Alan D. Waggoner

A new, simplified and accurate method for determining ejection fraction with two-dimensional echocardiography.

A new method to determine left ventricular (LV) ejection fraction (EF) with wide‐angle, twodimensional echocardiography (2‐D echo) has been developed using the parasternal long‐axis, apical fourchamber and apical long‐axis views. End‐diastolic and end‐systolic measurements of LV short axes at the base and mid‐LV cavity in the parasternal long‐axis view and at the upper, middle and lower thirds of the cavity in the apical views are made, from which an averaged minor axis at end‐diastole and at end‐systole is calculated. Fractional shortening of the LV long axis (ΔL) is estimated from apical contraction. Satisfactory 2‐D echoes were obtained in 55 of 58 nonselected patients (all three views in 32 patients, two views in 22 and one view in one); 42 of 55 patients had coronary artery disease. EF by 2‐D echo was compared with EF by gated cardiac blood pool imaging in all patients (r = 0.927, SEE = 6.7%) and to EF by single‐plane cineangiography (angio) in 35 of 55 patients (r = 0.913, SEE = 7.4%). LV dyssynergy was frequently present and involved the apex in 29 of 55 patients. Using angio as the standard for evaluating wall motion at the apex, 2‐D echo was 100% sensitive and specific in detecting abnormal apical wall motion. We condude that EF can be determined accurately with 2‐D echo in a large group of patients with and without dyssynergy by a simple method that eliminates the need for planimetry or computer assistance.

Detection of coronary artery disease with exercise two-dimensional echocardiography. Description of a clinically applicable method and comparison with radionuclide ventriculography.

Two-dimensional echocardiography (2-D echo) was performed in 73 patients evaluated for coronary artery disease (CAD) and in four normal volunteers before and immediately after a maximal treadmill exercise test. Diagnostic images were obtained from the apical and parasternal windows. In 17 patients with normal coronary arteriograms, ejection fraction (EF) increased from 66 9% (±4 SD) at rest to 73 8% after exercise (p < 0.001), while in 56 patients with proved CAD, EF fell from 56 13% at rest to 53 16% after exercise (p < 0.01). The sensitivity of postexercise 2-D echo for detecting CAD (based on abnormal EF response and/or regional dyssynergy) was 91% (51 of 56 patients) and the specificity was 88% (15 of 17). Sensitivity for one-, two- and three-vessel disease was 64% (seven of 11), 95% (20 of 21) and 100%, respectively. Patients with multivessel disease showed a significant fall in a wall motion score index, from 0.79 0.25 to 0.63 0.26. Exercise radionuclide ventriculography (RNV) was also performed in 41 of the subjects (17 normals and 24 CAD patients) on a bicycle ergometer. The overall sensitivity of 2-D echo in this subgroup was 92%, compared with 71% for RNV. The sensitivity of 2-D echo for one-vessel disease (n = 4) was 50%, that for two-vessel disease (n = 12) was 100% and that for three-vessel disease (n = 12) was 100%. Respective values for RNV were 0%, 80% and 90%. The specificity of 2-D echo was 88% and that of RNV was 82%. A significantly higher peak heart rate response was observed on the treadmill than on the bicycle ergometer in both CAD patients and normal subjects. We conclude that postexercise 2-D echo is a clinically applicable technique for the diagnosis and evaluation of CAD patients and compares favorably with exercise RNV.

Assessment of pulsed Doppler echocardiography in detection and quantification of aortic and mitral regurgitation.

