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Publications and source records attributed to C Y Choong.
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The Doppler transmitral velocity curve is commonly used to assess left ventricular diastolic function. Recent investigations, however, relating Doppler mitral indexes to ventricular compliance, relaxation, and preload have been inconclusive and at times contradictory. We used a mathematical formulation to study the physical and physiological determinants of the transmitral velocity pattern for exponential chamber pressure-volume relationships with active ventricular relaxation (2,187 combinations investigated). We showed that transmitral velocity is fundamentally affected by two principal physical determinants, the transmitral pressure difference and the net atrioventricular compliance, as well as the impedance characteristics of the mitral valve. These physical determinants in turn are specified by the compliance and relaxation parameters of physiological interest. We found that the peak mitral velocity is most strongly related to initial left atrial pressure but lowered by prolonged relaxation, low atrial and ventricular compliance, and systolic dysfunction. Peak acceleration varies directly with atrial pressure and inversely with the time constant of isovolumic relaxation, with little influence of compliance, whereas the mitral deceleration rate is approximately valve area divided by atrioventricular compliance. We then used these data to suggest possible strategies for improved analysis of noninvasive data (Doppler indexes, planimetered valve area, and isovolumic relaxation time) to estimate ventricular compliance and relaxation and atrial pressure.
Hemodynamic and metabolic changes were measured at rest and during exercise in 23 patients with chronic heart failure and in 6 control subjects. Exercise was limited by leg fatigue in both groups and capacity was 40% lower in the patients with failure. At rest, comparing patients with control subjects, heart rate and right atrial and pulmonary wedge pressure were higher; cardiac output, stroke volume and work indexes and ejection fraction were lower; mean arterial and right atrial pressure and systemic resistance were similar. During all phases of exercise in patients with heart failure, pulmonary wedge pressure and systemic vascular resistance were higher and pulmonary vascular resistance remained markedly elevated compared with values in control subjects. Cardiac output was lower in the patients with failure, but appeared to have the same physiologic distribution in both groups during exercise. Although arterial-femoral venous oxygen content difference was higher in patients with heart failure, this increase did not compensate for the reduced blood flow. Even though the maximal oxygen consumption was significantly reduced, femoral venous lactate and pH values were higher than values in control subjects, but femoral venous pH was similar in both groups at their respective levels of maximal exercise. Ejection fraction was lower in those with heart failure at rest and did not increase with exercise. Ventilation in relation to oxygen consumption was higher in patients with failure than in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Left ventricular filling (as assessed by Doppler echocardiography) has previously been shown to depend in a complex fashion on ventricular diastolic function (compliance and relaxation) as well as other variables, such as atrial pressure and compliance, ventricular systolic function and mitral valve impedance. To study the effect of isolated physiologic alterations on individual Doppler indexes, a mathematic model of mitral flow was analyzed. By varying one physiologic variable at a time, it was shown that mitral velocity acceleration is affected directly by atrial pressure and inversely by the ventricular relaxation time constant, with relatively little impact of chamber compliance. Deceleration rate was directly influenced by mitral valve area, atrial pressure and ventricular systolic dysfunction and inversely affected by atrial and ventricular compliance relations, with little impact of relaxation unless it was so delayed as to be incomplete during deceleration. Peak velocity was directly affected most strongly by initial left atrial pressure, and lowered somewhat by prolonged relaxation, low atrial and ventricular compliance and systolic dysfunction. Strikingly different filling patterns emerged when the primary physiologic alterations were accompanied by simultaneous compensatory changes in atrial pressure designed to maintain stroke volume constant. Low ventricular compliance with preload compensation produced characteristic E waves with very short acceleration and deceleration times and high peak velocity. Thus, mathematic analysis of ventricular filling helps to explain the physical and physiologic basis for the transmitral velocity curve.
