Long-term outcomes after cardiac transplantation: an experience based on different eras of immunosuppressive therapy.

BACKGROUND: Constantly changing practices in heart transplantation have improved posttransplant survival in patients with end-stage heart disease. The objective of this study was to evaluate long-term outcomes in different eras of immunosuppressive therapy after cardiac transplantation at a single center during a two-decade period. METHODS: A retrospective review of 1,086 consecutive cardiac allograft recipients who underwent transplantation between 1977 to 1999 was performed. Patients were divided into four eras based on type of immunosuppressive therapy: era 1 = steroids, azathioprine (n = 26, February 1977 to March 1983), era II = steroids, cyclosporine (n = 43, April 1983 to April 1985), era III = cyclosporine, steroids, azathioprine (n = 752, April 1985 to December 1995), era IV = cyclosporine, steroids, mycophenolate mofetil (n = 315, January 1996 to October 1999). RESULTS: The actuarial survival of the entire cohort of 1,086 patients undergoing cardiac transplantation was 79%, 66%, and 49% at 1, 5, and 10 years, respectively. There were significant trends in recipient age and gender distribution among the four eras with increasing proportion of older age (> 60 years) and female recipients in eras III and IV (p = 0.001 and 0.02). Early mortality and long-term survival improved significantly over all eras (p < 0.001). Rejection as a cause of death decreased over time (era I, 24%; era II, 21%; era III, 15%; era IV, 9%; p = 0.02), whereas the contribution of transplant coronary artery disease as a cause of death remained unchanged. CONCLUSIONS: Cardiac transplantation provides satisfactory long-term survival for patients with end-stage heart failure. The improving outcomes in survival correlate with improved immunosuppressive therapy in each era. Although the reasons for improvement in survival over time are multifactorial, we believe that changes in immunosuppressive therapy have had a major impact on survival as evidenced by the decreasing number of deaths due to rejection.

Factors affecting long-term survival (>10 years) after cardiac transplantation in the cyclosporine era.

OBJECTIVES: The aim of this study was to determine long-term survival (>10 years) after cardiac transplantation in the cyclosporine era and identify risk factors influencing long-term survival. BACKGROUND: Despite the availability of newer modalities for heart failure, cardiac transplantation remains the treatment of choice for end-stage heart disease. METHODS: Between 1983 and 1988, 195 patients underwent heart transplantation at a single center for the treatment of end-stage heart disease. Multivariable logistic regression analysis of pretransplant risk factors affecting long-term survival after cardiac transplantation included various recipient and donor demographic, immunologic and peritransplant variables. RESULTS: Among the group of 195 cardiac transplant recipients, actuarial survival was 72%, 58% and 39% at 1, 5 and 10 years respectively. In the 65 patients who survived >10 years, mean cardiac index was 2.91/m2 and mean ejection fraction was 58%. Transplant-related coronary artery disease (TRCAD) was detected in only 14 of the 65 patients (22%). By multivariable analysis, the only risk factor found to adversely affect long-term survival was a pretransplant diagnosis of ischemic cardiomyopathy (p = 0.04). CONCLUSIONS: Long-term survivors maintain normal hemodynamic function of their allografts with a low prevalence of TRCAD. It is possible that similar risk factors that lead to coronary artery disease in native vessels continue to operate in the post-transplant period, thereby contributing to adverse outcomes after cardiac transplantation. Aggressive preventive and therapeutic measures are essential to limit the risk factors for development of coronary atherosclerosis and enable long-term survival after cardiac transplantation.

Reinterventions after repair of common arterial trunk in neonates and young infants.

