Effects of Dobutamine Infusion on Mitral Regurgitation

Both intensity of mitral regurgitant murmur and color-coded Doppler regurgitant signal area have been reported to correlate with the degree of regurgitation. To evaluate the relationship between the intensity of regurgitant murmur and severity of mitral regurgitation, phonocardiography, echocardiography, and Doppler ultrasound were performed in 18 patients with mitral regurgitation before and during dobutamine infusion. Mitral regurgitation was due to mitral valve prolapse with ruptured chordae tendineae in 8 patients, rheumatic change in 5 patients, and dilated cardiomyopathy in 5 patients. With intravenous dobutamine infusion, heart rate (77–103 beats/min), systolic blood pressure (119–144 mmHg), peak mitral regurgitant jet velocity (4.5–5.4 m/sec), intensity of mitral regurgitant murmur (to 201% of that before infusion in early systole) increased, while left ventricular end-diastolic volume (124–102 mm), left ventricular end-systolic volume (57–42 mm), mitral anular diameter (33–28mm), and color Doppler mitral regurgitant signal area (704–416 mm²) decreased (P < 0.05). Total (forward + backward) left ventricular stroke volume (66–61 mL/beat) showed no change. Dobutamine decreased mitral regurgitant flow/beat, regardless of etiology of mitral regurgitation, which was probably due to the decrease of left ventricular size and mitral annular diameter. Although total (forward + backward) left ventricular stroke volume was unchanged, dobutamine effectively increased forward left ventricular stroke volume by decreasing backward regurgitation. Mitral regurgitant murmur became louder despite the decrease of mitral regurgation, indicating the uselessness of auscultation in the grading of the severity of mitral regurgitation.     

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.     

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.     

Dynamic changes in the canine mitral regurgitant orifice area during ventricular ejection.

We designed this study to test the hypothesis that in acute mitral regurgitation the mitral regurgitant area (MRA) is a dynamic quantity which varies with the time variation of ventricular volume. Mitral insufficiency was created in five open-chest dogs in which a portion of the anterior leaflet was excised. Phasic aortic and mitral flows were measured electromagnetically, along with left atrial and ventricular pressures. Filling, regurgitant, and stroke volumes, and systolic pressure gradient were determined by digital methods. MRA was calculated from the fluid dynamic equation of motion to give the temporal mean and the instantaneous value at three instants of time and at the time of peak flow (when inertia is negligible). Mean regurgitant fraction was 42 +/- 12% with no indication of left ventricular failure due to volume overload. MRA decreased monotonically with time to 59% of its initial value and closely paralleled the decrease in ventricular volume during systole. In a control study using a tilting-disc prosthesis with a hole 5 mm in diameter in the occluder, the calculated MRA was time invariant and equal to the measured area for regurgitation. We conclude that in acute mitral regurgitation the MRA is a function of ventricular volume.     

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.     

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.     

Mitral regurgitation in hypertrophic cardiomyopathy. Non-invasive study by two dimensional Doppler echocardiography.

Mitral regurgitation and its haemodynamic features were investigated non-invasively in cases of hypertrophic cardiomyopathy by means of two dimensional Doppler echocardiography. There were 28 patients, 14 of whom showed systolic anterior motion (SAM) of the mitral echo; the other 14 did not. The following results were obtained. (1) Mitral regurgitation was detected by the Doppler technique in all cases with systolic anterior motion of the mitral echo and in half of those without it. (2) Doppler signals of mitral regurgitation started immediately after the first heart sound. (3) Mitral regurgitant flow was often distributed from the entire mitral orifice over the entire or the posterior half of the left atrium in the cases with systolic anterior motion. In the cases without systolic anterior motion the regurgitation was usually localised near the mitral orifice. These features differ from those of regurgitation usually seen in rheumatic mitral valve disease and idiopathic mitral valve prolapse. (4) The Doppler technique and left ventriculography were equally efficient in detecting mitral regurgitation. (5) The early systolic component of the murmur of hypertrophic myopathy is considered to result in the main from concomitant mitral regurgitation, but not from turbulent blood flow in the left ventricular outflow tract, so that in cases with mitral regurgitation as a complication, mitral regurgitation may also contribute to the development of the midsystolic portion of the systolic murmur, while the main origin of this portion of the murmur is the left ventricular outflow obstruction.     