Pulsed Doppler echocardiography was employed to detect disturbed or turbulent flow diagnostic of aortic or mitral regurgitation. Sensitivity, specificity, diagnostic accuracy, and predictive value were assessed by the independent interpretation and comparison of aortic root angiograms (91 patients) and left ventriculograms (94 patients) to the time interval histogram display of the pulsed Doppler. Sensitivity of Doppler in detecting mitral regurgitation was 94 per cent, with specificity 89 per cent, predictive value 81 per cent, and diagnostic accuracy 90 per cent (32 patients with, 62 without regurgitation). In aortic regurgitation, sensitivity was also 94 per cent, specificity 82 per cent, predictive value 94 per cent, and the diagnostic accuracy was 91 per cent (69 patients with, 22 without aortic regurgitation). Additionally, no Doppler evidence of mitral or aortic regurgitation was present in 20 normal subjects. The aetiology of left-sided valvular regurgitation varied widely, with prosthetic valvular insufficiency being the cause of mitral and aortic regurgitation in seven and 10 patients, respectively. Sixteen of 17 (94%) paraprosthetic leaks were correctly identified by pulsed Doppler. In patients with aortic regurgitation the flow-velocity curve recorded in the ascending aorta frequently showed a negative (or reversed) diastolic component, the magnitude of which (expressed as percentage negative area) correlated significantly with angiographic severity of regurgitation. Thus, pulsed Doppler echocardiography is a highly accurate and objective non-invasive technique for detecting mitral and aortic regurgitation. In aortic regurgitation, estimation of severity is possible from inspection of the Doppler ascending aortic flow velocity curve.

Pulsed doppler echocardiographic detection of right-sided valve regurgitation. Experimental results and clinical significance

Abstract Pulsed Doppler echocardiography may allow noninvasive detection of tricuspid insufficiency as disturbed or turbulent systolic flow in the right atrium and pulmonary insufficiency as turbulent diastolic flow in the right ventricular outflow tract. Accordingly, six open chest mongrel dogs were examined with Doppler echocardiography before and after surgical creation of tricuspid and pulmonary insufficiency. The Doppler technique detected the appropriate lesion in all instances, with a specificity of 100 percent. In 121 patients (20 without heart disease, 101 with heart disease of various causes), pulsed Doppler echocardiography was used to detect right-sided valve regurgitation. Results were compared with right-sided pressure measurements and M mode echocardiographic findings in all, and with right ventricular angiography in 21 patients. Pulsed Doppler study detected tricuspid insufficiency in 61 of 100 patients, 12 (20 percent) of whom had clinical evidence of this lesion. Angiographic evidence of tricuspid regurgitation was present in 18 patients, 17 of whom had positive Doppler findings (sensitivity 94 percent), and absent in 3, all with negative Doppler findings. Pulmonary insufficiency was found on pulsed Doppler study in 47 of 91 patients, 3 of whom (all after pulmonary valvotomy) had clinical evidence of this lesion. Increased right ventricular systolic pressure (greater than 35 mm Hg) was noted more often in patients with (55 of 61 or 90 percent) than in those without (22 of 59 or 37 percent) tricuspid insufficiency (p Thus, pulsed Doppler echocardiography appears to be an accurate noninvasive technique for detection of right-sided valve regurgitation. The absence of diagnostic physical findings in many of the patients indicates that the hemodynamic severity of the Doppler-detected valve insufficiency was probably insignificant. However, because of its high incidence rate (87 percent) and association with pulmonary hypertension (87 percent), pulsed Doppler detection of tricuspid or pulmonary insufficiency, or both (in the absence of pulmonary stenosis) was found superior to M mode echocardiographic measurements (right ventricular size, pulmonary valve motion) in the prediction of pulmonary hypertension.

Importance of preoperative hypertrophy, wall stress and end-systolic dimension as echocardiographic predictors of normalization of left ventricular dilatation after valve replacement in chronic aortic insufficiency

