Validation of attenuation-corrected equilibrium radionuclide angiographic determinations of right ventricular volume: comparison with cast-validated biplane cineventriculography

To determine the accuracy of attenuation-corrected equilibrium radionuclide angiographic determinations of right ventricular volumes, we initially studied 14 postmortem human right ventricular casts by water displacement and biplane cineventriculography. Biplane cineventriculographic right ventricular cast volumes, calculated by a modification of Simpson's rule algorithm, correlated well with right ventricular cast volumes measured by water displacement (r = .97, y = 8 + 0.88x, SEE = 6 ml). Moreover, the mean volumes obtained by both methods were no different (73 +/- 28 vs 73 +/- 25 ml). Subsequently, we studied 16 patients by both biplane cineventriculography and equilibrium radionuclide angiography. The uncorrected radionuclide right ventricular volumes were calculated by normalizing background corrected end-diastolic and end-systolic counts from hand-drawn regions of interest obtained by phase analysis for cardiac cycles processed, frame rate, and blood sample counts. Attenuation correction was performed by a simple geometric method. The attenuation-corrected radionuclide right ventricular end-diastolic volumes correlated with the cineventriculographic end-diastolic volumes (r = .91, y = 3 + 0.92x, SEE = 27 ml). Similarly, the attenuation-corrected radionuclide right ventricular end-systolic volumes correlated with the cineventriculographic end-systolic volumes (r = .93, y = - 1 + 0.91x, SEE = 16 ml). Also, the mean attenuation-corrected radionuclide end-diastolic and end-systolic volumes were no different than the average cineventriculographic end-diastolic and end-systolic volumes (160 +/- 61 and 83 +/- 44 vs 170 +/- 61 and 86 +/- 43 ml, respectively). Comparison of the uncorrected and attenuation-corrected radionuclide right ventricular volumes demonstrated narrower 95% confidence intervals for the attentuation-corrected right ventricular volume determinations over a wide range of cineventriculographic volumes. Thus we conclude that: (1) attenuation-corrected radionuclide right ventricular end-diastolic and end-systolic volumes compare closely with those obtained by a cast-validated biplane cineventriculographic method and (2) attenuation-corrected radionuclide right ventricular volumes correspond more closely to determinations of biplane cineventriculographic right ventricular volumes and are thus likely to be more accurate than uncorrected radionuclide right ventricular volumes.     

Direct quantitation of right and left ventricular volumes with nuclear magnetic resonance imaging in patients with primary pulmonary hypertension.

To test the utility of electrocardiographically gated spin echo nuclear magnetic resonance (NMR) imaging in quantitating right and left ventricular volumes and function in patients with primary pulmonary hypertension, right and left ventricular end-diastolic and end-systolic volumes, stroke volumes and ejection fractions were determined in 11 patients with primary pulmonary hypertension and in 10 subjects with normal echocardiographic findings. Ventricular chamber volumes were computed by summing the ventricular chamber volumes of each NMR slice at end-diastole and end-systole. This technique was verified by comparison of results obtained by this method and with the water displacement volumes of eight water-filled latex balloons and ventricular casts of eight excised bovine hearts. In the patients with primary pulmonary hypertension, right ventricular volume indexes were 121 +/- 45 ml/m2 at end-diastole and 70.1 +/- 41.6 ml/m2 at end-systole; both values were significantly greater than values in the normal subjects (67.9 +/- 13.4 and 27.9 +/- 7.5 ml/m2, respectively). Left ventricular end-diastolic volume index was significantly less in the patients (44.9 +/- 9.7 ml/m2) than in the normal subjects (68.9 +/- 13.1 ml/m2). There was no significant difference in left ventricular end-systolic volume between the two groups (24.4 +/- 8.6 and 27.1 +/- 7.8 ml/m2, respectively). Right and left ventricular ejection fractions in the patients with primary pulmonary hypertension (0.43 +/- 0.21 and 0.46 +/- 0.15, respectively) were significantly less than values in normal subjects (0.59 +/- 0.09 and 0.6 +/- 0.11, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative angiographic right and left ventricular volumes

