Echocardiographic assessment of left ventricular outflow tract in d-transposition of the great arteries

The left ventricular outflow tract in 38 patients (aged 0.3 to 13 years) with complete d-transposition of the great arteries, 31 with intraatrial (Mustard) repair, was quantitated with echocardiography, and the findings were correlated with hemodynamic and angiographic data. The left ventricular outflow tract (LVO) was measured on the echocardiogram as an anteroposterior dimension between the closure point on the mitral valve below the pulmonary arterial root (PA) and the left endocardial surface of the interventricular septum. This measurement was expressed as an LVO/PA ratio and on the basis of these measurements three groups were recognized.Group I consisted of 14 patients who had an unobstructed left ventricular outflow tract and no significant pressure differences between the pulmonary artery and left ventricle. In Group II, the 16 patients had evidence of dynamic obstruction and mild to moderate pressure differences between the pulmonary artery and left ventricle, characterized in the echocardiogram by LVO/PA ratios comparable with those of Group I, but with an abnormally prominent early posterior systolic septal bulge in the left ventricular outflow tract, abnormal systolic anterior motion of the mitral valve and coarse fluttering of the pulmonary valve. In Group III the eight patients had anatomically fixed stenosis of the left ventricular outflow tract and severe left ventricular outflow pressure gradients characterized in the echocardiogram by a reduced LVO/PA ratio and fine vibrations of the pulmonary valve. Angiographically discrete or long segmental narrowing of the left ventricular outflow tract correlated well with the echocardiographic data. Echocardiographic measurements of left ventricular posterior wall thickness also correlated well with the severity of left ventricular outflow stenosis in these three groups. The echocardiogram provides clinically useful quantitative and qualitative analysis of the left ventricular outflow tract in patients with complete transposition of the great arteries.     

Echocardiographic spectrum of the hypoplastic left heart syndrome: A clinicopathologic correlation in 19 newborns

Ultrasonic studies were performed in 19 neonates with the hypoplastic left heart syndrome whose diagnosis was confirmed at angiography or autopsy, or both. The patients were classified in two echocardiographic groups: Group I, 10 infants whose ventricular septum could be recorded, and Group II, 9 infants whose septum could not be recorded. The findings in these groups were compared with those in 60 neonates without congenital heart disease also studied with ultrasound. Two additional neonates who presented with signs of shock were also studied.The diagnostic echocardiographic features of hypoplastic left heart syndrome were: (1) a left ventricular end-diastolic dimension of less than 9 mm; (2) an aortic root diameter of less than 6 mm; (3) a ratio of left ventricular end-diastolic to right ventricular end-diastolic dimension of less than 0.6; and (4) a mitral valve echo that is absent or greatly distorted and of small amplitude. These echocardiographic criteria differed significantly from findings in the normal group (P < 0.01). Echocardiography proved valuable in neonates with shock. It is a safe, reliable technique that can be used to delineate the intracardiac anatomy in sick neonates with the hypoplastic left heart syndrome.     

Double outlet left ventricle with intact ventricular septum

Two cases of double outlet left ventricle with intact ventricular septum are reported. Both patients presented with neonatal cyanosis and signs of right ventricular outflow tract obstruction. Both have hypoplastic right ventricles with suprasystemic pressures, pulmonary to mitral valve continuity and the aorta in left-sided position. These seem to be the second and third cases of the malformation to be described thus far.     

Echocardiographic assessment of left ventricular function in coronary arterial disease.

