Left atrial overload can be used to estimate mitral regurgitant volume

This study was conducted to assess the accuracy of the estimated mitral regurgitant volume using both the left atrial filling volume and the systolic component of pulmonary vein flow expressed as the percent of its total. Since mitral regurgitation fills the left atrial chamber, the variation in atrial volume during ventricular systole has been proposed as a means to evaluate the severity of regurgitation. Although the correlation with invasive grading of mitral regurgitation is good, there is an unacceptable overlap among grades caused by the absence of information concerning pulmonary vein flow, which enters the left atrium while regurgitation occurs. The Doppler regurgitant volume, or Dp-RVol (mitral stroke volume minus aortic stroke volume) was quantified in 74 patients with any degree and etiology of mitral regurgitation. Atrial volumes were measured from the four-chamber apical view (biplane area-length method). The systolic time-velocity integral of pulmonary vein flow was expressed as the percent of the total (PVs%) (systolic-diastolic) time-velocity integral. These parameters were subjected to multivariate analysis and a regression equation was obtained. The equation was subsequently applied to a group of 31 patients without mitral regurgitation, as evaluated by color Doppler or continuous-wave Doppler and to the overall population (105 patients) in order to estimate the mitral regurgitant volume. In 74 patients with mitral regurgitation, the Doppler regurgitant volume was univariately correlated with the left atrial filling volume (r= 0.74; p<0.0001) and the systolic pulmonary vein velocity integral expressed as the percent of the total (r=0.67; p<0.0001). In multiple regression analysis, the combination of atrial filling and the pulmonary vein velocity integral provided the more accurate estimation of the regurgitant volume (R2=0.84; standard error of the estimate [SEE], 13.9 mL; p<0.0001; Dp-RVol equals 7.84+[1.08*left atrial filling volume] 2 [0.839*PVs%]). In 31 patients with no mitral regurgitation detected by color Doppler or continuous wave Doppler the estimated regurgitant volume was 4.3±6.6 mL. In the overall population the estimated regurgitant volume and the Doppler regurgitant volume correlated well with each other (R2=0.85; SEE, 11.5 mL; p<0.0001). The equation was 100% sensitive and 98% specific in detecting a regurgitant volume higher than 55 mL. The combination of the atrial filling volume and the systolic pulmonary vein time-velocity integral expressed as the percent of the total allows reliable estimation of the regurgitant volume in patients with mitral regurgitation. (c)2001 CHF, Inc.     

Doppler evaluation of severity of mitral regurgitation: Relation to pulmonary venous blood flow patterns in an animal study

Objectives. This study examined the influence of regurgitant volume on pulmonary venous blood flow patterns in an animal model with quantifiable mitral regurgitation.Background. Systolic pulmonary venous blood flow is influenced by atrial filling and compliance and ventricular output and by the presence of mitral regurgitation. The quantitative severity of the regurgitant volume itself is difficult to judge in clinical examinations.Methods. Six sheep with chronic mitral regurgitation produced by previous operation to create chordal damage were examined. At reoperation the heart was exposed and epicardial echocardiography performed. Pulmonary venous blood flow waveforms were recorded by pulsed Doppler under color flow Doppler guidance using a Vingmed 750 scanner. The pulmonary venous systolic inflow to the left atrium was expressed as a fraction of the total inflow velocity time integral. Flows across the aortic and mitral valves were recorded by electromagnetic flowmeters balanced against each other. Pressures in the left ventricle and left atrium were measured directly with high fidelity manometer-tipped catheters. Preload and afterload were systematically manipulated, resulting in 24 stable hemodynamic states.Results. Simple logarithmic correlation between the regurgitant volume and size of a positive or negative pulmonary venous inflow velocity time integral during systole was good (r = −0.841). By stepwise linear regression analysis with pulmonary venous negative systolic velocity time integral as a dependent variable compared with the regurgitant volume, fractional shortening, left atrial νwave size, systemic vascular resistance and left ventricular systolic pressure, only contributions from νwave size and regurgitant volume (r = 0.80) reached statistical significance in determining pulmonary venous negative systolic flow.Conclusions. Evaluation of systolic pulmonary venous blood flow velocity time integral can give valuable information helpful for estimating the regurgitant volume secondary to mitral regurgitation.     

