Schwammenthal E, Chen C, Benning F, Block M, Breithardt G, Levine R A
Hospital of the Westfälische Wilhelms University of Münster, Germany.
Circulation. 1994 Jul;90(1):307-22. doi: 10.1161/01.cir.90.1.307.
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
近端血流会聚法是一种定量彩色多普勒血流技术,最近已被验证可用于计算反流流量和瓣口面积。我们通过评估反流流量和瓣口面积的时间进程,研究了该方法作为研究二尖瓣反流不同病理生理机制工具的潜力,并分析了其对二尖瓣反流定量的意义。
连续研究了56例不同病因的二尖瓣反流患者。从近端血流会聚区域的彩色M型记录计算瞬时反流流速Q(t),并除以相应的瓣口速度V(t)以获得瞬时瓣口面积A(t)。通过对Q(t)积分获得反流搏出量(RSV)。平均反流流速Qm通过RSV除以反流时间计算得出。计算峰值与平均反流流速之比Qp/Qm和瓣口面积之比Ap/Am以评估Q(t)和A(t)的阶段性特征。在最初的24例患者(第1组)中,将彩色多普勒记录计算的Qm和RSV与传统脉冲多普勒方法进行比较(r = 0.94,标准误 = 29.4 mL/s;r = 0.95,标准误 = 9.7 mL),并与血管造影进行比较(rs = 0.93和rs = 0.94,P < 0.001)。在接下来的32例患者(第2组)中研究了Q(t)和A(t)的时间变化:在扩张型心肌病的功能性反流患者(n = 12)中,整个收缩期A(t)持续减小,左心室舒张期增加;Ap/Am为5.49±3.17。在二尖瓣脱垂患者(n = 6)中,收缩早期A(t)较小,收缩中期大幅增加,左心室舒张期轻度减小;Ap/Am为2.48±0.26。在风湿性二尖瓣反流患者(n = 14)中,4例患者在大部分收缩期发现反流瓣口面积大致恒定。在其他患者中,A(t)有显著变化及其最大值出现的时间;Ap/Am为1.81±0.56。方差分析表明Ap/Am的差异与二尖瓣反流的病因有关(P < 0.0001)。为验证心动周期中计算的反流瓣口面积变化反映实际变化,在二尖瓣反流犬模型中通过实验测试了该方法预测整个收缩期恒定瓣口面积的能力。通过在二尖瓣前叶植入不同大小的固定索环瓣口产生五个血流阶段。整个收缩期正确预测了恒定的反流瓣口面积,平均百分比误差为 -1.8±4%(范围为 -6.9%至 +5.8%);收缩期以10%间隔计算的个体曲线标准差平均为13.3%(范围为3.6%至19.6%)。此外,对五只犬进行药物诱导心室功能障碍导致的功能性二尖瓣反流,并将换能器直接置于心脏而非胸部获取近端血流会聚区域的彩色M型记录,从而排除平移运动对观察到的血流模式的显著影响。反流血流变化模式与在患者中观察到的相同。
近端血流会聚法表明,反流流量和瓣口面积在整个收缩期以二尖瓣反流潜在机制特有的不同模式变化。因此,该方法除了有作为量化二尖瓣反流工具的潜力外,还允许分析个体患者反流的病理生理学,这可能有助于临床决策。从随时间变化的近端流场计算二尖瓣反流流速和容积(即不假设会导致个体患者高估的恒定瓣口面积)与独立技术具有极好的一致性。