This investigation was designed to determine the role of echocardiography in the assessment of left ventricular function in patients with significant coronary arterial disease. Satisfactory echocardiograms were obtained in 43 patients with coronary arterial disease. The ventriculographic ejection fraction was determined by the area length method. The echocardiographic left ventricular end-diastolic dimension was increased to more than 5-4 cm in 17 patients. Fifteen of these patients had an ejection fraction of 0-45 or less. Three patients had a normal left ventricular end-diastolic dimension but an ejection fraction of less than 0-45. Twenty-three patients had an ejection fraction of more than 0-45 and a normal left ventricular end-diastolic dimension. The left ventricular end-diastolic dimension index was increased (greater than 3 cm/m2) in 15 patients, all of whom had ejection fraction of less than 0-45. Three patients had a normal left ventricular end-diastolic dimension index and an ejection fraction of less than 0-45. Twenty-five patients had a left ventricular end-diastolic dimension index of less than 3 cm/m2 or less and an ejection fraction of more than 0-45. The percentage fractional shortening of the echocardiographic left ventricular dimension was reduced in 25 patients. In 18 of these the ejection fraction was 0-45 or less. The percentage fractional shortening of the left ventricle was normal in 18 patients. In 2 of them the ejection fraction was less than 0-45. In summary, increase of the left ventricular end-diastolic dimension or left ventricular end-diastolic dimension index is usually associated with a critical reduction of the ejection fraction as determined by ventriculography. Since the ejection fraction is an important determinant of mortality related to bypass graft surgery, echocardiography should be useful in the detection of patients with a poor prognosis.     

The association of fixed and dynamic left ventricular outflow obstruction.

Twelve patients were investigated echocardiographically and angiographically and were shown to have severe fixed obstruction to the left ventricular outflow tract. Eight had valvular stenosis, and four had discrete subvalvular membranes. Two of the patients had additional dynamic obstruction of the left ventricular outflow tract. This was recognized preoperatively by echocardiography because of abnormal systolic motion of the mitral leaflet. At the time of definitive surgery for relief of the fixed obstruction, the additional dynamic obstruction was identified and treated, since persistent residual obstruction may lead to death in the immediate postoperative period or to long-term symptoms. The dynamic left ventricular outflow obstruction is probably a result of the hypertrophy produced by the fixed obstruction.     

Progression to left ventricular dilatation in patients with hypertrophic obstructive cardiomyopathy

Congestive heart failure with dilated left ventricle developed in two patients with symptomatic hypertrophic obstructive cardiomyopathy. Both patients previously underwent cardiac surgery for relief of their outflow obstruction. Alterations in structure and function of the left ventricle during their episode of cardiac failure and thereafter were documented by echocardiography. The findings suggest that progression to left ventricular dilatation is a potential complication in patients with hypertrophic obstructive cardiomyopathy.     

Impact of gender on the left ventricular cavity size and contractility in patients with hypertrophic cardiomyopathy

BACKGROUND: The aim of the study was to assess gender-specific differences in left ventricular cavity size, contractility and left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy. METHODS: We studied retrospectively 129 referred patients with hypertrophic cardiomyopathy (77 males and 52 females). The echocardiographically measured left ventricular end-systolic, end-diastolic dimensions, fractional shortening and occurrence of left ventricular outflow tract gradient > or =30 mmHg were compared between sexes. Logistic regression analysis was used to calculate the predictive values of left ventricular dimensions and contractility for left ventricular outflow tract obstruction for each gender separately. RESULTS: Left ventricular end-diastolic and end-systolic dimensions were significantly smaller in females than males (41.7+/-5.3 vs. 45.1+/-4.9 mm, P=0.0003; 23.1+/-44 vs. 25.6+/-5.3 mm, P=0.007 respectively). On the contrary, the value of fractional shortening was comparable in both sexes (44.7+/-7.3 vs. 43.6+/-7.9%, P>0.05). The left ventricular outflow tract gradient occurred in females as frequently as in males (28.8 vs. 33.8%, P>0.05). By logistic regression analysis the predictors of left ventricular outflow tract gradient in females were left ventricular end-systolic diameter (relative risk=0.74; confidence interval (CI) 0.61 to 0.91; P=0.0038), left ventricular end-diastolic diameter (relative risk=0.82; CI 0.72 to 0.96; P=0.0061) and fractional shortening (relative risk=1.11; CI 1.01 to 1.22; P=0.036). The most potent predictor appeared to be left ventricular end-systolic dimension. In males none of these parameters identified patients with left ventricular outflow tract obstruction. Conclusions: Females with hypertrophic cardiomyopathy featured smaller left ventricular cavity size, which predisposed to left ventricular outflow tract obstruction (the most potent predictor of left ventricular outflow tract obstruction was left ventricular end-systolic dimension). Higher left ventricular contractility also determined left ventricular outflow tract gradient occurrence in females with hypertrophic cardiomyopathy. In males despite a larger left ventricular cavity size the left ventricular outflow tract obstruction occurred with a similar frequency as in females. Left ventricular outflow tract obstruction was not predicted by left ventricular cavity size or contractility in males.     