OBJECTIVES: To determine rates of reintervention after repair of common arterial trunk in the neonatal and early infant periods. BACKGROUND: With improving success in the early treatment of common arterial trunk, the need for reinterventional procedures in older children, adolescents and adults will become an increasingly widespread concern in the treatment of these patients. METHODS: We reviewed our experience with 159 infants younger than four months of age who underwent complete primary repair of common arterial trunk at our institution from 1975 to 1998, with a focus on postoperative reinterventions. RESULTS: Of 128 early survivors, 40 underwent early reinterventions for persistent mediastinal bleeding or other reasons. During a median follow-up of 98 months (range, 2 to 235 months), 121 reinterventions were performed in 81 patients. Actuarial freedom from reintervention was 50% at four years, and freedom from a second reintervention was 75% at 11 years. A total of 92 conduit reinterventions were performed in 75 patients, with a single reintervention in 61 patients, 2 reinterventions in 11 patients and 3 reinterventions in 3 patients. Freedom from a first conduit reintervention was 45% at five years. The only independent variable predictive of a longer time to first conduit replacement was use of an allograft conduit at the original repair (p = 0.05), despite the significantly younger age of patients receiving an allograft conduit (p < 0.001). Reintervention on the truncal valve was performed on 22 occasions in 19 patients, including 21 valve replacements in 18 patients and repair in 1, with a freedom from truncal valve reintervention of 83% at 10 years. Surgical (n = 29) or balloon (n = 12) reintervention for pulmonary artery stenosis was performed 41 times in 32 patients. Closure of a residual ventricular septal defect was required in 13 patients, all of whom underwent closure originally with a continuous suture technique. Eight of 16 late deaths were related to reintervention. CONCLUSIONS: The burden of reintervention after repair of common arterial trunk in early infancy is high. Although conduit reintervention is inevitable, efforts should be made at the time of the initial repair to minimize factors leading to reintervention, including prevention of branch pulmonary artery stenosis and residual interventricular communications.

Role of the endothelium in placental dysfunction after fetal cardiac bypass.

BACKGROUND: Fetal cardiac bypass causes placental dysfunction, characterized by increased placental vascular resistance, decreased placental blood flow, hypoxia, and acidosis. Vasoactive factors produced by the vascular endothelium, such as nitric oxide and endothelin 1, are important regulators of placental vascular tone and may contribute to this placental dysfunction. METHODS: To investigate the role of the vascular endothelium in placental dysfunction related to fetal cardiac bypass, we studied 3 groups of fetal sheep. In the first group (n = 7) we determined placental hemodynamic responses before and after bypass to an endothelium-dependent vasodilator (acetylcholine), an endothelium-independent vasodilator (nitroprusside), and endothelin 1. In the second group (n = 8) a nonspecific endothelin receptor blocker (PD 145065) was administered and placental hemodynamic values were measured before and after bypass. In the third group (n = 5) endothelin 1 levels were measured before and after bypass. RESULTS: Before fetal cardiac bypass exogenous endothelin 1 decreased placental blood flow by 9% and increased placental resistance by 9%. After bypass endothelin 1 decreased placental flow by 47% and increased resistance by 106%. There was also a significant attenuation of the placental vascular relaxation response to acetylcholine after bypass, whereas the response to nitroprusside was not significantly altered. In fetuses that received the PD 145065, placental vascular resistance increased significantly less than in control fetuses (28% versus 62%). Similarly, placental blood flow decreased significantly more (from 6. 3 +/- 3.1 to 28.3 +/- 10.4 pg/mL; P =.01) in control fetuses than in fetuses receiving PD 145065 (33% versus 20%). Umbilical venous endothelin 1 levels increased significantly in fetuses exposed to fetal bypass but did not change in control fetuses. CONCLUSIONS: The basal endothelial regulatory mechanisms of placental vascular tone were deranged after fetal cardiac bypass. Endothelin receptor blockade, which substantially reduced postbypass placental dysfunction, and other interventions aimed at preserving endothelial function may be effective means of optimizing fetal outcome after cardiac bypass.

Cardiac transplantation in over 1000 patients: a single institution experience from Columbia University.