To define and compare predictors of postoperative normalization of diastolic left ventricular dimension after aortic valve replacement, echocardiographic indexes of left ventricular size, function, degree of hypertrophy and systolic wall stress were examined in 43 patients with chronic and 14 with acute aortic insufficiency. In all of the latter 14 patients, left ventricular diastolic dimension returned to normal (mean 5.2 +/- 0.4 cm) in the postoperative follow-up period (mean 8.0 months). In contrast, of those with chronic insufficiency, 28 (group A) had postoperative normalization of diastolic dimension whereas the remaining 15 (group B) had persistent enlarged diastolic dimension. Preoperative end-systolic dimension, diastolic radius/thickness ratio, mean radius/thickness ratio, mean wall stress and end-systolic stress were 84 to 93 percent accurate in predicting normalization versus persistence of left ventricular dilatation postoperatively, and were superior to preoperative end-diastolic dimension and shortening fraction. Postoperatively, group A had complete normalization of end-systolic dimension and of mean and end-systolic wall stresses with persistence of a normal shortening fraction. Group B continued to have increases in end-systolic dimension, mean wall stress and end-systolic stress with a reduction in shortening fraction. Postoperatively there was a 43 and 29 percent incidence rate of heart failure and death by heart failure, respectively, in group B versus none in group A (p less than 0.01). These findings support the concept that inappropriate hypertrophy in chronic aortic insufficiency is associated with progressive increases in wall stress and end-systolic dimension and a reduction in shortening fraction that eventually result in irreversible cardiac dilatation and failure. Accurate and clinically relevant determination of reversible and irreversible alterations in left ventricular size and function may be obtained with these echocardiographic indexes.

Effect of cardiac surgery on ventricular septal motion: Assessment by intraoperative echocardiography and cross-sectional two-dimensional echocardiography

Echocardiographic evidence of paradoxical septal motion frequently occurs after cardiac surgery. To assess possible etiologic factors 17 patients were studied preoperatively, intraoperatively, and 7 days after surgery. Preoperative septal motion was normal in 14 and paradoxical in three (two with previous cardiac surgery, one with atrial septal defect [ASD]). Intraoperative septal motion prior to surgical procedure was normal in 16 and paradoxical in one (ASD). Septal motion (excursion and thickening fraction) was normal in all patients prior to chest closure. Echocardiograms of adequate quality were obtained at 7 days post surgery in 15 patients; septal motion was paradoxical in nine (group A) and normal in six (group B). No significant differences were seen between the two groups in ischemic time or in the preoperative to postoperative change in left ventricular (LV) and right ventricular diastolic dimension, shortening fraction, or septal and posterior wall thickening fraction. A significant postoperative decrease in septal excursion was seen in group A but not in group B; significant postoperative increases in posterior wall excursion were seen in both groups. Cross-sectional two-dimensional echocardiograms performed in 20 patients (8 normal, 12 postoperative paradoxical septal motion) were analyzed. In normal controls no significant change was detected in the LV centroid position during systole. In contrast, the 12 postoperative patients showed significant anterior displacement of the LV centroid and right septum during systole. Thus, paradoxical septal motion after cardiac surgery appears to relate to excessive anterior cardiac mobility due to pericardiotomy rather than to myocardial ischemia resulting from cardiopulmonary bypass.

Diagnosis and quantification of aortic stenosis with pulsed doppler echocardiography

