Early postoperative changes in left ventricular chamber size, architecture, and function in aortic stenosis and aortic regurgitation and their relation to intraoperative changes in afterload: a prospective two-dimensional echocardiographic study

We prospectively studied 16 patients with isolated aortic stenosis and eight with isolated aortic regurgitation undergoing aortic valve replacement, using two-dimensional echocardiography preoperatively, intraoperatively, and 41 +/- 7 days postoperatively to calculate the intraoperative change in afterload, quantify the postoperative changes in left ventricular chamber size, architecture, load and function, determine whether the postoperative left ventricular remodeling correlated with the intraoperative change in afterload in aortic stenosis and aortic regurgitation, and assess whether preoperative afterload excess precluded postoperative improvement in left ventricular function. Preoperative left ventricular mass, end-systolic meridional and circumferential wall stresses, ejection fraction, and stress-shortening relations in patients with aortic stenosis and aortic regurgitation were similar. However, our patients with aortic regurgitation had severe systolic dysfunction, with ejection fraction less than 55% in all but one patient, compared with only 10 of 16 patients with aortic stenosis. Left ventricular end-diastolic volume, mass/volume ratio, and chamber shape were significantly different in patients with aortic stenosis and aortic regurgitation (174 +/- 64 vs 294 +/- 140 ml, p less than .01; 1.81 +/- 0.63 vs 1.14 +/- 0.18, p less than .01; and 0.59 +/- 0.09 vs 0.69 +/- 0.09, p less than .05, respectively). Intraoperative end-systolic meridional and circumferential stresses fell significantly in patients with aortic stenosis but remained unchanged in those with aortic regurgitation. The changes in left ventricular volume and ejection fraction during early postoperative remodeling (6 weeks) correlated with the intraoperative change in afterload in patients with aortic stenosis. In contrast, there was no intraoperative change in afterload in patients with aortic regurgitation and no significant changes in left ventricular volume, architecture, or function at 6 weeks or at 6 months. The differences in left ventricular remodeling and changes in function between patients with aortic stenosis and aortic regurgitation in the early postoperative period most probably relates to the major difference in intraoperative reduction in afterload, although a contributory role may have been played by the preoperative left ventricular dysfunction in those with aortic regurgitation that was underestimated by measurement of ejection fraction.     

Mechanics of postextrasystolic potentiation in normal subjects and patients with valvular heart disease

To determine the relative influence of preload, afterload, and inotropic state on postextrasystolic potentiation (PESP) of ventricular performance in man, we computed angiographic left ventricular volume and wall stress frame by frame for a control and potentiated beat in each of 31 patients. In 10 normal subjects, PESP increased ejection fraction by 14%, while left ventricular end-diastolic volume increased by 8% (p less than .001) and end-systolic stress fell by 21% (p less than .005). Enhanced diastolic filling (+6%, p less than .005) with a small decline in end-systolic stress (-8%, p = NS) likewise contributed to potentiation of ejection fraction (+14%, p less than .001) in seven patients with aortic stenosis. Diastolic filling was not significantly augmented during the compensatory pause in six patients with isolated mitral regurgitation, nor in eight patients with aortic regurgitation (+2%, p = NS for both). Although afterload tended to fall for potentiated beats in patients with aortic (-11%, p = NS) and mitral regurgitation (-23%, p = NS), analysis of ejection fraction-end-systolic stress relationships demonstrated an independent effect of inotropic state on potentiated ejection performance. Thus, utilization of preload reserve contributed to PESP in normal subjects and patients with aortic stenosis, but not in those with volume overload imposed by chronic valvular regurgitation. Enhanced inotropic state independent of small changes in afterload was demonstrated in all subgroups.     

