Management of ventricular septal defect: a survey of practice in the United Kingdom.

BACKGROUND: A survey of pediatric cardiac surgeons was performed to establish current opinions in the United Kingdom concerning closure of ventricular septal defect. METHODS: Questionnaires were sent to 14 pediatric cardiac centers in 1995 (16 surgeons, 100% response), and again in 1997 (20 surgeons, 100% response). RESULTS: Results are presented for 1997, with findings from 1995 shown in parentheses. Eleven (6) surgeons used bypass exclusively, 9 (10) sometimes used circulatory arrest. Operative techniques were similar, although the material used for the patch varied. Multiple defects were approached via the transatrial route by 18 (15), right ventriculotomy by 11 (7) and left ventriculotomy by 7 (6). The juxta-arterial defect was approached via the transpulmonary route by 16 (13), a combination by 9 (11), transatrial by 10 (6), and transventricular by 9 (5). The most common indications for pulmonary arterial banding were "Swiss cheese" defect for 13 (13), and functionally single ventricle for 5 (6). Ventricular septal defect associated with coarctation was repaired in two stages by 13 (10), a single stage by 5 (3), or either by 1 (3). CONCLUSIONS: Pediatric cardiac surgeons in the United Kingdom demonstrate a uniform, evidence-based approach to the management of ventricular septal defect.

Acute right ventricular restrictive physiology after repair of tetralogy of Fallot: association with myocardial injury and oxidative stress.

BACKGROUND: Acute right ventricular (RV) restrictive physiology after tetralogy of Fallot repair results in low cardiac output and a prolonged stay in the intensive care unit (ICU). However, its mechanism remains uncertain. METHODS AND RESULTS: In the first 24 hours after tetralogy of Fallot repair (n=11 patients), serial prospective measurements were performed of cardiac troponin T, indexes of NO production (NO(2)(-) and NO(3)(-) combined as NOx), and iron metabolism and antioxidants. RV diastolic function was assessed by transthoracic Doppler echocardiography. Patients who had a long stay in the ICU were characterized by restrictive RV physiology (nonrestrictive group [n=7]: 3.0+/-0.6 days [mean+/-SD]; restrictive group [n=4]: 10.7+/-3.1 days). Troponin T peak concentration and the area under its concentration-time curve (AUC) were higher in the restrictive RV group (peak: restrictive group 17. 0+/-2.8 microg/L, nonrestrictive group 10.4+/-4.6 microg/L, P<0.03; AUC: restrictive group 268.8+/-73.6 microg. h(-1). L(-1), nonrestrictive group 136.2+/-48.3 microg. h(-1). L(-1), P<0.03). Plasma NOx/creatinine concentrations were higher in the restrictive group than the nonrestrictive group at 2 hours after bypass (restrictive group 1.3+/-0.4, nonrestrictive group 0.8+/-0.2; P=0. 04) but were similar by 24 hours. Iron loading peaked 2 to 10 hours after bypass and was more severe in the restrictive group (peak transferrin saturation: restrictive group 83.9+/-13.0%, nonrestrictive group 58.3+/-16.2%, P=0.05; minimum total iron-binding capacity: restrictive group 0.59+/-0.21%, nonrestrictive group 0.76+/-0.06%, P=0.04; minimum iron-binding antioxidant activity to oxyorganic radicals: restrictive group 9. 5+/-22.4%, nonrestrictive group 50.6+/-11.4%, P=0.01). CONCLUSIONS: After tetralogy of Fallot repair, acute restrictive RV physiology is associated with greater intraoperative myocardial injury and postoperative oxidative stress with severe iron loading of transferrin.

Modified ultrafiltration improves global left ventricular systolic function after open-heart surgery in infants and children.