We studied 130 patients undergoing percutaneous balloon mitral valvotomy. The relation between valvular morphology according to a previously described echocardiographic scoring system and hemodynamic outcome expressed as qualitative ("good" and suboptimal) and as absolute change in valve area was analyzed. The relative importance of the individual components of this echocardiographic score (valvular thickening, mobility, calcification, and subvalvular disease) to the change in valve area after valvotomy was also examined. Mean transmitral pressure gradient decreased from 16 +/- 6 to 6 +/- 3 mm Hg (p less than 0.0001), and mitral valve area increased from 0.9 +/- 0.3 to 1.8 +/- 0.7 cm2 (p less than 0.0001). Results in individual patients were variable. Eighty-four percent (61 of 73) of patients with an echocardiographic score of 8 or less had a "good" outcome (final valve area greater than or equal to 1.5 cm2 and an increase in valve area of greater than or equal to 25%), whereas 58% (33 of 57) of patients with an echocardiographic score of 8 or more had a suboptimal result (p less than 0.001). The sensitivity of an echocardiographic score of 8 or less for predicting a "good" outcome was 72%, and the specificity was 73%. The echocardiographic score correlated negatively (r = -0.40, p less than 0.0001) with the absolute increase in mitral valve area after valvotomy, but there was substantial scatter in the data. Of the four components of the total echocardiographic score, valvular thickening correlated best with the absolute change in value area (r = -0.47, p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
Mitral-valve prolapse is a common cardiac valvular disorder with a wide range of severity and diverse clinical outcomes. The lack of a standard definition of mitral-valve prolapse may explain the variation in reported complication rates. To identify high-risk and low-risk subgroups, we retrospectively analyzed clinical and two-dimensional echocardiographic data from 456 patients with mitral-valve prolapse. Mitral-valve prolapse was defined on the basis of echocardiographic findings as systolic displacement into the left atrium of one or both leaflets beyond the plane of the mitral annulus in the parasternal long-axis view. Two groups of patients were compared: those with thickening of the mitral-valve leaflets and redundancy (designated the classic form; n = 319) and those without leaflet thickening (designated the nonclassic form; n = 137). The two groups were similar in age and sex ratio. Complications or a history of complications was more prevalent in the classic than the nonclassic form: infective endocarditis, 3.5 percent and 0 percent, respectively (P less than 0.02); moderate-to-severe mitral regurgitation, 12 percent and 0 percent (P less than 0.001); and the need for mitral-valve replacement, 6.6 percent and 0.7 percent (P less than 0.02). However, the frequency of stroke was similar in the two groups: 7.5 percent and 5.8 percent (P not significant). We conclude that in a selected population of patients with mitral-valve prolapse, those with the classic form (leaflet thickening and redundancy) are at higher risk than those without these features for the infectious and hemodynamic complications of mitral-valve prolapse, but not for stroke.
We have previously reported that regional wall motion abnormalities in a canine model of acute myocardial infarction may show substantial improvement in the first 6 weeks after infarction. To determine whether the mechanism of this improvement in function is the result of scar contraction within the infarct, we studied the relationship between changes in regional wall motion defined by cross-sectional echocardiography and the regional concentration of radioactive microspheres injected immediately before coronary occlusion and sampled 6 weeks after occlusion. Eight dogs underwent serial echocardiographic and microsphere blood flow measurements immediately before and 30 minutes, 48 hours, 1 week, 3 weeks, and 6 weeks after ligation of the left anterior descending or the left circumflex coronary artery. Wall motion and blood flow were measured in the short-axis section of the left ventricle at the level of the midpapillary muscle in each 10-degree radial segment around the circumference of the ventricle. Infarct histology was assessed at 6 weeks by means of the same radial coordinate system. Control data were collected in a similar manner from four dogs that underwent sham operations and had no histologic evidence of infarction. In all of the animals with infarcts, but not in the sham animals, the calculated preocclusion endocardial and epicardial blood flow values in the histologic infarct zone (252 +/- 44 and 168 +/- 17 ml/min/100 gm, respectively, mean +/- SEM) were significantly higher than those in the normal opposite wall (endocardial: 106 +/- 3 ml/min/100 gm, p less than 0.01); epicardial: 108 +/- 3 ml/min/100 gm, p less than 0.01. The location and circumferential extent of myocardium showing this elevation of preocclusion blood flow correlated well (r = 0.93, p less than 0.001) with the location and circumferential extent of the histologic infarct. The amount of wall motion abnormality, measured from the "correlation plot area," decreased significantly from its maximum value of 39 +/- 3 degrees at 48 hours after coronary occlusion to 3 +/- 1 degrees (p less than 0.001) at 6 weeks after occlusion. The ratio of the preocclusion transmural blood flow in the infarct zone to that in the noninfarct zone, a measure of the condensation of the microspheres injected before coronary occlusion, and therefore of the degree of scar contraction at 6 weeks, correlated well (r = 0.83, p less than 0.01) with the recovery of wall motion 6 weeks after infarction.(ABSTRACT TRUNCATED AT 400 WORDS)