Preoperative left ventricular function: minimal requirement for successful late results of valve replacement for aortic regurgitation

Postoperative survival and left ventricular function were studied in 62 patients who underwent aortic valve replacement for isolated, chronic aortic regurgitation between 1978 and 1985. The average follow-up period was 3.8 years. There were three in-hospital and six late deaths. Five (56%) of the nine postoperative deaths were of cardiac-related causes. The mean 7 year survival rate was 83 +/- 5%. Preoperative left ventricular end-systolic volume index was the most important indicator (p less than 0.001) for subsequent cardiac death. The 6.5 year survival rate was 92 +/- 4% for patients with an end-systolic volume index less than 200 ml/m2 compared with 51 +/- 16% for those whose index was greater than 200 ml/m2. None of the 48 patients with an end-systolic volume index less than 200 ml/m2 died of cardiac-related causes. Twenty-three of the 48 patients with an end-systolic volume index less than 200 ml/m2 (Group 1) and 6 of the 12 patients with a higher index (Group 2) underwent repeat catheterization 26 months postoperatively. Preoperative afterload, assessed by end-systolic wall stress, was elevated in both groups, but decreased postoperatively, becoming identical to the afterload in 20 normal control subjects. Although the preoperative ejection fraction was depressed in both groups, the great majority of patients in Group 1, compared with none in Group 2, exhibited normal ejection fraction postoperatively. Thus, in patients who recently underwent surgery for aortic regurgitation, satisfactory late results in both long-term survival and reversal of left ventricular dysfunction were obtained when the preoperative end-systolic volume index was less than 200 ml/m2.     

Evaluation of relationship between myocardial contractile state and left ventricular function in patients with aortic regurgitation

We studied the relationship between myocardial contractile state and left ventricular functional response to exercise in 14 asymptomatic patients with isolated moderate-to-severe aortic regurgitation and six control subjects. The slope of the systolic blood pressure-left ventricular end-systolic volume (pressure-volume) relationship determined by radionuclide ventriculography during angiotensin infusion was used as an indirect measure of myocardial contractility and was compared with left ventricular ejection fraction at rest and during both isometric handgrip and dynamic bicycle exercise. The slope of the pressure-volume relationship was significantly lower in patients with aortic regurgitation than in the control subjects (1.75 +/- 0.57 vs 2.78 +/- 0.42, p less than 0.01). The slope correlated exponentially with resting ejection fraction and was linearly related to changes in left ventricular ejection fraction during both handgrip and bicycle exercise. In patients with aortic regurgitation, resting ejection fraction may overestimate myocardial function. The slope of the pressure-volume relationship measured during afterload stress and left ventricular ejection fraction response to exercise intervention more reliably reflect the degree of left ventricular dysfunction.     

Afterload mismatch in aortic and mitral valve disease: implications for surgical therapy

In the management of patients with valvular heart disease, an understanding of the effects of altered loading conditions on the left ventricle is important in reaching a proper decision concerning the timing of corrective operation. In acquired valvular aortic stenosis, concentric hypertrophy generally maintains left ventricular chamber size and ejection fraction within normal limits, but in late stage disease function can deteriorate as preload reserve is lost and aortic stenosis progresses. In this setting, even when the ejection fraction is markedly reduced (less than 25%), it can improve to normal after aortic valve replacement, suggesting that afterload mismatch rather than irreversibly depressed myocardial contractility was responsible for left ventricular failure. Therefore, patients with severe aortic stenosis and symptoms should not be denied operation because of impaired cardiac function. In chronic severe aortic and mitral regurgitation, operation is generally recommended when symptoms are present, but whether to recommend operation to prevent irreversible myocardial damage in patients with few or no symptoms has remained controversial. In aortic regurgitation, left ventricular function generally improves postoperatively, even if it is moderately impaired preoperatively, indicating correction of afterload mismatch. Most such patients can be carefully followed by echocardiography. However, in some patients, severe left ventricular dysfunction fails to improve postoperatively. Therefore, when echocardiographic studies in the patient with severe aortic regurgitation show an ejection fraction of less than 40% (fractional shortening less than 25%) plus enlarging left ventricular end-diastolic diameter (approaching 38 mm/m2 body surface area) and end-systolic diameter (approaching 50 mm or 26 mm/m2), confirmation of these findings by cardiac catheterization and consideration of operation are advisable even in patients with minimal symptoms. In chronic mitral regurgitation, maintenance of a normal ejection fraction can mask depressed myocardial contractility. Pre- and postoperative studies in such patients have shown a poor clinical result after mitral valve replacement, associated with a sharp decrease in the ejection fraction after operation. This response appears to reflect unmasking of decreased myocardial contractility by mitral valve replacement, with ejection of the total stroke volume into the high impedance of the aorta (afterload mismatch produced by operation).(ABSTRACT TRUNCATED AT 400 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)     