Color Doppler regurgitant jet area for evaluating eccenteric mitral regurgitation: An animal study with quantified mitral regurgitation

Objectives. The purpose of the present study was to rigorously evaluate the accuracy of the color Doppler jet area planimetry method for quantifying chronic mitral regurgitation.Background. Although the color Doppler jet area has been widely used clinically for evaluating the severity of mitral regurgitation, there have been no studies comparing the color jet area with a strictly quantifiable reference standard for determining regurgitant volume.Methods. In six sheep with surgically produced chronic mitral regurgitation, 24 hemodynamically different states were obtained. Maximal color Doppler jet area for each state was obtained with a Vingmed 750. Image data were directly transferred in digital format to a microcomputer. Mitral regurgitation was quantified by the peak and mean regurgitant flow rates, regurgitant stroke volumes and regurgitant fractions determined using mitral and aortic electromagnetic flow probes.Results. Mean regurgitant volumes varied from 0.19 to 2.4 liters/ min (mean [±SD] 1.2 ± 0.59), regurgitant stroke volumes from 1.8 to 29 ml/beat (mean 11 ± 6.2), peak regurgitant volumes from 1.0 to 8.1 liters/min (mean 3.5 ± 2.1) and regurgitant fractions from 8.0% to 54% (mean 29 ± 12%). Twenty-two of 24 jets were eccentric. Simple linear regression analysis between maximal color jet areas and peak and mean regurgitant flow rates, regurgitant stroke volumes and regurgitant fractions showed correlation, with r = 0.68 (SEE 0.64 cm²), r = 0.63 (SEE 0.67 cm²), r = 0.63 (SEE 0.67 cm²) and r = 0.58 (SEE 0.71 cm²), respectively. Univariate regression comparing regurgitant jet area with cardiac output, stroke volume, systolic left ventricular pressure, pressure gradient, left ventricular/ left atrial pressure gradient, left atrial mean pressure, left atrial vwave pressure, systemic vascular resistance and maximal jet velocity showed poor correlation (0.08 < r < 0.53, SEE > 0.76 cm²).Conclusions. This study demonstrates that color Doppler jet area has limited use for evaluating the severity of mitral regurgitation with eccentric jets.     

Simultaneous measurement of left atrial pressure by Doppler echocardiography and catheterization.

Simultaneous, continuous wave Doppler echocardiography, left ventricular systolic and mean pulmonary capillary wedge pressure measurements were performed during cardiac catheterization in 54 patients with mitral regurgitation. Doppler-derived left atrial pressure, which was calculated by subtracting mitral regurgitant gradient from brachial artery systolic pressure, correlated well with mean pulmonary capillary wedge pressure by catheter (r = 0.933, SEE = 2.9 mmHg, P < 0.001); a comparison between non-invasive and invasive systolic gradients across the mitral valve yielded a high correlation (r = 0.91, SEE = 6.0 mmHg, P < 0.001); and there was also a high correlation between brachial artery and left ventricular systolic pressures (r = 0.93, SEE = 4.9 mmHg, P < 0.01). It is concluded that Doppler echocardiography provides a reliable and accurate method for complete non-invasive assessment of left atrial pressure in patients with mitral regurgitation.     

Effects of heart rate on experimentally produced mitral regurgitation in dogs

The effects of increasing heart rate (HR) on the hemodynamics of acute mitral regurgitation (MR) were studied in 8 open-chest dogs. Filling volume, regurgitant volume and stroke volume were calculated from electromagnetic probe measurements of mitral and aortic flows. The left atrial-left ventricular systolic pressure gradient was measured with micromanometers. The calculated effective mitral regurgitant orifice area varied from 10 to 128 mm², with a consequent regurgitant fraction (regurgitant volume/filling volume) of 24 to 62%. After crushing the sinus node, HR was increased stepwise from 90 to 180 beats/min by atrial pacing while maintaining aortic pressure constant. With increasing HR, filling volume, stroke volume, regurgitant volume and regurgitant time decreased; total cardiac output, forward cardiac output, regurgitant output, systolic pressure gradient, regurgitant fraction and the regurgitant orifice did not change; left ventricular end-diastolic pressure decreased; and left atrial v-wave amplitude increased. These results indicate that in acute experimental MR with a wide spectrum of incompetence, the relative distribution of forward and regurgitant flows did not change with large increases in HR. At rates >150 beats/min the atrial contraction occurs early and increases the amplitude of the left atrial v wave. This may contribute to the severity of pulmonary congestion in patients with MR.     

