trauma to the anterior chest wall caused by a flying metal bar. On examination the only external evidence of 4~V injury was a transverse superficial laceration 3 cm long, overlying the second intercostal space. There was a soft systolic murmur at the cardiac apex and a few bilateral basal crepitations. Twenty-four hours later there was sudden deterioration in his condition and he developed signs of pulmonary oedema. He was transferred to our unit. On admission he had a regular pulse rate of 160 beats/min and a blood pressure of 100/80mm Hg. There (fig 1). At cardiac catheterisation severe mitral regurgitation into a normal left atrium was seen. There was no aortic regurgitation and the coronary arteries were normal.After these investigations the patient's condition deteriorated further and an emergency operation with cardiopulmonary bypass was performed. External and internal cardiac massage was necessary because of inadequate output, but proved ineffective owing to the severe mitral regurgitation. Through a left atriotomy the mitral leaflets appeared normal, but the anterior papillary muscle was found to be avulsed at the base ( fig 2). There was contusion of the anterior surface of the left upper lobe of the lung and the left ventricular outflow tract. The mitral valve was replaced with a Carpentier-Edwards porcine xenograft. The patient is alive eight months after surgery, though he has a residual neurological deficit consisting of bilateral lateral popliteal nerve palsy.~~~~~Fig 2 Papillary muscle avulsed at the base with intact chordae popliteal nerve palsy.tendinae. Discussionaccompanying non-penetrating trauma to the chest wall. TheCardiac lacerations may result from crush or stretch forces papillary muscles, the interventricular septum, or the free ventricular wall may be ruptured.'478 Experimental evidence Address for reprint requests: Mr R Pillai, Brompton Hospital, London indicates that intraventricular pressures of over 320 mm Hg are SW3 6HP.

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SUMMARY A 43-year-old man collapsed suddenly, with pericardial tamponade, seven weeks after an inferior myocardial infarction. Pericardiocentesis disclosed very heavily blood stained fluid. Left ventricular angiography 10 days later showed a left ventricular aneurysm. At operation a left ventricular false aneurysm was resected and the patient recovered uneventfully.Cardiac rupture occurs in 4 to 24% of all deaths from acute myocardial infarction.' It may occur from a few hours to several days after the infarction and is usually fatal. It is not usually an acute "blowout", but a gradual penetration of the necrotic myocardium by a dissecting haematoma,I leading to cardiac tamponade. Surgical treatment of this complication has occasionally been successful. We report a case of cardiac rupture that occurred seven weeks after myocardial infarction and was subsequently treated surgically. Case reportA 43-year-old mechanic was admitted to hospital with a two day history of praecordial pain radiating down both arms and up to the throat. The pain was intermittent but had gradually increased in intensity. There was no significant past medical history.On physical examination his general condition appeared good. His pulse rate was 80 per minute, regular, and his blood pressure was 160/110 mnmHg. There was no evidence of cardiac failure. The electrocardiogram confirmed an acute inferior myocardial infarction. The chest x-ray film showed slight cardiomegaly. From 180Two weeks later, he had a sudden onset of dizziness followed by two transient syncopal episodes. This was soon followed by upper chest pain which radiated to the throat and was aggravated by deep inspiration and lying flat. On examination he was pale, cold, clammy, and dyspnoeic. Pulse was 120 per minute, regular, and of low volume. The systolic blood pressure by palpation was 70 mmHg on expiration, falling to 50 mmHg on inspiration. The jugular venous pressure was raised 8 cm above the sternal angle. The heart sounds were inaudible. The electrocardiogram showed the presence of the previous inferior myocardial infarction. An anteroposterior portable chest x-ray film showed probable cardiomegaly. An echocardiogram showed a large echo-free space anteriorly and posteriorly, indicating a pericardial effusion.A diagnosis of pericardial tamponade was made and pericardiocentesis was carried out using the apical approach. On removal of 67 ml heavily bloodstained fluid, there was a dramatic clinical improvement and the blood pressure rose to 110/70 mmHg. The pericardial fluid haemoglobin was 10-4 g/dl and the circulating blood haemoglobin was 14-4 g/dl; the erythrocyte sedimentation rate was 22 mm/hour. He was transferred by ambulance to the Middlesex Hospital Cardiothoracic Surgical Unit, with a pericardial drain in situ but closed off. His general condition continued to improve so operation was deferred.Left ventricular angiography, 10 days after his collapse, showed a large saccular posteroinferior left ventricular aneurysm (Fig.). This showed paradoxical movement and...