Prevalence and significance of left ventricular outflow gradient during dobutamine echocardiography.

AIMS: This study investigated the clinical and physiological significance of the dynamic left ventricle outflow gradient observed in some patients during dobutamine stress echocardiography. METHODS: Three hundred and ninety-four consecutive patients completed dobutamine stress echocardiography using Doppler echocardiography to assess the presence of myocardial ischaemia and left ventricular outflow gradient. The prevalence of left ventricular outflow gradient was evaluated and correlated with echocardiographic and clinical findings. Fifteen patients with left ventricular outflow gradient during dobutamine infusion underwent exercise echocardiography for appearance of left ventricular outflow gradient. RESULTS: Sixty-nine of 394 (17.5%) patients developed a left ventricular outflow gradient of more than 36 mmHg. In nine of them (13%) the anterior mitral valve leaflet had a systolic anterior motion. In 60 of the 69 patients (87%) there was a dynamic obstruction at the level of the papillary muscles. The mean intracavitary gradient was 75.4 (range 36-175) mmHg. There was no correlation between the presence or absence of a dobutamine stress echocardiography-induced left ventricle outflow gradient and chest pain or shortness of breath. In patients who developed a left ventricular outflow gradient ischaemic wall motion abnormalities occurred at a significantly lower frequency during dobutamine stress echocardiography (2.9 vs 16.4% P<0.001). None of the 15 patients who underwent exercise echocardiography developed significant left ventricular outflow gradient. CONCLUSION: Left ventricular outflow gradient occurs occasionally during dobutamine stress echocardiography examination. Its presence is of no physiological or clinical significance.     

Two-dimensional echocardiographic evaluation of right ventricular size and function in newborns with severe right ventricular outflow tract obstruction

Critical pulmonary stenosis or atresia with intact ventricular septum represents a congenital cardiac lesion for which the long-term prognosis appears to depend partly on the size of the right ventricle. Thus, the capability of noninvasive assessment of right ventricular size to predict operative outcome was examined in 15 infants (aged 1 to 30 days, mean 5.6) with severe right ventricular outflow tract obstruction (either critical pulmonary stenosis [7 patients] or pulmonary atresia with intact ventricular septum [8 patients]). Using echocardiography in two orthogonal subxiphoid views, right ventricular volume, wall thickness, area change fraction, ejection fraction and tricuspid anulus dimension were measured. All patients with a normalized right ventricular enddiastolic volume of less than 5 ml/m2 and a normalized tricuspid anulus dimension of less than 1.0 cm/m2/3 required a shunt operation. Only one patient with a volume of more than 6 ml/m2 and a normalized tricuspid anulus dimension of more than 1.4 cm/m2/3 required more than relief of right ventricular outflow tract obstruction. In this patient, residual severe pulmonary stenosis necessitated the shunt procedure. One patient with a volume of more than 6 ml/m2 had an anulus diameter of less than 1.4 cm/m2/3 and one patient with an anulus diameter of more than 1.4 cm/m2/3 had a volume of less than 6 ml/m2; both required shunt procedures. It therefore appears that if either the ventricular volume or tricuspid anulus size is excessively small, a shunt procedure is necessary. Wall thickness, area change fraction and ejection fraction measurements were not significantly correlated with right ventricular volume or postoperative outcome.(ABSTRACT TRUNCATED AT 250 WORDS)     