Left ventricular ejection performance, wall stress, and contractile state in aortic regurgitation before and after aortic valve replacement

Left ventricular ejection performance, wall stress, and contractile state were evaluated in 35 patients with chronic aortic regurgitation. Cineangiography and pressure measurements were obtained before and a mean of 26 months after aortic valve replacement, and data were compared with those from 30 normal control subjects. The relation between quantitative changes in wall stress and changes in ejection fraction after surgery was determined. Preoperatively, end-systolic stress was elevated in patients with aortic regurgitation (218 +/- 45 vs. 160 +/- 23 kdynes/cm2 [mean +/- SD] for control subjects, p less than 0.01), and ejection fraction was depressed (0.46 +/- 0.11 vs. 0.65 +/- 0.05, p less than 0.01). End-systolic stress decreased postoperatively (151 +/- 41 kdynes/cm2, p less than 0.01) and ejection fraction increased (0.58 +/- 0.11, p less than 0.01). The magnitude of increase in ejection fraction correlated significantly and negatively (r = -0.65) with the quantitative change in end-systolic stress after surgery. Contractile function, as assessed by the ejection phase index-end-systolic stress relation, did not significantly change: 23 of 35 patients preoperatively and 18 of 35 patients postoperatively had values that clearly fell below the 95% confidence limit of the ejection fraction-end-systolic stress relation for controls. After surgery, individual ejection fraction-end-systolic stress relationships demonstrated a shift parallel to the regression curve for the control subjects. Moreover, persistent postoperative left ventricular hypertrophy was significantly associated with persistent contractile dysfunction. Thus, late improvement in left ventricular ejection performance after aortic valve replacement can be attributed to the reduction in end-systolic stress. Contractile function itself was not improved by surgery. Persistent postoperative hypertrophy may be a marker for myocardial contractile dysfunction.     

Impaired left ventricular functional reserve in hypertensive patients with left ventricular hypertrophy

To determine whether patients with hypertension and especially those with left ventricular hypertrophy have subtle changes in cardiac function, we measured the increase in left ventricular ejection fraction and in systolic blood pressure to end-systolic volume index ratio with exercise in 40 hypertensive patients and 16 age-matched normotensive volunteers. Twenty-two hypertensive patients without hypertrophy had normal end-systolic wall stress at rest and exercise responses. In contrast, the 18 patients with echocardiographic criteria for left ventricular hypertrophy demonstrated a significant increase in end-systolic wall stress at rest compared with normal subjects (69 +/- 16 vs. 55 +/- 15 10(3) x dyne/cm2, p less than 0.05) despite having normal resting left ventricular size and ejection fraction. In patients with left ventricular hypertrophy, the increase in ejection fraction with exercise was less than in the normotensive control subjects (7 +/- 7 vs. 12 +/- 8 units, p less than 0.05), and delta systolic blood pressure to end-systolic volume with exercise was reduced (3.3 +/- 3.8 vs. 8.3 +/- 7.7 mm Hg/ml/m2, p less than 0.05). The hypertensive patients with hypertrophy displayed a shift downward and to the right in the relation between systolic blood pressure to end-systolic volume ratio and end-systolic wall stress compared with control subjects and hypertensive patients without left ventricular hypertrophy. Thus, hypertensive patients with left ventricular hypertrophy by echocardiography and normal resting ejection fraction exhibit abnormal ventricular functional responses to exercise. This finding may have implications in identifying patients at higher risk for developing heart failure.     