OBJECTIVES: Modified ultrafiltration increases blood pressure and cardiac index following open-heart surgery in children, but it is unclear if this is secondary to an improvement in global left ventricular function. A previous report has suggested that left ventricular systolic function as assessed in a single chord is improved by ultrafiltration (Davies MJ, Nguyen K, Gaynor JW, Elliott MJ. Modified ultrafiltration improves left ventricular systolic function in infants after cardiopulmonary bypass. J Thorac Cardiovasc Surg 1998;115:361--370). The prominent vascular actions of modified ultrafiltration necessitate left ventricular assessment using load-independent indices of systolic and diastolic function. METHODS: In 22 consecutive infants and children undergoing open-heart surgery, left ventricular function was assessed following bypass and then 10 min later. Sixteen children (median weight 8.1 kg) underwent modified ultrafiltration during this period, the remainder (median weight 7.3 kg) were controls for spontaneous recovery without ultrafiltration. Real-time pressure-volume loops, with transient inferior caval vein snaring were generated from conductance and microtip pressure catheters inserted through the LV apex. From these, load-independent (slope of the end-systolic pressure-volume [Ees] and end-diastolic pressure-volume [Eed] relationships) and load-dependent (Pmax, maximum LV pressure; Ped, end-diastolic LV pressure; maximum [dP/dtmax] and minimum [dP/dtmax] time derivatives of LV pressure; tau, time constant of isovolumic relaxation) indices of left ventricular function were measured. RESULTS: Haemoconcentration was achieved in all modified ultrafiltration patients, median increase in haematocrit 34% (interquartile range 21%, 42%), final haematocrit 0.40 (0.35, 0.41). Ees increased 58% (9, 159, P = 0.005). The changes in Eed, Pmax, Ped, dP/dtmax, dP/dtmin, and tau were not significantly different from the control group. CONCLUSION: Modified ultrafiltration improves global left ventricular systolic function in infants and children following open-heart surgery.

Cardiorespiratory responses to negative pressure ventilation after tetralogy of fallot repair: a hemodynamic tool for patients with a low-output state.

OBJECTIVES: We hypothesized that a period of cuirass negative pressure ventilation (NPV) would augment the cardiac output of patients in the early postoperative period after complete correction of tetralogy of Fallot (TOF). BACKGROUND: Diastolic right ventricular dysfunction can lead to a low-output state in an important minority of patients after TOF repair. In these patients, the diastolic pulmonary arterial flow, which characterizes restrictive right ventricular physiology, and on which the cardiac output is so dependent, is highly sensitive to changes in intrathoracic pressure. METHODS: The effects of NPV on pulmonary blood flow were investigated in 23 intubated children who were initially ventilated using intermittent positive pressure ventilation after TOF repair. Eight patients had restrictive right ventricular physiology. All children received a 15-min period of NPV, and eight received a prolonged period (45 min) of NPV. RESULTS: A brief period of NPV increased pulmonary blood flow by 39%, and the improvement further continued if the study period was extended, with a total increase of 67% after 45 min. Patients with restrictive physiology had a somewhat delayed response to NPV, but the ultimate increase during an extended period of NPV was greater in restrictive patients (84%) than nonrestrictive patients (50%). CONCLUSIONS: By manipulating important cardiopulmonary interactions, NPV improves the cardiac output of patients after TOF repair, and has a role as a hemodynamic tool in the management of the low-output state in selected cases.

Intracardiac extension of tumour thrombus from a soft tissue sarcoma.

We present a case of malignant peripheral nerve sheath tumour in a patient with von Recklinghausen's neurofibromatosis with intracardiac extension of the tumour thrombus. This is the first reported case of a soft tissue sarcoma associated with transluminal propagation of a tumour thrombus to the heart.

Left ventricular dysfunction after open repair of simple congenital heart defects in infants and children: quantitation with the use of a conductance catheter immediately after bypass.

