Balloon valvuloplasty for recurrent aortic stenosis after surgical valvotomy in childhood: immediate and follow-up studies

The immediate and intermediate-term effects of balloon valvuloplasty were assessed at cardiac catheterization in nine children with recurrent stenosis after a previous surgical aortic valvotomy. At valvuloplasty the patients ranged in age from 0.35 to 16 years and had undergone surgical valvotomy 0.3 to 12.5 years previously. Balloon valvuloplasty immediately reduced the peak systolic aortic stenosis gradient by 53%, from 88 +/- 9 (mean +/- SEM) to 41 +/- 6 mm Hg (p = 0.004). The left ventricular systolic pressure was reduced from 189 +/- 8 to 157 +/- 8 mm Hg (p = 0.001) and the left ventricular end-diastolic pressure from 17 +/- 1 to 14 +/- 2 mm Hg (p = 0.025). The heart rate and cardiac index remained unchanged. Before valvuloplasty, one patient had 1 + and two patients had 2+ aortic insufficiency. In six of nine patients, balloon valvuloplasty caused no change in the degree of valvular insufficiency. Two patients had a 1 + increase (from 0 to 1 + insufficiency in both), and one patient with no insufficiency developed 2+ aortic insufficiency. Elective follow-up catheterization was performed 0.8 to 2.5 years (mean 1.5 +/- 0.2) after valvuloplasty. At follow-up, the peak aortic stenosis gradient remained significantly reduced from the gradient before valvuloplasty (37 +/- 5 versus 85 +/- 10 mm Hg, p = 0.002). The gradient had not changed significantly from that measured immediately after valvuloplasty (37 +/- 5 versus 38 +/- 5 mm Hg, p = 0.75). At follow-up, aortic insufficiency had decreased from that immediately after valvuloplasty in three patients and had increased in two.(ABSTRACT TRUNCATED AT 250 WORDS)     

Noninvasive determination of the valvar area in aortic valve disease by Doppler echocardiography and radionuclide angiography

To assess the severity of outlfow obstruction in patients with aortic valve disease, the aortic valvar area was noninvasively determined in 22 patients with isolated aortic stenosis or combined stenosis and regurgitation. The ejection time (ET), maximal velocity (Vmax), and systolic velocity integral (SVI) of the aortic flow was obtained by continuous wave Doppler ultrasound. Left ventricular stroke volume (SV) was determined by radionuclide angiography, using a counts-based nongeometric technique with individual attenuation correction. Aortic valve area (AVA) was calculated using a modified Gorlin formula; AVA = SV/(71.2 X ET X Vmax), and also by dividing the stroke volume by the systolic velocity integral; AVA = SV/SVI. The two noninvasive determinations correlated closely with the valve areas obtained by invasive measurements; r = 0.95, SEE = +/- 0.13 cm2 by the modified Gorlin formula, and r = 0.94, SEE = +/- 0.14 cm2 by the integration method. The two noninvasive calculations showed almost uniform results; r = 0.98, SEE = +/- 0.09 cm2. In conclusion, aortic valve area can be determined with reasonable accuracy by combining Doppler echocardiography and radionuclide angiography. This noninvasive approach may reduce the need for invasive measurements in patients with suspected aortic valve disease. In addition, radionuclide angiography provides important information about left ventricular function.     

Left ventricular remodeling after aortic valve replacement]

