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Cryopreserved aortic valve homografts have become an accepted aortic valve substitute, but long-term studies with echocardiographic assessment of valve function are largely unavailable. Between 1981 and January 1, 1991, a total of 178 patients aged 9 months to 80 years (median 46 years) underwent implantation of a cryopreserved aortic valve homograft. Serial two-dimensional Doppler echocardiographic studies were obtained in 149 patients. Overall survival was 91% at 1 year and 85% at 8 years. Survival of patients undergoing isolated primary infracoronary aortic valve replacement was 99% at 1 month and 94% at 8 years. Twelve patients underwent homograft explanation. Freedom from explantation for leaflet degeneration was 95% at 8 years. Freedom from presumed leaflet failure (valve degeneration at explantation or aortic insufficiency grade 3/4 or more without reoperation on echocardiography) was 94% at 5 years and 85% at 8 years. By multivariable analysis younger recipient age was the only risk factor identified for leaflet failure. Ninety-five percent of patients followed up for 4 or more years were in New York Heart Association class I or II.

The purpose of this study was to quantitate the uncertainty inherent in the electrophysiologic mapping of ventricular preexcitation as seen in Wolff-Parkinson-White syndrome. An ink-coated needle electrode was constructed to serve as a point source of unipolar stimulation along the atrioventricular junction. Activation times for 11 ventricular mapping sites at the atrioventricular junction were measured for each stimulation point. Maps were successfully completed for 18 right free wall and 14 posterior septal stimulation points. The activation time at the mapping site closest to the stimulation point was termed the index activation time. Activation times identical to the index activation time were noted at 1.3 +/- 0.5 mapping sites for each free wall stimulation point and 1.9 +/- 0.9 mapping sites for each septal stimulation point (p0.05, septal versus free wall stimulation points). Activation times falling within 5 msec of the index activation time were noted at 2.4 +/- 1.0 mapping sites for each free wall stimulation point and at 3.9 +/- 1.4 mapping sites for each septal stimulation point (p0.05, septal versus free wall stimulation points). The uncertainty of electrophysiologic mapping can be quantitated, and this error should be considered when making inferences regarding the anatomy of accessory pathways based on electrophysiologic data. A knowledge of the uncertainty inherent in the localization of accessory atrioventricular connections by electrophysiologic mapping can be used to plan borders of surgical dissection that will account for this uncertainty at a 95% confidence level.

Previous descriptions of the four anatomic regions of dissection in Wolff-Parkinson-White syndrome have been largely qualitative. In this study quantitative data describing this anatomy are presented, together with statistical analysis of selected anatomic relationships. Fourteen human hearts were dissected. The borders of the posteroseptal dissection along the mitral anulus, tricuspid anulus, and epicardium were measured. A positive correlation between the mitral and tricuspid annular dimensions was found (r = 0.55; p = 0.04); however, the length of epicardial dissection was more variable. The dimensions of the anteroseptal space and the position of the right coronary artery within this space were measured. These measurements emphasize the proximity of the aortic sinuses of Valsalva to the right atrial endocardium near the posteromedial extent of the dissection. The dimensions of the right and left free walls and the position of the coronary arteries within these spaces were measured. A positive correlation was found between the width of the atrioventricular groove and the length of the dissection necessary to separate the atrioventricular groove fat from the ventricular surface (r = 0.89; p = 0.0001, right free wall; r = 0.87; p = 0.0001, left free wall). The quantitative data presented in this article are intended to enhance the surgeon's appreciation of the anatomy relevant to the treatment of Wolff-Parkinson-White syndrome. The knowledge gained from this quantitative analysis may improve accuracy in the electrophysiologic localization and surgical disruption of accessory atrioventricular connections.

Survival after entry and survival after repair (94%, 91%, and 91% at 1 month, 1 year, and 5 years, respectively) were similar in two institutions treating 196 consecutive patients, and there was no advantage (and a possible disadvantage) of a protocol of preliminary shunting and later repair in very young patients. Size and configuration of the right and left pulmonary arteries had no demonstrable effect on survival, prevalence of transannular patching, or postrepair right ventricular-left ventricular pressure ratio. Small size of the pulmonary "anulus" and trunk were risk factors for death, transannular patching, and high postrepair pressure ratio. High postrepair pressure ratio was a risk factor for death after repair. Very young age (less than about 3 months) was a risk factor for death after repair, particularly when other risk factors coexisted. The prevalence of transannular patching in patients with mild infundibular and pulmonary anulus and trunk hypoplasia decreased across the time of the study, without ill effect. The usefulness of measuring postrepair right ventricular-left ventricular pressure ratio is emphasized by the data.