OBJECTIVE: Quantification of myocardial injury after the simplest pediatric operations by load-independent indices of left ventricular function, using conductance and Mikro-Tip pressure catheters (Millar Instruments, Inc., Houston, Tex.) inserted through the left ventricular apex. METHODS: Sixteen infants and children with intact ventricular septum undergoing cardiac operations had left ventricular function measured, immediately before and after bypass. Real-time pressure-volume loops were generated by conductance and Mikro-Tip pressure catheters placed in the long-axis via the left ventricular apex, and preload was varied by transient snaring of the inferior vena cava. RESULTS: Good quality pressure-volume loops were generated in 13 patients (atrial septal defects, n = 11; double-chambered right ventricle, n = 1; supravalvular aortic stenosis, n = 1; age 0.25 to 14.4 years, weight 3.1 to 46.4 kg). Their mean bypass time was 41 +/- 14 minutes and mean aortic crossclamp time 27 +/- 11 minutes. End-systolic elastance decreased by 40.7% from 0.34 +/- 0.17 to 0.21 +/- 0.15 mm Hg-1.ml-1.kg-1 (p < 0.001). There were no significant changes in the slope of the stroke work-end-diastolic volume relationship, end-diastolic elastance, time constant of isovolumic relaxation, and normalized values of the maxima and minima of the first derivative of developed left ventricular pressure. CONCLUSION: Load-independent indices of left ventricular function can be derived from left ventricular pressure-volume loops generated by conductance and Mikro-Tip pressure catheters during the perioperative period in infants and children undergoing cardiac operations. Incomplete myocardial protection was demonstrated by a deterioration in systolic function after even short bypass and crossclamp times.

Cardiopulmonary interactions after Fontan operations: augmentation of cardiac output using negative pressure ventilation.

BACKGROUND: The low-output state is the chief cause of morbidity and mortality after Fontan operations. An alternative hemodynamic tool would be a welcome addition for these patients, who are typically resistant to conventional therapeutic measures. METHODS AND RESULTS: The hemodynamic effects of conversion from conventional intermittent positive pressure ventilation (IPPV) to cuirass negative pressure ventilation (NPV) was investigated in nine acute postoperative Fontan patients on the pediatric intensive care unit and nine anesthetized patients undergoing cardiac catheterization in the convalescent phase after Fontan operations. Pulmonary blood flow was measured using the direct Fick method during IPPV and after a brief period of NPV. In one subgroup of patients, pulmonary blood flow was measured again after reinstitution of IPPV, and in a second subgroup, pulmonary blood flow was measured after an extended period of NPV. A brief period of NPV increased pulmonary blood flow from 2.4 to 3.5 L x min(-1) x /m(-2), with a mean increase of 42%. Pulmonary blood flow continued to improve, with a total increase of 54% after an extended period of NPV. Values fell toward baseline after reinstitution of IPPV. Heart rate was unchanged during NPV, and the improvement in pulmonary blood flow was achieved by an increase in stroke volume from 25 mL/m2 to 37 mL/m2. CONCLUSIONS: Through improvement of the stroke volume alone, NPV brought about a marked increase in the pulmonary blood flow and, hence, cardiac output of Fontan patients. An improvement in cardiac output of this order, and by this mechanism, is currently unmatched by any therapeutic alternatives.

Cardiopulmonary interactions in healthy children and children after simple cardiac surgery: the effects of positive and negative pressure ventilation.

OBJECTIVE: To investigate the effects of cuirass negative pressure ventilation on the cardiac output of a group of anaesthetised children after occlusion of an asymptomatic persistent arterial duct, and a group of paediatric patients in the early postoperative period following cardiopulmonary bypass. DESIGN: Prospective study. SETTING: The paediatric intensive care unit and catheter laboratory of a tertiary care centre. PATIENTS: 16 mechanically ventilated children were studied: seven had undergone surgery for congenital heart disease, and nine cardiac catheterisation for transcatheter occlusion of an isolated asymptomatic persistent arterial duct. INTERVENTIONS: Cardiac output was measured using the direct Fick method during intermittent positive pressure ventilation and again after a short period of negative pressure ventilation. In five of the postoperative patients a third measurement was made following reinstitution of positive pressure ventilation. RESULTS: Negative pressure ventilation was delivered without complication, with no significant change in systemic arterial oxygen and carbon dioxide tension. The mixed venous saturation increased from 74% to 75.8% in the healthy children, and from 58.9% to 62.3% in the postoperative group. Negative pressure ventilation increased the cardiac index from 4.0 to 4.5 l/min/m2 in the healthy children, and from 2.8 to 3.5 l/min/m2 in the surgical group. The increase was significantly higher in the postoperative patients (28.1%) than the healthy children (10.8%). CONCLUSIONS: While offering similar ventilatory efficiency to positive pressure ventilation, cuirass negative pressure ventilation led to a modest improvement in the cardiac output of healthy children, and to a greater increase in postoperative patients. There are important cardiopulmonary interactions in normal children and in children after cardiopulmonary bypass, and by having beneficial effects on these interactions, negative pressure ventilation has haemodynamic advantages over conventional positive pressure ventilation.