The aim of the study was the assessment of left ventricular (LV) systolic function and left ventricular mass following aortic valve replacement (AVR) due to aortic valve stenosis as well as the influence of regression of LV hypertrophy in patients with normal and impaired LV systolic function prior to surgery. 74 patients with severe aortic valve stenosis (29 female, 45 male, mean age 66 +/- 18 years) were divided into 2 groups according to LV ejection fraction (EF): Group 1 with EF > 50% (n = 40); Group 2 with EF < or = 50% (n = 34). Furthermore, patients were differentiated into a group A without (n = 53) and a group B with aortic regurgitation (< or = II degrees, n = 21). All patients were examined by transthoracic echocardiography before and 1 month after surgery. There was a significant decrease of LV enddiastolic and endsystolic volume indices following AVR in group 2 and group B. Patients with preoperatively lower EF (group 2) showed an increase in LV ejection fraction from 39 +/- 10% before AVR to 47 +/- 11% after AVR (p < 0.001), whereas patients with preoperative normal EF (group 1) showed a significant decrease in EF (from 62 +/- 8% to 57 +/- 10%, p < 0.05). Also patients with combined aortic valve disease before AVR had an increase of EF after surgery (from 45 +/- 14% to 56 +/- 14%, p < 0.03). There were significant decreases of interventricular septum thickness and LV posterior wall thickness in group 1 and group A, whereas a significant decrease of LV enddiastolic diameter index was noted only in group B. Improvement of the NYHA functional class could be demonstrated in group 2 from 2.8 +/- 0.7 before to 2.2 +/- 0.6 after AVR, as well as in group B from 2.9 +/- 0.7 before to 1.9 +/- 0.7 after surgery. In conclusion, patients with impaired LV function or combined aortic valve disease showed a significant improvement of left ventricular systolic function after AVR, while patients with normal LV function presented a slight decrease of EF. There was a significant regression of left ventricular muscle mass in all groups independent of the left ventricular functional status.     

Factors determining early improvement in mitral regurgitation after aortic valve replacement for aortic valve stenosis: a transthoracic and transesophageal prospective study

BACKGROUND: Mitral regurgitation (MR) is frequently associated with aortic stenosis. Previous reports have shown that coexisting mitral insufficiency can potentially regress after aortic valve replacement. HYPOTHESIS: This study sought to assess the frequency and severity of MR before and after aortic valve replacement for aortic stenosis and to define the determinants of its postoperative evolution. METHODS: For this purpose, 30 adult patients referred for aortic valve surgery underwent pre- and postoperative transthoracic and transesophageal echocardiography and color Doppler examination. RESULTS: Mean preoperative left ventricular ejection fraction was 57 +/- 16% and remained unchanged postoperatively. Preoperative MR was usually mild to moderate and correlated with aortic stenosis severity and left ventricular systolic dysfunction. The color Doppler mitral regurgitant jet area significantly decreased during the postoperative period (p = 0.016) as left ventricular loading conditions returned to normal, suggesting an early decrease of the functional part of MR. On the other hand, the mitral regurgitant jet width at the origin remained unchanged. Statistical analysis found pulmonary artery pressure (p = 0.02) an d indexed left ventricular mass (p = 0.009) to be preoperative predictive factors of postoperative MR improvement. Predictive factors of postoperative MR severity were left atrial diameter (p = 0.02), pulmonary artery pressure (p = 0.003), and the presence of mitral calcifications (p = 0.004). CONCLUSION: In our cohort of patients with normal left venticular ejection fraction, the majority of moderate MR, associated with severe aortic stenosis, regresses early after aortic valve replacement. Mitral calcifications and/or left atrial dilation seem to be predictive factors of fixed MR.     

Noninvasive estimation of the left ventricular pressure waveform throughout ejection in young patients with aortic stenosis

Validation of a totally noninvasive method for estimating instantaneous left ventricular pressure and constructing a pressure waveform throughout ejection in patients with aortic stenosis is reported. In 20 patients (aged 8.75 +/- 10 years) with congenital aortic stenosis (measured peak left ventricular pressure 120 to 260 mm Hg; transvalvular gradient 18 to 165 mm Hg), transaortic valve continuous wave Doppler ultrasound, indirect carotid pulse tracing, peripheral blood pressure and measured left ventricular pressure were recorded simultaneously at cardiac catheterization. Data were entered into a microcomputer using a digitizing tablet and the instantaneous Doppler gradient was calculated and added to instantaneous aortic pressure, derived from the time-corrected and calibrated carotid pulse tracing, to estimate instantaneous left ventricular pressure. Estimated left ventricular pressure waveforms reproduced measured left ventricular pressure closely. The mean error at peak left ventricular pressure was 0.2 +/- 4.8 mm Hg (r = 0.98, p = 0.001). The average error throughout ejection was 0.9 +/- 5.1 mm Hg. The error of estimated pressure was not related to age or the severity of aortic stenosis. The Doppler peak instantaneous gradient was observed to correlate closely (r = 0.97, p = 0.001) with peak to peak gradient. With this technique, the left ventricular pressure waveform throughout ejection can be accurately estimated noninvasively in patients with aortic stenosis. This methodology enables determination of mean, total and instantaneous systolic left ventricular pressure.     