Systolic aortic regurgitation in rheumatic carditis: Mechanistic insight by Doppler echocardiography

BackgroundAortic regurgitation (AR) usually occurs in diastole in presence of an incompetent aortic valve. Systolic AR is a rare phenomenon occurring in patients with reduced left ventricular systolic pressure and atrial fibrillation or premature ventricular contractions. Its occurrence is a Doppler peculiarity and adds to the hemodynamic burden.AimRheumatic carditis is often characterised by acute or subacute severe mitral regurgitation (MR) due to flail anterior mitral leaflet and elongated chords. In patients with acute or subacute MR, developed left ventricular systolic pressure may fall in mid and late systole due to reduced afterload and end-systolic volume and may be lower than the aortic systolic pressure, causing flow reversal in aorta and systolic AR.Material and methods17 patients with acute rheumatic fever were studied in the echocardiography lab during the period 2005–2015. Five patients had severe MR of which two had no AR and hence were excluded from the study. Three young male patients (age 8–24 years) who met modified Jones’ criteria for rheumatic fever with mitral and aortic valve involvement were studied for the presence of systolic AR.ResultsIn presence of acute or subacute severe MR, flail anterior mitral valve and heart failure, all three showed both diastolic and late systolic AR by continuous-wave and color Doppler echocardiography.ConclusionSystolic AR is a unique hemodynamic phenomenon in patients with acute rheumatic carditis involving both mitral and aortic valves and occurs in presence of severe MR.     

Mitral regurgitation in hypertrophic cardiomyopathy. Non-invasive study by two dimensional Doppler echocardiography

Mitral regurgitation and its haemodynamic features were investigated non-invasively in cases of hypertrophic cardiomyopathy by means of two dimensional Doppler echocardiography. There were 28 patients, 14 of whom showed systolic anterior motion (SAM) of the mitral echo; the other 14 did not. The following results were obtained. (1) Mitral regurgitation was detected by the Doppler technique in all cases with systolic anterior motion of the mitral echo and in half of those without it. (2) Doppler signals of mitral regurgitation started immediately after the first heart sound. (3) Mitral regurgitant flow was often distributed from the entire mitral orifice over the entire or the posterior half of the left atrium in the cases with systolic anterior motion. In the cases without systolic anterior motion the regurgitation was usually localised near the mitral orifice. These features differ from those of regurgitation usually seen in rheumatic mitral valve disease and idiopathic mitral valve prolapse. (4) The Doppler technique and left ventriculography were equally efficient in detecting mitral regurgitation. (5) The early systolic component of the murmur of hypertrophic myopathy is considered to result in the main from concomitant mitral regurgitation, but not from turbulent blood flow in the left ventricular outflow tract, so that in cases with mitral regurgitation as a complication, mitral regurgitation may also contribute to the development of the midsystolic portion of the systolic murmur, while the main origin of this portion of the murmur is the left ventricular outflow obstruction.     

Effects of isosorbide dinitrate on rheumatic and non-rheumatic mitral regurgitation

Isosorbide dinitrate was given to seven patients with isolated mitral regurgitation (three cases of rheumatic origin, four non-rheumatic) to assess its hemodynamic effects. The pulmonary capillary pressure, left ventricular end-diastolic pressure, left ventricular end-diastolic volume index, and the aortic pressure were all significantly reduced. The heart rate was significantly increased, while the systemic vascular resistance and the left ventricular contractility index were unchanged. The regurgitant flow increased by an average of 72.2% in the rheumatic group, but decreased by an average of 4.8% in the non-rheumatic group (p < 0.05). The forward cardiac output decreased slightly in both groups, but the difference was not significant (NS). It appears that isosorbide dinitrate has a more detrimental effect on cases of mitral regurgitation of rheumatic origin than on those of non-rheumatic origin. We suggest the difference in the responses is a consequence of the dynamic nature of the regurgitant orifice in the non-rheumatic group and the static nature of the orifice in the rheumatic group.     