Relationship between type of outflow tract repair and postoperative right ventricular diastolic physiology in tetralogy of Fallot. Implications for long-term outcome.

BACKGROUND: Restrictive right ventricular (RV) physiology can be present early and late after tetralogy of Fallot repair. It is associated with a complicated early postoperative course but is favorable late after repair because it is associated with less pulmonary regurgitation, better exercise tolerance, and less QRS prolongation and symptomatic ventricular arrhythmias. It is not known, however, whether in the current surgical era, this physiology is present in tetralogy of Fallot patients at mid-term follow-up and whether it is related to the type of RV outflow tract repair. Finally, the impact of this physiology on the early evolution of QRS prolongation has not been examined previously. In this study we attempted to address these issues in a cohort of recently operated patients. METHODS AND RESULTS: Ninety-five patients were studied 4.3 years after repair by Doppler echocardiography, serial electrocardiograms, and chest radiographs. Restrictive RV physiology defined by the presence of antegrade pulmonary artery flow in late diastole was present in 38% of the patients. It was more common in patients with transannular patch (TAP) repair compared with non-TAP repair (50% versus 21%, P < .05). QRS duration at follow-up was 121.2 +/- 17.6 and 132.6 +/- 11.8 ms in restrictive and nonrestrictive patients with TAP repair, respectively (P < .02). CONCLUSIONS: Restrictive RV physiology has been identified at mid-term follow-up in a contemporary surgical series. It is associated with less QRS prolongation, regardless of the technique used for outflow tract repair, and may be associated with fewer long-term complications. Nonrestrictive physiology is associated with the most marked QRS prolongation. This subgroup is most at risk from the late deleterious consequences of chronic pulmonary regurgitation.

Negative-pressure ventilation improves cardiac output after right heart surgery.

BACKGROUND: A low cardiac output state can complicate the postoperative course of patients undergoing Fontan-type operations and tetralogy of Fallot repair. METHODS AND RESULTS: We investigated the effect of negative-pressure ventilation on cardiac output in 11 children in the early postoperative period after right heart surgery. All patients were initially ventilated with volume-cycled intermittent positive-pressure ventilation, and negative-pressure ventilation was delivered with the Hayek external high-frequency oscillator. Cardiac output was calculated by the direct Fick method, oxygen consumption being measured by respiratory mass spectrometry. Cardiac output was measured during intermittent positive-pressure ventilation and after 15 minutes of negative-pressure ventilation. Negative-pressure ventilation improved the cardiac output by a mean of 46% (P = .005). Heart rate did not change, and stroke volume increased by a mean of 48.5% (P = .005). Mixed venous saturation increased by 4.6% (P < .02), and consequently arteriovenous oxygen content difference fell significantly (P = .01). The systemic and pulmonary vascular resistances were reduced significantly during negative-pressure ventilation (P < .05 and P < .03, respectively). CONCLUSIONS: Negative-pressure ventilation improves cardiac output in children after total cavopulmonary connection and tetralogy of Fallot repair and may prove to be an important therapeutic option in children with the low cardiac output state.

Intraoperative apical ventricular septal defect closure using a modified Rashkind double umbrella.

OBJECTIVE: To demonstrate the safety and efficacy of intraoperative apical ventricular septal defect (VSD) closure using a modified Rashkind double umbrella. DESIGN: Descriptive study of all patients in whom intraoperative device closure of apical VSDs was attempted. SETTING: A tertiary referral centre. PATIENTS: Four patients with an apical VSD requiring closure, during the period January 1993 to May 1995. INTERVENTIONS: Intraoperative placement of a modified Rashkind umbrella. RESULTS: Four successful placements resulting in apical VSD closure, as judged by transoesophageal colour flow mapping. Three patients received a 17 mm and one a 12 mm umbrella. Early complete closure was achieved in three patients. There was a small residual leak around the 12 mm device that had resolved at 5 month follow up. There was one early death, which was unrelated to VSD closure. CONCLUSION: Apical ventricular septal defects can be closed safely and effectively with intraoperative use of a modified Rashkind umbrella.