Pulmonary venous flow dynamics before and after balloon mitral valvuloplasty as determined by transesophageal Doppler echocardiography.

The pattern of left atrial filling was studied in 14 patients with severe mitral stenosis in sinus rhythm before and immediately after successful balloon mitral valvuloplasty by transesophageal pulsed Doppler echocardiography of the left superior pulmonary vein. Mean mitral valve orifice area increased from 0.8 +/- 0.1 to 2.2 +/- 0.3 cm2 (p less than 0.0001), and left atrial mean pressure decreased from 30 +/- 5 to 12 +/- 4 mm Hg (p less than 0.0001) after the procedure. After balloon mitral valvuloplasty, significant increases in peak systolic pulmonary velocity (35 +/- 16 to 44 +/- 10 cm/s; p less than 0.01), systolic flow velocity time integral (3.3 +/- 1.5 to 5.9 +/- 2.0 cm; p less than 0.001) and the ratio of systolic/diastolic pulmonary venous flow velocity time integrals (0.8 +/- 0.4 to 1.4 +/- 0.5; p less than 0.001) were observed. An acute increase in mitral valve orifice area caused no significant changes in peak diastolic forward flow velocity (40 +/- 7 to 41 +/- 9 cm/s; p = not significant [NS]), diastolic forward flow velocity time integral (4.3 +/- 1.7 to 4.6 +/- 1.8 cm; p = NS) and atrial flow reversal velocity (30 +/- 3 to 35 +/- 3 cm/s; p = NS) compared with at baseline. The results suggest that in patients with severe mitral stenosis and sinus rhythm, left atrial filling is biphasic with a diastolic preponderance, and successful mitral valvuloplasty is associated with an immediate increase in pulmonary venous systolic forward flow.     

Mechanism of reduction of mitral regurgitation with vasodilator therapy.

Acute mitral regurgitation was produced in six open chest dogs by excising a portion of the anterior valve leaflet. Electromagnetic flow probes were placed in the left atrium around the mitral anulus and in the ascending aorta to determine phasic left ventricular filling volume, regurgitant volume and stroke volume. The systolic pressure gradient was calculated from simultaneously measured high fidelity left atrial and left ventricular pressures. The effective mitral regurgitant orifice area was calculated from Gorlin's hydraulic equation. Infusion of nitroprusside resulted in a significant reduction in mitral regurgitation. No significant change occurred in the systolic pressure gradient between the left ventricle and the left atrium because both peak left ventricular pressure and left atrial pressure were reduced. The reduction of mitral regurgitation was largely due to reduction in the size of the mitral regurgitant orifice. Reduction of ventricular volume rather than the traditional concept of reduction of impedance of left ventricular ejection may explain the effects of vasodilators in reducing mitral regurgitation.     

Age-related increase in systolic fraction of pulmonary vein flow velocity-time integral from transesophageal Doppler echocardiography in subjects without cardiac disease.

The pulmonary vein flow velocity-time profile would be equivalent to the pulmonary vein flow volume-time profile, provided that the cross-sectional area of the pulmonary vein remains unchanged during 1 cardiac cycle. The systolic fraction of the pulmonary vein flow velocity-time integral, a ratio of velocity-time integral of the S wave to the sum of velocity-time integrals of the S and D waves, represents the ratio of left atrial storage volume to left ventricular stroke volume. This systolic fraction may help early filling of the left ventricle through an appropriate storage of blood and generation of driving pressure in the left atrium. Because early filling of the left ventricle is progressively impaired with age, it was hypothesized that this systolic fraction is increased with age. Forty-four noncardiac surgical patients (age range 17 to 70 years) who underwent transesophageal Doppler echocardiography under general anesthesia were studied, and left upper pulmonary vein flow and mitral inflow velocities were recorded. The ratio of peak velocity of the E wave to that of the A wave of mitral inflow velocity-time profile (y) decreased with age (y = -0.0245 x age + 2.41; r = -0.672, p < 0.01). Systolic fraction (y) increased with age (y = 0.00373 x age + 0.514; r = 0.656, p < 0.01). The age-related increase in the systolic fraction of pulmonary vein flow velocity-time integral may account for the compensation for impaired early filling of the left ventricle in elderly patients.     