The presence of disturbed or turbulent flow in the ascending aorta, as assessed with pulsed Doppler echocardiography, was correlated with the presence and severity of aortic stenosis in 95 patients: 18 normal subjects, 18 with a normal aortic prosthesis and 59 with clinically suspected aortic stenosis who underwent hemodynamic studies. Turbulence was defined as a frequency dispersion greater than 1.5 cm on a time interval histographic recording of the Doppler signal. Systolic turbulence was absent in all 18 normal subjects and present in the 59 patients with aortic stenosis. The patients were divided into a test group (Group I, 34 patients) and a prospective group (Group II, 25 patients). Five graphic indexes were evaluated indicative of either duration or amplitude of turbulence, amount of frequency dispersion above and below the 0 frequency shift baseline or degree of distortion of the “flow-curve” pattern of the analog signal. Chi square analysis of results in group I indicated significant (p < 0.001) differences in the magnitude of each index between patients with an aortic valve area greater than 1.0 cm2 (n = 12) and those with an area less than 1.0 cm2 (n = 22). When all five indexes were combined, 91 percent of patients with a valve area of less than 1.0 cm2 had three or more indexes suggesting reduced valve area (positive score of 3 to 5), whereas 92 percent of patients with an area greater than 1.0 cm2 had two or fewer positive indexes (p < 0.001). In Group II, 93 percent of patients with an aortic valve area of less than 1.0 cm2 (n = 14) had a positive score of 3 to 5 whereas 82 percent of patients with an area greater than 1.0 cm2 (n = 11) had a score of 0 to 2 (p < 0.001). The overall sensitivity of the technique (n = 59) in detecting valve areas of less than 1.0 cm2 was 92 percent with a specificity of 87 percent; the predictive values for distinguishing areas less than from those greater than 1.0 cm2 were 92 and 87 percent, respectively. The technique could not be used to distinguish patients with a valve area of 0.7 cm2 or less (n = 27) from those with an area greater than 0.7 but less than 1.0 cm2 (n = 9). Turbulence was either absent or mild (0 to 2 positive scores) in the patients with an aortic prosthesis. The presence of either aortic insufficiency (n = 17), increased age (65 years or older) (n = 20) or left ventricular dilatation or failure (n = 23) did not appear to alter the results significantly. Severity of aortic stenosis could not be assessed with M mode echocardiography in 30 of 59 patients (51 percent). Thus, pulsed Doppler echocardiography allows objective assessment of severity of aortic stenosis and may therefore be an excellent screening technique for detection of patients with an aortic valve area of less than 1.0 cm2.

Echo-phonocardiographic determination of left atrial and left ventricular filling pressures with and without mitral stenosis.

In mitral stenosis (MS) the interval between the second sound and the opening snap (A2-OS) is known to shorten, while the interval between the onset of the QRS and the first sound (Q-M1) lengthens with smaller mitral valve orifice size and higher left atrial pressures. Because M1 and OS are temporally related to the C and E points on the mitral valve echogram, respectively, the ratio of Q-C to A2-E may relate to left atrial pressure in MS and to left ventricular filling pressures (LVFP) in the absence of MS. To test this hypothesis the Q-C/A2-E ratio was measured in 22 patients without MS from simultaneous mitral valve echogram, ECG and phonocardiogram at cardiac catheterization. An excellent correlation between Q-C/A2-E and left ventricular end-diastolic pressure (LVEDP) was observed (r = 0.93; SEE = 2.6 mm Hg; LVEDP range 5–28 mm Hg). The resulting regression equation: LVEDP = 21.6 (Q-C/A2-E) + 1.1, was prospectively evaluated in a second group of 32 patients without MS and with echo-phonocardiograms performed at left-heart catheterization (25 patients) or right-heart catheterization with flow-directed, balloon-tip catheters for measurement of mean pulmonary capillary wedge pressure (PCWP) (seven patients); LVFP ranged from 5-40 mm Hg. Calculated LVFP correlated well with measured LVFP (r = 0.81; SEE = 4 mm Hg). Ten of 11 patients (91%) with LVFP > 14 mm Hg were correctly separated from 19 of 21 patients (90%) with LVFP < 14 mm Hg. In 10 patients, LVFPs were acutely altered by either volume expansion or vasodilators and in all instances, calculated LVFP moved in the same direction as measured LVFP. In addition, the same equation was used to estimate mean PCWP in 22 patients with MS and eight with prosthetic mitral valves. Estimated PCWP correlated well with measured PCWP (r = 0.78; SEE = 4 mm Hg) and correctly separated 18 of 19 patients (95%) with PCWP > 18 mm Hg from nine of 11 patients (87%) with PCWP < 18 mm Hg. Thus, the Q-C/A2- E ratio and left atrial pressure correlate closely. This relationship allows one to closely estimate LVFP in patients with various types of heart disease and to judge severity of MS noninvasively.