Ventriculographic and hemodynamic features of mitral regurgitation of cardiomyopathic, rheumatic and nonrheumatic etiology

Quantitative angiographic findings were reviewed in 40 patients with significant mitral regurgitation classified into three etiologic groups: group I, primary mitral regurgitation (prolapse, ruptured chordae); group II, mixed stenosis and regurgitation of rheumatic origin; and group III, cardiomyopathic mitral regurgitation. For patients in both groups I and II, left ventricular end-diastolic volume was directly related to regurgitant fraction, and ejection fraction was generally well maintained. In contrast, patients in group III had a depressed ejection fraction (less than 0.40) and end-diastolic volume that was disproportionately increased in relation to the degree of regurgitation. Left ventricular end-diastolic pressure was a poor indicator of severity of regurgitation in all patient groups. There was a significant negative correlation between forward cardiac index and regurgitant fraction. There was significant relation, although with considerable variation, between the normalized V wave and regurgitant fraction. The graphs of chamber size, ejection fraction and hemodynamic measures plotted against the severity of regurgitation in different patient groups provide a perspective for interpreting the findings in individual patients.     

PISA method for assessment of mitral regurgitation in children.

OBJECTIVE: The purpose of this study was to determine the feasibility and significance of the proximal isovelocity surface area (PISA) method in children with rheumatic mitral regurgitation (MR). METHODS: Thirty-one children (mean age 12.3+/-3.1 years), with chronic MR, were evaluated by semiquantitative and quantitative Doppler, quantitative two-dimensional echocardiography and the PISA methods. Also, we compared the effective regurgitant orifice area, regurgitation volume and systolic left ventricular functions in mild-moderate and severe MR. RESULTS: There were no statistically significant differences in the regurgitant orifice area and regurgitant volume values obtained by the PISA method and the quantitative Doppler (p>0.05) but they were different from the same values obtained by two dimensional echocardiography (p<0.05). There were excellent correlations between the regurgitant orifice area, regurgitant volume and the radius of the proximal flow convergence hemisphere (r=0.882, r=0.925, r=0.880; p<0.05). We found a very good correlation between the regurgitant orifice area obtained by the PISA and left ventricular end-diastolic diameters, the ratio of the jet/left atrial area, grading with color Doppler imaging (r=0.763, r=0.745, r=0.618; p<0.05). CONCLUSION: It is concluded that MR can be accurately predicted in children by using the PISA method as like as the Doppler method.     

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.     

Relation of Mitral Annular Dilation with Dynamic Mitral Regurgitation in Patients with Rheumatic Mitral Regurgitation

Introduction: Dynamic mitral regurgitation (MR) is frequently investigated in patients with left ventricular systolic dysfunction (LVSD). Data about the dynamic MR in patients with organic valve disease are limited. The aim of this study was to evaluate the alteration of MR by exercise in patients with rheumatic valve disease (RVD). Methods: Asymptomatic patients with rheumatic MR and normal left ventricular function had been included in our study. Transthoracic echocardiography and Doppler measurements were performed at rest and just after submaximal exercise test performed with treadmill. Severity of MR was evaluated quantitatively by measuring effective regurgitant orifice area (EROA) with flow convergence method. Results: A total of 34 patients with rheumatic MR had been included. Severity of MR increased in 10 patients with exercise (Group 1) and decreased in 24 of them (Group 2). When the variables of two groups were compared; diastolic blood pressure after exercise, EROA, left atrial volume, left ventricular diastolic volume and mitral annular area values were significantly higher in Group 1 patients. A linear regression model was constructed by considering change of EROA by exercise the dependent, and the variables showing significant differences as the independents. Mitral annular area was found to be independently associated with EROA increase with exercise (R²= 0.499; P < 0.001). Conclusion: Mitral annular dilation is independently associated with increase of MR with submaximal exercise in asymptomatic patients with MR due to RVD with normal left ventricular function.     

Doppler echocardiography distinguishes between physiologic and pathologic “silent” mitral regurgitation in patients with rheumatic fever