Anatomo-functional correlations of changes in electrocardiographic repolarization in aortic and mitral valve insufficiency. Comparison of indices based on QRS voltages

Electrocardiographic repolarization changes and voltage criteria for left ventricular hypertrophy were examined, in relation to hemodynamic, echocardiographic and angiographic data. This was done to evaluate their association with abnormalities in cardiac function and structure in 53 patients with chronic aortic regurgitation and 36 patients with chronic mitral regurgitation. No patient showed evidence of coronary artery disease. Of the patients with aortic regurgitation, the 27 patients with an abnormal repolarization pattern at ECG had worse NYHA functional class when compared to the 24 patients with normal repolarization (2.4 +/- 1 vs 1.6 +/- 0.9; p less than .01). They also had greater left ventricular dimensions (end-diastolic volume: 162 +/- 57 ml/m2 vs 109 +/- 15 ml/m2, p less than .01; end-systolic volume: 85 +/- 46 ml/m2 vs 44 +/- 31 ml/m2, p less than .01), lower left ventricular ejection fraction (.50 +/- .12 vs .63 +/- .14; p less than .01), greater left ventricular mass (170 +/- 56 gr/m2 vs 119 +/- 29 gr/m2; p less than .01) and higher end-diastolic left ventricular pressure (21 +/- 11 mmHg vs 11 +/- 8 mmHg; p less than .01). QRS voltage was less closely related to cardiac function and structure and thus, did not modify the conclusions based on repolarization findings alone. Furthermore, repolarization patterns identified patient subgroups with high or low prevalences of previously described predictors of poor surgical outcome. The presence or absence of the "strain" pattern was not related to differences in cardiac structure and function, in patients with mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Supernormal ejection performance is isolated to the ipsilateral congenitally pressure-overloaded ventricle

Congenital left ventricular pressure overload is associated with "excessive" hypertrophy that leads to subnormal afterload (wall stress), permitting enhanced ventricular ejection performance. Whether congenital right ventricular pressure overload is associated with a similar phenomenon is uncertain. It is also unknown whether supranormal ejection performance affects only the overloaded ventricle or is a general process affecting both ventricles. Conflicting data exist about whether the hypertrophic process associated with pressure overload is induced primarily by local loading conditions or by neuroendocrine influences. If the former postulate is true, the hypertrophic response should be confined to the overloaded ventricle; if the latter is true, one might predict that both ventricles would be affected by a less specific response to circulating catecholamines. To help resolve these issues, both right and left ventricular performance was examined in seven patients with isolated congenital pulmonary stenosis (average pulmonary pressure gradient 78 +/- 13 mm Hg), six patients with isolated congenital aortic stenosis (average gradient 80 +/- 10 mm Hg) and six normal subjects. Right ventricular ejection fraction was increased in patients with pulmonary stenosis (61 +/- 2%) compared with the value in normal subjects (53 +/- 2%, p less than 0.01) and in patients with aortic stenosis (50 +/- 3%, p = 0.007). Left ventricular ejection fraction was increased in patients with congenital aortic stenosis (84 +/- 4%) compared with the value in normal subjects (70 +/- 4%, p less than 0.01) and in patients with congenital pulmonary stenosis (65 +/- 2%, p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular arrhythmias in aortic valve disease before and after surgery.

In order to evaluate the incidence and prognostic value of ventricular arrhythmias in patients with aortic valve disease, 24 hour ambulatory electrocardiographic recordings were obtained in 374 patients without coronary artery disease (aortic stenosis n = 194, aortic regurgitation n = 103, combined aortic stenosis and regurgitation n = 77). Following aortic valve replacement, repeat recordings were obtained in a subgroup of 96 patients at 13 +/- 4 days and 18 +/- 7 months. Ventricular arrhythmias were classified in all cases according to Lown and were compared with clinical, echocardiographic and hemodynamic data. Preoperatively, ventricular premature beats were observed in 329 patients (88%), and were found to be frequent (>30 ventricular premature beats/hour) in 83 (22%). Multiformity was found in 105 (28%), couplets in 75 (20%) and ventricular tachycardia in 45 (12%). The occurrence of ventricular arrhythmias was not related to the type or severity of the valve lesions. Patients with severe ventricular arrhythmias (Lown class 3 or 4: 36.5%) had a higher ventricular wall thickness (interventricular septum thickness 14.2 +/- 1.8 mm vs. 11.9 +/- 2.0 mm, p < 0.01, a higher LV mass (178 +/- 32 g/m2 vs. 142 +/- 35 g/m2, p < 0.001) and a lower left ventricular ejection fraction (48% +/- 9% vs. 56.5% +/- 10%, p < 0.001); while in patients with aortic regurgitation a higher end-diastolic LV volume (224 +/- 38 ml/m2 vs. 178 +/- 42 ml/m2, p < 0.02) and a higher end-systolic LV diameter (56 +/- 7 mm vs. 46 +/- 8 mm, p < 0.02) were observed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Echocardiographic evaluation of the response to afterload stress test in young asymptomatic patients with chronic severe aortic regurgitation: sensitivity of the left ventricular end-systolic pressure-volume relationship

