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Surgical repair of Tetralogy of Fallot (TOF) is followed by very good early and medium-term results (perioperative mortality < or =5%), but there is increasing awareness of the occurrence of late adverse events: many patients experience progressive right ventricular (RV) dilatation/dysfunction leading to symptomatic right ventricular failure, arrhythmias, need for reoperation(in 5-15% of patients within 5-20 years after initial correction ), and late death. Although some predisposing factors such as complexity of anatomy (borderline pulmonary artery (PA) size, right ventricular outflow tract (RVOT) hypoplasia), age at operation, or prior shunting appear to affect early or late outcome adversely, it is debatable if other factors such as type of repair or use of a transannular patch correlate with poor late outcome or increased reoperation rates. Obviously, if careful study reveals specific modifiable factors predisposing to adverse late events (e.g. component of surgical technique), appropriate modification in surgical management may lead to improved late outcome.

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OBJECTIVES: Postcardiotomy acute severe heart failure cannot be managed by medical treatment alone and most often requires some form of mechanical support. In this study we evaluate the efficacy of postoperative extracorporeal membrane oxygenation (ECMO) support following surgery for congenital heart disease (CHD) in infants and children. METHODS: Over a 6-year period from October 1997 to October 2003, 10 patients aged 5 days to 28.5 months (median 3 months) who underwent surgical procedures for CHD received postoperative mechanical support for failing cardiac function despite optimal medical therapy. In 3 patients ECMO was instituted in the operating room (OR) and in 7 patients this was introduced in the intensive care unit (ICU) 2 to 48 (median 20) hours postoperatively. RESULTS: Four patients (40%) were successfully weaned, while support was withdrawn in the remaining 6 due to irreversible vital organ damage. Following successful weaning, one of the survivors died 8 hours later from barotrauma and intrapulmonary hemorrhage, and another died 4 months later from persistent heart failure. The other two patients remain well in NYHA class II. CONCLUSIONS: Despite the adverse effects of ECMO, the methodology provided the necessary support and allowed the failing heart to recover in a number of patients where inotropic support alone proved inadequate.

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OBJECTIVES: Right ventricular (RV) dysfunction is a significant cause of morbidity and mortality after surgical correction of tetralogy of Fallot (TOF). Transatrial/transpulmonary repair avoids a ventriculotomy (in contrast to the transventricular approach) emphasizing maximal preservation of RV structure and function. We have adopted this technique as less traumatic for the right ventricle. This study evaluates the early surgical results of our approach. METHODS: Between September 1997 and July 2001, 110 consecutive patients with TOF were referred to our unit for surgical therapy. Of these, 14 were unsuitable for repair and underwent aortopulmonary shunting+/-pulmonary artery patching. In the remaining 96 patients (median age 1.4 years), complete transatrial/transpulmonary repair was performed. Previously placed shunts (ten patients) were taken down and any secondary stenoses or branch pulmonary artery distortion repaired. In all cases, subpulmonary resection and ventricular septal defect (VSD) closure were accomplished transatrially. Whenever pulmonary valvotomy and valve ring widening were necessary, it was achieved through a pulmonary arteriotomy. In 84 patients the main pulmonary artery was augmented with an autologous pericardial patch, and in 23 the patch was extended to pulmonary artery branch(es). A limited (<1cm ) or extended (>1cm, but