Effective regurgitant orifice area: A noninvasive Doppler development of an old hemodynamic concept

Objectives. The purpose of this study was to determine the feasibility, relation to other methods and significance of the effective regurgitant orifice area measurement.Background. Assessment of the severity of valvular regurgitation (effective regurgitant orifice area) has not been implemented in clinical practice but can be made by Doppler echocardiography.Methods. Effective regurgitant orifice area was calculated by Doppler echocardiography as the ratio of regurgitant volume/ regurgitant jet time-velocity integral and compared with color flow Doppler mapping, angiography, surgical classification, regurgitant fraction and variables of volume overload.Results. In 210 consecutive patients examined prospectively, feasibility improved from the early to the late experience (65% to 95%). Effective regurgitant orifice area was 28 ± 23 mm²(mean ± SD) for aortic regurgitation (32 patients), 22 ± 13 mm²for ischemic/functional mitral regurgitation (50 patients) and 41 ± 32 mm²for organic mitral regurgitation (82 patients). Significant correlations were found between effective regurgitant orifice and mitral jet area by color flow Doppler mapping (r = 0.68 and r = 0.63, p < 0.0001, respectively) and angiographic grade (r = 0.77, p = 0.0004). Effective regurgitant orifice area in surgically determined moderate and severe lesions was markedly different in mitral regurgitation (35 ± 12 and 75 ± 33 mm², respectively, p = 0.009) and in aortic regurgitation (21 ± 8 and 38 ± 5 mm², respectively, p = 0.08). Strong correlations were found between effective regurgitant orifice area and variables reflecting volume overload. A logarithmic regression was found between effective regurgitant orifice area and regurgitant fraction, underlining the complementarity of these indexes.Conclusions. Calculation of effective regurgitant orifice area is a noninvasive Doppler development of an old hemodynamic concept, allowing assessment of the lesion severity of valvular regurgitation. Feasibility is excellent with experience. Effective regurgitant orifice area is an important and clinically significant index of regurgitation severity. It brings additive information to other quantitative indexes and its measurement should be implemented in the comprehensive assessment of valvular regurgitation.     

Physiopathology and etiology of mitral insufficiency

Mitral regurgitation has a complex pathophysiology. It should be assessed from the study of factors influencing regurgitant volume and the evaluation of hemodynamics effects downstream (impact on left ventricular function) and upstream (level of left atrial compliance and pulmonary pressure). The regurgitant volume is larger when the regurgitation time is longer, the regurgitant orifice is bigger and the magnitude of the left ventrico-atrial systolic gradient higher. The study of left ventricular function is difficult, especially in chronic mitral regurgitation where the apparently normal left ventricular systolic function can hide a significant worsening in myocardiacs fibres contractile abilities. With the increase in life expectancy and with the decrease in the incidence of rheumatic fever, aetiologies of mitral regurgitation have changed in the past 30 years. They are now dominated by dystrophic mitral regurgitation and infective endocarditis while rheumatic fever becomes less frequent.     

Left Atrial Contribution to Left Ventricular Filling in Patients with Mitral Stenosis: Combined Analysis of Transmitral and Pulmonary Venous Flow Velocities

We recorded transmitral and pulmonary venous flow velocities using transthoracic continuous-wave and transesophageal pulsed Doppler echocardiography, respectively, in 36 patients with mitral stenosis who were in sinus rhythm to investigate the left atrial contribution to left ventricular filling in mitral stenosis. The mitral valve area was determined by transthoracic two-dimensional short-axis echocardiography. Patients were classified as having mild stenosis (± 1.5 cm², n = 17) or moderate stenosis (< 1.5 cm², n = 19). The mean pulmonary capillary wedge pressure and left atrial maximal diameter were significantly larger, and left atrial volume change during atrial contraction was significantly smaller in the moderate group than in the mild group. The percent left atrial contribution to left ventricular filling, estimated from the transmitral flow velocity, the peak atrial systolic velocity, and the percent ratio of left atrial systolic regurgitation to left atrial filling, estimated from the pulmonary venous flow velocity, were significantly lower in the moderate group than in the mild group. The percent left atrial contribution to left ventricular filling, the peak atrial systolic velocity, and the percent ratio of left atrial systolic regurgitation to left atrial filling were positively correlated with the mitral valve area and negatively correlated with the mean pulmonary capillary wedge pressure. These results suggest that the left atrial contribution to left ventricular filling in patients with mitral stenosis in sinus rhythm decreases as the severity of valve stenosis increases, and that analysis of the atrial systolic waves of the transmitral and pulmonary venous flow velocities provides important information for evaluation of left atrial systolic performance in patients with mitral stenosis.     