Comparative angiographic right and left ventricular volumes and right and left ventricular ejection fractions have been reported in the same normal infants and children. This relationship was assessed in adult patients to determine if these pediatric observations persist in later life. Seventeen adults, who had both right and left ventricular angiograms and who had no demonstrable organic heart disease, were studied. Right ventricular end-diastolic volume ranged from 54 to 98 (76 +/- 14, mean +/- SD) cc/m2 and left ventricular end-diastolic volume ranged from 48 to 90 (70 +/- 12) cc/m2; p less than 0.03. Right ventricular end-systolic volume ranged from 22 to 47 (33 +/- 8.0) cc/m2 and left ventricular end-systolic volume ranged from 13 to 34 (22 +/- 5.3) cc/m2; p less than 0.00005. Calculated right ventricular stroke volume ranged from 31 to 60 (43 +/- 8.3) cc/m2 and left ventricular stroke volume ranged from 29 to 70 (48 +/- 11) cc/m2; p = NS. Calculated right ventricular ejection fraction ranged from 0.48 to 0.62 (0.57 +/- 0.04) and the left ventricular ejection fraction ranged from 0.57 to 0.84 (0.68 +/- 0.07; p less than 0.00005. Both right ventricular end-systolic and end-diastolic volumes were greater than left ventricular end-systolic and end-diastolic volumes. This resulted in decreased right ventricular ejection fraction compared to left ventricular ejection fraction. The difference between the two ventricles may be due to compliance, muscle mass, and anatomic configuration with a net result of one chamber more completely emptying than the other. Thus it appears that the relationships between right and left ventricular volumes noted in infancy and childhood persist in adult life.     

Precision of measurements of right and left ventricular volume by cine computed tomography

Precise determination of left and right ventricular stroke volumes is limited with conventional imaging techniques. We determined whether right and left ventricular stroke volumes could be precisely measured with cine computed tomography (CT). Cine CT enables simultaneous imaging of the right and left ventricles at an 8 mm slice thickness with a maximal scanning rate of 17 frames/sec (50 msec acquisition intervals). In eight dogs, true right ventricular and left ventricular stroke volumes were determined by dividing thermodilution cardiac output by heart rate and/or with the use of an aortic electromagnetic flow probe implanted over a long term. After at least 5 sec of suspended respiration, cine CT images were acquired during central venous injection of a nonionic contrast agent. Multiple perturbations in stroke volume were induced in each dog by the administration of dobutamine, sodium pentobarbital, or sodium nitroprusside or by coronary artery occlusion. Right and left ventricular stroke volumes were obtained by Simpson's reconstruction of end-diastolic and end-systolic short-axis tomograms from apex to base. The cine CT left ventricular stroke volume (range 11 to 45 ml) correlated highly with the true left ventricular stroke volume (r = .99, slope = 1.01, y intercept = -0.2 ml, SEE = 1.5 ml, n = 25). The cine CT right ventricular stroke volume (range 11 to 34 ml) also correlated highly with the true right ventricular stroke volume (r = .98, slope = 0.9, y intercept = 2.2 ml, SEE = 1.7 ml, n = 15). In 12 studies, the mean difference between nearly simultaneous right and left ventricular stroke volumes by cine CT was 1.1 ml (range 0.1 to 3.2 ml). Calculation of right and left ventricular stroke volumes from data from cine CT were highly reproducible. Intraobserver variability in measurements of right ventricular stroke volume (r = 1.0, slope = 0.99, y intercept = 0.19 ml) and left ventricular stroke volume (r = 1.0, slope = 1.02, y intercept = -0.21 ml) was minimal. Interobserver variability in measurements of right ventricular stroke volume (r = .98, slope = 0.90, y intercept = 1.66 ml) and left ventricular stroke volume (r = .99, slope = 0.97, y intercept = -0.02 ml) was likewise minimal. Thus, precise and highly reproducible measurements of right and left ventricular stroke volumes can be obtained with cine CT.     

Relationship between echocardiography, cardiac output, and abnormally contracting segments in patients with ischemic heart disease.

Twenty-four patients with proven coronary artery disease and abnormally-contracting segments were studied by both echocardiography and biplane angiographic techniques. Comparison was made between the left ventricular biplane angiographic volumes and those obtained from echocardiographic measurements which were calculated from cubed function and regression equaltion methods. The percent abnormally contracting segment (ACS) was obtained from biplane left ventricular angiography and was calculated from the diastolic and systolic anteroposterior and lateral angiocardiograms. The angiographic end-diastolic volume correlated with that calculated from the echocardiographic dimensions with an r value of 0.865 and SEE of +/- 22.64 ml. The angiographic end-systolic volume and echo end-systolic volume did not correlate as well, with an r = 0.7063. The difference in stroke volume predicted by the diastolic and systolic echocardiographic dimensions and the actual stroke volume determined by Fick technique was related to the percent abnormally contracting segment of the left ventricle (r = 0.8967). The percent ACS could be estimated from echo and Fick stroke volume measurements by the cube function and regression equations. Echo ventricular volume determinations were analyzed for the cube function method and the regression equations of Fortuin et al. and Teichholz and coworkers, with the method of Fortuin et al. producing the most sensitive relationship: % ACS = 0.32 (SVecho - SVFick) % + 8.9%. The correlation coefficient for the estimate was 0.8967 with a SEE of +/- 4.78%. In patients with coronary artery disease and abnormally contracting segments, echocardiography can provide reliable measurements of left ventricular end-diastolic volume but estimates of end-systolic volume are less accurate. If mitral regurgitation or a ventricular aneurysm can be excluded, the difference in echocardiographic and forward stroke volume by an independent method is related to the angiographic and forward stroke volume by an independent method is related to the angiographic abnormally contracting segment, and this relationship permits estimation of the size of the abnormally, contracting segment.     