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INTRODUCTION: The ligament of Marshall is a left atrial neuromuscular bundle with sympathetic innervation that may be a source of atrial fibrillation (AF)-inducing automatic activity. METHODS AND RESULTS: Twenty-four patients with paroxysmal AF (including 18 with adrenergic AF) and 25 with other arrhythmias underwent catheter mapping. In cases of adrenergic AF, radiofrequency ablation was attempted when Marshall potentials were recorded. Patients were followed for 2 months before and 11.2 +/- 4.2 months after the procedure. Catheterization of the distal superoposterior coronary sinus was feasible in 14 patients with AF (10 with adrenergic AF) and 12 patients without AF. A discrete Marshall potential was recorded in 12 patients with AF versus 3 patients without AF (P = 0.004). In 10 patients with adrenergic AF, this potential followed the atrial electrogram during sinus rhythm by 26 +/- 5 msec on left atrial recordings and 24 +/- 4 msec on coronary sinus recordings, and preceded it during atrial ectopy by 29 +/- 5 msec and 26 +/- 5 msec, respectively. It was abolished by epicardial (n = 1), endocardial (n = 4), or combined epicardial and endocardial ablation (n = 5). Seven patients with ablation showed significant reductions in adrenergic AF, whereas no significant change was seen in 8 adrenergic AF patients not undergoing ablation (P = 0.004). No improvement was seen in 3 of 4 patients with only endocardial ablation, whereas all 6 patients with epicardial ablation improved (P = 0.033). CONCLUSION: Recording of Marshall potential is feasible in patients with paroxysmal AF. Combined epicardial and endocardial catheter ablation of ligament of Marshall tissue may reduce the paroxysms of adrenergic AF.

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During surgical repair of a neonatal coarctation it was recognized that this was a rare, previously undescribed form of stenosis of the entire descending thoracic aorta. A few hours after the end-to-end surgical repair, the child underwent successful balloon angioplasty, involving the entire descending thoracic aorta, and in which we intentionally avoided the surgical site.

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BACKGROUND: Despite improved surgical results for truncus arteriosus, overall mortality rates, remain higher than those reported for other complex congenital heart diseases, especially with truncal valve regurgitation or an interrupted aortic arch. METHODS: Seventeen patients had complete repair of the truncus arteriosus at the Cleveland Clinic Foundation between August 1993 and June 1997. The age at operation ranged from 2 days to 4.5 years. Associated abnormalities included interrupted aortic arch in 3 patients and abnormal coronary artery anatomy in 3. Four patients had more than moderate truncal valve insufficiency requiring concomitant truncal valve repair. RESULTS: There were no early deaths and only one late death at a mean follow-up of 24 months. The death occurred 3 months postoperatively and resulted from refractory pulmonary vascular obstructive disease in a patient who was referred at 1 year of age. Reoperation was required in 4 patients. CONCLUSIONS: Even in the presence of associated anomalies complete repair was performed with a low mortality rate. Truncal valve repair can be performed safely in the neonate with good results.

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A case of double-outlet right ventricle, unbalanced complete atrioventricular canal, hypoplastic aortic arch, coarctation of the aorta, and atrioventricular valve regurgitation was treated with a staged approach. At 4 days of life the patient underwent aortic arch repair, atrial septectomy, common atrioventricular valve regurgitation repair, and pulmonary artery banding. When she was 14 months of age a biventricular repair was accomplished by two-patch complete atrioventricular canal repair and arterial switch procedure.