The mechanism of decrease in dynamic mitral regurgitation during heart failure treatment: importance of reduction in the regurgitant orifice size

Objectives. The purpose of this study was to quantify and characterize the regurgitant flow pattern and regurgitant orifice area in patients undergoing therapy for severe heart failure using contemporary echocardiographic techniques.

Background. Mitral regurgitation may be dynamic in patients with heart failure and ultimately correlate with outcome in a group of patients.

Methods. Fourteen patients with severe heart failure felt to require hemodynamic monitoring for the optimization of medical therapy were enrolled. Two-dimensional and Doppler echocardiograms were performed before and following invasively guided therapy. Hemodynamics and standard echocardiographic dimensions were determined as well as regurgitant volume and regurgitant orifice area derived from color M-mode and Doppler measurements.

Results. Invasively guided therapy for heart failure was associated with a reduction in weight, filling pressures of the left and right heart, systemic vascular resistance, and echocardiographic left atrial, left ventricular and mitral annular dimensions. The mitral regurgitant volume decreased from 47 ± 27 ml before therapy to 14 ± 14 ml after therapy; p < 0.001. While therapy for heart failure markedly attenuated the volume of regurgitation, the pattern of regurgitant flow across the mitral valve was not significantly altered. In contrast, there was no difference in the velocity time integral of the continuous-wave Doppler spectra of mitral regurgitation with therapy (128 ± 23 cm to 123 ± 25 cm, p = 0.23). In all patients, the regurgitant orifice area decreased with therapy from 0.55 ± 0.38 cm² to 0.21 ± 0.20 cm² (p < 0.001).

Conclusions. Pharmacologic reduction in filling pressure and systemic vascular resistance leads to a reduction in the dynamic mitral regurgitation of heart failure through a reduction in the regurgitant orifice area but not through a change in the gradient across the mitral valve. Reduction of the regurgitant orifice area is likely related to decreased left ventricular volumes and decreased annular distention.     

Coincidental Finding of Cor Triatriatum by Intraoperative Transesophageal Echocardiography in a Patient with Severe Mitral Regurgitation from Myxomatous Degeneration

Cor triatriatum is a rare congenital cardiac anomaly consisting of a left atrial membrane dividing the atrium into proximal and distal chambers. The anomaly usually presents in childhood, but can present later in life, in which case it is often associated with mitral regurgitation. We report a patient in whom cor triatriatum was found coincidentally by intraoperative transesophageal echocardiography before surgery for severe mitral regurgitation. An interesting finding was preservation of antegrade systolic pulmonary vein flow by Doppler possibly due to shielding of the pulmonary veins from the regurgitant jet by the left atrial membrane.     

Large V waves in the pulmonary capillary wedge pressure tracing without mitral regurgitation: the influence of the pressure/volume relationship on the V wave size