Peak left ventricular pressure during percutaneous aortic balloon valvuloplasty: clinical and echocardiographic correlations

Peak left ventricular pressure during balloon inflation was measured in 20 patients who underwent balloon valvuloplasty for severe aortic stenosis to define the determinants of ventricular pressure development in response to increased loading conditions. The peak left ventricular pressure ranged from 150 +/- 5 to 386 +/- 22 mm Hg (mean +/- SD), was reproducible in each patient with each balloon inflation (mean coefficient of variation 7.8%) and correlated with concurrent echocardiographic measurements of ejection fraction (r = 0.89, p = 0.0001) and mass/volume ratio in systole (r = 0.91, p = 0.0001) or diastole (r = 0.88, p = 0.0001). Thirteen patients with class II or more severe congestive heart failure had lower values for peak left ventricular pressure than did those without failure (225 +/- 46 versus 305 +/- 45 mm Hg, p = 0.002), whereas no difference in rest left ventricular systolic pressure was seen between the two groups. The measurement of peak left ventricular pressure was inversely related to rest mean circumferential end-systolic wall stress (r = 0.52, p = 0.046). Thus, peak left ventricular systolic pressure measured during aortic valvuloplasty in humans correlates closely with traditional measures of left ventricular function. This measurement, which previously has been obtained only in experimental animal studies, is a simple and reproducible hemodynamic index that may provide new insights in studies of ventricular function and congestive heart failure in aortic stenosis.     

Serial assessment of mitral regurgitation by pulsed Doppler echocardiography in patients undergoing balloon aortic valvuloplasty

Mitral regurgitation was serially assessed by pulsed Doppler echocardiography in 144 patients undergoing balloon aortic valvuloplasty for symptomatic aortic stenosis. Regurgitant scores of 0, 1, 2 and 3 were assigned to pulsed Doppler patterns corresponding to no, mild, moderate and severe mitral regurgitation, respectively. Before balloon aortic valvuloplasty, mitral regurgitant score correlated significantly (p less than 0.005) but weakly with aortic valve area (r = -0.24), left ventricular ejection fraction (r = -0.34) and left ventricular systolic pressure (r = 0.23). There was no significant correlation between mitral regurgitation and either mean catheterization or mean Doppler aortic valve gradient. Balloon aortic valvuloplasty produced significant decreases in both catheterization and Doppler mean transvalvular aortic valve gradients (56 +/- 19 to 31 +/- 12 and 60 +/- 19 to 48 +/- 16 mm Hg, respectively; both p less than 0.0001) and a significant increase (p less than 0.0001) in aortic valve area assessed by catheterization (0.6 +/- 0.2 to 0.9 +/- 0.3 cm2). Left ventricular ejection fraction did not change, but cardiac output increased (p less than 0.001) and pulmonary capillary wedge pressure decreased (p less than 0.0001). Pulsed Doppler findings of mitral regurgitation were present in 102 of the 144 patients. Eighty-eight patients had a score compatible with mild or more severe degrees of mitral regurgitation, and 49 had a score indicative of moderate or severe valvular insufficiency. In the entire group of 144 patients, mitral regurgitant score decreased significantly from 1.1 +/- 1.0 to 1.0 +/- 1.0 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular arrhythmias in aortic valve disease before and after aortic valve replacement.