Two-dimensional echocardiographic assessment of left ventricular function in chronic obstructive pulmonary disease

In 10 patients undergoing therapy for a mild exacerbation of their chronic obstructive pulmonary disease (COPD), a quantitative two-dimensional echocardiographic (2DE) study was performed together with hemodynamics to assess left ventricular (LV) function. From the 2DE examination, which was made up of parasternal, subcostal, and apical views, measurements of LV short axis end-diastolic and end-systolic areas (A) at the high papillary muscle level and long axis end-diastolic and end-systolic length (L) permitted us to calculate LV end-systolic and end-diastolic volumes (V) using the formula V = 5/6 AL. Compared with the same measurements obtained in a group of 12 normal volunteers, patients with COPD exhibited a markedly reduced LV cavity (LVES, 28.9 +/- 14.6 ml/m2 versus 51.5 +/- 11.0 ml/m2; LVEDV, 67.7 +/- 24.6 ml/m2 versus 103.2 +/- 19.9 ml/m2). An increased thickness of both left ventricular free wall and interventricular septum was also evidenced in patients with COPD. Left ventricular systolic function, assessed using both peak systolic blood pressure/end-systolic volume ratio and calculated left ventricular ejection fraction, was found to be clearly enhanced in patients with COPD. The influence of right ventricular enlargement on left ventricular diastolic function was also investigated in patients with COPD using progressive volume loading and 2DE right ventricular measurements. After a given threshold of volume loading, reduction in stroke index, opposite variations in right and left ventricular size and septal flattening, suggested the occurrence of ventricular interaction.     

Pericardial influences on right and left ventricular filling dynamics

The influence of the pericardium on right and left ventricular filling was studied using two-dimensional and Doppler echocardiography in 14 open-chest dogs. Doppler echo parameters of filling included early (E) and late (A) velocities and their ratio (E/A) for the mitral and tricuspid valves. Right and left ventricular volumes were calculated from orthogonal two-dimensional echocardiographic images. Data were compared at three levels of left ventricular end-diastolic pressure (6 +/- 2, 13 +/- 3, and 21 +/- 4 mm Hg) at matched heart rates before and after pericardiectomy. The instantaneous diastolic pressure gradient was measured in 12 of the dogs. Pericardiectomy resulted in an increase in early mitral velocity, peak early diastolic pressure gradient, and E/A but not early mitral velocity normalized for end-diastolic volume. In contrast, for the tricuspid valve flow, pericardiectomy did not change E but caused a marked increase in A and a decrease in E/A. Right ventricular end-diastolic volumes at matched left ventricular end-diastolic volumes were similar before and after the pericardium was removed. However, removal of the pericardium caused a significant decrease of the slope for the right (86.0 +/- 27.0 x 10(-4) versus 50.0 +/- 19.5 x 10(-4) mm Hg/ml, p less than 0.01), but not left, ventricular ln end-diastolic pressure-volume relation (21.2 +/- 9.2 x 10(-3) versus 21.4 +/- 5.3 x 10(-3) mm Hg/ml, p = NS), and a decrease of the pressure intercept for the left (3.0 +/- 2.0 versus 1.6 +/- 0.9 mm Hg, p less than 0.05), but not right, ventricular ln end-diastolic pressure-volume relation (2.8 +/- 1.4 versus 1.4 +/- 0.8 mm Hg, p = NS). In conclusion, filling of the two ventricles is affected by the pericardium over a wide range of physiological ventricular volumes and pressures. At matched left ventricular end-diastolic volume, pericardiectomy causes a fundamental alteration in right, but not left, ventricular filling.     