We have previously demonstrated that a large V wave in the pulmonary capillary wedge tracing may occur in the absence of mitral regurgitation. This study evaluates the role of left atrial and pulmonary vein compliance on such a finding. We studied 11 patients with coronary disease, without clinical or angiographic mitral regurgitation. Heart rate, pulmonary capillary wedge mean, A and V waves, V-wave slope, left ventricular and aortic pressures, cardiac output, and left atrial echo and apical phonocardiogram were recorded simultaneously. Preload was modified acutely by volume overload and by the administration of i.v. nitroglycerine. Volume administration induced a marked increase in V-wave pressure (13.0 +/- 9.6 vs. 27.0 +/- 9.6 mmHg, p less than 0.05), without producing mitral regurgitation, and without appreciable change in left atrial dimension by echo (33.0 +/- 4.9 vs. 35.5 +/- 5.2 mm, NS), or stroke volume (101.7 +/- 26.2 vs. 97.8 +/- 34.3 ml, NS). An increase was also seen in the A wave (13.6 +/- 8.9 vs. 23.3 +/- 8.5 mmHg, p less than 0.05), pulmonary capillary wedge mean pressure (9.8 +/- 7.2 vs. 20.6 +/- 7.8 mmHg, p less than 0.05), and left ventricular diastolic pressure (7.4 +/- 5.5 vs. 14.6 +/- 6.3 mmHg, p less than 0.05). All values returned to baseline after nitroglycerine. The compliance of the left atrium/pulmonary veins decreased with increasing pulmonary capillary wedge pressures. With large filling volumes, a small stroke volume brings on a large pressure change, thus explaining the finding of large V waves in patients with elevated pulmonary capillary wedge pressure and without mitral regurgitation.     

Dynamic aspects of acute mitral regurgitation: effects of ventricular volume, pressure and contractility on the effective regurgitant orifice area.

The dynamics of acute mitral regurgitation were studied in six open-chest dogs in whom a portion of the anterior leaflet was excised. Phasic mitral and aortic flows were measured electromagnetically and left ventricular filling volume, regurgitant volume (RV) and forward stroke volume (SV) were calculated. The systolic pressure gradient (SPG) between the left ventricle (LV) and left atrium (LA) was obtained from high-fidelity pressure transducers. The effective mitral regurgitant orifice area (MRA) was calculated from the hydraulic equation of Gorlin. Volume infusion resulted in significant increases in both left atrial and left ventricular pressures; thus, the SPG was unchanged and the increase in RV was due primarily to the increase in MRA. Angiotensin infused to raise arterial pressure resulted in greater increments in left ventricular than left atrial pressure, so that SPG rose significantly. The increase in RV was due to increases in both MRA and SPG. Norepinephrine infusion increased systolic left ventricular pressure and SPG, while left ventricular end-diastolic pressure and left atrial pressure diminished. Despite a significant increase in SPG, RV did not increase, due to a substantial decrease in MRA. Thus, angiotensin and volume infusion induced a substantial increase in regurgitation due to the increase in MRA, while augmentation of contractility after norepinephrine infusion resulted in a decrease in regurgitation through reduction of MRA. These findings support the clinical view that maintaining a small LV with sustained myocardial contractility will reduce mitral regurgitation. Alternatively, left ventricular dilatation can enhance mitral regurgitation by increasing the effective regurgitant orifice independent of SPG.     

Echocardiographic Evaluation of Hemodynamics in Patients With Systolic Heart Failure Supported by a Continuous-Flow LVAD

BackgroundHemodynamics assessment is important for detecting and treating post-implant residual heart failure, but its accuracy is unverified in patients with continuous-flow left ventricular assist devices (CF-LVADs).ObjectivesWe determined whether Doppler and 2-dimensional transthoracic echocardiography reliably assess hemodynamics in patients supported with CF-LVADs.MethodsSimultaneous echocardiography and right heart catheterization were prospectively performed in 50 consecutive patients supported by using the HeartMate II CF-LVAD at baseline pump speeds. The first 40 patients were assessed to determine the accuracy of Doppler and 2-dimensional echocardiography parameters to estimate hemodynamics and to derive a diagnostic algorithm for discrimination between mean pulmonary capillary wedge pressure ≤15 versus >15 mm Hg. Ten patients served as a validation cohort.ResultsDoppler echocardiographic and invasive measures of mean right atrial pressure (RAP) (r = 0.863; p < 0.0001), systolic pulmonary artery pressure (sPAP) (r = 0.880; p < 0.0001), right ventricular outflow tract stroke volume (r = 0.660; p < 0.0001), and pulmonary vascular resistance (r = 0.643; p = 0.001) correlated significantly. Several parameters, including mitral ratio of the early to late ventricular filling velocities >2, RAP >10 mm Hg, sPAP >40 mm Hg, left atrial volume index >33 ml/m², ratio of mitral inflow early diastolic filling peak velocity to early diastolic mitral annular velocity >14, and pulmonary vascular resistance >2.5 Wood units, accurately identified patients with pulmonary capillary wedge pressure >15 mm Hg (area under the curve: 0.73 to 0.98). An algorithm integrating mitral inflow velocities, RAP, sPAP, and left atrial volume index was 90% accurate in distinguishing normal from elevated left ventricular filling pressures.ConclusionsDoppler echocardiography accurately estimated intracardiac hemodynamics in these patients supported with CF-LVAD. Our algorithm reliably distinguished normal from elevated left ventricular filling pressures.     

