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This analysis summarizes the first report of the Society of Thoracic Surgeons National Congenital Heart Surgery Database Committee in association with Summit Medical Systems. Twenty-four centers joined the program at various dates of entry resulting in 18,894 enrolled patient records. This report compiled the relevant clinical features of 18 congenital heart categories over a 4-year period (1994-1997), which included 8,149 patient records. The data analyses are largely descriptive in character. Missing data points were described and not omitted in the analysis. Statistical analysis was not performed due to missing data points in some categories. Certain trends, however, could be identified and are discussed. The first Society of Thoracic Surgeons National Congenital Heart Surgery Database Report has succeeded in establishing a finite record that can be improved to establish universal national and international utility, risk stratification, and scholarly outcome analyses.

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We retrospectively reviewed the 26-year National Institutes of Health experience with operative treatment of obstructive hypertrophic cardiomyopathy in pediatric patients. Operative criteria were either severe obstructive symptoms (New York Heart Association functional class III or IV) or sudden death. Seventeen patients underwent 19 open procedures, of which the present study is comprised. Complete follow-up was available 10.1 +/- 1.4 years (mean +/- standard error; range, 0.8 to 26.2 years) after operation. The mean ages at diagnosis and operation were 11.9 +/- 1.3 years (range, 1 to 17 years) and 14.8 +/- 0.7 years (range, 9 to 17 years), respectively. The preoperative intraventricular septum mean dimension was 23.2 +/- 1.3 mm (range, 11 to 36 mm). The left ventricular outflow tract gradient was 74 +/- 9 mm Hg (range, 20 to 175 mm Hg) at rest and 94 +/- 7 mm Hg (range, 55 to 175 mm Hg) with provocation. Fifteen patients (88%) underwent left ventricular myotomy and myectomy, and 2 underwent mitral valve replacement. Two patients who initially received left ventricular myotomy and myectomy later underwent mitral valve replacement. There were one perioperative death (6%) and five late sudden deaths (31%) at 3.8, 8.7, 9.6, 14.1, and 21 years postoperatively. Kaplan-Meier survival was 86% +/- 8% at 5 years and 77% +/- 12% at 10 years. After operation, the left ventricular outflow tract gradient decreased almost 80% to 21 +/- 15 mm Hg (p = 0.0001). In 8 patients, the left ventricular outflow tract gradient completely resolved.(ABSTRACT TRUNCATED AT 250 WORDS)

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The mechanism by which obstruction to right ventricular (RV) outflow occurs in patients with hypertrophic cardiomyopathy (HC) is not well understood. To clarify this issue, 5 severely symptomatic patients (aged 18 to 55 years, mean 30) with HC and marked subpulmonic obstruction (basal peak systolic pressure gradients 60 to 118 mm Hg) were studied. Four patients also had obstruction to left ventricular outflow (maximal basal or provocable pressure gradient 12 to 110 mm Hg). The RV outflow obstruction in each patient resulted from greatly hypertrophied musculature comprised of crista supraventricularis, moderator band or trabeculae. Operative resection of portions of this muscle resulted in abolition or substantial reduction of the RV outflow gradient (to 0 to 11 mm Hg) in the 3 patients with both pre- and postoperative hemodynamic studies. The left ventricular wall and ventricular septum also were massively thickened (32 to 40 mm) in each patient. These findings support the view that marked RV outflow tract obstruction in patients with HC is due to greatly hypertrophied RV muscle, and that operative resection will relieve the outflow gradients and normalize RV systolic pressure. The muscular RV hypertrophy causing obstruction appeared to constitute a primary and excessive hypertrophic process involving both ventricles.