Background: The diagnosis of rheumatic fever is based on physical findings (major) and supporting laboratory evidence (minor) as defined by the Jones criteria. Rheumatic carditis is characterized by auscultation of a mitral regurgitant murmur. Doppler echocardiography, however, may detect mitral regurgitation when there is no murmur (“silent” mitral regurgitation), even in normal individuals. Hypothesis: The hypothesis of this study was that physiologic mitral regurgitation can be differentiated from pathologic “silent” mitral regurgitation by Doppler echocardiography. Methods: The study group consisted of 68 patients (2–27 years) with normal two-dimensional imaging and Doppler evidence of mitral regurgitation but no murmur. Patients with rheumatic fever (n = 37) met Jones criteria (chorea in 20, arthritis in 17). Patients without rheumatic fever (n = 31) were referred for innocent murmur (n = 7), abnormal electrocardiogram (n = 13), and chest pain (n = 11). Echoes were independently reviewed by two cardiologists blinded to the diagnosis. Pathologic mitral regurgitation was defined as meeting the following four criteria: (1) length of color jet > 1 cm, (2) color jet identified in at least two planes, (3) mosaic color jet, and (4) persistence of the jet throughout systole. Jet orientation was also noted. Results: Using the above criteria, there was agreement in echo interpretation of pathologic versus physiologic mitral regurgitation in 67 of 68 patients (interobserver variability of 1.5%). Pathologic regurgitation was found in 25 (68%) patients with rheumatic fever but in only 2 (6.5%) patients without rheumatic fever (p<0.001). The specificity of Doppler for detecting pathologic regurgitation was 94% with a positive predictive value of 93%. The color mitral regurgitant jet was posteriorly directed in all 25 patients with rheumatic fever. Conclusion: Pathologic “silent” mitral regurgitation of rheumatic fever can be distinguished from physiologic mitral regurgitation using strict Doppler criteria, particularly when the jet is directed posteriorly. These data support the use of Doppler echocardiography as a minor criterion for evaluating patients with suspected rheumatic fever.     

Left atrial filling volume can be used to reliably estimate the regurgitant volume in mitral regurgitation

Objectives. The objective was to analyze the accuracy and diagnostic value of the estimated regurgitant volume of mitral regurgitation using 1) left atrial volume variation during ventricular systole (left atrial filling volume) and 2) the percent of systolic pulmonary vein velocity integral compared with its total.Background. Left atrial filling volume (LAfill), which represents the atrial volume variation during ventricular systole, has been used for the assessment of mitral regurgitation severity. A good correlation with invasive semiquantitative evaluation was found, but with an unacceptable overlapping among grades. The reason could be the absence of information concerning the contribution of blood entering into the left atrium from the pulmonary veins.Methods. Doppler regurgitant volume (Dpl-RVol) (mitral stroke volume − aortic stroke volume) was measured in 30 patients with varying degrees and etiological causes of mitral regurgitation. In each patient atrial volumes were measured from the apical view, using the biplane area-length method. The systolic time-velocity integral of pulmonary vein flow was expressed as a percentage of the total (systolic-diastolic) time-velocity integral (PVs%). These parameters were used in this group of patients to obtain an equation whose reliability in estimating Dpl-RVol was tested in a second group of patients.Results. In the initial study group, with linear regression analysis the following parameters correlated with Dpl-RVol: end-systolic left atrial volume (R²= 0.37, p = 0.0004); LAfill (R²= 0.45, p < 0.0001); PVs% (R²= 0.56, p < 0.0001). In multiple regression analysis the combination of LAfill and the percent of the systolic pulmonary vein velocity integral (PVs%) provided a more accurate estimate of regurgitant volume (R²= 0.88; SEE 10.6; p < 0.0001; Dpl-RV = 6.18 + (1.01 × LAfill) − (0.783 × PVs%). The equation was subsequently tested in 54 additional patients with mitral regurgitation with a mean Dpl-RVol 27 ± 37 ml. Estimated regurgitant volume and Dpl-RVol correlated well with each other (R²= 0.90; SEE 12.1; p < 0.0001). In the test population, the equation was 100% sensitive and 98% specific in detecting a regurgitant volume higher than 55 ml.Conclusions. Left atrial filling volume and pulmonary vein flow give a reliable estimate of regurgitant volume in mitral regurgitation.     

Use of Cardiac Magnetic Resonance Imaging in Assessing Mitral Regurgitation: Current Evidence

Accurate quantification of regurgitant volume is a central component to the management of mitral regurgitation. Cardiac magnetic resonance imaging (CMR) accurately quantifies mitral regurgitation as the difference between left ventricular stroke volume and forward stroke volume using steady state free precession and phase contrast imaging. The CMR measurement of mitral regurgitant volume is reproducible and can quantify mitral regurgitation in patients without regard to regurgitant jet morphology, such as patients with multiple and eccentric jets. It can be used to quantify regurgitant volume in patients with multiple valve lesions and concomitant intracardiac shunts without the use of intravenous contrast. Studies have highlighted the accuracy and reproducibility of CMR in quantifying mitral regurgitation and have begun to link CMR to clinical outcomes.     