Significance of left ventricular outflow tract cross-sectional area in hypertrophic cardiomyopathy: a two-dimensional echocardiographic assessment

The morphologic determinants of subaortic obstruction in patients with hypertrophic cardiomyopathy are not completely understood. To define the relation between left ventricular outflow tract orifice size and presence or absence of subaortic obstruction, we studied 65 patients with hypertrophic cardiomyopathy and 16 normal controls by quantitative two-dimensional echocardiography. Left ventricular outflow tract area was measured at the onset of systole in the short-axis view in the stop-frame mode. Left ventricular outflow tract area was significantly smaller in patients with hypertrophic cardiomyopathy and subaortic obstruction (2.6 +/- 0.7 cm2) than in patients without obstruction (5.9 +/- 1.6 cm2, p less than 0.001). Twenty of 21 patients with obstruction had a left ventricular outflow tract area smaller than 4.0 cm2, whereas 28 of 30 patients without obstruction had a left ventricular outflow tract area of 4.0 cm2 or greater. The outflow tract area in patients with provocable obstruction (4.6 +/- 1.6 cm2) was intermediate between the areas of patients with and without obstruction. Left ventricular outflow tract area was significantly smaller in patients with hypertrophic cardiomyopathy (4.6 +/- 2.0 cm2) than in normal subjects (10.4 +/- 1.2 cm2, p less than 0.001). We conclude that the cross-sectional outflow tract area is closely related to the presence or absence of subaortic obstruction in patients with hypertrophic cardiomyopathy. Hence, the size of the outflow tract at the level of the mitral valve appears to be of major pathophysiologic significance in producing obstruction in these patients.     

Noninvasive study of left ventricular performance in obese patients: influence of duration of obesity

We studied the performance of the left ventricle in 35 obese patients by means of noninvasive methods, including echocardiography, carotid arterial pulse tracing, and phonocardiography. Patients were divided into two groups according to the duration of obesity: group 1 included patients who had been obese for less than 15 years, and group 2 comprised patients who had been obese for more than 15 years. There were no differences in the degree of obesity and cellularity of adipose tissue between two groups. Left ventricular dimension and wall thickness, stroke volume, and cardiac output were significantly greater in both groups of obese patients than in nonobese control subjects. Group 2 had a significantly increased end-diastolic dimension index (DdI, calculated as end-diastolic dimension/cube root of body surface area), stroke index (SI), and radius/wall thickness ratio (R/Th) of the left ventricle compared with group 1. Multiple regression analysis showed that DdI, SI, and R/Th correlated significantly with the duration of obesity. We conclude that alterations of cardiac performance in obese patients with left ventricular enlargement and wall thickening is attributed not only to the excess of body weight but also to the duration of obesity.     

Complete transposition of the great arteries: visualization of left and right outflow tract obstruction by oblique subcostal two-dimensional echocardiography

Subcostal oblique 2-dimensional echocardiography was performed in 64 infants younger than 2 years with complete transposition of the great arteries (TGA) (situs solitus, concordant atrioventricular and discordant ventriculoarterial connections). All patients examined before cardiac catheterization had a correct diagnosis by 2-dimensional echocardiography using the subcostal oblique views. Twelve patients had associated left ventricular (LV) outflow tract obstruction and 7 had right ventricular (RV) outflow obstruction. The standard parasternal views failed to diagnose obstruction in 1 patients with LV outflow obstruction and 5 with RV outflow obstruction; the subcostal left oblique cut and long axis of the left ventricle visualized all left-sided obstructions, and right-sided obstructions were correctly displayed in 5 of 7 cases using a combination of left oblique and right oblique cuts. Two-dimensional echocardiographic subcostal oblique views allow an excellent definition of the morphologic characteristics of RV and LV outflow tracts in patients with TGA and improve the diagnosis of the outflow obstruction in these malformations.     