The prevalence of valvular regurgitation in a large population with structurally normal hearts remains unknown. From the computer database of the echocardiography laboratory of the hospital, 7209 records containing results of both two-dimensional and Doppler echocardiographic examinations were identified, from which 867 (12%) with no structural abnormality on two-dimensional echocardiograms were obtained for analysis. Of these 867 records, 291 (34%) had evidence of regurgitation by Doppler technique in at least one cardiac valve. Mitral regurgitation was found in 167 (19%), tricuspid regurgitation in 151 (17%), pulmonic regurgitation in 45 (5%), and aortic regurgitation in 29 records (3%). Regurgitation of just one valve was the most common and occurred in 207 records (24%). This was followed by regurgitation of two valves (69 records, 8%), three valves (13 records, 2%), and four valves (two records, 0.2%). The prevalence of mitral, tricuspid, and aortic regurgitation was found to increase significantly with increasing age, as was the prevalence of regurgitation involving multiple valves. In 98% and 95% of mitral and tricuspid regurgitations, respectively, the jets were confined to the proximal one fourth of the atria, suggesting only trivial or mild regurgitation. Thus valvular regurgitation occurs not uncommonly in patients with structurally normal hearts referred for echocardiographic evaluation. These findings caution against the inappropriate diagnosis of clinical disease in the many patients who fall into this category. The increasing prevalence of valvular regurgitation with increasing age suggests that a wear-and-tear phenomenon rather than a congenital cause is involved in most instances.
To assess the electrophysiologic effects of acute hemodynamic improvement in patients with left ventricular systolic dysfunction, 12 patients with a left ventricular ejection fraction less than 0.40 and a history of sustained monomorphic ventricular tachycardia were studied. All patients had underlying coronary artery disease. Patients underwent programmed cardiac stimulation in random order during a baseline period and with nitroprusside infusion. Mean pulmonary capillary wedge pressure decreased from 20 +/- 8 mm Hg at baseline study to 8 +/- 3 mm Hg during nitroprusside infusion (p less than 0.0001). Pulmonary artery, right atrial and systemic arterial pressures also decreased with nitroprusside (p less than 0.01). Cardiac output did not change. Left ventricular dimensions, determined by two-dimensional echocardiography, decreased significantly during nitroprusside infusion. The right ventricular effective refractory period, measured during ventricular drive trains at cycle lengths of 400 and 600 ms, were similar during baseline and nitroprusside periods (271 +/- 30 versus 274 +/- 31 ms at 600 ms, and 249 +/- 25 versus 246 +/- 18 ms at 400 ms). In 2 patients no ventricular arrhythmias were induced during either study period; in the other 10, ventricular tachyarrhythmias were induced during both periods. The mean number of extrastimuli required to induce a ventricular tachyarrhythmia was similar during the baseline period (1.8 +/- 0.6) and during nitroprusside infusion (1.9 +/- 0.7). As well, the mean cycle length of ventricular tachycardia induced was similar during the baseline period (347 +/- 61 ms) and during nitroprusside infusion (342 +/- 70 ms).(ABSTRACT TRUNCATED AT 250 WORDS)
To investigate the antianginal action of nitroglycerin and nifedipine, systemic and right heart pressures, cardiac output, oxygen consumption, and radionuclide left ventricular ejection fraction and volume were measured in 14 men with stable effort angina and a positive exercise electrocardiogram. Exercise tests were performed on a semiupright bicycle ergometer on no therapy and after intravenous nitroglycerin and sublingual nifedipine, which lowered mean arterial pressure by 20 mm Hg. Exercise tolerance improved from 50 +/- 4 to 61 +/- 5 W on nifedipine and to 79 +/- 4 W on nitroglycerin (p less than 0.01, nitroglycerin vs. nifedipine). At submaximal workloads, both drugs decreased arterial pressure and ventricular volumes, but heart rate was higher on nifedipine. At peak exercise on nitroglycerin (79 W), oxygen consumption, cardiac index, heart rate, and rate-pressure product were significantly increased over peak control and nifedipine values, while systolic pressure and end-diastolic volume were unchanged. Nitroglycerin reduced pulmonary wedge pressure more and systemic diastolic pressure less than nifedipine, so the coronary perfusion gradient was reduced by nifedipine and maintained by nitroglycerin. Also, there was less angina and ST-segment depression after nitroglycerin compared to control or nifedipine, and the left ventricular diastolic pressure-volume relationship was improved only by nitroglycerin. This suggests that the action of nitroglycerin in reducing ischemia is not only due to reduced myocardial oxygen demand, but that myocardial oxygen delivery may also be increased.