Elevated pulmonary vascular resistance is a known risk factor for early death from acute right ventricular failure after orthotopic cardiac transplantation. Patients in whom the elevated pulmonary vascular resistance is due primarily to increased left atrial pressure ("reactive") frequently have normalization of resistance after transplantation, but few studies have detailed the time course and magnitude of these changes. To analyze the response of pulmonary vascular resistance to cardiac transplantation, we analyzed data from 4353 right heart catheterizations on all 182 patients undergoing cardiac transplantation between 1981 and Jan. 1, 1990. Before transplantation 18% of patients had a pulmonary vascular resistance greater than 4 WU, 16% had a pulmonary artery systolic pressure greater than 60 mm Hg, and 16% had a transpulmonary gradient greater than 14 mm Hg. In the overall group of patients, pulmonary vascular resistance (mean value 2.63 WU), transpulmonary gradient (mean value 9.9 mm Hg), and pulmonary artery systolic pressure (mean value 48.0 mm Hg) were normalized within 1 week of cardiac transplantation. In patients with a high preoperative pulmonary vascular resistance (greater than or equal to 4 WU), the resistance fell promptly within 1 week of transplantation but continued to be slightly elevated throughout the period of follow-up. By multiple regression analysis, pulmonary vascular resistance at 1 week and 1 year after transplantation was significantly correlated with the pretransplantation resistance. Pulmonary vascular resistance anytime after transplantation was related to preoperative resistance, body surface area, and pulmonary artery diastolic pressure. Inferences: (1) As a group, cardiac transplant recipients have a normal pulmonary vascular resistance, transpulmonary gradient, and pulmonary artery systolic pressure within 1 week after transplantation with little change thereafter for at least several years. (2) Patients with reversible elevation of pulmonary vascular resistance before cardiac transplantation typically have a reactive and a fixed component. Cardiac transplantation relieves the reactive but not the fixed component. As a result, pulmonary vascular resistance early (within 1 week) and late after transplantation will have fallen but not completely normalized.

The value of prophylactic monoclonal or polyclonal antibody therapy early after cardiac transplantation is controversial. Between Jan. 1, 1987, and July 1, 1988, 32 consecutive patients underwent cardiac transplantation (cyclosporine, azathioprine, and prednisone maintenance therapy) with either early prophylactic rabbit antithymocyte globulin (n = 17) or monoclonal OKT3 (Ortho Diagnostic Systems, Inc., Raritan, N.J.) (10 days) (n = 15). Follow-up was through Sept. 1, 1988, for morbid events and through Jan. 1, 1989, for survival. All patients (100%) survived the study period (follow-up of 6 to 24 months). The efficacy of rabbit antithymocyte globulin and OKT3 prophylaxis was similar regarding median time (days) to first rejection (16 versus 21 days, p = 0.5), number of rejection episodes during first 2 months (1.5 versus 1.3 days, p = 0.8), and freedom from rejection at 2 months (18% versus 27%, p = 0.8). Early infections were slightly less common in the rabbit antithymocyte globulin group than the OKT3 group (median time to first infection: 318 versus 250 days, p = 0.5; freedom from rejection at 2 months: 82% versus 64%, p = 0.21), although differences were likely due to chance. Cytomegalovirus syndrome was common, with one case of cytomegalovirus pneumonia. T-cell markers during OKT3 treatment did not predict subsequent rejection (within 2 weeks after OKT3) as assessed by mean T3-lymphocyte count during OKT3 use (p = 0.3) or T3-lymphocyte count during the last 3 days of OKT3 use (p = 0.4). Inferences: (1) Prophylactic rabbit antithymocyte globulin or OKT3 with triple-drug immunosuppression yields excellent intermediate survival after heart transplantation. (2) These protocols for rabbit antithymocyte globulin and OKT3 provide similar protection against early rejection with a relatively low risk of early infection. (3) T-cell markers do not predict early rejection after OKT3.

A 3-year-old boy underwent successful surgical correction of double-outlet right ventricle (S, D, D), noncommitted ventricular septal defect (VSD) of the endocardial cushion type, and pulmonary stenosis. The operation consisted of an internal baffle connecting the left ventricle to the aorta through the VSD. The pulmonary outflow tract was widened with a Dacron patch. Surgical options in this and other subsets of DORV are discussed.