In order to evaluate the effect of aortic valve replacement on the incidence of ventricular arrhythmias in patients with aortic valve disease, 24-hour ambulatory electrocardiographic recordings were obtained before surgery in 96 patients without coronary artery disease (aortic stenosis n = 50, combined aortic stenosis and regurgitation n = 19 and aortic regurgitation n = 27). Following aortic valve replacement, repeat recordings were obtained after 13 +/- 4 days and 18 +/- 7 months. Ventricular arrhythmias were in all cases classified according to Lown and were compared with clinical, echocardiographic and hemodynamic data. Preoperatively, ventricular premature beats were observed in 85 patients (89%) and were frequent (greater than 30 ventricular premature beats/hour) in 20 (21%). Multiformity was found in 27 (28%), couplets in 18 (19%) and ventricular tachycardia in 11 (11.5%). The occurrence of ventricular arrhythmias was not related to the type or severity of valve lesions. Patients with severe ventricular arrhythmias (Lown class 3 or 4: 37%) had a greater thickness of their interventricular septum 13.9 +/- 2.5 mm, vs 11.7 +/- 2.6 (p less than 0.05); a higher LV mass 176 +/- 34 g/m2, vs 134 +/- 39 (p less than 0.05) and a lower left ventricular ejection fraction 47 +/- 12%, vs 57 +/- 11, (p less than 0.01). Two weeks postoperatively, the incidence and severity of ventricular arrhythmias had increased: ventricular premature beats were noted in 92% and were severe in 50%. No correlation was found between ventricular arrhythmias and preoperative or operative data. Eighteen months after surgery, ventricular premature beats were still observed in 81% of patients but remained frequent in 7% only. Severe ventricular arrhythmias were noted in 27%. Patients with severe ventricular arrhythmias had at the time of this late recording a lower radionuclide left ventricular ejection fraction 57 +/- 14%, vs 73 +/- 9 (p less than 0.02) and a higher enddiastolic diameter 63 +/- 15 mm, vs 48 +/- 7, (p less than 0.01). This study indicates that ventricular arrhythmias are common in patients with aortic valve disease. The severity of arrhythmias is influenced by the LV consequences of valve lesion both pre- and late postoperatively. The frequency and severity of ventricular arrhythmias increase early after surgery and do not correlate with preoperative or operative data.     

Alterations in left ventricular geometry, wall stress, and ejection performance after correction of congenital aortic stenosis

Children with congenital aortic stenosis have "excessive" left ventricular hypertrophy with reduced resting systolic wall stress that allows for supernormal ejection performance. If aortic stenosis is uncorrected, this pattern persists until adulthood. The effect of removing the aortic pressure gradient on left ventricular hypertrophy and wall stress in children with congenital aortic stenosis is unknown. To test the hypothesis that removal of the stimulus for hypertrophy by aortic valve replacement or repair would normalize left ventricular mass and wall stress, we measured left ventricular ejection performance, wall stress, and contractile function in seven patients at cardiac catheterization before and 36 +/- 7 months after surgical correction of congenital aortic stenosis. After aortic valve replacement or repair, the aortic valve gradient fell from 87 +/- 12 to 7 +/- 4 mm Hg, and peak left ventricular pressure fell from 187 +/- 14 to 128 +/- 8 mm Hg. Left ventricular ejection fraction decreased postoperatively from 86 +/- 4% to 74 +/- 4% (p less than 0.001), whereas velocity of circumferential fiber shortening decreased from 2.15 +/- 0.15 to 1.6 +/- 0.11 (p less than 0.002). Left ventricular mass remained unchanged preoperatively (121 +/- 14 g/m2) and postoperatively (121 +/- 16 g/m2), but wall thickness (h) decreased in relation to ventricular radius (r) (h/r = 0.55 +/- 0.05 preoperatively, 0.36 +/- 0.02 postoperatively; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

The molecular phenotype of human cardiac myosin associated with hypertrophic obstructive cardiomyopathy