Two-dimensional echocardiographic determination of ventricular volumes in the fetal heart. Validation studies in fetal lambs

The determination of ventricular volumes in the fetal heart from two-dimensional echocardiography (2DE) may give a better estimate of fetal ventricular size than simple diameter measurements, but the accuracy of this method has not been established. In fetal lambs, we tested whether ventricular volume calculations from 2DE using a biplane Simpson's rule algorithm are accurate. Calculations of left and right ventricular end-diastolic volumes from 2DE were compared with cast volumes of these ventricles. Also, at different levels of left atrial pressure, left ventricular stroke volumes calculated from 2DE were compared with stroke volumes measured simultaneously by an electromagnetic flowmeter. There was a good correlation between volumes determined from 2DE (y axis) and from casts (x axis) for both the left (r = 0.92; y = 0.2 + 1.1x; SEE = 0.19 ml) and right ventricle (r = 0.90; y = 0.7 + 0.9x; SEE = 0.21 ml). Left ventricular stroke volumes calculated from 2DE correlated well with those measured by the electromagnetic flowmeter (r = 0.87; y = 0.2 + 0.9x; SEE = 0.27 ml). Thus, calculation of fetal ventricular volumes from 2DE images using a biplane Simpson's rule method is feasible and accurate.     

Noninvasive evaluation of the ratio of pulmonary to systemic flow in ventricular septal defect by means of Doppler two-dimensional echocardiography

Left ventricular inflow volume (LVIV) and outflow volume (LVOV) were determined by pulsed Doppler echocardiography, and the ratio of pulmonary to systemic flow (Qp/Qs) was estimated as a ratio of LVIV to LVOV (LVIV/LVOV). Seventy-seven patients were studied, 47 control subjects and 30 patients with ventricular septal defect (VSD). LVOV was calculated from the left ventricular ejection flow velocity and left ventricular outflow tract diameter; LVIV was calculated from the transmitral flow velocity and mitral valve motion as traced by M-mode echocardiography. Cardiac input (COin) and cardiac output (COout) were calculated as the product of LVIV or LVOV and heart rate. Cardiac output was also determined by the dye dilution method (COdye) in control subjects. A close correlation was observed between COdye and COin (y = 1.18x - 243, r = 0.85, p less than 0.005, SEE = 1026 ml/min) and COdye and COout (y = 1.16x - 323, r = 0.90, p less than 0.005, SEE = 639 ml/min). LVIV and LVOV were highly correlated in control subjects (y = 0.95x + 5.3, r = 0.94, p less than 0.005, SEE = 6.6 ml). LVIV/LVOV was 0.97 +/- 0.1 (mean +/- SD) in control subjects, whereas LVIV/LVOV (1.87 +/- 0.88) was significantly higher in patients with VSD (p less than 0.01). In patients with VSD, LVIV/LVOV correlated with Qp/Qs determined invasively (y = 0.97, SEE = 0.23, n = 16). Thus with our method LVIV and COin can be accurately determined, and we suggest that Doppler-determined LVIV/LVOV is clinically useful for evaluating the shunt flow magnitude in VSD.     

The importance of pericardial constraint in experimental pulmonary embolism and volume loading.

To clarify the magnitude of the contribution of pericardial constraint to the hemodynamic deterioration that is observed during acute pulmonary embolism, hemodynamics and chamber dimensions (sonomicrometry) were measured during pulmonary embolization and subsequent volume loading in six anesthetized and instrumented open-chest, open-pericardium dogs. Embolization markedly increased peak right ventricular systolic pressure (38 +/- 5 mm Hg before embolism to 64 +/- 12 mm Hg after repeated embolization, p less than 0.05). However, right ventricular stroke volume decreased by only an insignificant amount (17 +/- 7 ml to 15 +/- 6 ml, p = not significant). Indices of left ventricular end-diastolic volume (left ventricular area = anteroposterior x septum-to-left ventricle free wall diameters) and stroke work (stroke work = area of the left ventricular pressure-area loop) were also similar before and after repeated embolization. Volume loading after repeated embolization resulted in increased right ventricular stroke volume (15 +/- 6 ml to 20 +/- 4 ml, p = 0.06), left ventricular area (3320 +/- 600 mm2 to 3470 +/- 580 mm2, p less than 0.05) and stroke work (261 +/- 158 mm Hg to 425 +/- 170 mm Hg x mm2, p less than 0.05). These results are in marked contrast to those in a previously reported study in a closed-chest and closed-pericardium model in which there was a decrease in left ventricular preload and systolic function after similar embolization-induced right ventricular pressure loading. Moreover, there was a further decrease in these parameters as a result of volume loading after embolism in the closed pericardium experiments. In conclusion, pericardial constraint contributes to hemodynamic deterioration during both acute right ventricular pressure loading and subsequent volume loading. The hemodynamic response to both interventions in the intact animal is determined not only by the degree of right ventricular dysfunction but also by the degree of direct ventricular interaction.     