Since 1977, the cardiac transplantation program at Columbia has performed 1,137 heart transplant operations with a current one-year survival rate of approximately 90% and a 5-year survival rate of approximately 75% representing the largest single institution experience in North America. Over 2 decades of experience in the selection of donors and recipients has permitted us to expand eligibility limits and relax conventional exclusion criteria allowing us to transplant high-risk donors and medically complex recipients with excellent results. Recipient characteristics, rather than those of the donor, substantially impact outcome following OHT and use of extended donors will improve allocation of donor organs particularly with marginal recipients. During the 2-decade long evolution in our transplant experience, substantial improvements have been made in the areas of immunosuppression, treatment of rejection, and handling of sensitized recipients. Frequent causes of late mortality such as graft rejection, infection, malignancy, and TCAD, have been significantly diminished in the modern area of immune manipulation but remain major causes of death and barriers to long-term survival. The single biggest impediment to growth in OHT is the shortage of donor organs. We have attempted to address this issue by identifying patients who may be better served with a bridging surgical procedure such as a mechanical assist device, or alternative procedures such as transmyocardial laser revascularization, high-risk reparative surgery, or myocardial volume reduction operations. Ongoing research interests at Columbia including LVADs, immunologic sensitization, xenotransplantation, and vasculogenesis offer the potential for continued growth for treatment of end-stage heart disease into the next millennium.

Trends in the management of truncal valve insufficiency.

BACKGROUND: The single semilunar valve in patients with truncus arteriosus frequently is dysplastic and dysfunctional. Truncal valve insufficiency has been associated with poor outcome. Although the management of truncal valve insufficiency has evolved over the years, approaches to this problem vary considerably and remain a serious dilemma in many cases. METHODS: We reviewed the records of 89 patients with unrepaired truncus arteriosus and mild (n = 37), moderate (n = 33), or severe (n = 19) truncal valve insufficiency who were admitted to our institution between 1975 and 1995. Eight patients (7 neonates) with moderate or severe insufficiency died before surgical intervention, and 4 patients underwent palliative pulmonary artery banding. The remaining 77 patients underwent repair. The median age at repair was 3.2 months (range, 2 days to 15 years; 83% infants), and it decreased from 4 months between 1975 and 1985 to 1 month between 1986 and 1995. Truncal valve replacement (mechanical = 6, allograft = 4) was performed in 10 patients, and 5 patients underwent valve repair. RESULTS: All 4 patients who underwent pulmonary artery banding died either early or late. The hospital (or 30-day) mortality rate after repair was 34% (26/77). At a median follow-up of 10 years, 11 hospital survivors had died, with overall 1- and 10-year actuarial survival rates of 56% and 48%, respectively, and poorer survival among patients with severe truncal valve insufficiency (p = 0.02). Late truncal valve replacement (n = 24) had been performed in 21 patients. Freedom from truncal valve replacement was better in patients with mild truncal insufficiency than in those with moderate or severe preoperative insufficiency (p < 0.001). Four late deaths were related directly to reoperation for truncal valve replacement or to prosthetic valve dysfunction. Three of the 4 neonates who received allograft root replacements died within 7 months of repair, and severe allograft valve insufficiency requiring replacement 1 year after operation developed in the fourth. CONCLUSIONS: The prospects for patients with truncal valve insufficiency have been improving over time. Nevertheless, the results in patients with severe insufficiency continue to be poor.

Long-term follow-up of truncus arteriosus repaired in infancy: a twenty-year experience.