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The purpose of this study was to determine if the combination of a mechanical and bioprosthetic valve in the aortic and mitral positions influences late morbidity and mortality when compared with patients who had dual mechanical or dual bioprosthetic valves inserted. We reviewed the course of 89 hospital survivors of combined aortic and mitral valve replacement. The mean postoperative follow-up interval was 6.6 years, with a total follow-up of 583 years (98% complete). At 12 months after operation, mean functional class decreased from 3.1 to 1.7 (p < 0.05) and mean cardiac index increased from 2.1 to 2.5 L.min-1.m-2 (p < 0.05). Actuarial survival for the 89 patients (exclusive of < 30-day or in-hospital mortality, 14%) was 70%, 51%, and 33% at 5, 10, and 15 years. Freedom from reoperation was 93%, 78%, and 68%, and freedom from combined thromboembolism and anticoagulant-related hemorrhage was 82%, 60%, and 50%. These results show that there was no difference in overall survival in patients with dual mechanical valves, dual bioprosthetic valves, or a combination of both types at 15 years. There was, however, a lower reoperation rate in the group with dual mechanical valves as compared with the group with dual bioprosthetic valves (p < 0.05 at 10 years) or with a combination of valves (p < 0.05 at 15 years). The higher the number of mechanical valves the higher the combined risk of thromboembolism and anticoagulant-related hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)

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The purpose of this study was to determine what influence various combinations of mechanical and bioprosthetic valves in the aortic, mitral, and tricuspid positions had on late morbidity and mortality of 40 hospital survivors of triple-valve replacement. At operation the patients ranged in age from 27 to 69 years; 73% were women. The mean postoperative follow-up interval was 8.3 years, with a total follow-up of 331 years (100% complete). At 12 months after operation, functional class decreased from 3.3 to 1.6 (p < 0.05), cardiac index increased from 2.0 to 2.6 L.min-1 x m-2 (p < 0.05), and pulmonary artery pressures decreased from 59/27 to 40/17 mm Hg (p < 0.05). There were no differences in preoperative variables between groups. Actuarial survival for the 40 patients (exclusive of 30-day or in-hospital mortality, which was 31%) was 78% and 74% at 5 and 10 years. At the same milestones, freedom from reoperation was 96% and 54%, freedom from combined thromboembolism and anticoagulant-related hemorrhage was 68% and 56%, and freedom from all late valve-related morbidity and mortality was 64% and 25%. Comparison of the patients with two or more mechanical prostheses with the patients having two or more bioprostheses indicated no significant differences in actuarial freedom from late death, thromboembolic events, or anticoagulant-related hemorrhage. However the actuarial freedom from reoperation in the groups with two or more mechanical valves was lower than that of the groups with two or more bioprosthetic valves (0/10 versus 13/30; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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BACKGROUND: Several operations (most commonly ventricular septal myotomy-myectomy and also mitral valve replacement) have been performed to relieve symptoms and obstruction to left ventricular outflow in patients with hypertrophic cardiomyopathy (HCM). METHODS AND RESULTS: In an effort to establish an alternative to mitral valve replacement, combined septal myotomy-myectomy and suture plication of the anterior mitral valve leaflet was performed in a subgroup of 36 severely symptomatic patients with obstructive HCM. These patients were selected primarily because the mitral leaflets were judged morphologically at the time of operation to be of sufficient size relative to that of the outflow tract to represent a risk for residual systolic septal contact and outflow obstruction. The effects of operation were assessed in 34 patients; of the 33 with preoperative symptoms, 28 (85%) reported substantial functional improvement after surgery over an average follow-up of 2.2 years. Of 29 patients with complete hemodynamic data, basal outflow gradient was obliterated or reduced substantially by surgery (to < or = 35 mm Hg) in 26 patients (90%) and for the group from 81 +/- 42 to 16 +/- 24 mm Hg (p < 0.001); provocable gradient with isoproterenol infusion also decreased considerably (from 109 +/- 50 to 47 +/- 25 mm Hg; p < 0.001). Echocardiographic studies showed that plication limited the systolic anterior motion of anterior mitral leaflet. There was no hemodynamic evidence of mitral stenosis, and in only one patient did mitral regurgitation increase after surgery. CONCLUSIONS: Mitral valve plication combined with myotomy-myectomy in obstructive HCM 1) can be performed safely and does not adversely alter mitral valve function, 2) relieves symptoms and outflow obstruction under basal and provocable conditions, and 3) may represent an alternative to mitral valve replacement in selected patients with elongated and enlarged mitral leaflets.