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OBJECTIVE: To retrospectively examine a 4 year policy of restoring the morphologically left ventricle to the systemic circuit in patients presenting after 3 months of age with ventriculo-arterial discordance with or without associated atrio-ventricular discordance. This policy was stimulated by the known tendency of the morphologically right ventricle to develop dysfunction sooner or later when left in the systemic circuit. Such a policy dictates a more complex surgical approach and, at this point, it remains controversial whether or not the increased surgical complexity is warranted. METHODS: From July 1, 1993 to March 31, 1997, a total of 29 patients were entered into a protocol for placement of the morphologically left ventricle into the systemic circuit. Three groups of patients were identified. Group I; congenitally corrected transposition in 14 patients -- were treated with either a Senning plus arterial switch operation or Senning plus Rastelli procedure. Group II; failed atrial switch procedure in 12 patients of which nine proceeded to arterial switch operation with Senning or Mustard takedown and atrial reseptation. Group III; D-transposition of the great vessels presenting more than 1 year after birth in three patients who underwent arterial switch operation alone. A deconditioned morphologically left ventricle required reconditioning by means of preparatory pulmonary artery banding in 17 of 29 patients. In the patients requiring pulmonary artery banding, an average of 2.1 pulmonary artery bandings was required to prepare the morphologically left ventricle for a systemic pressure workload. RESULTS: In those patients with a deconditioned morphologically left ventricle requiring preparatory pulmonary artery banding, the mean ratio between the left ventricular and right ventricular systolic pressure increased from 0.48 to 0.95. The left ventricular mass increased from 46.6 to 81.8 g/m2 in five patients subjected to serial MRI measurement. Three patients failed the preparatory pulmonary artery banding and did not proceed to anatomical correction. Two subsequently died at a later time. In the patients proceeding to complete anatomical correction: group I -- there were no early or late deaths. Two patients required pacemaker implantation post-operatively. Group II -- there were two in-hospital deaths, one early due to intrapulmonary hemorrhage and one late, secondary to postoperative left ventricular failure with a stormy post-operative course requiring successful ECMO placement and weaning. These patients were 18 and 25 years old, respectively. One patient proceeded to cardiac transplantation 3 months after surgery due to ongoing morphologically left and right ventricular dysfunction. Group III -- all patients continue to do well. CONCLUSIONS: Late anatomic correction of ventriculo-arterial discordance with or without atrio-ventricular discordance can be performed at a relatively low risk. Reconditioning of the morphologically left ventricle can be achieved by sequential pulmonary banding but is not without risk. Failure to achieve adequate reconditioning of the morphologically left ventricle by pulmonary artery banding in the older patient probably increases the risk of non-survival and may be offset by timely transplantation. Longer follow-up and an assessment of the functional status of these patients is required to assess whether or not this complex surgical approach is indeed warranted.

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A case of branch retinal artery occlusion due to an embolus from a retained left atrial catheter is presented. Removal was accomplished by reoperation. Prompt removal of any retained intracardiac catheter is recommended.

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An infant with hypoplastic left heart syndrome presented for surgical repair at 9 months of age, the ductus having remained open in the presence of a restrictive atrial septal defect. In addition, an anomalous left coronary artery originating from the right pulmonary artery was found. After preliminary blade/balloon atrial septostomy, a successful modified Norwood procedure with concomitant reimplantation of the anomalous coronary artery was performed.

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We assessed the long-term results of our experience with 109 patients with end-stage cardiopulmonary disease who underwent primary combined heart-lung transplantation at Stanford University Medical Center between March 1981 and January 1994. Average recipient age was 31 +/- 10 years (mean +/- standard deviation) median, 31 years; range, 1 month to 52 years. Recipient diagnoses included primary pulmonary hypertension (31%), Eisenmenger's syndrome (39%), complex congenital heart disease (8%), cystic fibrosis (14%), bronchiectasis (2%), and emphysema (3%). Immunosuppression was with cyclosporine and a tapering regimen of corticosteroids. In 1986 azathioprine was added, and since 1987 induction therapy with OKT3 has been employed. Actuarial survival rates at 1, 5, and 10 years were 68% +/- 4.6%, 43% +/- 5.4%, and 23% +/- 8.1%, respectively (mean +/- 1 standard error of the mean). Fourteen deaths occurred in the hospital for an operative mortality rate of 12.8% +/- 3.3%, and 61 deaths occurred overall. Causes of death included hemorrhage (five patients), infection (21), rejection (one), nonspecific pulmonary failure (four), graft coronary artery disease (six), and obliterative bronchiolitis (eight). Infection, rejection, and obliterative bronchiolitis were the major complications. Only 20% +/- 3.9% of patients were free from any infection 3 months after transplantation. Heart and lung rejection commonly occurred asynchronously; actuarial estimates of freedom from isolated lung rejection at 1 and 5 years were 47% +/- 5.2% and 40% +/- 5.6%, respectively. For simultaneous heart and lung rejection these estimates were 87% +/- 3.5% and 86% +/- 3.8%, and for isolated heart rejection 63% +/- 5.1% and 51% +/- 6.4%, respectively. Although graft coronary artery disease developed less frequently than in patients after isolated heart transplantation (90% +/- 4.6% of patients were free of graft coronary artery disease at 5 years), obliterative bronchiolitis remains a major long-term complication and cause of morbidity and mortality. Actuarial estimates of freedom from obliterative bronchiolitis at 1, 5, and 10 years were 71% +/- 5.1%, 51% +/- 6.1%, and 42% +/- 7.8%, respectively. These results show satisfactory early and medium-term outcome after combined heart-lung transplantation but also underscore that much progress is needed in controlling infection, rejection, and obliterative bronchiolitis, all of which remain as major impediments to long-term survival.

