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Two-dimensional echocardiography has been a decisive advance in the investigation of rheumatic valvular disease. In mitral stenosis, short axis views enable a quantitative evaluation of mitral surface area by planimetry. Long axis views contain additional important information on the state of the subvalvular apparatus and on the possible presence of left atrial thrombosis. The quantitative assessment of regurgitant flow in mitral incompetence is difficult and can only be approximative. On the other hand, the mechanism of mitral incompetence may be clearly demonstrated in: - mitral valve prolapse with the characteristic bowing of the posterior leaflet; - rheumatic mitral incompetence with the abnormal valvular thickening showing the post-rheumatic retractile fibrosis; - ruptured chordae with eversion of the tip of one of the values in the left atrium; - infective endocarditis with ruptured chordae and vegetations; - cogenital mitral incompetence where the superiority of 2D echo over M mode is most marked, the apical incidences demonstrating the high VSD, ostium primum defect and cleft mitral valve. The limitations of the method are also discussed.

Forty-eight patients underwent M-Mode, 2D and pulsed Doppler echocardiography with systematic apical and subcostal examination of the mitral and tricuspid orifices to determine the value of pulsed Doppler echo in the detection of tricuspid regurgitation. The fourty-eight patients, aged 12 to 69 years, were divided into 2 groups: Group I: 27 patients referred for cardiac catheterisation usually with a view to surgery. The majority of patients had rheumatic valvular, congenital heart disease or cardiomyopathies. All of these patients had phonocardiography, right and left heart catheterisation, right ventricular angiography and measurement od cardiac output. Group II: 21 control patients with no auscultatory, radiological or electrocardiographic changes. This group was studied to determine the specificity of pulsed Doppler examination of the tricuspid valve and the patients only underwent echocardiography. Selective right ventricular angiography was selected as the reference. The sensitivity, specificity and predictive value of pulsed Doppler echocardiography in the positive diagnosis of tricuspid regurgitation were determined. Its value in quantifying tricuspid regurgitation was also analysed. The sensitivity of pulsed Doppler was 93 p. 100 in this series: all but one case of angiographically proven tricuspid regurgitation were detected by the finding of unequivocal systolic turbulence in the right atrium. The specificity of pulsed Doppler was 91 p. 100. The positive predictive value of systolic turbulence in the right atrium was 81 p. 100. The only reliable criteria for quantifying the regurgitation were the intensity of the acoustic signal and the spatial extension of intraatrial turbulent flow: all patients with turbulent flow propagating as far as the superior wall of the right atrium or the inferior vena cava had angiographically severe tricuspid regurgitation. A comparison with other paraclinical methods of detecting tricuspid regurgitation showed that pulsed Doppler echocardiography is the most sensitive tool at the clinician's disposal for diagnosing this lesion: the sensitivity of auscultation and phonocardiography was 50 p. 100, jugular pulse tracings 54 p. 100, right heart catheterisation 50 p. 100, and pulsed Doppler echocardiography 93 p. 100. Pulsed Doppler echocardiography may even be superior to angiography which has, until now, been the method of reference for diagnosing tricuspid regurgitation.

This study concerns 51 cases of mitral valve prolapse demonstrated on bidimensional 4 cavities sonography according to Gilbert's criteria and aims to determine the frequency of the associated valvular involvement, anatomically with sonography and functionally with the Doppler test. Sonography demonstrates a tricuspid valve prolapse in 79 p. cent of the cases and an aortic valve prolapse in 10 p. cent. The Doppler test demonstrates a tricuspid leakage in 52 p. cent of the cases, a pulmonary leakage in 62 p. cent, and an aortic leakage in 18 p. cent. The myxoid degeneration found in 60 p. cent of the cases is a major factor in the occurrence of complications, especially progressive cardiac insufficiency (A). The myxoid degeneration defines therefore the "isolated prolapse disease" as opposed to "the prolapse without myxoid degeneration" which is a pure sonographic entity and probably a variation of the normal (A). This cardiac insufficiency occurs late during the 6th or 7th decade and is due to mechanical factors: prolapse, chords rupture and annular dilatation.