The detection of myocardial depression is an important goal in the management of patients with chronic severe aortic regurgitation but may be quite difficult at an early stage by the conventional basal measures of contractility. The response to afterload stress determined by angiotensin challenge and the end-systolic pressure-volume relationship was evaluated echocardiographically in 16 asymptomatic or mildly symptomatic patients with chronic severe aortic regurgitation, ages 15 to 56 years (mean 32 +/- 12). Nine normal subjects, ages 25 to 41 years (mean 31 +/- 5), served as a control group. In the group with aortic regurgitation, end-systolic dimensions were greater than 55 mm in five of 16 patients and fractional shortening was 25% or less in two of 16. In the control group angiotensin caused a decrease of stroke volume index in six out of nine patients (15% at the most) and a mild increase in three. In the group with aortic regurgitation stroke volume index decreased by 15% or more of the basal value in nine of 16 patients and increased or decreased by less than 15% in seven of 16. Ejection fraction decreased in both groups, from 61 +/- 6% to 52 +/- 7% in the control group and from 56 +/- 6% to 45 +/- 5% in the group with aortic regurgitation. Ventricular function curves were derived by relating end-diastolic volume index to stroke work index; seven of 16 patients had abnormal responses reflecting an afterload mismatch.(ABSTRACT TRUNCATED AT 250 WORDS)     

Improvement in forward cardiac output without a change in ejection fraction during nitroglycerin therapy in patients with functional mitral regurgitation

Left ventricular volumes and forward aortic flow were measured using combined two-dimensional echocardiography and doppler cardiography in seven patients with decompensated congestive heart failure and functional mitral regurgitation prior to and during intravenous administration of nitroglycerin. Total stroke volume was calculated from the difference between end-diastolic and end-systolic volumes, and regurgitant mitral volume from the difference between total stroke volume and forward aortic flow. Regurgitant mitral volume fell from 19 +/- 9 to 3 +/- 3 mL/beat (p less than 0.001), while forward stroke volume increased from 35 +/- 8 to 45 +/- 9 mL/beat (p less than 0.001). The changes were well correlated (r = 0.8, p less than 0.001). Total stroke volume decreased from 54 +/- 12 to 48 +/- 6 mL/beat (p less than 0.05), and ventricular end-diastolic volume from 173 +/- 66 to 158 +/- 66 mL (p less than 0.05). Left ventricular ejection fraction did not change significantly: 33 +/- 9% vs 32 +/- 9% (NS). Thus, in patients with severe congestive heart failure and functional mitral regurgitation, intravenous nitroglycerin redistributes blood flow within the heart by decreasing mitral regurgitation and increasing forward aortic flow, without affecting left ventricular ejection fraction.     

Quantitative evaluation of left ventricular systolic function using bidimensional echocardiography: comparison with cineangiography