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BACKGROUND: Cardiac transplantation for children with endstage heart disease has become an accepted form of therapy and is being practiced with increasing frequency and improving short-term outcome. METHODS AND RESULTS: To assess the medium-term outcome of pediatric cardiac transplantation, we analyzed our experience with 72 patients under the age of 18 (range, 0.1 to 17.7 years; mean, 9 +/- 6.4 [SD]) who underwent orthotopic cardiac transplantation at Stanford University between 1977 and 1993. There were 38 male and 34 female patients. Preoperative diagnoses included congenital heart disease in 24 (33%), idiopathic cardiomyopathy in 27 (37%), viral cardiomyopathy in 12 (17%), and familial cardiomyopathy in 7 (10%) patients. Immunosuppressive management has evolved over time and has included a tapering schedule of steroids, azathioprine, rabbit antithymocyte globulin, cyclosporine in all patients after 1980, and induction with OKT3 since 1987. Operative mortality rate was 12.5 +/- 4.0% (mean +/- 70% confidence intervals). Actuarial survival estimates at 1, 5, and 10 years are 75 +/- 7.1%, 60 +/- 6.4%, and 50 +/- 8.1% (mean +/- 1 SEM), respectively. Causes of death included infection in 8 (28% of deaths), rejection in 7 (24%), graft coronary disease in 5 (17%), pulmonary hypertension in 4 (14%), and nonspecific graft failure in 2 (7%) patients. Survival rates were similar for patients over and those under age 10 years (including the infant cohort of 18 patients transplanted since 1986). Currently, there are 43 patients alive, all in New York Heart Association functional class I. Only 22 +/- 5.6% of patients were free of rejection at 1 year, but 86 +/- 5.4% were free of rejection-related death at 10 years. At 1 year, only 37 +/- 6% of patients were free from any infection, but 88 +/- 4.2% remained free of infection-related death at 5 years. Actuarial freedom from graft coronary artery disease (angiographic or autopsy proven) was 85 +/- 6.6% at 5 years and from coronary artery disease-related death was 91 +/- 4.7%. CONCLUSIONS: These data demonstrate satisfactory medium-term outcome of cardiac transplantation in selected pediatric patients with end-stage heart disease, but further progress is necessary to more effectively control rejection, infection, and graft coronary disease.