BACKGROUND: There have been few reports of long-term follow-up after truncus arteriosus repair in infancy. METHODS: A retrospective review was performed to assess long-term outcomes among 165 patients who survived the initial hospital stay after complete repair of truncus arteriosus since 1975. The median age at truncus repair over this 20-year experience was 3.5 months (range 2 days to 36 years), and 81% of patients were less than 1 year of age. Previous pulmonary artery banding had been performed in 15 patients, and two patients had undergone prior repair of interrupted aortic arch. Significant procedures performed along with truncus repair included truncal valve replacement (n = 10) or repair (n = 5) and repair of interrupted aortic arch (n = 4). RESULTS: Patients were followed up for up to 20.4 years (median 10.5 years). Twenty-five patients were lost at cross-sectional follow-up, with a total of 67 patient-years of follow-up available on these patients. There have been 23 late deaths, eight of which occurred within 6 months of repair and 13 of which occurred within 1 year. Ten of the late deaths were related to reoperations. Actuarial survival among all hospital survivors was 90% at 5 years, 85% at 10 years, and 83% at 15 years and was essentially identical for infants alone. A significant independent risk factor for poorer long-term survival was truncus with moderate to severe truncal valve insufficiency before repair. During the follow-up period, 107 patients underwent 133 conduit reoperations. Median time to conduit reoperation was 5.5 years, and the only factor significantly associated with shorter time to conduit replacement was smaller conduit size at initial repair. In addition, 26 patients underwent 30 truncal valve replacements. Six patients required truncal valve replacement before any conduit-related reintervention, with two associated deaths. Actuarial freedom from truncal valve replacement among patients with no prerepair truncal valve insufficiency was 95% at 10 years. Actuarial freedom from truncal valve replacement was significantly lower among patients with truncal insufficiency before initial repair (63% at 10 years). At follow-up, all patients except three were in New York Heart Association functional class I. CONCLUSIONS: Ten- to 20-year survival and functional status are excellent among infants undergoing complete repair of truncus arteriosus. Conduit replacement or revision is almost inevitably necessary in this group of patients.

Measurement of collateral blood flow in a porcine model of aortic coarctation by velocity-encoded cine MRI.

The purpose of this study was to investigate the time course of development of collateral blood flow in an animal model of aortic coarctation. A juxtaductal aortic stenosis (model coarctation) was surgically created in five juvenile pigs. MRI was performed preoperatively, 1 to 2 days postoperatively, and 2 to 10 weeks postoperatively. Aortic blood flow was measured by velocity-encoded cine MR (VENC-MR). The percent change in aortic blood flow (delta BF) from proximal to distal descending thoracic aorta was calculated, and a multiple-comparison paired t test used to assess changes in delta BF over time. Invasive flow measurements were obtained in one animal before sacrifice using an ultrasonic probe. delta BF preoperatively was -2 +/- 8% (mean +/- SE). delta BF increased to 32 +/- 7% (mean +/- SE, P = .022) 2 days postoperatively and 55 +/- 19% (P = .032) 2 to 8 weeks postoperatively. Invasive measurements were in qualitative agreement with the VENC-MR data. VENC-MR is an accurate noninvasive method of measuring collateral blood flow in aortic coarctation. Recruitment and development of collateral flow pathways occur rapidly in an animal model.

Post-cardiopulmonary bypass pulmonary hypertension in lambs with increased pulmonary blood flow. A role for endothelin 1.

BACKGROUND: After cardiopulmonary bypass (CPB), pulmonary hypertension and its associated increased vascular reactivity are a major source of morbidity, particularly for children with increased pulmonary blood flow. Although post-CPB pulmonary hypertension is well described, its mechanisms remain incompletely understood. Plasma levels of endothelin 1. a potent vasoactive substance implicated in pulmonary hypertension, are increased after CPB. The purpose of the present study was threefold: to characterize the changes in pulmonary vascular resistance and vascular reactivity induced by hypothermic CPB; to investigate the effects of preexisting increased pulmonary blood flow on these changes; and to better define the role of endothelin 1 in the pathogenesis of post-CPB pulmonary hypertension. METHODS AND RESULTS: Vascular pressures and blood flows were monitored in 14 1-month-old lambs with increased pulmonary blood flow (after in utero placement of an aortopulmonary shunt) and 6 age-matched control lambs. During the 2-hour study period after 105.3 +/- 20.6 minutes of hypothermic CPB the increase in pulmonary vascular resistance was significantly augmented in lambs with increased pulmonary blood flow compared with control lambs (P < .05). Pretreatment with PD 145065 (a nonselective endothelin receptor blocker; 50 micrograms.kg-1.min-1) completely blocked this increase in pulmonary vascular resistance and blocked the increase in pulmonary vascular resistance in response to acute alveolar hypoxia after CPB (96.3 +/- 88.5% versus -9.7 +/- 16.4%; P < .05). Plasma endothelin 1 levels increased after CPB in all lambs. CONCLUSIONS: Preexisting increased pulmonary blood flow alters the response of the pulmonary circulation to hypothermic CPB; the increase in pulmonary vascular resistance induced by CPB is augmented in lambs with increased pulmonary blood flow. Pretreatment with endothelin 1 receptor blockers eliminated the increase in pulmonary vascular resistance and the pulmonary vasoconstricting response to alveolar hypoxia, suggesting a role for endothelin 1 in post-CPB pulmonary hypertension. Endothelin 1 receptor blockers may decrease morbidity in children at risk for pulmonary hypertension after surgical repair with CPB and warrants further study.