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To determine predictors of exercise benefit in patients with hypertrophic cardiomyopathy after operative relief of left ventricular (LV) outflow tract obstruction, 30 patients underwent catheterization and exercise testing before and 6 months after operation, and hemodynamic measurements were obtained. The increase in maximal oxygen consumption (VO2max) during treadmill exercise testing was chosen as an index of exercise benefit. Univariate analysis showed a significant positive correlation of operative change in VO2max with preoperative LV end-diastolic and pulmonary arterial wedge pressures, operative change in exercise duration, and operative reductions in LV end-diastolic and pulmonary arterial wedge pressures and resting LV outflow tract gradient, and a significant negative correlation with preoperative VO2max and percent predicted VO2max. Multivariate analysis by stepwise linear regression of only significant univariate variables selected only preoperative percent predicted VO2max, and operative reduction in LV end-diastolic pressure and resting LV outflow tract gradient as significant predictors of postoperative change in VO2max. Stepwise regression analysis, applied only to preoperative exercise and catheterization hemodynamic variables, selected only preoperative percent predicted VO2max and preoperative LV end-diastolic pressure as predictors of improvement in exercise capacity. Thus, patients with obstructive hypertrophic cardiomyopathy, after failing medical therapy, are most likely to demonstrate improvement in exercise capacity if preoperative exercise testing demonstrates limited exercise capacity and if surgery achieves reduction in elevated resting LV outflow tract gradients and LV filling pressures.

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BACKGROUND: To assess the impact of surgical relief of left ventricular outflow obstruction on myocardial perfusion abnormalities in patients with obstructive hypertrophic cardiomyopathy, 20 symptomatic patients who underwent a septal myectomy or mitral valve replacement were studied with assessment of myocardial perfusion during exercise by 201Tl emission computed tomography before and 6 months after surgery. METHODS AND RESULTS: Before surgery, 15 patients had myocardial perfusion defects during exercise that completely normalized at rest, one patient had both reversible and fixed perfusion defects, two patients had fixed defects only, and two patients had normal exercise and rest thallium scans. After surgical relief of left ventricular outflow obstruction (basal gradient reduced from 62 +/- 40 to 7 +/- 12 mm Hg, p less than 0.001; peak provokable gradient reduced from 131 +/- 27 to 49 +/- 36 mm Hg, p less than 0.001), repeat exercise thallium studies showed complete normalization of perfusion defects in 11 patients, including the two patients with fixed defects alone before surgery, and improvement in the magnitude and distribution of perfusion defects in five additional patients. This was associated with a significant reduction in the number of patients with reversible regional defects (five patients compared with 13 patients before surgery, p = 0.026) and of patients with endocardial hypoperfusion (four patients compared with 12 patients before surgery, p = 0.024). Furthermore, increased lung uptake of thallium was noted in five patients after surgery, compared with 12 patients before surgery (p = 0.055). Only two patients with reversible perfusion defects before surgery had unchanged postoperative studies. However, four patients acquired new fixed defects as a consequence of surgery, and two of these four had the greatest severity and distribution of left ventricular hypertrophy by echocardiography. These four patients experienced a substantially greater decrease in ejection fraction (-26 +/- 15%) after surgery than the remaining patients (-3 +/- 14%, p less than 0.01). CONCLUSIONS: Surgical relief of left ventricular outflow obstruction results in normalization or improvement of myocardial perfusion in the majority of patients with reversible and fixed perfusion defects by 201Tl scintigraphy. However, surgery may result in myocardial injury and scarring, with consequent decreased left ventricular ejection fraction in some patients.

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Certain clinical and morphologic findings are described in 11 patients with hypertrophic cardiomyopathy complicated by infective endocarditis that produced severe mitral or aortic valve regurgitation, or both, necessitating valve replacement. All 11 patients had changes in the operatively excised valve or valves characteristic of healed infective endocarditis. The infection involved only the mitral valve in seven patients, only the aortic valve in three patients and both valves in one patient. Study of the operatively excised mitral valves indicated that the healed vegetations were located most commonly on the left ventricular aspects of the anterior mitral leaflet, indicating that vegetation had formed at contact points of this leaflet with mural endocardium of the left ventricular outflow tract. In all 11 patients, the infective endocarditis either worsened preexisting valve regurgitation or initiated valve regurgitation and led to worsened signs and symptoms of cardiac dysfunction, necessitating valve replacement. Functional class improved in the nine patients who survived 7 to 101 months after valve replacement. Hypertrophic cardiomyopathy appears to be a factor predisposing to infective endocarditis. Patients with hypertrophic cardiomyopathy should receive prophylactic antibiotic therapy during procedures that predispose to infective endocarditis.