Quantification of regurgitant lesions by MRI

We examined 46 patients with angiographically documented regurgitant lesions (26 patients with mitral regurgitation, 20 patients with aortic regurgitation) using an 0.5 Tesla magnet. In each patient a multislice-multiphase spinecho sequence in sagittal-coronal double angulated plane was performed to assess left and right ventricular volumes, ejection fraction and regurgitant fraction. Additionally a blood flow sensitive gradient echo technique was done to visualize direction and extension of the regurgitant jet. MRI data were compared with quantitative and qualitative assessment of regurgitation by angiography and echocardiography. Using the gradient echo technique MRI could demonstrate the regurgitant jet in all patients. A linear correlation for volume parameters by MRI and angio was found with best correlation for the left ventricular stroke volume (r=0.82, p<0.0001). Furthermore MRI regurgitant fraction correlated with angiographically determined regurgitant fraction in patients with aortic regurgitation (r=0.91, p<0.0001) and mitral regurgitation (r=0.67, p<0.001), respectively. Semiquantitative assessment of regurgitation by gradient echo technique showed an agreement with angiographic grading by Sellers in 70% of mitral and 75% of aortic regurgitation, respectively. The comparison of MRI and color Doppler sonography showed only moderate correlation of r=0.72 (p<0.01).     

Detection, localization, and quantitation of bioprosthetic mitral valve regurgitation. An in vitro two-dimensional color-Doppler flow-mapping study

The usefulness of two-dimensional color-Doppler flow-imaging (2D Doppler) in the detection, localization, and quantitation of bioprosthetic mitral valve regurgitation is uncertain. Mitral bioprostheses, before and after the creation of transvalvular (n = 33), paravalvular (n = 17), or combined (n = 23) defects, were mounted in a pulsed duplication system (flow rates, 2.5-6.5 l/min; pulse rate, 70 beats/min). An Aloka 880 2D Doppler system (Japan) was used to image the regurgitant jets in the simulated left atrial chamber, analogous to images obtained with transesophageal echocardiography. Jet area was corrected to an estimate of stroke volume: 2D Doppler measurements were divided by [(valve effective orifice area) X (continuous-wave Doppler-determined mean diastolic filling velocity)]/pulse rate. Regurgitant fraction and regurgitant volume were measured by an electromagnetic flow probe. 2D Doppler correctly identified the presence and location of paravalvular regurgitation. In transvalvular and combined transvalvular-paravalvular defects, there were six incorrect interpretations, all having transvalvular regurgitant volumes less than 4 ml/beat. In the presence of transvalvular regurgitation, jet area, length, and width correlated linearly with regurgitant volume (r = 0.82, 0.80, and 0.68, respectively; p less than 0.0001) and regurgitant fraction (r = 0.62, 0.61, and 0.45, respectively; p less than 0.001). Correlations with regurgitant fraction were improved when 2D Doppler measurements were corrected for stroke volume (r = 0.78, 0.79, and 0.67, respectively; p less than 0.0001). Mitral bioprostheses with transvalvular defects were also studied at varying flow rates (3.2-7.5 l/min) and pulse rates (70, 90, and 110 beats/min). The correlation between jet area and regurgitant volume was improved with a second-order polynomial regression (r = 0.93, p less than 0.0001). Our conclusions are that 1) in this in vitro model analogous to transesophageal imaging, 2D Doppler accurately detects and localizes bioprosthetic mitral valve regurgitation; 2) in transvalvular bioprosthetic mitral valve regurgitation, 2D Doppler measurement of jet area has a curvilinear relation with regurgitant volume, and correlation with regurgitant fraction is improved with correction for stroke volume; and 3) in paravalvular bioprosthetic mitral valve regurgitation, correlations between 2D Doppler measurements and regurgitant volumes are weaker, possibly because of jet eccentricity.     