Key role of the alternate complement pathway in hyperacute rejection of rat hearts transplanted into fetal sheep.

Hyperacute rejection (HAR) mediated by xenoreactive natural antibodies (XNA), which are thought to develop in early infancy, is a major impediment to transplantation between widely disparate species. The ability to diagnose certain forms of congenital heart defects early in prenatal life suggests the potential for these defects to be corrected by cardiac transplantation, prior to the development of XNA and host immunocompetence. This study investigated whether discordant cardiac xenotransplantation into fetal and neonatal recipients might obviate HAR due to the relative lack of XNA. Six neonatal lambs at 3 days (n=3) or 7 days (n=3) of life, and two fetal lambs at 125 and 142 days of gestation (term = 145 days) received cardiac grafts from adult Wistar-Furth (275-350 g) rats. All eight cardiac xenografts showed clinical evidence of HAR, with rapid swelling, loss of contractility, and ecchymosis and a mean survival time of 12.5 +/- 6.4 min. Sections of explanted grafts showed classical histologic features of HAR, including interstitial hemorrhages, platelet microthrombi, and edema, without leukocyte infiltration. Immunopathology of grafts harvested from fetal recipients showed a lack of significant intragraft deposition of sheep IgM, IgG, or C1q, but widespread endothelial labeling for C3, factor B, and properdin. In contrast, grafts in neonatal recipients showed IgM, IgG, and C1q deposition, as well as C3, factor B, properdin, and terminal complement (C) components. Fibrin deposition and platelet thrombi were seen in both groups of recipients. Injection of cobra venom factor resulted in prolongation of cardiac xenograft survival in neonatal lambs (n=3) to 12 hr. Analysis by immunohistology showed that normal sera from neonatal and adult, but not fetal, sheep contained IgM and IgG XNA reactive with rat cells. In conclusion, rodent grafts transplanted into fetal sheep undergo HAR, likely through direct activation of the alternate pathway of C, whereas neonatal lambs acquire XNA in the very early postnatal period and reject rat hearts through activation of both the classical and alternate pathways of C. Thus, at least in some species combinations, cardiac transplantation during the early postnatal period, or even in utero, may still be subject to development of HAR.

Coarctation repair using end-to-side anastomosis of descending aorta to proximal aortic arch.