Should atrial septal defects in adults be closed?

BACKGROUND: By assessing current surgical outcome and symptomatic relief, this study attempts to answer whether atrial septal defects in adults should be closed. METHODS: Thirty-nine adult patients aged 35.2 +/- 13.6 years underwent operation for an atrial septal defect between June 1988 and June 1994. Indications for closure were symptoms (33 patients) or a significant left-to-right atrial shunt (6 patients). Data were obtained from hospital records, and the latest status of the patients was determined by a written questionnaire. RESULTS: There were no deaths. Pulmonary embolism in 1 patient was the only complication observed. The QRS duration on the surface electrocardiogram decreased immediately (p < 0.001), and the cardiothoracic ratio on chest radiographs was significantly lower 3 to 6 months after operation (p < 0.001), both findings reflecting improved hemodynamics. No residual shunts were seen on follow-up (mean follow-up, 3.3 +/- 2.2 years). Twenty-seven (81.8%) of the 33 symptomatic patients improved clinically in terms of exercise performance, atrial arrhythmias, or both. Three (50%) of the 6 previously asymptomatic patients reported improved functional capacity post-operatively. CONCLUSIONS: Today, operation for atrial septal defects in adults can be performed with no mortality and low morbidity and results in symptomatic improvement in the majority of patients. Clinical improvement was seen even in patients who considered themselves asymptomatic preoperatively. We advocate closure of atrial septal defects in adult patients with symptoms or significant atrial shunts.

Effects of inhibition of complement activation using recombinant soluble complement receptor 1 on neutrophil CD11b/CD18 and L-selectin expression and release of interleukin-8 and elastase in simulated cardiopulmonary bypass.

The inflammatory response to cardiopulmonary bypass includes activation of complement and induction of several neutrophil activation pathways. A recombinant soluble form of complement receptor 1 was used as a specific inhibitor of complement activation in simulated cardiopulmonary bypass circuits. Substantial complement activation was observed in these circuits with progressive accumulation of both plasma C3a and terminal complement complex. Soluble complement receptor 1 resulted in a significant reduction in C3a levels (p < 0.01) but did not inhibit terminal complement complex generation. A marked rise in neutrophil CD11b/CD18 expression, simultaneous loss of L-selectin expression, and a progressive accumulation of plasma elastase-alpha 1-antitrypsin occurred and were not affected by soluble complement receptor. However, generation of interleukin-8 in the circuits was inhibited (p < 0.05) by pretreatment with soluble complement receptor. These data suggest that changes in neutrophil activation seen during cardiopulmonary bypass may not be induced directly by anaphylatoxin generation.

Increasing cyanosis early after cavopulmonary connection caused by abnormal systemic venous channels.

OBJECTIVE: To show that abnormal systemic venous channels in patients who undergo cavopulmonary anastomoses can become manifest and haemodynamically important only after surgery despite detailed preoperative investigation. DESIGN: Descriptive study of patients fulfilling the above criteria selected from hospital records over the past three years. SETTING: A tertiary referral centre. PATIENTS: Of the three cases identified, two were isomeric, one with left atrial isomerism and hemiazygos continuation of the inferior vena cava who underwent bilateral bidirectional Glenn anastomoses and one with right isomerism who underwent total cavopulmonary anastomosis. Case 3 had absent left atrioventricular connection with a hypoplastic left lung and underwent a classic right Glenn procedure. All three cases presented with progressive cyanosis in the early postoperative period. INTERVENTIONS AND RESULTS: Postoperative angiography in case 1 showed a remnant of a left inferior vena cava draining to the atrium to have become grossly dilated causing cyanosis, which resolved after redirection of this vessel and of the hepatic veins into the right pulmonary artery with an intra-atrial baffle. Cyanosis in case 2 was caused by intra-hepatic shunting to a hepatic vein draining to the left of the intra-atrial baffle. The diagnosis was made at necropsy, being overlooked on postoperative angiography. Repeat angiography in case 3 showed progressive dilatation of a small left superior vena cava to coronary sinus. Test occlusion with a view to embolisation revealed hitherto an undemonstrated hemiazygos continuation of inferior caval to brachiocephalic vein. The patient underwent surgical ligation of these two venous channels. CONCLUSIONS: Despite appropriate investigation some "abnormal" venous pathways manifest themselves, dilate, and become haemodynamically important only after surgical cavopulmonary anastomoses. In the presence of early postoperative cyanosis "new" systemic venous collateral channels should be considered as a possible cause, which may require reintervention.