Approaches to determination of left ventricular volume and ejection fraction by real-time two-dimensional echocardiography.

Left ventricular volumes and ejection fraction were derived from real time two-dimensional echocardiographic images (2 DE) and single plane (RAO) left ventricular cineangiograms in a series of 50 patients. Prospective application of a series of 6 alternate algorithms showed that a modified Simpson's rule approach using mitral and papillary muscle cross sections and an apical four chamber view provided the best 2 DE - angiographic correlations: for end-diastolic volume r = 0.82, SEE = 39 ml; for end-systolic volume r = 0.90, SEE = 29 ml and for ejection fraction r = 0.80, SEE = 0.09. The large SEE for volume determination indicates that further refinements are necessary to predict left ventricular volumes adequately; however, ejection fraction can be derived with an accuracy which allows practical clinical decisions in patients with satisfactory 2 DE images.     

Effect of alteration of left ventricular activation sequence on the left ventricular end-systolic pressure-volume relation in closed-chest dogs

We investigated the effect of pacing from the atrium and various ventricular sites on the left ventricular end-systolic pressure-volume relation following autonomic blockade in a total of 10 dogs chronically instrumented to measure left ventricular pressure and determine left ventricular volume from three ultrasonic endocardial dimensions. During ventricular pacing, left ventricular end-diastolic volume, stroke volume, and end-systolic pressure were decreased, while the end-systolic volume was relatively unchanged. Left ventricular end-systolic pressure-volume relations were generated by vena caval occlusions during pacing at a constant rate from the left atria, and the epicardium of the right ventricular free wall, right ventricular apex, and left ventricular free wall. The left ventricular end-systolic pressure-volume relations were described by straight lines for each site (r greater than 0.96 and SEE less than 2.9 mm Hg in all but one instance). Compared to atrial pacing, the left ventricular end-systolic pressure-volume relations were shifted (P less than 0.001) to the right during pacing from ventricular sites. During atrial pacing, the volume intercept of the left ventricular end-systolic pressure-volume relation was 16.0 +/- 7.2 ml (mean +/- SD), and increased to 18.7 +/- 7.8 ml (P less than 0.05) during pacing from the right ventricular free wall, to 19.6 +/- 7.7 ml (P less than 0.05) during pacing from the right ventricular apex, and to 20.0 +/- 7.5 ml (P less than 0.05) during pacing from the left ventricular free wall. These volume intercepts correlated roughly with the extent of dyssynchronous activation as estimated by the QRS duration (r = 0.59 to 0.93) and the time for left ventricular endocardial activation (r = 0.92 and 0.95). During ventricular pacing, the slope of the left ventricular end-systolic pressure-volume relation changed only slightly. Similar results were obtained during pacing from right ventricular endocardial sites. We conclude that alterations of the normal activation sequence produced by ventricular pacing depress left ventricular pumping function independent of loading conditions, as indicated by a rightward shift of the left ventricular end-systolic pressure-volume relation. The extent of this shift appears to be in proportion to the degree of dyssynchronous activation. The decreased stroke volume during ventricular pacing is due both to a decreased end-diastolic volume (decreased preload) and the rightward shift of the end-systolic pressure-volume relation (decreased pump function).     

Effects of epoprostenol on right ventricular hypertrophy and dilatation in pulmonary hypertension

OBJECTIVES: To gain more knowledge of changes in main pulmonary artery flow and right ventricular mass and volumes in patients with pulmonary hypertension during epoprostenol therapy. METHODS: Eleven patients (9 women) were evaluated before the start of therapy and every 4 months thereafter. Right and left ventricular volumes and masses were measured by cine MRI. Flow was measured with MRI velocity quantification. At the same times, 6-min walking tests were performed. Right-heart catheterizations were performed at baseline and after 1 year. RESULTS: Right ventricular mass in the patient group was significantly higher from that in a control group of healthy volunteers (95 +/- 26 g vs 42 +/- 10 g, p < 0.05 [mean +/- SD]), whereas the stroke volume was lower (34 +/- 11 mL vs 81 +/- 11 mL, p < 0.05). The greatest improvement in right ventricular stroke volume (to 41 +/- 11 mL, p < 0.05) took place in the first 4 months. During the 1-year follow-up, right ventricular end-diastolic volume and mass did not change, and mean pulmonary artery pressure remained nearly stable at 55 mm Hg at baseline and 53 mm Hg after 1 year. Pulmonary vascular resistance decreased by 12.5% (p = 0.06). CONCLUSIONS: From these data we conclude that epoprostenol lowers pulmonary vascular resistance, leading to an increase in pulmonary artery flow. This increase in pulmonary artery flow corresponds well with the increase in 6-min walking distance and can be noninvasively monitored by MRI (flow quantification). Right ventricular dilatation and hypertrophy are not reversed by epoprostenol therapy, but do not progress either.     