BACKGROUND: Recurrent aortic coarctation after primary operative repair in the neonate and small infant is seen most commonly within the first year of life. Inadequate removal of ductal tissue, failure to address hypoplasia of the aortic arch, and suture line tension have been cited as important factors in early recurrence. METHODS: To address these issues, we have used a technique of coarctation resection and extended anastomosis of the descending aorta to the undersurface of the aortic arch. THe salient features of this approach include extensive mobilization of the aortic arch and neck vessels, careful trimming of all ductal tissue, ligation of the isthmus just beyond the left subclavian artery, and end-to-side anastomosis of the descending aorta to a separate incision in the undersurface of the aortic arch proximal to all tubular hypoplasia. Between July 1992 and January 1995, 19 consecutive neonates (median age, 13 days) and 4 consecutive infants under 3 months of age (median age, 69 days) with a mean peak systolic upper to lower extremity resting gradient of 27.9 +/- 16.9 mm Hg underwent repair of aortic coarctation and tubular hypoplasia of the arch. Other procedures performed at the time of repair included ligation of a patent ductus arteriosus (n = 19), pulmonary artery banding (n = 3), and closure of ventricular septal or atrial septal defect (n = 3). RESULTS: There were no perioperative deaths. Early postoperative complication included a recurrent laryngeal nerve injury and a transient focal tonic clonic seizure. There was one late death, after a subsequent intracardiac surgical procedure, at a median follow-up of 16 months (range, 1 to 29 months). Twenty-one of 22 late survivors were free of recurrent aortic coarctation by echocardiography findings and clinical examination, with a median upper to lower extremity gradient of 0 mm Hg. Reintervention for recurrent aortic coarctation was not required in any survivor. CONCLUSIONS: The technique described herein completely removes all potentially abnormal tissue from the aorta, including ductal tissue and all tubular hypoplastic tissue proximal to the coarctation site.

Aortoventriculoplasty with the pulmonary autograft: the "Ross-Konno" procedure.

BACKGROUND: For patients with complex left ventricular outflow tract obstruction, including hypoplastic aortic anulus with or without severe diffuse subaortic stenosis, various aortoventriculoplasty procedures (e.g., Konno procedure and its modifications; extended aortic allograft root replacement) are important management options. In younger patients, however, reoperation for valve replacement is inevitably required, and anticoagulation issues pose additional problems. The pulmonary autograft provides a promising option for aortic valve replacement as part of the aortoventriculoplasty procedure in children. Long-term follow up shows that the pulmonary autograft functions well as the systemic arterial (neoaortic) valve and that valve growth occurs. METHODS: Between July 1993 and May 1995, 11 patients 4 days to 17 years old (median 12 months) underwent aortoventriculoplasty with pulmonary autograft (Ross-Konno procedure). The diagnoses were aortic stenosis with or without subaortic stenosis (n = 8), Shone complex (n = 2), and interrupted aortic arch with subaortic stenosis (n = 1). On average, 1.9 previous interventions had been performed per patient, including a previous Konno procedure in one patient. The aortic root was replaced with a pulmonary autograft valve. The left ventricular outflow tract was enlarged with a Dacron polyester fabric patch in two patients, with an allograft aortic patch in two patients and a right ventricular infundibular free wall muscular extension harvested in continuity with the autograft in seven patients. RESULTS: Intraoperative transesophageal echocardiographic assessment revealed mild aortic insufficiency in one patient. One patient had a residual left ventricular outflow tract gradient of 15 mm Hg. Significant complications were cardiac tamponade from bleeding (n = 1) and complete heart block necessitating a permanent pacemaker (n = 1). Follow-up ranged from 2 weeks to 16 months. To date, there have been no late deaths or reoperations. Follow-up echocardiography revealed mild autograft insufficiency in one patient and a 16 mm Hg residual left ventricular outflow tract gradient in one patient. CONCLUSIONS: Initial experience suggests that aortoventriculoplasty with the pulmonary autograft is an excellent alternative for young patients with complex left ventricular outflow tract obstruction. Because the pulmonary autograft has been shown to grow after implantation, reoperation on the left ventricular outflow tract is likely to be avoided.

Extending the limits of the Ross procedure.