A new approach to noninvasive evaluation of aortic regurgitant fraction by two-dimensional Doppler echocardiography

The aortic regurgitant fraction was estimated noninvasively in 20 patients with aortic regurgitation from systolic aortic and pulmonary volume flow determined by duplex Doppler echocardiography. By assuming that an excess of the aortic volume flow (AF) compared with the pulmonary volume flow (PF) is due to aortic regurgitant flow, the aortic regurgitant fraction (RF) was calculated as follows: RF(%) = (AF - PF)/AF X 100. The aortic and pulmonary volume flows were determined as products of systolic integrals of ejection flow velocities and cross-sectional areas of the left and right ventricular outflow tracts, respectively. The Doppler estimate of the regurgitant fraction was compared by semiquantitative grading (1+ to 4+) by cineaortography and with the measurement of regurgitant fraction by catheter technique. The mean Doppler-determined aortic regurgitant fraction was 2.4% for normal subjects, 28.0% for the patients with 1+, 32.6% for the patients with 2+, 53.3% for the patients with 3+, and 62.4% for the patients with 4+. A fair correlation was found between Doppler estimates of regurgitant fraction and semiquantitative cineaortographic grades (r = .80, p less than .01). In the patients without associated mitral regurgitation, a close correlation was observed between Doppler and catheter estimates of regurgitant fraction (r = .96, p less than .01; y = 1.0x - 0.08). In the patients with associated mild mitral regurgitation, however, Doppler estimates of regurgitant fraction substantially underestimated those determined by the conventional catheter technique, which cannot separately quantitate the aortic regurgitant fraction in the presence of mitral regurgitation. These observations indicate that the proposed Doppler technique provides a useful method to evaluate the aortic regurgitant fraction specifically regardless of the presence of associated mitral lesions.     

Quantitation of functional mitral regurgitation during bicycle exercise in patients with heart failure.

OBJECTIVES: We sought to examine the feasibility and reliability of quantifying mitral regurgitation (MR) during exercise by Doppler echocardiography in patients with heart failure and to assess the relationship between dynamic MR and systolic pulmonary artery pressure changes. BACKGROUND: The severity of MR can be quantified by using several echocardiographic methods. Quantitation of MR during dynamic exercise has not yet been performed. METHODS: Symptom-limited, semi-supine two-dimensional and Doppler echocardiograms during bicycle exercise were obtained in 27 consecutive patients with heart failure and functional MR. Regurgitant volume was measured at rest and during exercise by the proximal isovelocity surface area (PISA) method and by quantitative Doppler echocardiography. Exercise-induced changes in regurgitant volume were compared with changes in the regurgitant jet area to left atrial area ratio, vena contracta width and trans-tricuspid pressure gradient. RESULTS: The regurgitant volume measured by the PISA method increased from 21 +/- 12 ml (range 5 to 55) at rest to 39 +/- 23 ml (range 8 to 85) during exercise (p < 0.0001). The difference between two observers was low for both rest (2.0 +/- 2.7 ml) and exercise measurements (3.5 +/- 6.2 ml). The regurgitant volume measured by quantitative Doppler echocardiography increased from 29 +/- 13 to 49 +/- 24 ml (p = 0.0001). Excellent correlation between the two methods was obtained with exercise (r = 0.92). Exercise-induced changes in regurgitant volume, as measured by the PISA method, correlated well with regurgitant volume changes measured by quantitative Doppler echocardiography (r = 0.88), changes in vena contracta width (r = 0.82) and changes in trans-tricuspid pressure gradient (r = 0.73), but not with changes in regurgitant jet area to left atrial area ratio (r = 0.29). Seventeen patients stopped exercise because of fatigue and 10 because of dyspnea. These 10 patients exhibited greater increases in regurgitant volume (34 +/- 6 vs. 11 +/- 8 ml), corresponding to a significant elevation of the trans-tricuspid gradient (48 +/- 14 vs. 20 +/- 14 mm Hg). CONCLUSIONS: Quantitation of functional MR during exercise is feasible in patients with heart failure. There is a good correlation between regurgitant volume measured during exercise by the PISA method and that obtained by quantitative Doppler echocardiography, suggesting that the technique is reliable. An increase in mitral regurgitant volume during dynamic exercise correlates well with elevation of systolic pulmonary artery pressure.