Over the past few years there has been a gradual recognition that obstruction to outflow from the left ventricle may be determined by lesions other than fusion of the aortic valve cusps or congenital diaphragms below or above the cusps. This syndrome has been described by Brock (1957Brock ( , 1959, under the title of Functional obstruction of the left ventricle, and he instances a patient in whom hypertension produced left ventricular hypertrophy that narrowed the outflow tract of the left ventricle in systole. Bercu et al. (1958) used the term Pseudo-aortic stenosis to describe a patient with apparent aortic stenosis who at autopsy had gross generalized ventricular hypertrophy only. Morrow and Braunwald (1959), under the heading Functional aortic stenosis, instance two patients with apparent sub-aortic stenosis who at open operation were found to have no anatomical obstruction.Recently Teare (1958), from autopsy studies, gave the first adequate description of Asymmetrical hypertrophy of the heart, a condition in which the interventricular septum in particular is grossly hypertrophied and bulges into both ventricular cavities. One of his cases presented with signs of mitral stenosis; another was studied by us during life and found to have signs of obstruction to right ventricular inflow tract, and fourteen members of her family also had heart disease with similar signs (Hollman et al., 1960). Fig. 1 shows the heart in one of these patients.We have now seen 8 patients in whom we believe that hypertrophy of the left ventricle of undetermined cause has caused obstruction to left ventricular outflow (pseudo-aortic stenosis). Some have had signs suggesting inflow obstruction of one or both ventricles in addition, and we propose the term Obstructive cardiomyopathy as being a suitable descriptive title for the whole group. In one of our patients the obstruction was successfully dealt with by open-heart surgery. THE PATIENTS Case 1. A man, aged 42 years, had rheumatic fever at the age of 11 years and was told afterwards that his heart was affected. He was, however, perfectly well until the age of 36, when he began to experience tight prmcordial pain on exertion which, at the age of 40, became worse and came on whenever he tried to hurry. Also, for 6 years he had lost consciousness on several occasions when persisting in fairly strenuous effort. Dyspncea on effort had been minimal up to the last year when it had become more noticeable. He had a paroxysm of tachycardia at the age of 32. There was no family history of heart disease.On examination he was a stocky man. The pulse was rather small in volume. On most occasions the upstroke was quite normal, while on others it appeared to be anacrotic. The blood pressure was 140/80 mm. The heart was quiet with a tapping apex beat and there was no thrill. A moderately loud aortic ejection murmur was heard at all areas and was louder at the apex than at the right second space. An ejection click was heard at the apex and the second sound was single. Phonocardiography showed an ejec...

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