[Cardiogenic shock complicating extensive infarction with ventricular septal defect. Circulatory assistance and heart transplantation]. / Choc cardiogénique sur infarctus étendu, compliqué d'une communication interventriculaire. Assistance circulatoire et greffe cardiaque.

A 47 year old man had a massive anterior myocardial infarction with cardiogenic shock with a left parasternal murmur. Coronary angiography showed occlusion of the left anterior descending artery for which angioplasty resulted in failure. There was antero-lateral-apical akinesia and a ventricular septal defect (VSD) with a left-right shunt (Qp/Qs = 1.54). Persistence and aggravation of haemodynamic instability led to intra-aortic balloon pumping with inotropic pharmacological support followed by biventricular assistance with a MEDOS device. Under transoesophageal echocardiographic monitoring, the outcome was marked over 7 days by the progressive increase in the shunt volume of the VSD, a decrease of drainage and injection flow, progressive increase in spontaneous contrast echos followed by the presence of fibrin in the cardiac chambers and canulae, the presence of thrombus in the external ventricles, blockage of the right external valve which only opened after increasing the degree of anticoagulation, and, finally, cardiac tamponade which required drainage before the patient's state improved. On the 8th day, the patient being stable with a normal neurological status, the availability of a donor heart led to the decision to transplant, which was carried out without complications. This case poses the problem of cardiac assist devices and their daily monitoring, and then that of cardiac transplantation in this indication.

[Emergency angioplasty for total thrombosis of the left main coronary artery. Apropos of a case]. / Angioplastie en urgence d'une thrombose complète du tronc coronaire. A propos d'un cas.

Complete thrombosis of the left main coronary artery is a rare angiographic finding and usually gives rise to cardiogenic shock during unstable angina or myocardial infarction. The prognosis of this condition is very dependent on the collateral coronary circulation and the myocardial protection seems to depend on the rapidity of revascularisation. Two therapeutic approaches may be envisaged; emergency coronary bypass grafting or percutaneous angioplasty, the natural history being particularly disastrous. The authors report the case of a 42-year-old patient with complete occlusion of the left main stem responsible for unstable angina and acute pulmonary oedema. The outcome with angioplasty in the acute phase associated with surgical revascularisation four days later, was good.

[Changes in myocardial metabolism induced by drugs used during intensive care]. / Modifications du métabolisme myocardique par les médicaments utilisés en réanimation.

More and more patients with coronary heart disease (CAD) are admitted to intensive care units. The drugs used to treat these patients have various effects on the myocardium which must be known in order to avoid worsening the CAD. This review examines the metabolic effects on the myocardium of the most commonly used drugs in intensive care. The physiology of myocardial oxygen supply is first recalled with regard to the coronary circulation, myocardial oxygen extraction and consumption. Digitalis glycosides do not affect the coronary circulation, but the decrease myocardial oxygen consumption in patients with heart failure, mainly by lowering heart rate. Dihydropyridine calcium blockers (nifedipine, nicardipine) increase coronary blood flow, despite a decrease in arterial blood pressure. Their effects on myocardial oxygen consumption are mediated by a sympathetic reflex. Verapamil decreases the heart rate and myocardial inotropism, and is responsible for coronary vasodilation. The result is a decrease in myocardial oxygen consumption. Diltiazem and bepridil have almost similar effects: they decrease myocardial oxygen consumption and increase blood supply to the heart. It has been recently shown that verapamil was the most depressant calcium channel blocking agent, and that it resulted in the most important decrease in myocardial metabolism. Beta-blocking agents decrease myocardial metabolism, except those with an important intrinsic sympathomimetic activity, such as pindolol. Amiodarone can be considered as an alpha and beta blocking drug: its main effect is to counteract the effects of endogenous catecholamines on myocardial metabolism. The sympathomimetic amines (noradrenaline, adrenaline, isoprenaline, dopamine, dobutamine) increase, to different extents, myocardial oxygen consumption. Vasodilators, such as the nitrates or sodium nitroprusside, decrease cardiac filling pressures, and increase myocardial blood flow, thus lowering myocardial oxygen consumption. Phosphodiesterase inhibitors (amrinone, enoximone) have both an inotropic and a vasodilating effect. They decrease cardiac afterload, and increase blood supply to the myocardium; this compensates for the increase in myocardial oxygen consumption due to the increase in myocardial contractility. Because all the drugs used in intensive care have different effects on myocardial metabolism, their reasoned use should avoid an inappropriate increase in oxygen demand.