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We analyzed our experience with 496 patients who underwent primary cardiac transplantation since the introduction of cyclosporine immunosuppression (Dec. 16, 1980, to Jan. 7, 1993). There were 388 male and 108 female patients. Mean recipient age was 40 +/- 16 years (range 0.1 to 70 years, median 44 years). Recipient diagnoses included coronary disease in 188, idiopathic cardiomyopathy in 196, viral cardiomyopathy in 35, and congenital heart disease in 28 patients. Donor age was 25 +/- 10 years (range 1 to 53 years, median 24 years). Graft ischemic time was 148 +/- 57 minutes (range 38 to 495 minutes, median 149 minutes). Operative mortality (hospital death) rate was 7.9% +/- 1.3% (70% confidence intervals). Multivariate logistic regression analysis revealed that (higher) pulmonary vascular resistance and gender (female) were the only independent predictors of hospital death (p < 0.05). Actuarial survival estimates for all patients at 1, 5, and 10 years are 82% +/- 1.7% (83% +/- 1.8% adult, 77% +/- 5.2% pediatric), 61% +/- 2.5% (65% +/- 2.5% adult, 64% +/- 6.6% pediatric), and 41% +/- 3.7% (40% +/- 4% adult, 54% +/- 8.6% pediatric), respectively. For 232 patients treated with triple-drug immunosuppression and induction with OKT3 since 1987, survival estimates at 1 and 5 years are 82% +/- 2.6% and 67% +/- 3.7%, respectively. Causes of death for the entire group were rejection in 29 (14% of deaths), infection in 69 (34%), graft coronary disease in 36 (18%), nonspecific graft failure in 6 (3%), malignancy in 19 (10%), stroke in 6 (3%), pulmonary hypertension in 6 (3%), and other causes in 30 (15%) patients. Actuarial freedom from rejection at 3 months, 1 year, and 5 years was 21% +/- 1.9%, 14% +/- 1.7%, and 7.2% +/- 1.5%, respectively (+/- 1 standard error of the mean). Estimates of freedom from rejection-related death at 1, 5, and 10 years were 96% +/- 1%, 93% +/- 1.4%, and 93% +/- 1.4%, respectively. Actuarial freedom from any infection at 3 months and at 1 and 5 years was 40% +/- 2.3%, 27% +/- 2.1%, and 15% +/- 2.0% and from infection-related death, 95% +/- 1.0%, 93% +/- 1.2%, and 85% +/- 1.9%, respectively. Actuarial freedom from (angiographic or autopsy proved) graft coronary artery disease at 1, 5, and 10 years was 95% +/- 1.2%, 73% +/- 2.7%, and 65% +/- 3.6% and from coronary disease-related death or retransplantation 98% +/- 0.7%, 84% +/- 2.2%, and 66% +/- 4.3%, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

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BACKGROUND: Although the major limitation of porcine valves is their finite durability, no controlled clinical data exist regarding the relative durability of the two porcine bioprostheses implanted most commonly today, the Carpentier-Edwards (C-E) and Medtronic Hancock I (H) valves. METHODS AND RESULTS: To assess this question, 174 patients undergoing aortic (AVR) or mitral (MVR) valve replacement with a bioprosthesis between March 1980 and March 1982 were randomized to receive either a C-E or a H valve. There were 102 AVRs (54 C-E and 48 H) and 74 MVRs (39 C-E and 35 H). For both the AVR and MVR cohorts, the average patient age was 58 +/- 14 years (+/- SD). The male/female ratio was 2.2:1 for AVR and 0.57:1 for MVR. Clinical follow-up was undertaken periodically; the most recent follow-up closing interval was July through October 1992, and current follow-up was 96% complete. Cumulative follow-up totaled 1369 patient-years (mean, 7.7 +/- 3.6 years; median, 9.1 years; maximum, 12.0 years). The main focus of this analysis was bioprosthetic durability, using the AATS/STS guidelines defining "Structural Valve Deterioration" (SVD). Multivariate analysis revealed that (younger) age was the only significant (P = .024) independent predictor of SVD. Valve manufacturer (C-E versus H) and valve site (aortic versus mitral) did not emerge as significant independent risk factors for SVD. Actuarial rates (Cutler-Ederer) expressed as percent free of SVD (+/- SEM) at 10 years (n = number of patients remaining at risk) were 71 +/- 7% and 59 +/- 9% for the C-E (n = 26) and H (n = 17) groups, respectively, for the AVR cohort; for the MVR cohort, these estimates were 60 +/- 10% (n = 12) and 72 +/- 10% (n = 11), respectively, but these differences were not statistically significant (P = NS, Lee-Desu). CONCLUSIONS: After 10 years, there was no statistically significant difference in durability or other valve-related complications between the H and C-E aortic or mitral valves. Based on current information, the choice of a porcine bioprosthesis should be based on factors other than durability, including ease of implantation, hemodynamic performance, and cost.