AIM: The aim of the study was to compare the functional and structural properties of the motor protein, myosin, and isolated myocyte contractility in heart muscle excised from hypertrophic cardiomyopathy patients by surgical myectomy with explanted failing heart and non-failing donor heart muscle. METHODS: Myosin was isolated and studied using an in vitro motility assay. The distribution of myosin light chain-1 isoforms was measured by two-dimensional electrophoresis. Myosin light chain-2 phosphorylation was measured by sodium dodecyl sulphate-polyacrylamide gel electrophoresis using Pro-Q Diamond phosphoprotein stain. RESULTS: The fraction of actin filaments moving when powered by myectomy myosin was 21% less than with donor myosin (P = 0.006), whereas the sliding speed was not different (0.310 +/- 0.034 for myectomy myosin vs. 0.305 +/- 0.019 microm/s for donor myosin in six paired experiments). Failing heart myosin showed 18% reduced motility. One myectomy myosin sample produced a consistently higher sliding speed than donor heart myosin and was identified with a disease-causing heavy chain mutation (V606M). In myectomy myosin, the level of atrial light chain-1 relative to ventricular light chain-1 was 20 +/- 5% compared with 11 +/- 5% in donor heart myosin and the level of myosin light chain-2 phosphorylation was decreased by 30-45%. Isolated cardiomyocytes showed reduced contraction amplitude (1.61 +/- 0.25 vs. 3.58 +/- 0.40%) and reduced relaxation rates compared with donor myocytes (TT(50%) = 0.32 +/- 0.09 vs. 0.17 +/- 0.02 s). CONCLUSION: Contractility in myectomy samples resembles the hypocontractile phenotype found in end-stage failing heart muscle irrespective of the primary stimulus, and this phenotype is not a direct effect of the hypertrophy-inducing mutation. The presence of a myosin heavy chain mutation causing hypertrophic cardiomyopathy can be predicted from a simple functional assay.     

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.     

Coronary atherosclerosis is associated with left ventricular dysfunction and dilatation in aortic stenosis

Patients with aortic stenosis develop widely variable patterns of left ventricular hypertrophy and dysfunction. We postulated that coronary atherosclerosis (CAD) may be associated with impaired left ventricular function and chamber dilatation in patients with aortic stenosis. Left ventricular mass and volumes were quantified from two-dimensional echocardiography and correlated with coronary angiography in 78 patients with severe aortic stenosis and no previous myocardial infarction or regional wall motion abnormalities. Eighteen patients (group 1) had smooth coronary arteries, 25 patients had irregular coronary arteries with 50% or less stenosis (group 2), and 35 patients had obstructive CAD (group 3). Even though the calculated valve area was similar in all three study groups, group 1 patients had higher values for ejection fraction (65 +/- 9%, 51 +/- 17%, and 48 +/- 13%; p = 0.0002), systolic mass-to-volume ratio (9.2 +/- 3.9, 5.6 +/- 2.8, and 5.2 +/- 2.2; p = 0.0001), and cardiac index (2.9 +/- 0.7, 2.5 +/- 0.7, and 2.3 +/- 0.6 l/min.min2; p = 0.015) than patients in groups 2 and 3, respectively (mean +/- SD). Mean circumferential wall stress was inversely related to severity of CAD. Multivariate analysis showed that CAD is an independent predictor of ejection fraction and mass-to-volume ratio in this group of patients. Thus, in an elderly population with severe aortic stenosis, patients with both obstructive and nonobstructive CAD have an increased incidence of left ventricular enlargement and systolic dysfunction.     

Increased expression and regional differences of atrial myosin light chain 1 in human ventricles with old myocardial infarction. Analyses using two monoclonal antibodies.