Humoral and cellular activation in a simulated extracorporeal circuit.

Endothelial injury consequent upon widespread humoral and cellular activation is probably a major contributor to the phenomenon of cardiopulmonary bypass-induced organ dysfunction. This article reviews some of the mechanisms by which complement and neutrophil activation and interleukin-8 may be involved in this inflammatory response. In a model consisting of a simulated extracorporeal circulation we were able to demonstrate complement activation, profound and specific changes in neutrophil adhesion molecule expression, and interleukin-8 generation. The importance of these changes and their potential interactions are discussed.

Brain damage after profoundly hypothermic circulatory arrest: correlations between neurophysiologic and neuropathologic findings. An experimental study in vertebrates.

Five groups of neonatal pigs were subjected to cardiopulmonary bypass with circulatory arrest periods that varied from 70 to 120 minutes for the investigation of brain changes in induced deep-core hypothermia (15 degrees C) with circulatory arrest. The parameters that were analyzed were (1) microscopy of the brain in animals at 6 hours after bypass procedures and (2) intraoperative monitoring of somatosensory evoked potentials. Microscopic cellular damage appeared in all animals with a circulatory arrest period of more than 70 minutes. These changes involved mainly Purkinje's cells of the cerebellum, and they affected particularly the inferior half of the cerebellum. The prolongation of latency in the cortical responses, which reflects a slowing of the neural transmission with hypothermia, occurred in all animals. The late evoked potentials remained absent in all piglets with circulatory arrest periods of 90, 105, and 120 minutes, but they were fully recovered in all piglets of the control group and those with 70-minute arrest times. We concluded that the cerebellar region is the most sensitive site in which ischemic lesions attain their maximal severity and extent, and the maximum time of circulatory arrest without histopathologic and neurophysiologic sequelae should not exceed 70 minutes.

Neuropathological features of profoundly hypothermic circulatory arrest: an experimental study in the pig.

Twenty-four neonatal pigs were exposed to periods of circulatory arrest of between 70 and 120 min under profound hypothermia at 15 degrees C. Brain tissue taken 6h after cardiopulmonary bypass was examined histologically and by electron microscopy for evidence of hypoxic damage. Specimens from control pigs and animals subjected to 70 min arrest showed no morphological changes in the cerebral or cerebellar neurones. The earliest changes were seen after 90-min arrest; these were highly significant after 120 min. The changes involved mainly the Purkinje cells of the cerebellum with vacuolation in the cytoplasm; the inferior half of the cerebellum was particularly affected. The frequency and pattern of selective vulnerability of the cerebellum may be related primarily to the nature of its blood supply.

Organ dysfunction and cardiopulmonary bypass: the role of complement and complement regulatory proteins.