Postoperative regression of left ventricular dimensions in aortic insufficiency: a long-term echocardiographic study

The ability of preoperative M-mode echocardiography to predict the clinical course and the decrease in left ventricular size was assessed in 42 patients after uncomplicated valve replacement for isolated aortic insufficiency. During follow-up study, one patient died of chronic heart failure. The New York Heart Association functional class of the 41 survivors improved from 2.4 to 1.2. All patients had a preoperative M-mode echocardiogram. Serial echocardiographic measurements, available in 33 patients, showed a sustained decrease in left ventricular end-diastolic dimension after the first postoperative year from 73 +/- 8 to 57 +/- 9 mm at 6 to 12 months and to 53 +/- 9 mm at 3 years postoperatively (p less than 0.01). Left ventricular cross-sectional area decreased from 31 +/- 8 to 26 +/- 7 cm2 and then to 23 +/- 5 cm2 at the latest follow-up study (p less than 0.01). At 3 years postoperatively, M-mode echocardiograms were available in 37 patients: 24 had a normal left ventricular dimension (group 1), while 13 still had an enlarged left ventricle (group 2). The clinical course in these two groups was similar. The best preoperative predictor of persistent left ventricular enlargement was the end-diastolic dimension (p less than 0.05), whereas fractional shortening and the end-diastolic radius/thickness ratio were not predictive.(ABSTRACT TRUNCATED AT 250 WORDS)     

Alterations in left ventricular volumes and ejection fraction at rest and during exercise in patients with aortic regurgitation

This study was performed (1) to determine the changes in left ventricular volumes during exercise in patients with aortic regurgitation, and (2) to evaluate the importance of these alterations in characterizing left ventricular function in these patients. In 15 normal subjects (Group I) and in 17 patients with aortic regurgitation (Group II), left ventricular end-diastolic volume index, end-systolic volume index, ejection fraction and the ratio of peak systolic blood pressure to end-systolic volume index were measured at rest and during supine exercise. The patients with aortic regurgitation were classified into two groups on the basis of symptoms and chest radiographs: Group IIA, minimal or no symptoms, no cardiomegaly or pulmonary venous congestion; Group IIB, definite symptoms, with cardiomegaly and pulmonary venous congestion. Patients with aortic regurgitation had greater left ventricular end-diastolic and end-systolic volume indexes at rest and during exercise (p <0.05) than did normal subjects. During exercise, left ventricular end-diastolic volume index increased in normal subjects (53 ± 13 ml/m² [mean ± standard deviation] at rest, 67 ± 18 ml/m² during exercise, p <0.01), demonstrated a heterogeneous response in patients in Group IIA and increased in patients in Group IIB (180 ± 96 ml/m² at rest, 209 ± 102 ml/m² during exercise, p <0.05). During exercise, left ventricular end-systolic volume index decreased in normal subjects (18 ± 5 ml/m² at rest, $\text{15}\text{\$}\text{?}\text{6}$ ml/m² with exercise, p <0.01), increased in patients in Group IIB (82 ± 60 ml/m² at rest, 118 ± 93 ml/m² during exercise, p <0.05), and showed a variable response in those in Group IIA. At rest, left ventricular ejection fraction was similar in the three groups, but during exercise it increased in Group I (0.71 ± 0.07 at rest, 0.82 ± 0.07 with exercise, p <0.001), was unchanged in Group IIA and decreased in Group IIB (0.59 ± 0.15 at rest, 0.50 ± 0.16 during exercise, p <0.05). During exercise, there was an inverse relation between changes in left ventricular ejection fraction and endsystolic volume, but no relation between changes in end-diastolic volume and ejection fraction. Changes in the systolic pressure-volume ratio provided no more information than changes in end-systolic volume alone. Thus, abnormal alterations in left ventricular volumes occur during exercise in patients with aortic regurgitation and may be helpful in the further characterization of left ventricular performance in these patients.     