BACKGROUND. This study was designed to examine the expression of atrial/fetal-type myosin light chain 1 (ALC1) in human ventricles with old myocardial infarction and in control hearts. METHODS AND RESULTS. The expression of immunoreactive (ir) ALC1 was examined in the subendocardial and subepicardial myocardium of the infarcted and the noninfarcted regions in the left ventricles with old myocardial infarction (n = 12) and of the control left ventricles (n = 8). For the analysis, we prepared two monoclonal antibodies, KA1 and KB1, that were specific for only ALC1 and for both ALC1 and ventricular myosin light chain 1 (VLC1), respectively. The ir-ALC1 expression ratio [ALC1/(ALC1 + VLC1), %] of the subendocardial myocardium, determined densitometrically by Western blotting with KB1, was significantly higher in the infarcted region (11.4 +/- 7.3%) than in the noninfarcted region (4.7 +/- 2.3%, p < 0.001) and the control ventricle (1.0 +/- 1.5%, p < 0.0001). In the infarcted region, the subendocardial myocardium contained a significantly greater percentage of ir-ALC1 than the subepicardial myocardium (5.8 +/- 6.7%, p < 0.005). The ir-ALC1 expression ratio had a significant negative correlation with the value of tissue protein concentration (milligrams protein per gram wet weight). The immunohistochemical study with KA1 revealed that the surviving myocytes included in the infarcted region, especially in the ventricular aneurysm, expressed ir-ALC1 strongly in comparison with those in the noninfarcted or the control ventricles. CONCLUSIONS. These results demonstrate increased expression of ALC1 and the regional differences in the failing left ventricles with old myocardial infarction. We conclude that the reexpression of ALC1 in infarcted ventricles occurs as one of the regional responses to increased load and may be a useful biochemical marker for the appearance of fetal-type myocytes.     

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.     

Diastolic function in patients with aortic stenosis: influence of left ventricular load reduction

Pressure overload hypertrophy of the left ventricle due to aortic stenosis is associated with abnormalities of left ventricular isovolumic relaxation and early diastolic filling. The relative contribution of the hemodynamic load on the left ventricle to the impairment of diastolic function observed in this disorder remains poorly understood. To study this relation, the vasodilator nitroprusside was administered to eight patients with aortic stenosis and normal systolic function. The effect of a short-term reduction in left ventricular preload and afterload on left ventricular isovolumic relaxation and early diastolic filling was assessed by analysis of simultaneous micromanometer left ventricular pressure and radionuclide angiographic volume measurements. At baseline, left ventricular systolic and end-diastolic pressures were markedly elevated, and associated with prolongation of the time constant of left ventricular relaxation and depression of the left ventricular peak filling rate. Infusion of nitroprusside resulted in reduction of left ventricular systolic (204 +/- 31 to 176 +/- 31 mm Hg, p less than 0.05) and end-diastolic (31 +/- 8 to 18 +/- 6 mm Hg, p less than 0.05) pressures, with no associated improvement in time constant of left ventricular pressure decay (T) (68 +/- 25 to 80 +/- 37 ms, p = NS), T 1/2 (34 +/- 8 to 34 +/- 14 ms, p = NS), left ventricular peak filling rate (2.3 +/- 0.5 to 2.3 +/- 0.8 end-diastolic volume/s, p = NS) or time to left ventricular peak filling rate (150 +/- 50 to 144 +/- 37 ms, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Determination of the stenotic aortic valve area in adults using Doppler echocardiography

The severity of aortic stenosis was evaluated by Doppler echocardiography in 48 adults (mean age 67 years) undergoing cardiac catheterization. Maximal Doppler systolic gradient correlated with peak to peak pressure gradient (r = 0.79, y = 0.63x + 25.2 mm Hg) and mean Doppler gradient correlated with mean pressure gradient (r = 0.77, y = 0.59x + 10.0 mm Hg) by manometry. The transvalvular pressure gradient is flow dependent, however, and associated left ventricular dysfunction was common in our patients (33%). Thus, of the 32 patients with an aortic valve area less than or equal to 1.0 cm2 at catheterization, 6 (19%) had a peak Doppler gradient less than 50 mm Hg. To take into account the influence of volume flow, aortic valve area was calculated as stroke volume, measured simultaneously by thermodilution, divided by the Doppler systolic velocity integral in the aortic jet. Aortic valve areas calculated by this method were compared with results at catheterization in the total group (r = 0.71). Significant aortic insufficiency was present in 71% of the population. In the subgroup without significant coexisting aortic insufficiency, closer agreement of valve area with catheterization was noted (n = 14, r = 0.91, y = 0.83x + 0.24 cm2). Transaortic stroke volume can be determined noninvasively by Doppler echocardiographic measures in the left ventricular outflow tract, just proximal to the stenotic valve. Aortic valve area can then be calculated as left ventricular outflow tract cross-sectional area times the systolic velocity integral of outflow tract flow, divided by the systolic velocity integral in the aortic jet.(ABSTRACT TRUNCATED AT 250 WORDS)     