Early improvement in left ventricular diastolic function after relief of chronic right ventricular pressure overload

Chronic right ventricular pressure overload is associated with left ventricular diastolic dysfunction. Whether or not an abrupt reduction in pulmonary artery pressure in patients with chronic pulmonary hypertension results in early improvement of left ventricular diastolic function is unknown. To assess this, the Doppler indexes of left ventricular diastolic function and echocardiographic measures of left ventricular volume were analyzed in 22 patients (age, 41 +/- 14 years, mean +/- SD) before and within 1 week after pulmonary thromboendarterectomy for chronic thromboembolic pulmonary hypertension. Mean duration of cardiopulmonary symptoms was 37 months (range, 4 months to 9 years). After operation, mean pulmonary artery pressure and pulmonary vascular resistance decreased (50 +/- 13 to 29 +/- 9 mm Hg and 904 +/- 654 to 283 +/- 243 dynes.sec/cm5, respectively, both p less than 0.001), pulmonary artery wedge pressure was unchanged (11 +/- 5 to 12 +/- 5 mm Hg), and cardiac index increased (2.0 +/- 0.5 to 2.8 +/- 0.7 l/min/m2 p less than 0.001). Left ventricular end-diastolic volume and stroke volume increased significantly (58.5 +/- 18.0 to 76.6 +/- 25.0 ml and 30.3 +/- 12.3 to 41.8 +/- 12.5 ml, respectively, both p less than 0.001) after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Biventricular function in the adult respiratory distress syndrome

We examined biventricular function in patients with the adult respiratory distress syndrome (ARDS) by a combination of invasively determined pressures and flows and concomitant radionuclide angiography. Right (RVEF) and left (LVEF) ventricular ejection fractions were measured; right and left ventricular end-diastolic (EDVI) and end-systolic (ESVI) volume indices were calculated from the respective ejection fraction and measured thermodilution stroke volume. With an increase in the outflow pressure load on the right ventricle, measured as the mean pulmonary artery pressure (PAP), the RVEF fell (Y = 66.25 -1.01X; r2 = .42; p less than .001) and both the RVEDVI (y = 13.39 + 3.66X; r2 = .33; p less than .001) and RVESVI (Y = 23.9 + 3.57X; r2 = .41; p less than .001) increased. Progressive increases in the PAP also seemed associated with a change in left ventricular end-diastolic pressure-volume relationships: without pulmonary artery hypertension (PAP less than 20 mm Hg) the mean LVEDVI was 87.2 +/- 31.3 ml/m2 (mean +/- SD) and the mean PCWP was 5.0 +/- 2.8 mm Hg; with a mean PAP exceeding 30 mm Hg, the LVEDVI remained constant (90.4 +/- 26.9 ml/m2) although the PCWP was greater than previous (18.5 +/- 5.7 mm Hg; p less than .01). Analysis of right ventricular peak-systolic pressure end-systolic volume ratios implied a concurrent depression in right ventricular contractility at high levels of PAP. However, right ventricular "pump" function to maintain an adequate left ventricular preload remained unaltered regardless of the presence of pulmonary artery hypertension.     

Clinical Determinations of Volumes of Normal and Aneurysmatic Left Ventricles by Three-Dimensional Transesophageal Echocardiography