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Arterial wall perforation and chronic restenosis represent important factors limiting the clinical application of laser angioplasty. Discrimination of normal and atherosclerotic vessels by laser-excited fluorescence spectroscopy may offer a means of targeting plaque ablation, thereby reducing the frequency of restenosis and transmural perforation. In this study, with use of a 325 nm low power helium-cadmium laser, in vivo endogenous surface fluorescence was excited through a flexible 200 microns optical fiber within a 0.018 in. (0.046 cm) guide wire in contact with the intima of 268 vascular interrogation sites from 48 patients either during open heart surgery or during percutaneous catheterization procedures. Fluorescence spectra could be recorded in all patients in bloodless and blood-filled arteries. Endogenous surface fluorescence was analyzed measuring peak intensity, peak position and shape index of the spectra. Compared with normal wall, noncalcified and calcified coronary atheroma showed a 42% (p less than 0.001) and a 58% (p less than 0.001) decrease of peak intensity, and higher shape index (p less than 0.001 and p less than 0.01, respectively). In addition, peak position was shifted to longer wavelengths for noncalcified coronary atheroma (p less than 0.001). Compared with normal aorta sites, aortic plaques demonstrated a 46% decrease of peak intensity, longer peak position wavelengths (p less than 0.05) and a higher shape index (p less than 0.001). Using an atheroma detection algorithm, prospective analysis of aorta and coronary spectra showed a specificity of 100% for identifying normal sites and a sensitivity of 73% for recognizing atherosclerotic sites.(ABSTRACT TRUNCATED AT 250 WORDS)

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Five hundred twenty-five patients with hypertrophic cardiomyopathy underwent left ventricular myotomy and myectomy (LVMM) from 1960 to 1990. Four hundred ninety-six had nonregurgitant trileaflet aortic valves before LVMM. In 19 (4%) of these patients, aortic regurgitation developed after LVMM. Age of the 19 patients ranged from 10 to 58 years (mean age, 35 +/- 3 [+/- standard error of the mean]]. Seven were male and 12, female. Five patients underwent LVMM followed immediately by aortic valve replacement or valvuloplasty. Aortic regurgitation developed in 14 patients at a later date. The average New York Heart Association functional class improved from 3.2 +/- 0.1 to 1.3 +/- 0.1 (p less than 0.05, Student's t test) after operation. The average peak systolic left ventricular outflow tract gradient at rest and with provocation decreased from 65 +/- 8 to 14 +/- 5 mm Hg (p less than 0.05) and 108 +/- 9 to 45 +/- 7 mm Hg (p less than 0.05), respectively, 6 to 8 months after operation. Aortic regurgitation occurred in 7 of the 14 patients at 6 months or less after operation, and 3 required operative repair. In the other 7 patients, aortic regurgitation developed 3 years or more after LVMM, and 3 of them also required operative repair. All 12 patients in whom aortic regurgitation developed at operation or within 6 months postoperatively had either a very small aortic annulus (less than or equal to 21 mm, 5 patients), a low mitral-septal contact lesion (greater than or equal to 35 mm below the aortic annulus, 3 patients), or both (4 patients).(ABSTRACT TRUNCATED AT 250 WORDS)