Quantification of aortic valve area and left ventricular muscle mass in healthy subjects and patients with symptomatic aortic valve stenosis by MRI

MRI allows visualization and planimetry of the aortic valve orifice and accurate determination of left ventricular muscle mass, which are important parameters in aortic stenosis. In contrast to invasive methods, MRI planimetry of the aortic valve area (AVA) is flow independent. AVA is usually indexed to body surface area. Left ventricular muscle mass is dependent on weight and height in healthy individuals.We studied AVA, left ventricular muscle mass (LMM) and ejection fraction (EF) in 100 healthy individuals and in patients with symptomatic aortic valve stenosis (AS). All were examined by MRI (1.5 Tesla Siemens Sonate) and the AVA was visualized in segmented 2D flash sequences and planimetry of the performed AVA was manually.The aortic valve area in healthy individuals was 3.9+/-0.7 cm(2), and the LMM was 99+/-27 g. In a correlation analysis, the strongest correlation of AVA was to height (r=0.75, p<0.001) and for LMM to weight (r=0.64, p<0.001). In a multiple regression analysis, the expected AVA for healthy subjects can be predicted using body height: AVA=-2.64+0.04 x(height in cm) -0.47 x w (w=0 for man, w=1 for female).In patients with aortic valve stenosis, AVA was 1.0+/-0.35 cm(2), in correlation to cath lab r=0.72, and LMM was 172+/-56 g.We compared the AS patients results with the data of the healthy subjects, where the reduction of the AVA was 28+/-10% of the expected normal value, while LMM was 42% higher in patients with AS. There was no correlation to height, weight or BSA in patients with AS.With cardiac MRI, planimetry of AVA for normal subjects and patients with AS offered a simple, fast and non-invasive method to quantify AVA. In addition LMM and EF could be determined. The strong correlation between height and AVA documented in normal subjects offered the opportunity to integrate this relation between expected valve area and definitive orifice in determining the disease of the aortic valve for the individual patient. With diagnostic MRI in patients with AS, invasive measurements of the systolic transvalvular gradient does not seem to be necessary.     

Aortic valve repair versus replacement in bicuspid aortic valve disease

BACKGROUND AND AIM OF THE STUDY: The study aim was to compare the results of aortic valve repair and replacement with biological valves in adult patients with aortic insufficiency (AI) caused by congenital bicuspid aortic valve (BAV) METHODS: Forty-four patients who had aortic valve repair were matched for age and left ventricular function to 44 patients who had aortic valve replacement (AVR) with biological valves. Patients were followed annually using echocardiography. The mean follow up was 2.6 +/- 2.1 years for the repair group, and 3.5 +/- 2.1 years for the replacement group. Follow up was complete. RESULTS: There was no operative or late death in either group. Early postoperative echocardiography showed trace or no AI in 35 patients and mild AI in nine who had repair, and trace or no AI in 38 patients and mild AI in five who had AVR. The mean peak systolic gradient was 16.2 +/- 7.6 mmHg for repair and 13.2 +/- 7.2 mmHg for AVR. Four patients who had valve repair and two who had AVR, needed repeat aortic valve surgery because of progressive AI or endocarditis. Freedom from reoperation at five years was 91 +/- 5% for repair and 94 +/- 6% for replacement (p = 0.2), while freedom from moderate or severe AI at five years was 79 +/- 8% for repair and 94 +/- 6% for replacement (p = 0.024). The peak systolic gradient at follow up was 11.7 +/- 6.8 mmHg after repair and 13.3 +/- 9.6 mmHg after AVR (p = 0.4). There were no thromboembolic complications in either group. CONCLUSION: Repair of BAV is feasible in certain patients with AI, but the hemodynamics and clinical outcomes do not appear to be superior to AVR with biological valves during the first five years of follow up.     

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)     

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)