Biplane methods of determining left ventricular volumes are inaccurate in the presence of aneurysmal distortions. Multiplane transesophageal echocardiography, which provides multiple, unobstructed cross-sectional views of the heart from a single, stable position, has the potential for more accurate determinations of volumes of irregular cavity forms than the biplane methods. The aim of the study was to determine the feasibility of three-dimensional measurements of ventricular volumes in patients with normal and aneurysmatic left ventricles by using multiplane transesophageal echocardiography. With the echotransducer in the mid-esophageal (transesophageal) position, nine echo cross-sectional images of the left ventricle in approximately 20 degrees angular increments were obtained from each of 29 patients with coronary artery disease who had undergone biplane ventriculography during diagnostic cardiac catheterization. In 17 of these 29 patients, echo cross-sectional images of the left ventricle with the echotransducer in transgastric position were also obtained. End-diastolic volume, end-systolic volume, and ejection fraction were determined from multiplane transesophageal echocardiographic images and biplane ventriculographic images by the disc-summation method and compared with each other. In another ten patients with indwelling pulmonary artery catheters, stroke volumes calculated from multiplane transesophageal echocardiographic images were compared with those derived from thermodilution cardiac output measurements. Correlations between biplane ventriculographic and multiplane transesophageal echocardiographic measurements were higher in the ten patients with normal ventricular shape [for end-diastolic volumes, r = 0.91, SEE = 19 ml; for end-systolic volumes, r = 0.98, SEE = 9.3 ml; for ejection fractions (EFs), r = 0.91, SEE = 5.4%] than in the 19 patients with ventricular aneurysms (for end-diastolic volumes, r = 0.61, SEE = 31.5 ml; for end-systolic volumes, r = 0.66, SEE = 32.5 ml; for EFs, r = 0.79, SEE = 8%). Correlations between echocardiographic volumes from the transesophageal and transgastric transducer positions were high independent of left ventricular geometry (for end-diastolic volumes, r = 0.84, SEE = 13.1 ml; for end-systolic volumes, r = 0.98, SEE = 9.6 ml; for EFs, r = 0.97, SEE = 3.4%). In 12 observations (4 normal and 8 aneurysmal) from the ten patients with indwelling pulmonary artery catheters, correlation between stroke volumes determined from thermodilution cardiac output measurements and those derived from multiplane transesophageal echocardiographic images was high (r = 0.91, SEE = 6 ml). The results indicate that three-dimensional measurements of volumes of irregular and distorted left ventricles are feasible with multiplane transesophageal echocardiography. This method may be more accurate than biplane methods, especially in the presence of left ventricular aneurysms.     

Validation of the angiographic accuracy of digital left ventriculography

Digital subtraction angiography enhances the contrast to background signal, enabling the performance of angiography with reduced doses of contrast medium. The objectives of the present study were (1) to validate the accuracy of digital left ventriculography for measurement of left ventricular volumes and segmental contraction; and (2) to compare the hemodynamic effects resulting from low-and high-dose intraventricular contrast injections. Twenty-eight patients underwent digital left ventriculography, performed by intraventricular injection of 7 ml of contrast medium diluted in saline solution, followed by conventional cineangiography of the left ventricle performed with 45 ml of undiluted contrast medium. Left ventricular volumes calculated from digital ventriculograms correlated well with volumes calculated from conventional ventriculograms: end-diastolic volume (r = 0.97, standard error of estimate [SEE] 23.4 ml; end-systolic volume (r = 0.97, SEE 15.4 ml); stroke volume (r = 0.95, SEE 14.7 ml); and ejection fraction (r = 0.97, SEE 3.8%). Segmental left ventricular contraction, measured as percent chordal shortening of hemiaxes, correlated moderately well (r = 0.81, SEE 11.5%). After injection of undiluted contrast medium, left ventricular systolic pressure decreased (133 +/- 31 to 123.5 +/- 27 mm Hg; p less than 0.01) and left ventricular end-diastolic pressure increased (12.0 +/- 7 to 16.9 +/- 10 mm Hg; p less than 0.001). Left ventricular systolic and end-diastolic pressures did not change significantly after injection of diluted contrast medium, and patients had no discomfort. Thus, digital subtraction angiography permits the performance of left ventriculography with markedly reduced doses of contrast medium, obviating the hemodynamic effects resulting from injection of conventional doses of contrast medium. This new approach to left ventriculography provides high resolution ventriculograms for accurate measurement of left ventricular volumes, stroke volume, and ejection fraction.     

