Dynamics of mitral regurgitant flow and orifice area. Physiologic application of the proximal flow convergence...

The proximal flow convergence method, a quantitative color Doppler flow technique, has been validated recently for calculating regurgitant flow and orifice area. We investigated the potential of the method as a tool to study different pathophysiological mechanisms of mitral valve incompetence by assessing the time course of regurgitant flow and orifice area and analyzed the implications for quantification of mitral regurgitation.

Fifty-six consecutive patients with mitral regurgitation of different etiologies were studied. The instantaneous regurgitant flow rate Q(t) was computed from color M-mode recordings of the proximal flow convergence region and divided by the corresponding orifice velocity V(t) to obtain the instantaneous orifice area A(t). Regurgitant stroke volume (RSV) was obtained by integrating Q(t). Mean regurgitant flow rate Qm was calculated by RSV divided by regurgitation time. Peak-to-mean regurgitant flow rates Qp/Qm and orifice areas Ap/Am were calculated to assess the phasic character of Q(t) and A(t). In the first 24 patients (group 1), computation of Qm and RSV from the color Doppler recordings was compared with the conventional pulsed Doppler method (r = .94, SEE = 29.4 mL/s and r = .95, SEE = 9.7 mL) as well as with angiography (rs = .93 and rs = .94, P < .001). The temporal variation of Q(t) and A(t) was studied in the next 32 patients (group 2): In functional regurgitation in dilated cardiomyopathy (n = 12), there was a constant decrease in A(t) throughout systole with an increase during left ventricular relaxation; Ap/Am was 5.49 +/- 3.17. In mitral valve prolapse (n = 6), A(t) was small in early systole, increasing substantially in midsystole, and decreasing mildly during left ventricular relaxation; Ap/Am was 2.48 +/- 0.26. In rheumatic mitral regurgitation (n = 14), a roughly constant regurgitant orifice area during most of systole was found in 4 patients. In the other patients there was significant variation of A (t) and the time of its maximum; Ap/Am was 1.81 +/- 0.56. ANOVA demonstrated that the differences in Ap/Am were related to the etiology of mitral regurgitation (P < .0001). To verify that the calculated variation in regurgitant orifice area during the cardiac cycle reflects an actual variation, the ability of the method to predict a constant orifice area throughout systole was tested experimentally in a canine model of mitral regurgitation. Five flow stages were produced by implanting fixed grommet orifices of different sizes into the anterior mitral leaflet. A constant regurgitant orifice area was correctly predicted throughout systole with a mean percent error of -1.8 +/- 4% (from -6.9% to +5.8%); the standard deviation of the individual curves calculated at 10% intervals during systole averaged 13.3% (from 3.6% to 19.6%). In addition, functional mitral regurgitation caused by ventricular dysfunction was produced pharmacologically in five dogs, and the color M-mode recordings of the proximal flow convergence region were obtained with the transducer placed directly on the heart instead of the chest, thus ruling out a significant effect of translational motion on the observed flow pattern. The pattern of regurgitant flow variation was identical to that observed in patients.

The proximal flow convergence method demonstrates that regurgitant flow and orifice area vary throughout systole in distinct patterns characteristic of the underlying mechanism of mitral incompetence. Therefore, in addition to the potential of the method as a tool to quantify mitral regurgitation, it allows analysis of the pathophysiology of regurgitation in the individual patient, which may be helpful in clinical decision making. Calculating mitral regurgitant flow rate and volume from the time-varying proximal flow field (ie, without assuming a constant orifice area that would produce overestimation in individual patients) provides excellent agreement with independent te