Cardiogenic shock is a frequent and threatening complication in the course of acute myocardial infarction. Besides the well known causes (left ventricular failure, acquired interventricular defect, papillary muscle rupture, free wall rupture) other less frequent mechanisms recognize a functional substrate. The recognition of such mechanisms makes us to revert to the treatments with completely different prognostic implications. In our Coronary Care Unit we encountered, in a period of 12 months, 4 patients who presented clinical, electrocardiographic and/or echographic signs and symptoms of acute myocardial infarction, with different degrees of heart failure up to cardiogenic shock. Only 1 patient showed a severe stenosis of the left anterior descending coronary artery and a significant creatine kinase reduction. Left ventriculography, performed at admission, was unable to disclose the true mechanism of clinical presentation. Only a thorough echographic examination disclosed the presence of a dynamic left ventricular outflow tract obstruction as the cause of heart failure culminating in cardiogenic shock. Once recognized, pathophysiological treatment (administration of beta-blockers and withdrawal of vasodilators, inotropic drugs and intra-aortic balloon pump) led to a dramatic improvement, with an almost complete left ventricular function recovery. Left ventricular outflow tract obstruction is a mechanism that can lead to severe heart failure as a complication of an acute myocardial infarction. Conversely such a mechanism can be precipitated by other causes (hypotension, hypovolemia, especially in hypertensive patients) and can mimic an acute myocardial infarction. Its incidence is not negligible: in our Coronary Care Unit it accounted for about 15% of all cases of myocardial infarction requiring inotropic support. An accurate echocardiographic examination is mandatory even after coronary angiography, and always permits the physician to select the appropriate therapy.