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We evaluated subepicardial and subendocardial two-dimensional finite deformations in the left ventricular (LV) anterior, lateral, and posterior regions in the closed-chest, conscious dog heart. Eight dogs underwent placement of 22 radiopaque markers in the LV myocardium. Sets of three markers were implanted in the anterior, lateral, and posterior subepicardium and subendocardium at the mid-ventricular level; reference markers were placed at apical and basal sites. Eight hours later, biplane videofluoroscopy was performed. Finite deformations for each subepicardial and subendocardial region were analyzed during three consecutive beats at end expiration. Circumferential shortening occurred in all layers and regions; similarly, longitudinal shortening occurred in all layers except that of the posterior endocardium. Values of principal strain were -0.19 +/- 0.08 (SD) and -0.10 +/- 0.03 for the anterior subendocardium and subepicardium, -0.20 +/- 0.07 and -0.10 +/- 0.02 for the lateral subendocardium and subepicardium, and -0.13 +/- 0.02 and -0.10 +/- 0.03 for the posterior subendocardium and subepicardium respectively (P less than 0.05 subendocardium vs. subepicardium). Second principal strain tended to be near zero or positive (from -0.01 +/- 0.05 to 0.04 +/- 0.05) in all regions. The end-systolic direction of principal strain was -29 +/- 32 degrees and -34 +/- 29 degrees in the anterior subepicardium and subendocardium, -47 +/- 10 degrees and -30 +/- 37 degrees in the lateral subepicardium and subendocardium, and -4 +/- 29 degrees and +7 +/- 23 degrees in the posterior subepicardium and subendocardium. Anterior and lateral directions of principal strain were similar in the subepicardial and subendocardial layers and oriented along the epicardial fiber axis, but the posterior direction tended to be circumferentially oriented.(ABSTRACT TRUNCATED AT 250 WORDS)

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With the advent of cyclosporin A, accelerated coronary arteriosclerosis has become the major impediment to the long-term survival of heart transplant recipients. Due to epidemiologic reports suggesting a salutary effect of fish oil, the dose response of fish oil on graft coronary arteriosclerosis in a rabbit heterotopic cardiac allograft model was assessed using safflower oil as a caloric control. Seven groups of New Zealand White rabbits (n = 10/group) received heterotropic heart transplants from Dutch-Belted donors and were immunosuppressed with low-dose cyclosporin A (7.5 mg/kg/day). Group 1 animals were fed a normal diet and served as control. Group 2, 3, and 4 animals received a daily supplement of low- (0.25 mL/kg/day), medium- (0.75 mL/kg/day), and high- (1.5 mL/kg/day) dose fish oil (116 mg n-3 polyunsaturated fatty acid/mL), respectively. Group 5, 6, and 7 animals were supplemented with equivalent dose of safflower oil (i.e., 0.25, 0.75, and 1.5 mL/kg/day). Oil-supplemented rabbits were pretreated for 3 weeks before transplantation and maintained on the same diet for 6 weeks after operation. The extent of graft coronary arteriosclerosis was quantified using computer-assisted, morphometric planimetry. When the animals were killed, cyclosporin A was associated with elevated plasma total cholesterol and triglyceride levels in the control group. While safflower oil prevented the increase in plasma lipids at all dosages, fish oil ameliorated the cyclosporin-induced increase in total cholesterol only with high doses. Compared to control animals, there was a trend for more graft vessel disease with increasing fish oil dose, as assessed by mean luminal occlusion and intimal thickness. A steeper trend was observed for increasing doses of safflower oil; compared to the high-dose safflower oil group, animals supplemented with low-dose safflower oil had less mean luminal occlusion (16.3% +/- 5.9% versus 41.4% +/- 7.6%, p less than 0.017) and intimal thickness (7.9 +/- 1.9 microns versus 34.0 +/- 13.0 microns, analysis of variance: p = 0.054). Low-dose safflower oil also had a slight, but nonsignificant, beneficial effect on graft vessel disease when compared to control rabbits. The same trends were observed in the degree of histologic rejection (0 = none to 3 = severe) in fish oil- and safflower oil-treated animals. Rejection score correlated weakly but significantly (p = 0.0001) with mean luminal occlusion (r = 0.52) and intimal thickness (r = 0.46). Therefore allograft coronary disease in this model appeared to exhibit an unfavorable, direct-dose response to fish oil and safflower oil, independent of effects on plasma lipids.(ABSTRACT TRUNCATED AT 400 WORDS)

