Cardiovascular ImagingMitral regurgitation
systolic flow of blood from the left
ventricle into the left atrium due to insufficient closure of the mitral valve. It may be caused by pathology of the mitral leaflets, subvalvular mechanism (chordae or papillary muscles) or mitral annulus. There are a large number of aetiologies for mitral
regurgitation including
rheumatic heart disease, infectious
endocarditis,
ischaemic
papillary muscle rupture or traumatic papillary muscle rupture,
degenerative
cordal rupture,
mitral valve prolapse,
mitral annular calcification, and
congenital lesions such as parachute mitral valve and
atrioventricular septal defect.
The haemodynamic consequence of mitral regurgitation is systolic increase in left atrial pressure and pulmonary venous pressure during systole. The increase in pulmonary venous pressure is usually less severe than with mitral stenosis. However, severe elevation in pulmonary venous pressure occurs with acute onset of regurgitation. Mitral regurgitation imposes a volume load on the left atrium and ventricle. Left ventricular end-diastolic volume is increased. The total stroke volume of the left ventricle is increased since it includes the effective stroke volume (blood ejected to the aorta) and the regurgitant volume.
Imaging
Plain radiography shows various degrees of pulmonary venous hypertension and cardiomegaly. The severity of pulmonary venous hypertension is generally less than in predominant mitral stenosis. Cardiomegaly is a consequence of left atrial and left ventricular enlargement (Fig.1). right-sided chamber enlargement may be caused by pulmonary arterial hypertension or concurrent tricuspid regurgitation. In the absence of associated aortic valve decrease, the ascending aorta is inconspicuous. The left atrial appendage is usually enlarged in rheumatic mitral regurgitation but may not be recognizable with nonrheumatic aetiologies. Acute mitral regurgitation such as occurs with ruptured papillary muscle may cause severe alveolar pulmonary oedema, sometimes with a normal heart size.
The M-mode echocardiogram shows abnormal mitral leaflet closure patterns depending upon the type of mitral regurgitation. These consist of incomplete closure, mitral valve prolapse, ruptured chordae tendineae or flail mitral valve. The flail valve shows erratic systolic motion into the left atrium.
Two-dimensional echocardiography (V:2) shows the above signs described for M-mode echocardiography. This study may reveal the aetiology of the regurgitation by showing mitral valve prolapse; papillary muscle rupture or cordal rupture; thickened leaflet with fused commissure and decreased motion in rheumatic disease; vegetations or perforated leaflet in infectious endocarditis; parachute or cleft mitral valve in congenital disease; or mitral annular calcification. In chronic mitral regurgitations left ventricular volumes are increased and can be effectively monitored with two-dimensional echocardiography. The extent of the increase in left ventricular volumes is a prognostic indicator for surgical outcome. A left ventricular systolic volume over 60 ml/m2 is associated with a worse prognosis. Left ventricular dimensions at end diastole greater than 7 cm and at end systole greater than 5 cm are indicative of severe diseases.
Pulse wave Doppler echocardiography is extremely sensitive for detecting mitral regurgitation; it appears as a turbulent systolic signal within the left atrium directed away from the transducer. The extent of the penetration and area of the regurgitant jet can be used to estimate the severity. Colour flow Doppler provides a nearly real-time flow map of the origin and direction of mitral regurgitation. Large colour jets that occupy more than half of the left atrium, extend to the posterior portion of the atrium or into the appendage or pulmonary veins indicate significant regurgitation. Transoesophageal echocardiography is usually essential for the evaluation of prosthetic valve regurgitation. Transoesophageal echocardiography with colour flow Doppler can usually discriminate between valvular and perivalvular leaks of prosthetic valves.
Transoesophageal echocardiography also provides additional precision in the evaluation of the morphology of the native mitral valve and is highly effective for detecting vegetation, perforations, perivalvular abscess and ruptured chordae.
Left ventriculography shows escape of contrast media from the left ventricle into the left atrium during systole. Comparison of the intensity of opacification of the left atrium with left ventricle provides a semiquantitative estimate of severity. Quantitative left ventriculography reveals increased left ventricular end diastolic, end systolic and stroke volumes. The regurgitant volume in isolated mitral disease can be calculated as the difference in stroke volume calculated from left ventriculography (end-diastolic end-systolic volume) and the stroke volume measured with the Fick technique or indicator dilution method. Structural abnormalities of the valve such as flail valve or vegetations are revealed by left ventriculography. For the most part, echocardiography has supplanted angiography for the diagnosis and assessment of severity of mitral regurgitation.
Preoperative catheterization is performed mainly for the purpose of coronary arteriography in patients over 40 years of age.
Cine MRI displays the regurgitant jet as a signal void emanating from the mitral valve projecting into the left atrium during systole (Fig.2). The size of the signal void bears a rough relationship to the severity of regurgitation. Cine MR images encompassing the entire heart can be used to measure left atrial and ventricular volumes with high precision and reproducibility. Velocity-encoded cine MRI can be used to measure the volume of regurgitation. It can be measured as the difference in the inflow volume across the mitral annulus in diastole and the outflow volume through the ascending aorta in systole.
CBH