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This study compares results of a second left ventricular myotomy and myectomy (M + M) with those of mitral valve replacement (MVR) as reoperative procedures for persistent left ventricular outflow obstruction after M + M in hypertrophic cardiomyopathy. Comparison of the second M + M group (n = 12) with the MVR group (n = 11) disclosed significant difference (p less than 0.05) in mean age at the initial operation (29 +/- 11 years versus 40 +/- 8 years), interval between operations (46 +/- 57 months versus 18 +/- 13 months), and age at reoperation (33 +/- 10 years versus 42 +/- 8 years); and insignificant differences in mean preoperative functional class, cardiac index, left ventricular outflow gradients at rest or with provocation, and hospital mortality at reoperation (2/12 versus 1/11). At 6 months after reoperation, comparison of results of a second M + M with MVR showed that mean functional class, cardiac index, and left ventricular outflow gradient at rest were similarly improved, but the outflow gradient with provocation was significantly higher in the second M + M group (57 +/- 44 mm Hg versus 14 +/- 9 mm Hg, p less than 0.05). Total follow-up was 108 patient-years (100% complete) with an average of 5.9 years per patient in the second M + M group and 3.4 years per patient in the MVR group. Actuarial survival, including hospital mortality, at 3 and 5 years was 83% and 76%, respectively, after the second M + M, which was similar to 92% and 77% after MVR.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cardiopulmonary bypass is associated with postoperative humoral and cellular immune changes. Postoperative decrease in T helper (CD4), T suppressor (CD8), and B lymphocyte counts; decrease or reversal of the CD4/CD8 ratio; and poor in vitro response to mitogens have also been observed. Similar changes in lymphocyte number and function have also been noted in patients receiving transfusions. To determine whether observed changes after cardiopulmonary bypass are related to the bypass itself or to associated blood transfusions, we conducted a study of lymphocyte subsets in transfused and nontransfused patients. A flow cytometric analysis of seven lymphocyte subpopulations was conducted in 18 patients undergoing bypass, eight of whom did not receive a transfusion. The transfused group comprised recipients of both homologous (n = 8) and autologous (n = 2) blood. Total lymphocytes and lymphocytes with markers for CD3 (pan-T cells), CD4, and CD8 decreased significantly postoperatively independent of transfusion. B lymphocytes decreased postoperatively in both the autologous transfusion and no transfusion groups. However, this trend was not seen in patients receiving homologous blood, and three of these patients had evidence of T cell activation, suggestive of an immune response to homologous transfusion. Bypass produces significant changes in selected lymphocyte subsets. Furthermore, simultaneous homologous blood transfusion may specifically elicit an immune response in some patients undergoing cardiopulmonary bypass.

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The clinical course and hemodynamic results in patients undergoing operation for obstructive hypertrophic cardiomyopathy with preoperative pulmonary arterial hypertension were unknown. The hypothesis tested in this retrospective study was that operative relief of left ventricular outflow tract obstruction resulted in a substantial reduction in pulmonary artery pressures and mitral regurgitation without necessitating mitral valve replacement. Patients were included if their preoperative pulmonary systolic pressure was greater than 35 mm Hg and if they were without concomitant cardiac disease, with the exception of mitral regurgitation. Since 1962, 49 patients who fit our criteria underwent left ventricular myotomy and myectomy with 98% follow-up. Mean follow-up was 7.9 +/- 0.7 (mean +/- standard error of the mean) years with a range of 0.8 to 18.4 years. Early hospital mortality rate was 12% (n = 6); two deaths from low cardiac output and four from arrhythmia. There were 43 (88%) hospital survivors and 18 late deaths. Actuarial survival rate after operation was 87% +/- 5% (n = 31) at 5 years and 55% +/- 8% (n = 9) at 10 years. Thirty-nine of 43 survivors (91%) returned 9 +/- 1 months postoperatively for follow-up evaluation including cardiac catheterization. The majority (83%) were in New York Heart Association functional class I or II postoperatively. Cardiac catheterizations indicated a fall in pulmonary arterial systolic pressure from 62 +/- 3 (range = 36 to 105) to 38 +/- 2 (range = 21 to 65) mm Hg (p = 0.0001) with no difference in right atrial pressure or cardiac output. Pulmonary arterial wedge mean pressure decreased from 24 +/- 1 to 16 +/- 5 mm Hg (p = 0.0002) and preoperative mitral regurgitation improved or was abolished in 85% of patients studied (n = 13). Rest and maximal provocable left ventricular outflow tract gradients decreased from 81 +/- 7 and 103 +/- 5 to 14 +/- 3 and 45 +/- 8 mm Hg, respectively (p = 0.0001). Comparison of the above-mentioned patients, operated on since 1982, with a preoperatively matched group who underwent mitral valve replacement in the same interval showed no statistically significant difference in mortality, morbidity, hemodynamic outcome, or functional outcome with a mean follow-up of 2 years. We conclude that a consistent, significant reduction (mean = 40%) in preoperative pulmonary arterial systolic pressure, clinical symptoms, and mitral regurgitation occurs with relief of outflow tract obstruction by left ventricular myotomy and myectomy and that pulmonary hypertension and mitral regurgitation are not indications for mitral valve replacement in these patients.

