Anomalous course of the left anterior descending coronary artery between the aorta and pulmonary trunk: a rare cause of myocardial ischaemia at rest.

When the left anterior descending coronary artery follows an anomalous course between the aorta and pulmonary artery it can cause myocardial ischaemia or sudden death during exercise in young people. Coronary arteriography in a 27 year old man with angina pectoris at rest showed a left anterior descending coronary artery arising from a common right trunk and running from the aorta to the pulmonary artery. Follow up after revascularisation was uneventful.

[Course of unstable angina and therapeutic implications. Apropos of 74 cases]. / Evolution de l'angor instable et implications thérapeutiques. A propos de 74 cas.

The role of thrombosis in the pathogenesis of unstable angina has been demonstrated experimentally. This retrospective study was designed to identify the potential usefulness of fibrinolytic treatment in this situation. The following parameters were evaluated in 74 patients (62 men, 12 women; mean age: 60 +/- 10.2) with primary unstable angina: the course of unstable angina (Braunwald classification), risk factors, electrocardiographic changes, echocardiographic segmental kinetics, coronary arteriography findings, treatment used and outcome with a minimum follow-up of 3 months (mean: 6.3 months). Thirty nine per cent of class I patients and 18% of classes II and III were stabilised by medical treatment only. This accounted for 18 patients in our series (24%). The other patients (76%) required one or more reperfusion techniques (thrombolysis: 5 patients; angioplasty: 42; bypass: 19). Serious complications were seen in 3 patients: myocardial infarction: 2 postoperative (including one fatal) and 1 occurring 24 hours after angioplasty followed by cardiogenic shock and death. Five patients required thrombolytic treatment leading to clinical stabilisation enabling an additional procedure (angioplasty or bypass). No complications of thrombolytic treatment were seen. Thus thrombolytic treatment appears to be useful for the stabilisation of unstable angina and enables subsequent radical treatment under better conditions.

[Platelet hyperaggregation induced by low molecular weight heparin in adult respiratory distress syndrome]. / Hyperagrégabilité plaquettaire induite par une héparine de bas poids moléculaire au cours d'un syndrome de détresse respiratoire de l'adulte.

A case is reported of a 68-year-old woman admitted to the intensive care unit with an adult respiratory distress syndrome (ARDS) due to accidental poisoning with anhydrous phthalic acid. She was given prophylactic low molecular weight heparin (Fraxiparine). During the period of intensive care (mechanical ventilation with positive end-expiratory pressure), the patient experienced a stroke from which she recovered only partially. During pleurectomy for persistent pneumothorax, a lung biopsy was carried out. It confirmed the diagnosis of ARDS and recognized multiple pulmonary arterial thrombi. Because of these two thrombotic phenomena, a coagulation defect was searched for. Platelet aggregation tests were all positive with heparin and two low molecular weight fractions. The patient recovered remarkably once she was no longer given Fraxiparine, being extubated nine days afterwards. Six months after discharge, the patient's platelets still aggregated with heparin. The possible mechanism was a heparin-platelet-endothelium complex. It is noteworthy that, in this case, no thrombocytopaenia was found. It may have been countered by thrombocytosis, induced by cellular factors released during ARDS.