Percutaneous balloon mitral valvuloplasty is a new technique used in the treatment of adult patients with mitral stenosis. To evaluate the occurrence and severity of mitral regurgitation after balloon valvuloplasty, 24 patients (20 women and 4 men, mean age 57 years) were studied using two-dimensional and Doppler echocardiography before and less than 24 h after this procedure. Mitral valve area increased after valvuloplasty in all patients, from 0.89 +/- 0.07 to 1.61 +/- 0.09 cm2 (p less than 0.001). Before valvuloplasty, 10 patients had no mitral regurgitation, 4 had 1+, 4 had 2+ and 6 had 3+ mitral regurgitation. After valvuloplasty, new mitral regurgitation occurred in six patients. Regurgitation grade did not change in 13 patients (54%), increased by one grade in 8 patients (33%) and by two grades in 3 patients (13%). Left atrial volume decreased in all except one patient from 100 +/- 12 to 83 +/- 12 cm3 (p less than 0.001). Neither age, sex, cardiac rhythm, initial mitral valve area, increase in mitral valve area, morphologic characteristics of the valvular and subvalvular apparatus, previous mitral commissurotomy nor effective balloon dilating area discriminated between those patients with and without an increase in mitral regurgitation after valvuloplasty. Thus, mitral balloon valvuloplasty is frequently associated with an increase in mitral regurgitation. However, in this series, no patient developed severe mitral regurgitation, and left atrial volume decreased in nearly all patients. An increase in mitral regurgitation could not be predicted from any features of the valve or subvalvular apparatus, clinical characteristics of the patients or technical aspects of the procedure.
Although beneficial results have been reported immediately after percutaneous mitral balloon valvuloplasty, little information is available concerning the longer-term outcome of this procedure. The anatomic and functional results of percutaneous mitral valvuloplasty were assessed in 20 patients, in whom two-dimensional and Doppler echocardiographic examination could be obtained both immediately and 6 to 11 months (mean 7.5 +/- 2.0) after balloon dilation. Mean valve area measured by planimetry decreased slightly but significantly from 1.90 +/- 0.59 cm2 immediately after valvuloplasty to 1.62 +/- 0.55 cm2 (p less than 0.001) at follow-up. Individual changes in valve area were variable, and in four patients valve area decreased by greater than 25%. Echocardiographic scores of valvular morphology were obtained by assigning scores of 0 to 4 (with increasing abnormality) to each of four morphologic characteristics of the valve, namely, leaflet mobility, thickening, calcification and subvalvular thickening. This score was higher in the four patients with a decrease in valve area greater than 25% at follow-up than in the other patients (11 +/- 2 versus 7 +/- 2, p less than 0.002). Multiple regression analysis of several hemodynamic and echocardiographic factors identify first the echocardiographic score and second the valve area postvalvuloplasty as the only significant predictors of the percent decrease in valve area (r = 0.70, p less than 0.006). Mitral regurgitation graded by pulsed Doppler ultrasound decreased from 1.9 +/- 1.2 immediately after valvuloplasty to 1.0 +/- 0.9 (p less than 0.003) at follow-up, whereas there was no change in mean transmitral pressure gradient by Doppler echocardiography (5 +/- 2 versus 6 +/- 3 mm Hg, p = NS) and left atrial volume (74 +/- 34 versus 72 +/- 27 cm3, p = NS). Thus, 6 to 11 months after balloon mitral valvuloplasty, mean mitral valve area decreases slightly. Individual changes in valve area, however, are variable. Valvular morphology assessed by two-dimensional echocardiography may be useful for identifying those patients who have an increased likelihood of developing valvular restenosis.