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To assess the importance of the intact mitral subvalvular apparatus for left ventricular (LV) energetics, data from nine open-chest ejecting canine hearts were analyzed using piezoelectric crystals to measure LV volume. After mitral valve replacement with preservation of all chordae tendineae, baseline LV function was assessed during transient caval occlusion: A quadratic fit of the LV end-systolic pressure-volume data was used to determine the curvilinear end-systolic pressure-volume relationship (ESPVR). All chordae were then divided with exteriorized snares. Reassessment revealed deterioration of global LV pump function: (a) the coefficient of nonlinearity, decreased (less negative) by 90% (P = 0.06); (b) slope of the curvilinear ESPVR at the volume axis intercept, decreased by 75% (P = 0.01); and V100, end-systolic volume at 100 mmHg end-systolic pressure, increased by 42% (P less than 0.02). Similarly, preload recruitable stroke work fell significantly (-14%) and Vw1,000 (end-diastolic volume [EDV] at stroke work [SW] of 1,000 mmHg.ml) rose by 17% (P less than 0.04). With respect to LV energetics, the total mechanical energy generated by the ventricle decreased, as indicated by a decline in the slope of the pressure volume area (PVA)-EDV relationship (120 +/- 13 [mean +/- SD] vs. 105 +/- 13 mmHg, P less than 0.001). Additionally, comparison of LV SW and PVA from single beats with matched EDV showed that the efficiency of converting mechanical energy to external work (SW/PVA) declined by 14% (0.65 +/- 0.13 vs. 0.56 +/- 0.08, P less than 0.03) after chordal division. While effective systemic arterial elastance, Ea, also fell significantly (P = 0.03) after the chordae were severed, the Ea/Ees ratio (Ees = slope of the linear ESPVR) increased by 124% (0.91 +/- 0.53 vs. 2.04 +/- 0.87, P = 0.001) due to a proportionally greater decline in Ees. This indicates a mismatch in ventriculo-arterial interaction, deviating from that required for maximal external output (viz., Ea/Ees = 1). These adverse effects of chordal division may be related to the observed changes in LV geometry (i.e., eccentricity). We conclude that the intact mitral subvalvular apparatus is important in optimizing LV energetics and ventriculo-vascular coupling in addition to the enhancement of LV systolic performance.

