The spectrum of rheumatic mitral valve disease that is hemodynamically severe in developing countries differs from that currently reported in the United States. Severe, pure rheumatic mitral regurgitation is as prevalent as pure stenosis but has an entirely different time course, surgical anatomy, and relation to disease activity, suggesting a separate pathophysiologic mechanism.

Evidence has previously been produced from this laboratory (Barlow and Pocock, 1963;Barlow, 1965) that apical late systolic murmurs denote mitral regurgitation, and that the commonly associated non-ejection systolic clicks also have an intracardiac, and probably chordal, origin. It has also been suggested that the association of these auscultatory features with a distinctive electrocardiographic pattern and a billowing posterior leaflet of the mitral valve constitutes a specific syndrome (Barlow, 1965;Barlow and Bosman, 1966).In this paper we present an analysis of 90 subjects with either a late systolic murmur, a nonejection click, or both. The intracardiac origin of these murmurs and clicks is reaffirmed and their possible mode of production is considered. The abnormal electrocardiogram, the probable structural abnormality of the mitral valve mechanism, the various underlying aetiological factors, and the prognosis are discussed. SUBJECTS AND METHODSOf the 90 subjects, 65 were referred to the Cardiac Clinic for assessment of their auscultatory signs. Seven were found during hospital admission for a non-cardiac illness; 6 were detected after closed mitral valvotomy, and 5 others after other forms of mitral valve surgery. One 30-year-old woman complaining of palpitations, who regularly attended the Clinic, developed a late systolic murmur and click a year after observation began. Examination of relatives of patients with late systolic murmurs or non-ejection clicks produced a further 6 cases.The 90 subjects ranged in age from 4 to 63 years; 45 of them, including 13 children, were under the age of 30;

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