Blood flow patterns in the left ventricle in patients with myocardial infarction and ventricular aneurysm: evaluation using real-time two-dimensional Doppler echocardiography

To evaluate how the intraventricular blood flow is affected by the size of a left ventricular aneurysm and ventricular dysfunction, systolic left ventricular blood flow patterns were evaluated using two-dimensional Doppler flow images (real-time 2-D Doppler echo). The subjects consisted of 10 normal controls, 35 patients with anteroseptal infarction, two patients with inferior infarction and five patients with anteroseptal-inferior infarctions. The systolic period was divided into three subsets; early, mid- and end-systole. Forty-two patients with myocardial infarction were classified into three groups according to the left ventricular inflow patterns on real-time 2-D Doppler echo using the apical left ventricular long-axis approach; i.e., inflow signals confined to early systole (Group I), visualized up to mid-systole (Group II) and end-systole (Group III). Left ventricular end-diastolic dimension (LVDd), left ventricular end-systolic dimension (LVDs), and % non-contractile circumference (delta L) were calculated by the same echocardiographic approach. Ejection fraction (EF) was calculated by left ventricular cineangiography using the Simpson's method. The left ventricular inflow Doppler signals in the normal controls and Group I turned in the apex and then directed toward the left ventricular outflow tract during late diastole and early systole. Significant differences in EF were observed among the three groups. EF in Group I, II and III was 53 +/- 9%, 41 +/- 8% and 29 +/- 7%, respectively. However, LVDd, LVDs and delta L had the largest values in Group III and the smallest values in Group I. LVDd, LVDs and delta L were smallest in Group I and largest in Group III. In the normal controls, the left ventricular inflow signals proceeded to the apex and directed toward the left ventricular outflow tract in the early systolic period. Various changes in the inflow pattern were observed in patients with myocardial infarction and severe wall motion abnormalities, including delayed timing in proceeding from the apex to the left ventricular outflow tract, stagnant blood at the apex and further inflow of blood toward the apex even during end-systole. The patients with sustained inflow during late systole had hypofunction of the left ventricle as demonstrated by smaller EF and larger LVDd, LVDs, and delta L. In conclusion, the observation of intracardiac blood flows by real-time 2-D Doppler echo is of help in evaluating the severity of myocardial infarction.     

Bulboventricular foramen size in infants with double-inlet left ventricle or tricuspid atresia with transposed great arteries: influence on initial palliative operation and rate of growth.

Bulboventricular foramen obstruction may complicate the management of patients with single left ventricle. Bulboventricular foramen size was measured in 28 neonates and infants greater than 5 months old and followed up for 2 to 5 years in those patients whose only systemic outflow was through the foramen. The bulboventricular foramen was measured in two planes by two-dimensional echocardiography, its area calculated and indexed to body surface area. One patient died before surgical treatment. The mean initial bulboventricular foramen area index was 0.94 cm2/m2 in 12 patients (Group A) in whom the foramen was bypassed as the first procedure in early infancy. The remaining 15 patients underwent other palliative operations but the bulboventricular foramen continued to serve as the systemic outflow tract. There was one surgical death. Six (Group B) of the 14 survivors developed bulboventricular foramen obstruction during follow-up (mean initial bulboventricular foramen area index 1.75 cm2/m2). The remaining eight patients (Group C) did not develop obstruction during follow-up and had an initial bulboventricular foramen larger than that in the other two groups (mean initial bulboventricular foramen area index 3.95 cm2/m2). All patients with an initial bulboventricular foramen area index less than 2 cm2/m2 who did not undergo early bulboventricular foramen bypass developed late obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Adverse effect of nifedipine on left ventricular obstruction detected by pulsed Doppler echocardiography

The effect of nifedipine on the ejection flow pattern in the left ventricular outflow tract was observed using pulsed Doppler echocardiography in 6 patients with hypertrophic cardiomyopathy. After sublingual administration of nifedipine (10 mg) to 1 patient, the turbulent ejection flow pattern became more marked and increased in duration compared with the initial state. An increase in turbulence in the left ventricular outflow tract may increase the pressure gradient between the left ventricle and the aorta. Nifedipine appeared to have the potential of adverse action on left ventricular outflow obstruction.     