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The incidence of peripheral vascular complications in 272 patients with aortic dissection during a 25-year span was determined, as was outcome after a uniform, aggressive surgical approach directed at repair of the thoracic aorta. One hundred twenty-eight patients (47%) presented with acute type A dissection, 70 (26%) with chronic type A, 40 (15%) with acute type B, and 34 (12%) with chronic type B dissections. Eighty-five patients (31%) sustained one or more peripheral vascular complications: Seven (3%) had a stroke, nine (3%) had paraplegia, 66 (24%) sustained loss of a peripheral pulse, 22 (8%) had impaired renal perfusion, and 14 patients (5%) had compromised visceral perfusion. Following repair of the thoracic aorta, local peripheral vascular procedures were unnecessary in 92% of patients who presented with absence of a peripheral pulse. The operative mortality rate for all patients was 25% +/- 3% (68 of 272 patients). For the subsets of individuals with paraplegia, loss of renal perfusion, and compromised visceral perfusion, the operative mortality rates (+/- 70% confidence limits) were high: 44% +/- 17% (4 of 9 patients), 50% +/- 11% (11 of 22 patients), and 43% +/- 14% (6 of 14 patients), respectively. The mortality rates were lower for patients presenting with stroke (14% +/- 14% [1 of 7 patients]) or loss of peripheral pulse (27% +/- 6% [18 of 66 patients]). Multivariate analysis revealed that impaired renal perfusion was the only peripheral vascular complication that was a significant independent predictor of increased operative mortality risk (p = 0.024); earlier surgical referral (replacement of the appropriate section of the thoracic aorta) or more expeditious diagnosis followed by surgical renal artery revascularization after a thoracic procedure may represent the only way to improve outcome in this high-risk patient subset. Early, aggressive thoracic aortic repair (followed by aortic fenestration and/or abdominal exploration with or without direct visceral or renal vascular reconstruction when necessary) can save some patients with compromised visceral perfusion; however, once visceral infarction develops the prognosis is also poor. Increased awareness of these devastating complications of aortic dissection and the availability of better diagnostic tools today may improve the survival rate for these patients in the future. The initial surgical procedure should include repair of the thoracic aorta in most patients.

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We assessed the reversibility of functional and morphological changes of arterialized vein segments by returning them to the venous circulation. Thirteen dogs underwent right carotid and femoral veno-arterial grafting. After 12 weeks, veno-arterial grafts were removed for contractility (norepinephrine [NE] and 5-hydroxytryptamine [5-HT]), luminal prostacyclin (PGI2), and morphometric analyses; the remaining segments were used as left jugular and femoral veno-venous grafts. After another 12 weeks, the veno-venous grafts were harvested. To NE, veno-arterial grafts (ED50, 5.4 +/- 0.1 [-log M]) were less sensitive than control veins (ED50, 6.0 +/- 0.2) or veno-venous grafts (ED50, 6.4 +/- 0.2) but were more sensitive than control arteries (ED50, 4.0 +/- 0.1); the maximum tension of veno-arterial grafts (6.2 +/- 0.6 g) was greater than that of veins, less than that of arteries (9.8 +/- 1.0 g), and comparable with that of veno-venous grafts (5.1 +/- 1.1 g). To 5-HT, veno-arterial (ED50, 7.5 +/- 0.1) and veno-venous (ED50, 7.3 +/- 0.2) grafts were more sensitive than arteries (ED50, 6.0 +/- 0.3), while the vein was unresponsive; the maximum tension of veno-arterial grafts (5.0 +/- 0.7 g) was less than that of arteries (6.9 +/- 0.9 g) and greater than that of veno-venous grafts (1.4 +/- 0.3 g). PGI2 production in veins (3.6 +/- 0.8 ng/ml), veno-arterial grafts (3.9 +/- 0.8 ng/ml), and veno-venous grafts (3.3 +/- 0.9 ng/ml) was comparable and less than that of arteries (6.4 +/- 0.9 ng/ml). Veno-arterial graft intimal thickness (127 +/- 8 microns) and intimal area (15.6 +/- 1.8 x 10(3) microns 2) tended to be greater than that in the veno-venous graft (113 +/- 9 microns and 12.4 +/- 1.8 x 10(3) microns 2); also, the veno-arterial graft medial area (103.0 +/- 7.3 x 10(3) microns 2) was greater than that of the veno-venous graft (80.3 +/- 6.9 x 10(3) microns 2), thereby resulting in a similar relative intimal area (13 +/- 1%). Therefore, some changes associated with arterialization, for example, adrenergic sensitivity, maximum tension to 5-HT, medial thickening, and perhaps intimal hyperplasia, reverted toward venous values when replaced in the venous environment, possibly due to variations in pressure, flow, shear stress, and/or graft preparation techniques. Luminal PGI2 was unchanged in the grafts, implying that graft contractility was not modulated by luminal PGI2.

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