Cardiopulmonary bypass-induced organ dysfunction remains a clinical problem in certain groups of patients. Although the pathogenesis is multifactorial, it is likely that a panendothelial injury consequent upon widespread humoral and cellular activation is a major contributor to this process. The biologically active products of complement activation are certainly capable of inducing many of the features of the post-perfusion syndrome. The complex interactions between complement and many of the other proposed mediators of this response also supports this contention. However, it is equally certain that many of the other proposed mediators have some role to play. Inhibition of one cell type or inflammatory cascade is therefore unlikely to abolish all the adverse effects of CPB but will, at least in experimental systems, permit a more precise determination of the pathogenesis of this problem. The temptation to simply measure elevated circulating levels of newly identified mediators must be resisted and more effort applied to examining the pathophysiological effects of specific inhibitors. This type of investigation should initially be effected in experimental models where reproducible conditions can be ensured. In conjunction with this, far more precise end-points are required in order to assess the effect of any potential therapeutic intervention in a clinical setting. In particular, new techniques of evaluating endothelial injury need to be developed. In clinical studies careful consideration must be given to the patient population studied. Whilst patients undergoing routine coronary artery surgery form a relatively homogeneous group, the magnitude of endothelial injury sustained is probably small and, especially in terms of lung function, the signal will be diluted by other non-bypass-related events. The study of high risk groups would seem more appropriate despite their heterogeneity. An important unanswered question is why certain sub-populations of patients are at increased risk of clinically relevant bypass-induced injury. The endothelium of these patients may be different: the neonatal pulmonary microcirculation is not the same as that of an adult (with increased fluid filtration pressure and a higher microvascular surface area per unit lung mass [5,6]), children with pulmonary hypertension have histological evidence of an altered/damaged endothelium (S.G. Haworth, Personal Communication) whilst pre-existing sepsis could clearly induce a degree of endothelial dysfunction. A further possibility is that the inflammatory response in these patients is already "primed". Some patients with heart failure have been shown to have elevated circulating TNF.(ABSTRACT TRUNCATED AT 400 WORDS)

Assessment of neurological injury due to circulatory arrest during profound hypothermia. An experimental study in vertebrates.

To investigate brain changes in induced deep core hypothermia (15 degrees C) with circulatory arrest, five groups of neonatal pigs were subjected to cardiopulmonary bypass (CPB), with circulatory arrest (CA) periods varying from 70-120 min. The parameters analysed were: 1. Histology and electron microscopy of the brain six hours post-CPB, 2. Creatinophosphokinase (CPK) from cerebrospinal fluid (CSF), 3. Vasointestinal neuropeptide (VIP) and 7B2 specific neuropeptide both in plasma and brain tissue. The earliest morphological changes were seen after 90 min CA and were highly significant after 120 min arrest. These changes involved mainly the Purkinje cells of the interior half of the cerebellum with vacuolation in their cytoplasm. A rise in CPK in CSF occurred in all piglet-groups. The differences among the various groups were highly significant at 2 and 5 h post-CPB. (P < 0.05). Statistically significant differences were not exhibited among the various groups both in serum and brain tissue total mean values of VIP and 7B2 neuropeptides. We suggest that 1. The cerebellar region is the most sensitive where ischemic lesions attain their maximal severity and extent; the frequency and pattern of selective vulnerability of the cerebellum may be related primarily to its pattern of blood supply 2. The maximum time of CA without histopathological sequelae should not exceed 70 min.

Twelve year experience with the modified Blalock-Taussig shunt in neonates.

Between 1978 and 1990, 53 consecutive modified Blalock-Taussig (MBT) shunts were performed on 51 neonates with cyanotic congenital heart disease using 3 mm-5 mm Gore-Tex grafts. Only 4 of these children had uncomplicated tetralogy of Fallot. The remainder had more complicated pathology requiring urgent intervention. Retrospective analysis of the acute and long term results was performed with 100% follow-up, ranging from 1 month to 12 years (mean 3 years). There were 3 (6%) early deaths (within 30 days of operation) and 17 (33%) late deaths. Of the late deaths, 2 died after further palliation, 2 died after total correction and 13 died suddenly at home. Post mortem examination of the 13 sudden deaths revealed blocked shunts in only 3. Actuarial survival at 2 years was 58%. Shunt patency at 12 months was 87% and at 2 years, 62%. No patient used their initial MBT shunt for more than 40 months. Although this shunt provides good initial palliation, there is a high incidence of late sudden death. We are also concerned about the limited life span of the shunt which partly (3/13) explains the sudden deaths. Therefore we have adopted an aggressive approach to re-study by angiography within 3 months of surgery.