Accessory mitral valve tissue causing left ventricular outflow tract obstruction

Although left ventricular outflow tract obstruction is commonly associated with congenitally corrected transposition of the great vessels, this obstruction is seldom caused by accessory mitral valve tissue. Three cases in which accessory mitral valve tissue caused left ventricular outflow tract obstruction in children are described. Two had congenitally corrected transposition and one had normally connected great vessels. The accessory leaflet tissue, which was identified by echocardiography and angiography, was attached by chordae tendineae to normally sited papillary muscles and herniated into the left ventricular outflow tract during systole. Operation was successful in these patients. The accessory valve tissue was excised via an arteriotomy in the great vessel that arose from the left ventricle. The obstructive tissue was excised close to its peripheral attachments in the outflow tract and its chordae tendineae were divided. Resection was performed without injury to the abnormally placed conduction system or to the normal valve structures.     

Mechanism of left ventricular outlfow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis).

Left ventricular outflow obstruction in patients with idiopathic hypertrophic subaortic stenosis or obstructive asymmetric septal hypertrophy is due to abnormal forward motion during systole of the anterior mitral leaflet. To determine why some patients with this disease hav left ventricular outflow obstruction whereas others do not, we studied a large number of patiens with assymetric septal hypertrophy using both one- and two-dimensional echocardiography. In 100 patients with asymmetric septal hypertrophy and 22 normal subjects, mitral valve position at the onset of systole was quantitated by measuring the distance from the ventricular septum to the mitral valve and the distance from the mitral valve to the posterior left ventricular wall. None of the normal subjects and only 3 (6 percent) of 51 patients with nonobstructive asymmetric septal hypertrophy had a septal-mitral valve distance of less than 20 mm compared with 23 (66 percent) of 35 patients with obstructive asymmetric septal hypertrophy. Moreover, the mitral valve at the onset of systole was actually positioned forward in the left ventricular activity. Two-dimensional studies in 11 patients with obstructive asymmetric septal hypertrophy revealed that contraction of the malaligned papillary muscles did not cause the abnormal forward mitral valve motion. We propose that the left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy occurs as a result of two factors: (1) narrowing of the left ventricular outflow tract at the onset of systole, and (2) hydrodynamic forces generated by contraction on the left ventricle.     

Reversal of left ventricular dilatation, hypertrophy, and dysfunction by valve replacement in aortic regurgitation

Although aortic valve replacement for aortic regurgitation relieves left ventricular volume overload, ventricular geometry does not consistently normalize. To assess the extent, determinants, and functional consequences of reversal of left ventricular dilatation and hypertrophy, 38 patients with severe aortic regurgitation were studied pre- and postoperatively by serial echocardiography and radionuclide cineangiography. Left ventricular end-diastolic dimension normalized in 58% of patients by 9 +/- 6 months postoperatively, at which time 50% of patients had normalized mass; cumulative normalization rose to 66% for end-diastolic dimension and 68% for left ventricular mass during further follow-up. All patients who had normalized end-diastolic dimension also had normal postoperative ejection fractions (mean 61 +/- 8%). In contrast, patients in whom the left ventricle remained dilated had a 42% prevalence of subnormal postoperative left ventricular ejection fraction. Preoperative left ventricular end-systolic dimension less than or equal to 55 mm identified 86% of patients in whom end-diastolic dimension normalized, whereas end-systolic dimension exceeded 55 mm in 81% of those with persistent dilatation; other proposed preoperative predictors of operative outcome correctly identified lower proportions (from 59% to 71%) of patients in whom left ventricular size did or did not normalize. In conclusion, aortic valve replacement resulted in normalized left ventricular chamber size and mass in two thirds of the patients selected for operation by current criteria; favorable geometric outcome is associated with persistence or recovery of normal left ventricular function.