BACKGROUND: The potential for growth and the proven long-term durability of the native pulmonary valve make it ideal for replacement of the diseased aortic valve, especially in growing children. The use of the autologous pulmonary valve can be further extended to patients with complex left ventricular outflow tract obstruction and to neonates and infants. METHODS: Between June 1993 and May 1995, 35 patients underwent the Ross procedure at our center. Of these, 15 (43%) had complex left ventricular outflow tract obstruction and 7 (20%) were infants, including 3 neonates. The autologous pulmonary valve was implanted as a root replacement with coronary reimplantation in all patients. Additional left ventricular outflow tract procedures performed were ventricular myectomy in 7 patients and a Konno type aortoventriculoplasty in 11 patients. RESULTS: There was one early death in a patient with borderline hypoplastic left heart syndrome. At a median follow-up of 9 months (range, 0.2 to 22 months) there were no late deaths or reinterventions. The autologous pulmonary valve function was excellent, with 1 (2.8%) patient having moderate insufficiency. CONCLUSIONS: Autologous pulmonary valve is an excellent option for aortic valve replacement in all age groups. Its use can be readily extended to neonates, infants, and patients with complex left ventricular obstruction requiring additional left ventricular outflow tract procedures.

Performance of right ventricle to pulmonary artery conduits after repair of truncus arteriosus: a comparison of Dacron-housed porcine valves and cryopreserved allografts.

Repair of complex congenital heart defects often requires the use of extracardiac conduits. These repairs can be technically accomplished with excellent early results. However, the long-term performance of various conduits is less than optimal. In this report, we examined the long-term outcome of xenograft valved Dacron conduits and cryopreserved allograft valved conduits used for reconstruction of the right ventricular outflow tract in young patients with truncus arteriosus. A retrospective review was performed on 222 patients who underwent primary surgical repair of truncus arteriosus between January 1975 and December 1994 using a xenograft valved synthetic conduit (group I; n = 175) or with a cryopreserved valved allograft conduit (group II; n = 47). Median age at repair was 121 days in group I and 70 days in group II; median weight of patients in both groups was the same (4.2 kg). Conduit-related early deaths occurred in 5.7% (10/175) of patients in group I and none in group II. In a cohort of age-matched patients, actuarial freedom from conduit-related reintervention at 5 years follow-up was significantly better (P = .037) for the cryopreserved valved allograft conduits when compared with xenograft valved synthetic conduits. However, this difference was not apparent by 7 years. Multivariate analysis showed conduit size (P = .0005) as a significant predictor of early conduit-related reintervention. This study shows that mid-term performance of cryopreserved allografts (which have the advantage of technical ease of insertion of availability of small sizes for use in neonates), is better than the xenograft Dacron conduits.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmogenic ventricular aneurysms unrelated to coronary artery disease.

Malignant ventricular tachycardia occurs most frequently in patients with coronary artery disease who have had a previous myocardial infarction and in whom a ventricular aneurysm subsequently develops in the scarred section of myocardium. Ventricular tachycardia in the presence of normal coronary arteries and a left ventricular aneurysm is unusual and can be refractory to medical therapy. We retrospectively reviewed our experience of 10 patients treated at our institution from 1983 to 1993. Age ranged from 22 to 76 years, and all patients presented with sustained ventricular tachycardia. All patients underwent complete electrophysiologic testing. Cardiac catheterization was performed in 9 patients, and each had normal coronary artery anatomy without evidence of significant fixed lesions. A left ventricular aneurysm, diagnosed by either echocardiography, thoracic cine computed tomography or magnetic resonance imaging, or ventricular angiography was present in all patients. Ventricular tachycardia could not be suppressed pharmacologically in 7 of 10 patients using multiple agents including procainamide, quinidine, flecanide, tocainide, propaferone, and amiodarone. Six patients were treated surgically by intraoperative electrophysiologic mapping, endocardial resection of foci, and left ventricular aneurysmectomy. An implantable cardiac defibrillation device was implanted in 2 patients. One patient died on the second postoperative day after simultaneous mapping -guided aneurysmectomy and implantable cardioverter defibrillator placement. There was one late postoperative death. All other surgically treated patients had postoperative electrophysiologic studies demonstrating no inducible ventricular tachycardia, and these patients remain without antiarrhythmic therapy in follow-up extending from 29 to 86 months (mean, 56 months).(ABSTRACT TRUNCATED AT 250 WORDS)