One hundred two patients, aged 0.7 to 38 years, with a wide variety of cardiac malformations underwent the Fontan operation (1975 to April, 1985). Several different techniques were used. All but 17 had previously undergone one or more palliative operations. Follow-up information was obtained in all patients. Overall actuarial survival rate, with time zero being the time of the operation, was 63% at 6 years with no deaths after that in patients followed as long as out to 9.4 years; that for patients with tricuspid atresia was 81%. The hazard function (instantaneous risk) for death was highest immediately after operation and merged after about 6 months with a constant hazard extending as long as the patients were followed. Elevated post-repair right atrial pressure was correlated (p = 0.002) with the probability of death in the early phase, with the risk rising rapidly with pressures above 14 mm Hg. Hypertrophy of the ventricular main chamber was a risk factor for death in both the early (p = 0.007) and late (p = 0.008) phases of hazard, which explained in part the lesser risk of the Fontan operation in patients with tricuspid atresia. Younger age, but not older age, was a risk factor for early postoperative death, but this risk was neutralized by recent date of operation. Thus currently there is not a predicted increased risk associated with younger age at operation. In general, the Fontan operation should be done at a young age (2 to 4 years) to avoid increasing ventricular hypertrophy, but older age per se is not a contraindication to the operation.

The 1 month, 1 year, and 10 year actuarial survival rates after operation among 99 consecutive patients with discordant atrioventricular connection who underwent intracardiac repair are 86%, 75%, and 68%, respectively. The hazard function of death declines rapidly after operation to reach a low level 6 months postoperatively, and it becomes indistinguishable from that of a matched general population by 4 years. Risk factors for premature death include double-outlet right ventricle, complete heart block preoperatively or developing perioperatively, very young or older (greater than 25 years) age, a high hematocrit value, and earlier date of operation. The last indicates improvement in results in recent years. Eleven (11%) of 99 patients had complete heart block preoperatively, and 23 (26% of 88) developed it perioperatively. Patients with discordant ventriculoarterial connection (i.e., corrected transposition) had a lesser probability of developing heart block after repair than did those with other ventriculoarterial connections. Seventeen (17%) patients required tricuspid (pulmonary venous) valve replacement or repair at the original intracardiac operation, and eight additional patients developed important incompetence after repair. Among the risk factors for incompetence was an Ebstein-like anomaly of the tricuspid valve. Reoperations (three) for conduit obstruction have been no more common than in patients with concordant atrioventricular connection. Fifty-seven (81%) of 70 surviving patients are in New York Heart Association Class I and 12 (17%) in Class II. This, and the single-phase hazard function, indicate that the overall results of cardiac repair in patients with atrioventricular discordant connection could become excellent if the early risks were overcome.

The anatomic and functional characteristics of 310 consecutive patients undergoing repair of atrioventricular (AV) septal defects were studied. The characteristics of the six leaflets of the common (139 patients) or two-orifice (171 patients) AV valve are described. Interventricular communications were present in 156 patients and major associated cardiac anomalies in 73 (tetralogy of Fallot 20, double-outlet right ventricle nine, and others). Fifty-one patients (16%) died in hospital. The incremental risk of young age disappeared after 1976. Severity of preoperative AV valve incompetence and New York Heart Association (NYHA) functional class affected hospital mortality. Current risks for patients without major associated cardiac anomalies are 0.6% to 4% for patients in NYHA Class III without an interventricular communication, depending on the degree of preoperative AV valve incompetence, and 5% to 13% for such patients with an interventricular communication. Actuarial survival at 12 1/2 years postoperatively is 95% when preoperative AV valve incompetence is absent or mild and 88% when it is more severe (Grade 3, 4, or 5). Actually, 92% of hospital survivors are alive and in NYHA class I or II. Failure of the AV valve repair occurred in 32 (10%) of the 310 patients and occurred more frequently when AV valve incompetence was severe preoperatively. Its frequency is reduced by current repair techniques, except in patients without interventricular communication.

Recent follow-up of 127 patients having repair of double-outlet right ventricle during an 18 year experience (1967 to July, 1984) indicated an overall actuarial survival rate at 12 years of 38%. However, multivariate analysis supported by contingency tables indicated that currently the early (2 week) survival rate after the intraventricular tunnel repair for double-outlet right ventricle with subaortic ventricular septal defect in 6-month-old infants is 99% and the 10 year survival rate 97%. Reoperation of the tunnel repair was rarely required (one of 56 patients), and the functional results were excellent. Results were similar in patients with doubly committed ventricular septal defect, except that two of 10 patients developed typical discrete localized subaortic stenosis late postoperatively. Early and late results in patients with double-outlet right ventricle and subpulmonary ventricular septal defect were poor when an atrial switch operation was part of the repair; when an intraventricular tunnel repair between the left ventricle and aorta was combined with a right ventricular-pulmonary arterial conduit, no early deaths occurred, but three patients died late postoperatively. Several techniques of repair of double-outlet right ventricle with noncommitted ventricular septal defect have provided only a 22% overall 10 year survival rate. These data are used to derive inferences as to optimal treatment protocols.