The aim of the study was to compare the evaluation of the left ventricular systolic function performed both by angiography and 2D-echocardiography on 80 subjects (31 with coronary artery disease, 18 with left ventricular volume overload, 10 with left ventricular pressure overload, 14 with mitral valve disease and 7 normal controls). The 2D-echocardiograms of the left ventricle with simultaneous measurement of the right arm systolic blood pressure was performed within 24 hours of the angiographic examination. The following parameters were obtained using the two methods: end-diastolic volume index, end-systolic volume index, ejection fraction, left ventricular mass index, mass/volume ratio, end-systolic circumferential stress, contractility expressed as end-systolic circumferential stress/end-systolic volume ratio; the end-systolic circumferential stress/ejection fraction ratio was calculated only by 2D-echocardiography. The afterload and contractility were not calculated in subjects with coronary artery disease and left ventricular outflow gradient. No statistically significant differences were shown between the two methods, except a slight under-estimation by echocardiography of the angiographic end-diastolic volume index (93.1 +/- 38.9 ml/m2 vs 115 +/- 39.9 ml/m2; p less than 0.01) and over-estimation of the mass/volume ratio (1.38 +/- 0.33 g/ml vs 1.2 +/- 0.44 g/ml; p less than 0.01) was shown between the two methods for all parameters. A depressed contractile state was also demonstrated by the end-systolic circumferential stress/ejection fraction ratio. The inter and intraobserver variability was 6.6 +/- 4.4% (range 0.16%) and 4.2 +/- 3% (range 1.11%) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of additional valve lesions on left ventricular ejection time in aortic stenosis.

Rate-corrected left ventricular ejection time was measured from the aortic pressure tracings of 171 catheterised patients with aortic valve area less than or equal to 1.2 cm2. In 50 patients with pure aortic stenosis, left ventricular ejection time in increased with decreasing valve area and was significantly higher (468 +/- 5 ms, mean +/- SEM) than in 13 normal subjects (435 +/- 5 ms). Additional aortic regurgitation in 72 patients further increased the left ventricular ejection time to 484 +/- 4 ms. Significant mitral stenosis (mitral valve are less than or equal to 1.2 cm2) in 6 patients with aortic stenosis and 33 patients with aortic stenosis and regurgitation reduced the left ventricular ejection time to normal. Similarly, severe mitral regurgitation in 3 patients with aortic stenosis and regurgitation reduced left ventricular ejection time to normal, though slight or moderate mitral regurgitation in 4 of these patients did not. These data show that the prolonged left ventricular ejection time in aortic valve disease may be restored to normal in the presence of coexisting significant mitral disease.     

Abnormal exercise hemodynamics in patients with normal systolic function late after aortic valve replacement

We studied the hemodynamic response to supine bicycle exercise in 20 patients late (10 +/- 2 years) after aortic valve replacement (for aortic stenosis in 12 patients, aortic insufficiency in six patients, and for combined stenosis and insufficiency in two patients). The pulmonary artery wedge pressure was obtained with a pulmonary artery balloon catheter, and left ventriculography was performed by digital-subtraction angiography after injection of radiographic contrast into the pulmonary artery. These patients were compared with 11 control subjects with no or minimal cardiac disease studied routinely for evaluation of chest pain in whom left ventricular end-diastolic pressure and a direct contrast ventriculogram were obtained. Compared with the control population, the study population had similar left heart filling pressures (7 +/- 3 vs 9 +/- 3 mm Hg, NS), but higher left ventricular ejection fractions (75 +/- 7% vs 67 +/- 7%, p less than .02) and higher left ventricular muscle mass indexes (106 +/- 28 vs 85 +/- 9 g/m2, p less than .01). Elevated myocardial muscle mass led to lower systolic wall stress in the study population than in the control subjects (254 +/- 65 vs 320 +/- 49 10(3).dynes/cm2, p less than .01) and might explain the higher ejection fraction observed. Fourteen patients had a normal response to exercise (with left heart filling pressures of 16 +/- 4 vs 18 +/- 2 mm Hg for control subjects, NS; and left ventricular ejection fraction of 77 +/- 8% vs 73 +/- 5% for control subjects, NS). However, while the remaining six patients had a normal exercise left ventricular ejection fraction (72 +/- 9%, NS), they had an abnormal rise in left heart filling pressure (33 +/- 8 mm Hg, p less than .01). Preoperatively these patients also had higher left ventricular mid- and end-diastolic pressures at similar diastolic volumes, suggesting a decrease in chamber compliance. Thus, late after aortic valve replacement there is a subgroup of patients who, despite normal hemodynamics and normal left ventricular systolic function as assessed by the left ventricular ejection fraction at rest, have an abnormal response to exercise characterized primarily by a substantial rise in left heart filling pressures. Preoperatively this group also has a decrease in diastolic chamber compliance despite nearly normal left ventricular ejection fractions. This abnormality appears to result from a primary derangement of diastolic function that is not evident at rest.     