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Fifty-one patients, aged 1 to 18 years, having aortic valvotomy for congenital valvar aortic stenosis between 1956 and 1986 were followed up. The average age at operation was 11.5 years, with an operative mortality of 3.9%. The aortic valve gradient decreased from a mean preoperative value of 91 mm Hg to 27 mm Hg postoperatively. Current follow-up was 90% and averaged 16.8 years. Late cardiac mortality was 17.6%, with actuarial survival of 93.7% at 10 and 15 years, 81.8% at 20 and 25 years, and 70.9% at 28 years. Nineteen patients required reoperation (39%) at a mean of 17.7 years postoperatively, with a reoperation-free survival of 98% at 10 years. The reoperation rate accelerated in the following decade to 3.3% per year. Ten patients without reoperation were evaluated by continuous-wave Doppler echocardiography. The mean gradient was 21.6 mm Hg, and 90% had mild to moderate aortic insufficiency. This study confirms the efficacy of valvotomy in this age group and suggests that long-term survival and time to reoperation may be longer than previously reported.

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Left ventricular function often deteriorates after mitral valve replacement for mitral regurgitation. It has been postulated that disruption of the mitral valve apparatus at operation is a major mechanism of postoperative dysfunction. The hypothesis tested in this investigation was that chordal preservation results in more favorable left ventricular function. Sixty-nine patients with isolated mitral regurgitation who underwent mitral valve replacement were studied before and 6 months after operation by treadmill exercise testing, catheterization, echocardiography, and radionuclide angiography. Nine patients underwent mitral valve replacement with preservation of the entire mitral apparatus and five with preservation of the posterior leaflet and attached chordae. The remaining 55 had mitral valve replacement with complete excision of the native valve. Preoperatively, there were no differences among groups in age, gender, exercise capacity, cardiac index, rest or exercise ejection fraction, fractional shortening, or pulmonary artery pressures. There were four perioperative deaths (7%) and eight late deaths among the 55 patients with chordal resection but no early or late deaths of patients whose chordae were preserved (p = 0.05). In patients in whom the chordae were excised, exercise capacity, left ventricular systolic dimensions, and cardiac index did not improve after mitral valve replacement, and left ventricular function deteriorated, as evidenced by a reduction of both the resting and exercise ejection fractions (from 46% +/- 13% to 31% +/- 13%, p = 0.0001, and from 49% +/- 12% to 37% +/- 14%, p = 0.0007, respectively) and fractional shortening (from 34% +/- 10% to 26% +/- 14%, p = 0.0001). In contrast, exercise capacity improved after mitral valve replacement in patients in whom the entire apparatus was spared (by 4 +/- 3 minutes, p = 0.05), left ventricular systolic dimensions decreased (from 44 +/- 8 to 36 +/- 9 mm, p = 0.03), and left ventricular function was maintained or improved, as evidenced by preservation of the resting ejection fraction (preoperative, 50% +/- 14%; postoperative, 54% +/- 11%; p = no significant difference), exercise ejection fraction (46% +/- 16% versus 52% +/- 9%, p = no significant difference), fractional shortening (from 31% +/- 9% to 28% +/- 9%, p = no significant difference), and an increase in the cardiac index (from 2.0 +/- 0.3 to 2.7 +/- 0.5 L/min/m2, p = 0.05). No statistically significant differences between posterior chordal resection only and preservation of the entire apparatus were found.(ABSTRACT TRUNCATED AT 250 WORDS)

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Little information is available regarding coronary artery morphology after endarterectomy. In this report, we describe coronary artery morphology seen at necropsy 10 years after coronary artery endarterectomy and compare it with the morphology of the original endarterectomy specimen. Surprisingly, in some areas, all of the internal elastic membrane and most of the media were observed in the "endarterectomy" specimen.

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