The usefulness of digitized echocardiographic borders in quantitative regional left ventricular function analysis has been limited by the wide reported range for normal wall motion with this technique. We postulated that random error in endocardial border positioning is a major cause of this limitation. To test this hypothesis, we traced the endocardial borders field by field from 17 complete echocardiographic cycles in six dogs. These cycles showed a great deal of random movement, with each endocardial point reversing its motion an average of 18.5 times per cardiac cycle. Spatiotemporal Fourier analysis of these sequences demonstrated that most of the valid information on endocardial motion was contained in the first four temporal harmonics and the first seven spatial harmonics and that beyond these points the Fourier transform has the spectral characteristics of noise. Reconstruction of these 17 cycles eliminating all Fourier components above the sixth temporal and eighth spatial harmonics reduced the mean number of endocardial reversals per cycle to 2.3 (p less than .00001). To derive the optimal temporal and spatial cutoffs, we compared reconstructions of each of the 17 cycles with three M mode echocardiograms obtained simultaneously with the cross-sectional images. Fourier cutoffs were varied between two and 20 harmonics and demonstrated that the optimal temporal cutoff was 5.5 harmonics and optimal spatial cutoff 6.9. With optimal filtering, the correlation between ventricular diameter derived from the M mode and from the cross-sectional images was r = .965, compared with .877 for the M mode vs unfiltered cross-sectional data (p less than .0001). We conclude that two-dimensional filtered Fourier reconstruction significantly improves the accuracy of traced echocardiographic borders. This technique should be useful in the postprocessing of endocardial borders extracted by automated edge detection schemes and should also be applicable to cardiac images derived from modalities other than echocardiography.
We previously developed a cross-sectional echocardiographic technique for quantitatively mapping the endocardial surface of the left ventricle and on which regions of abnormal wall motion can be superimposed in their correct spatial distribution. This endocardial mapping technique (EMT) provides a measure of the left ventricular endocardial surface area (ESA in cm2), the area of abnormal wall motion (AWM in cm2), and the overall percent dysfunction (%AWM) as a measure of the functional "infarct size." To test this approach, we compared the EMT measurements with the actual endocardial surface area (in cm2) and pathologic infarct size (both percent infarct by volume and percent endocardial surface overlying infarct) measured at later autopsy in 20 adults (14 men, six women) ranging in age from 47 to 76 years (mean 64 +/- 9.6 years). The median interval from echocardiographic study to death was 19 days (range 1 to 269 days). Patients were divided into two groups based on the age of their infarcts at the time of death: (1) recent (infarct age less than 14 days; mean age 5.3 +/- 4.6 days) and (2) old (infarct age greater than 6 months; mean age 3.6 +/- 3 years). When the left ventricular endocardial surface area at autopsy was compared with the EMT-derived ESA, a close correlation was found (EMT area = 1.17 X autopsy area + 20.4; r = .94, p = .0001), with the systematic difference in the measurements accounted for by systolic arrest, loss of distending pressure, and specimen shrinkage. The echocardiographic measure of infarct size (%AWM) correlated well with the autopsy percent infarction by volume (%AWM = 1.1 X infarct volume + 5.5; r = .82, p = .0001). Similarly, a good correlation was found for the percent abnormal wall motion and the autopsy percent endocardial surface area overlying infarction (%AWM = 0.89 X infarct area - 0.9; r = .89, p = .0001). When the data were examined in relation to the age of the myocardial infarct, the echocardiographic %AWM appeared to overestimate the autopsy infarct size (by percent infarct volume) in the recent infarct group (n = 6), and underestimate the extent in the old infarct group (n = 13). The findings suggest that the EMT will provide a useful quantitative measure of left ventricular endocardial surface area and the extent of ischemic/infarct-related dysfunction.