Left ventricular performance in patients with coexistent mitral stenosis and aortic insufficiency

Isolated mitral stenosis and isolated aortic insufficiency impose unique and opposite loading conditions on the left ventricle. To assess these combined effects, hemodynamic and angiographic factors were compared among normal subjects and patients with isolated mitral stenosis, isolated aortic insufficiency or combined mitral stenosis and aortic insufficiency. Left ventricular end-diastolic volume index was lower in patients with combined lesions and severe or moderate aortic insufficiency than in patients with isolated severe or moderate aortic insufficiency (138 +/- 19 versus 206 +/- 20 cc/m2 and 87 +/- 5 versus 145 +/- 22 cc/m2, respectively) (p less than 0.05 for both). Left ventricular end-diastolic and end-systolic volume indexes were normal in two-thirds of patients with combined lesions and moderate or severe aortic insufficiency, whereas these indexes were high in all but one patient with isolated moderate or severe aortic insufficiency. Among patients with moderate or severe aortic insufficiency, 8 of 14 with isolated insufficiency had a reduced ejection fraction or circumferential fiber shortening rate compared with 5 of the 9 patients with combined lesions. Among patients with isolated aortic insufficiency, left ventricular end-systolic wall stress and end-diastolic and end-systolic volume indexes were higher (p less than 0.05) in those with reduced ejection performance than in those with normal ejection performance. These variables did not differ between patients with reduced or normal ejection performance in the group with combined lesions. The contractile index (ratio of end-systolic wall stress to end-systolic volume index) was significantly depressed in patients with severe aortic insufficiency in the groups with isolated aortic insufficiency or combined lesions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Time course of regression of left ventricular hypertrophy after aortic valve replacement

To assess the time course and extent of regression of myocardial hypertrophy after removal of the inciting hemodynamic stress, 21 patients with either aortic stenosis or aortic insufficiency were studied preoperatively, after an intermediate period (1.6 +/- 0.5 years), and late (8.1 +/- 2.9 years) after aortic valve replacement, and results were compared with those in 11 control patients. After aortic valve replacement there was significant hemodynamic improvement, with a fall in the left ventricular end-diastolic volume index (164 +/- 73 to 105 +/- 35 ml/m2, p less than .01), a fall in left heart filling pressure (19 +/- 9 to 12 +/- 5 mm Hg, p less than .01), and maintenance of the cardiac index (3.3 +/- 0.8 to 3.5 +/- 0.8 liters/min/m2, NS) and left ventricular ejection fraction (60 +/- 13% to 64 +/- 10%, NS). By the late study the cardiac index (4.0 +/- 0.6 liters/min/m2, p less than .01) and left ventricular ejection fraction (66 +/- 15%, p less than .05) had further increased and were significantly greater than before surgery. For the group as a whole, the left ventricular muscle mass index fell 31% after surgery by the time of the intermediate postoperative study (174 +/- 38 vs 120 +/- 29 g/m2, p less than .01), and a further 13% from the intermediate to the late study (105 +/- 32 g/m2, p less than .05). At the preoperative study left ventricular muscle mass index was greatest in those patients with aortic insufficiency (191 +/- 36 g/m2), and greater in those with aortic stenosis (158 +/- 33 g/m2) than in control subjects (85 +/- 9 g/m2, p less than .05). At the intermediate postoperative study left ventricular muscle mass index remained significantly higher in both those with preoperative aortic insufficiency (128 +/- 29 g/m2) and those with stenosis (114 +/- 27 g/m2) than in the control subjects (p less than .01). By the time of the late postoperative study there were no longer any significant differences in left ventricular muscle mass index. Thus, the regression of myocardial hypertrophy is a process that occurs over many years after correction of the primary hemodynamic abnormality. As this process of myocardial remodeling occurs, continued improvement in cardiac function may occur, and the improvement occurring between the intermediate and late postoperative studies at a slight but constant afterload excess (inherent in the relative stenosis of the aortic prosthesis) suggests that the hypertrophied myocardium is operating at a reduced level compared with normal myocardium.     

