Acute non-ischaemic mitral regurgitation (MR) has recently generated considerable interest because of its causal relationship to ruptured chordae tendineae and infective endocarditis, advances in its diagnosis by echo Doppler studies, and its management by afterload reduction and reconstructive surgery. It is fundamentally different from chronic MR because the previously normal, unprepared left ventricle (LV) and left atrium (LA) confront a sudden dramatic increase in volume. As the normal-sized left atrium suddenly receives a marked regurgitant flow, its pressure rises and is transmitted into the pulmonary capillaries causing pulmonary congestion and oedema. At onset, the LV function is usually well preserved and the pulmonary oedema does not reflect LV failure. In acute MR, the LV empties into the left atrium, thus reducing its radius and its systolic pressure, resulting in a decline in wall tension according to Laplace's law. With a reduction in LV wall tension, there is a marked increase in contractile shortening with marked increase in total LV output. The left ventricle may fail early in acute severe MR because it is forced to dilate rapidly before hypertrophy can occur, whereas in chronic MR both the LV diastolic volume and mass increase proportionately. With chronic persistence of MR, LV dysfunction and failure occur as a manifestation of the 'cardiomyopathy of overload'. Fortunately because of the low energy cost per unit of work in shortening, as opposed to that used for tension development, there is only a slight increase in myocardial oxygen consumption in acute MR. In patients with LV failure secondary to acute MR, the ejection fraction may be only slightly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)