The relation of the Doppler transmitral flow velocity profile to left ventricular loading conditions and diastolic properties remains poorly described. We studied seven adult mongrel dogs with an open-chest right heart bypass model in which left atrial pressure, representing preload, was varied by controlling blood flow into the pulmonary artery and left ventricular systolic pressure, representing afterload, was controlled independently by pumping blood into or from the femoral arteries. Heart rate was kept constant by crushing the sinus node and pacing the right atrium. Mitral inflow velocity profiles were measured by pulsed-wave Doppler echocardiography at multiple left atrial and left ventricular systolic pressures. In individual dogs, the peak E-wave velocity increased linearly with increasing left atrial V-wave pressure at constant left ventricular systolic pressure and decreased with increasing left ventricular systolic pressure at constant left atrial pressure. Stepwise multiple linear regression analysis of data pooled from all experimental stages in all dogs identified left atrial V-wave pressure, the time constant of relaxation (TL), and left ventricular systolic pressure, in order of decreasing significance, as predictors of the peak E-wave velocity (n = 82, multiple r = 0.87, p less than 0.0001). Multivariate analysis with the same three factors in individual dogs yielded higher r values (mean r = 0.89; range, 0.85-0.97), suggesting the presence of important interdog differences that were not accounted for by these three factors alone. When the values of codeterminant hemodynamic factors were kept within narrower limits, correlations between peak E-wave velocity and left atrial V-wave pressure (n = 35, multiple r = 0.83, p less than 0.0001), TL (n = 76, multiple r = -0.54, p less than 0.0001) and left ventricular systolic pressure (n = 20, multiple r = -0.59, p less than 0.005) improved substantially. In the pooled data, the relation of the peak E-wave velocity to left atrial V-wave pressure was shifted downward by an increase in TL (reduced relaxation rate), and the relation of the peak E-wave velocity to TL was shifted upward by an increase in left atrial V-wave pressure. Multivariate analysis also selected left atrial V-wave pressure and TL as the two most significant correlates of the velocity-time integral and deceleration rate of the E wave.(ABSTRACT TRUNCATED AT 400 WORDS)
Mitral pressure half-time (T1/2) is widely used as an independent measure of mitral valve area in patients undergoing percutaneous mitral valvotomy. However, fluid dynamics theory predicts T1/2 to be strongly dependent on chamber compliance and the peak transmitral gradient, which are variables that change dramatically with valvotomy. These theoretical predictions were tested in an in vitro model of the left heart where valve area, chamber compliance, and initial gradient were independently adjusted. Measured T1/2 was observed to vary inversely with orifice area and directly with net chamber compliance and the square root of the initial pressure gradient. Theoretical predictions of T1/2 agreed with observed values with r = 0.998. To test this theory in vivo, the hemodynamic tracings of 18 patients undergoing mitral valvotomy were reviewed. Predictions were made for T1/2 assuming dependence only on valve area; these showed some correlations before valvotomy (r = 0.48-0.64, p less than 0.05) but none after valvotomy (r = 0.05-0.28, p = NS). Predictions for T1/2 based on the theoretical derivation (and thus including compliance and pressure in their calculation) were much better: before valvotomy, r = 0.93-0.96, p less than 0.0001; after valvotomy, r = 0.52-0.66, p less than 0.05. These data indicate that T1/2 is not an independent inverse measure of mitral valve area but is also directly proportional to net chamber compliance and the square root of the initial transmitral gradient. These other factors render T1/2 an unreliable measure of mitral valve area in the setting of acute mitral valvotomy.
In 14 patients during exercise, intravenous nitroglycerin improved anginal threshold and increased workload compared with control subjects. At similar workloads, the decreased left ventricular volumes suggested decreased myocardial oxygen consumption due to peripheral unloading. At maximal exercise with nitroglycerin (50 +/- 17 to 79 +/- 15 watts), rate-pressure product and end-diastolic volumes were higher with less ischemia, suggesting myocardial supply was improved by nitroglycerin.
To determine the effect of filling pressure on the pattern of left ventricular filling in humans, the mitral flow velocity profile was measured by pulsed wave Doppler echocardiography during right and left heart catheterization in 11 patients before and during nitroglycerin infusion. Nitroglycerin reduced mean arterial pressure from 90 +/- 9 to 80 +/- 11 mm Hg (p less than 0.001) and mean pulmonary capillary wedge pressure from 9 +/- 4 to 4 +/- 2 mm Hg (p less than 0.001). Cardiac output fell from 6.6 +/- 1.5 to 5.5 +/- 1.4 liters/min (p less than 0.001) and heart rate increased from 60 +/- 13 to 65 +/- 14 beats/min (p less than 0.002). The time constant of isovolumic relaxation (TI.) decreased from 51 +/- 9 to 46 +/- 8 ms (p less than 0.01), indicating faster left ventricular relaxation. Nitroglycerin altered the Doppler characteristics of the early filling (E) wave but not those of the atrial contraction (A) wave. Peak velocity of the E wave decreased from 56 +/- 14 to 44 +/- 9 cm/s (p less than 0.001), peak velocity of the A wave did not change and the ratio of peak velocities of the E and A waves decreased from 0.97 +/- 0.33 to 0.77 +/- 0.20 (p less than 0.02). The deceleration of the E wave decreased from 289 +/- 138 to 186 +/- 71 cm/s2 (p less than 0.02). The ratio of velocity-time integral of the A wave to total velocity-time integral (that is, contribution of atrial contraction to total filling) increased from 0.31 +/- 0.09 to 0.36 +/- 0.08 (p less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)