Persisting volume overload of the left ventricle following surgical correction of chronic aortic insufficiency

After aortic valve replacement for chronic aortic regurgitation, complete normalization of the left ventricular end-diastolic volume can rarely be observed. We therefore investigated the role of continual volume overload caused by persisting concomitant mitral regurgitation. 20 patients who received an aortic valve for chronic aortic regurgitation (group 1), 5 patients after operation for aortic stenosis (group 2) and 6 patients with double valve replacement because of aortic and mitral valve lesions were included in the study 1 to 108 months after operation. All patients were examined clinically and by combined first pass/equilibrium radionuclide ventriculography. In the case of significant regurgitation (greater than 20%) 2-dimensional colour-coded Doppler-echocardiography was performed in patients of group 1 to localize the regurgitant lesion. 15 patients of group 1 had a typical systolic murmur indicating mitral regurgitation. 14 of these patients had significant scintigraphic left-sided heart regurgitation: 7 patients had regurgitant fractions between 21 and 40%; 6 patients between 41 and 60%; in 1 patient RF was 64%. Echocardiography confirmed mitral regurgitation in 9 of 11 of these cases. No significant regurgitation was observed in patients of group 2; mild regurgitation was measured in 5 of 6 patients of group 3 (26 to 31%). We conclude that in patients with chronic aortic regurgitation complete normalization of the left ventricular end-diastolic volume after valve replacement may not occur in some patients because of persisting mitral regurgitation.     

Measurement of aortic regurgitation by Doppler echocardiography

In an attempt to develop a new approach to the non-invasive measurement of aortic regurgitation, transmitral volumetric flow (MF) and left ventricular total stroke volume (SV) were measured by Doppler and cross sectional echocardiography in 23 patients without aortic valve disease (group A) and in 26 patients with aortic regurgitation (group B). The transmitral volumetric flow was obtained by multiplying the corrected mitral orifice area by the diastolic velocity integral, and the left ventricular total stroke volume was derived by subtracting the left ventricular end systolic volume from the end diastolic volume. The aortic regurgitant fraction (RF) was calculated as: RF = 1 - MF/SV. In group A there was a close agreement between the transmitral volumetric flow and the left ventricular total stroke volume, and the difference between the two measurements did not differ significantly from zero. In group B the left ventricular total stroke volume was significantly larger than the transmitral volumetric flow, and there was good agreement between the regurgitant fractions determined by Doppler echocardiography and radionuclide ventriculography. Discrepancies between the two techniques were found in patients with combined aortic and mitral regurgitation or a low angiographic left ventricular ejection fraction (less than 35%). The effective cardiac output measured by Doppler echocardiography accorded well with that measured by the Fick method. Doppler echocardiography provides a new and promising approach to the non-invasive measurement of aortic regurgitation.     

Measurement of aortic regurgitation by Doppler echocardiography.

In an attempt to develop a new approach to the non-invasive measurement of aortic regurgitation, transmitral volumetric flow (MF) and left ventricular total stroke volume (SV) were measured by Doppler and cross sectional echocardiography in 23 patients without aortic valve disease (group A) and in 26 patients with aortic regurgitation (group B). The transmitral volumetric flow was obtained by multiplying the corrected mitral orifice area by the diastolic velocity integral, and the left ventricular total stroke volume was derived by subtracting the left ventricular end systolic volume from the end diastolic volume. The aortic regurgitant fraction (RF) was calculated as: RF = 1 - MF/SV. In group A there was a close agreement between the transmitral volumetric flow and the left ventricular total stroke volume, and the difference between the two measurements did not differ significantly from zero. In group B the left ventricular total stroke volume was significantly larger than the transmitral volumetric flow, and there was good agreement between the regurgitant fractions determined by Doppler echocardiography and radionuclide ventriculography. Discrepancies between the two techniques were found in patients with combined aortic and mitral regurgitation or a low angiographic left ventricular ejection fraction (less than 35%). The effective cardiac output measured by Doppler echocardiography accorded well with that measured by the Fick method. Doppler echocardiography provides a new and promising approach to the non-invasive measurement of aortic regurgitation.