Between Jan. 1, 1973, and June 1, 1979, 29 patients underwent surgical closure of multiple ventricular septal defects (VSDs). Included are 19 patients with VSDs only (one death), five with tetralogy of Fallot (TF) (0 deaths), two with transposition of the great arteries and VSD (TGA/VSD) (one death), two with complete atrioventicular (AV) canal (one death), and one with common atrium (one death). The overall hospital mortality rate was 14% (4/29) and was significantly related to the complexity of the underlying malformation (p = 0.01) and the presence of major associated cardiac lesions (p = 0.005). The incidence of reoperation for overlooked VSDs was 28% (8/29) and was significantly related to the presence of muscular VSDs (all overlooked defects were muscular) and the failure preoperatively to diagnose multiple VSDs (p = 0.05). Of patients with shunt data available after the final operation, 85% (17/20) had a Qp/Qs less than or equal to 1.5, and no patient had a final Qp/Qs2.0. This experience indicates that satisfactory results usually can be achieved after operation for multiple VSDs and emphasizes the value of early assessment for residual shunting and reoperation when indicated.

Postoperative cardiac, pulmonary, renal and coagulation dysfunction, along with C3a levels, were studied prospectively in 116 consecutive patients undergoing open cardiac operations and 12 patients undergoing closed operations in the same time period. The level of C3a 3 hours after open operation was high (median value 882 ng X ml-1 plasma) and was related to the C3a level before cardiopulmonary bypass (CPB) (p = 0.03), the level at the end of CPB (p less than 0.0001), elapsed time of CPB (p = 0.07), and older age at operation (p less than 0.0001). It was inversely related to the cardiac output as reflected by the strength of the pedal pulses (p = 0.006). In contrast, C3a levels did not rise in patients undergoing closed operations. The probability of postoperative cardiac dysfunction after open operations (present in 27 of 116 patients) was predicted by C3a levels 3 hours after operation (p = 0.02), the CPB time (p = 0.02), and younger age (p less than 0.0001). The same risk factors pertained for postoperative pulmonary dysfunction (present in 41 of the 116 patients); renal dysfunction (present in 24 of the 116 patients) except that CPB time was not a risk factor here; abnormal bleeding (present in 21 of the 116 patients); and important overall morbidity (present in 26 of 116 patients). As regards important overall morbidity, the C3a level effect became evident at about 1,900 ng X ml-1 (a level reached by 9% of patients); the effect of increasing time of CPB became evident at about 90 minutes of CPB time; and the effect of young age became evident as age decreased from 10 to 4 years. This study demonstrates the damaging effects of CPB, relates them in part to complement activation by the foreign surfaces encountered by the blood, and supports the hypothesis that the mechanisms of the damaging effects include a whole-body inflammatory reaction.

Among 139 patients who underwent repair of tetralogy with pulmonary atresia, survival rates at 1 month and at 1, 5, 10, and 20 years were 85%, 82%, 76%, 69%, and 58%, respectively. The hazard function (instantaneous risk of dying) was greatest immediately after operation and declined thereafter, but a low constant hazard persisted for as long as the patients were followed up. Multivariately, the postrepair ratio between peak right ventricular and left ventricular pressures measured in the operating room provided the most information relative to the probability of death after repair, and cardiopulmonary bypass time the next. When morphologic abnormalities of the pulmonary circulation were considered in the multivariate analysis for risk factors for death, the size of the pulmonary arteries provided the most information, followed by the number of large aortopulmonary collateral arteries. The postrepair peak right ventricular/left ventricular pressure ratio was lower the day after operation than in the operating room in 65% of the patients in whom the measurements were made. Recurrent or residual ventricular septal defects necessitating rerepair occurred in four patients (3% of hospital survivors). Most surviving patients were in New York Heart Association class I at the time of follow-up.Early, intermediate, and long-term survival is less good after repair of tetralogy with pulmonary atresia than after repair of tetralogy with pulmonary stenosis. This is related primarily to the greater prevalence of high peak right ventricular/left ventricular pressure ratio measured in the operating room in the former group. Both the postrepair peak right ventricular/left ventricular pressure ratio in the operating room and the probability of death are inversely related to the size of the pulmonary arteries and directly to the number of large aortopulmonary collateral arteries. This and inferences from other risk factors may be helpful in achieving better results in the future.