Barlow J B
Department of Cardiology, University of the Witwatersand, Parktown, South Africa.
Aust N Z J Med. 1992 Oct;22(5 Suppl):541-9. doi: 10.1111/j.1445-5994.1992.tb00474.x.
Three decades after it was demonstrated that nonejection systolic clicks and late systolic murmurs have a mitral valve origin and that a specific syndrome is associated with the primary degenerative mitral lesion, numerous questions remain unanswered. A principal cause of confusion is the use of the term 'prolapse', which essentially implies a pathological state, in many patients with minimal evidence of a mitral valve anomaly. It should be recognised that no specific feature, whether evaluated by high standard echocardiography or indeed by careful morphological and histological examination, can be defined which distinguishes a normal variant from a pathological valve. There is a gradation from the normal billowing during ventricular systole of mitral leaflet bodies to marked billowing. With advanced billowing or floppy leaflets, failure of leaflet edge apposition supervenes (true prolapse). This is functionally abnormal and allows mitral regurgitation. Prolapse in turn may progress to a flail leaflet and hence gross regurgitation. Relatively rare complications of this degenerative mitral valve anomaly include systemic emboli, infective endocarditis, arrhythmias and, arguably, autonomic nervous system abnormalities. An attempt is made to clarify the management of some symptoms and other aspects of mitral prolapse-including rheumatic anterior leaflet prolapse (without billowing) which remains prevalent in South Africa and Third World countries.