Effects of reduced left ventricular mass on chamber architecture, load, and function: a study of anorexia nervosa

We investigated the effects of reduction in left ventricular mass on cavity geometry, afterload, pump function, and exercise performance in 17 patients with anorexia nervosa and in 10 age-and sex-matched normal subjects. Left ventricular mass index determined by two-dimensional echo-cardiography was significantly lower than that in normal subjects (53 +/- 15 vs 79 +/- 18 g/m2; p less than .005). Left ventricular end-diastolic and end-systolic volume indexes were also reduced in patients with anorexia nervosa compared with normal subjects (49 +/- 11 vs 65 +/- 17 ml/m2, p less than .005; 14 +/- 5 vs 19 +/- 4 ml/m2, p less than .025). In spite of the reductions in left ventricular mass and volume indexes, left ventricular chamber architecture described as h/R ratio, mass to volume ratio, and short/long left ventricular axis ratio were normal. Left ventricular afterload assessed as end-systolic meridional and circumferential wall stress was normal (59 +/- 18 vs 79 +/- 19 dyne/cm2 X 10(3) and 170 +/- 26 vs 167 +/- 23 dyne/cm2 X 10(3)). Ejection fraction, percent fractional shortening, and the relationship between end-systolic wall stress and ejection fraction were all within normal limits. In seven patients restudied after a 15% to 20% weight gain, left ventricular mass and volume indexes increased significantly but end-systolic wall stress and ejection fraction did not change. Ten patients with anorexia nervosa and resting heart rates and systolic blood pressures significantly lower than control values underwent treadmill testing. Exercise duration, peak heart rate, peak systolic blood pressure, and peak oxygen consumption in these patients were all significantly lower than normal. The hypotensive effect of fasting resulted in an initial decrease in afterload, which was the stimulus for reduction in left ventricular mass. The left ventricular remodeling associated with the mass reduction occurred in such a way that (1) orthogonal, meridional, and circumferential wall stresses were normalized, (2) normal chamber shape and architecture were maintained, and (3) chamber function and stress-shortening relationships were preserved. Thus down-regulation of left ventricular mass per se, like up-regulation of left ventricular mass, is not associated with abnormal left ventricular function.     

Ejection fraction response to supine exercise in asymptomatic aortic regurgitation: relation to simultaneous hemodynamic measurements

The change in ejection fraction during exercise is frequently employed as a measure of left ventricular functional reserve in patients with aortic regurgitation. However, little information is available about its relation to invasive measurements of cardiac performance. Therefore, simultaneous hemodynamic measurements and supine exercise blood pool scintigraphy were performed in 14 patients with severe, asymptomatic or minimally symptomatic aortic regurgitation associated with cardiomegaly but preserved left ventricular function at rest. Their hemodynamic measurements at rest were normal and their exercise capacity was excellent. When the patients were categorized into those patients whose ejection fraction increased or did not decrease by more than 0.05 (Group 1) and those whose ejection fraction decreased by more than 0.05 (Group 2), important differences were apparent. Echocardiographic, radionuclide and hemodynamic measurements at rest in the two patient groups were similar, but Group 1 exhibited a greater increase in cardiac index during supine exercise (2.8 +/- 0.4 to 10.0 +/- 1.8 versus 2.7 +/- 0.5 to 6.9 +/- 1.0 liters/min per m2; p less than 0.005) and a lesser increase in pulmonary capillary wedge pressure (13 +/- 4 to 19 +/- 7 versus 12 +/- 4 to 31 +/- 8 mm Hg; p less than 0.01). The severity of regurgitation decreased during exercise in all patients, but end-diastolic volume decreased and end-systolic volume decreased or was unchanged in Group 1, whereas end-diastolic volume was unchanged and end-systolic volume increased in Group 2.(ABSTRACT TRUNCATED AT 250 WORDS)