Percentage of shortening of the echocardiographic left ventricular dimension. Its use in determining ejection fraction and stroke volume

The percentage of shortening of the echocardiographic left ventricular dimension (% delta D) was prospectively evaluated in 42 patients without detectable asynergy during diagnostic cardiac catheterization and was found to correlate well with angiographic ejection fraction (r = 0.90). Ejection fraction was calculated as the product of % delta D X 1.7 or as % delta (D2), both formulae having similar degrees of accuracy and a better correlation with the angiographic determination than conventional formulae. Ejection fractions (angiographic and echocardiographic) of 51 percent or greater were always associated with a % delta D of 30 percent or more. In five patients the echocardiographically derived ejection fractions were normal (greater than or equal to 51 percent), while the angiographic ejection fractions were reduced; four of these patients had valvular regurgitation. End-diastolic volumes were calculated from end-diastolic echocardiographic dimensions utilizing a linear regression equation derived from correlating the end-diastolic echocardiographic dimension with the end-diastolic volume in 27 patients without valvular regurgitation (end-diastolic echocardiographic dimension ranged from 3.7 to 8.2 cm). The value for stroke volume determined as the product of calculated end-diastolic volume times ejection fraction correlated with the angiographically determined stroke volume (r = 0.88; standard error of estimate, +/- 11 ml) better than the value for stroke volume derived from conventional echocardiographic formulae.     

Left ventricular volume characteristics and its relationship with right ventricle after repair of tetralogy of Fallot

In order to study the left ventricular volume characteristics and right ventricular influence on left ventricle, cardiac catheterization and biplane cineangiography was performed in 61 patients after repair of tetralogy of Fallot. Preoperative left ventricular volume size was also measured in 25 patients. Postoperative left ventricular end-diastolic volume index (LVEDVI) was 93 +/- 22 ml/m2 (mean +/- standard deviation) and it was 140 +/- 29% of normal left ventricular volume. Left ventricular ejection fraction (LVEF) was 60 +/- 6%. Left ventricular size significantly increased from 109 +/- 25% to 140 +/- 23% of normal by corrective surgery (p less than 0.001). Left ventricular volume characteristics are correlated with right ventricle. LVEDVI increased with increasing right ventricular end-diastolic volume index (RVEDVI) and decreased right ventricular ejection fraction (RVEF). LVEDVI (ml/m2) = 60 + 0.29 RVEDVI (ml/m2), r = 0.52, p less than 0.001, LVEDVI (ml/m2) = 141 - 0.90 RVEF (%), r = -0.30, p less than 0.02. LVEF decreased with increasing RVEDVI and decreased RVEF. LVEF (%) = 68 - 0.075 RVEDVI (ml/m2), r = -0.51, p less than 0.001, LVEF (%) = 43 + 0.32 RVEF (%), r = 0.40, p less than 0.001. On the contrary there was no relationship between right ventricular volume characteristics and right ventricular systolic pressure. There were two cases whose LVEF was less than 50%. In one case right ventricular systolic pressure was as high as 98 mmHg. In the other patient RVEDVI was 299 ml/m2 (453% of normal right ventricular volume) because of severe pulmonary regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of volume load of the left ventricle in aortic and mitral insufficiency on the geometry and function of the right ventricle

To investigate the effect of chronic left ventricular enlargement on right ventricular geometry and function, biplane cineventriculograms were analyzed in 23 patients with aortic regurgitation (AR) and in 17 patients with mitral regurgitation (MR). Left ventricular end-diastolic volume indices (LVEDVI) were elevated and significantly (p less than 0.05) different in patients with aortic regurgitation (AR) (190.2 +/- 65.2 ml/m2) and mitral regurgitation (MR) (148.7 +/- 40.1 ml/m2). Right ventricular end-diastolic volume indices (RVEDVI), however, were comparable and within the normal range (AR: 96.6 +/- 18.3 ml/m2, MR: 100.2 +/- 33.7 ml/m2). Mean pulmonary artery pressure was significantly (p less than 0.05) higher in patients with mitral regurgitation with 24.7 +/- 12.8 mm Hg (AR: 17.5 +/- 6.6 mm Hg). Six patients with mitral insufficiency had concomitant tricuspid valve insufficiency. In five out of six patients with tricuspid insufficiency, right ventricular afterload was significantly elevated. Only in patients with mitral regurgitation was a significant correlation (r) between left and right ventricular end-diastolic volume index found (RVEDVI = 0.7 X LVEDVI +1, r = 0.80). Moreover, in patients with MR, left ventricular end-diastolic volume index correlated with right ventricular end-systolic volume index (RVESVI = 0.4 X LVEDVI -8, r = 0.73). Right ventricular ejection fraction was significantly different (p less than 0.05) between patients with aortic and mitral insufficiency (AR: 53.7 +/- 8.9%, MR: 46.7 +/- 10.7%). Particularly in patients with normal left ventricular ejection fraction (greater than 50%) and mitral regurgitation, the incidence of a reduced right ventricular ejection fraction (less than 50%) was significantly higher (p less than 0.01) compared to patients with aortic regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)