Biomedical subjects
Publications and source records attributed to L N Benson.
A patient with partial anomalous pulmonary venous connection complicated by postoperative occlusion of the distal superior vena cava and a baffle leak causing right-to-left shunt is described. Surgery was avoided by balloon dilation and stenting of the superior vena cava. The baffle leak was closed with a Rashkind double-umbrella device.
OBJECTIVES: This study intended to evaluate application of transcatheter occlusion of the patent ductus arteriosus in children < 10 kg body weight. BACKGROUND: Transcatheter occlusion of the patent ductus arteriosus in the child weighing > 10 kg has been proved safe and effective. METHODS: We reviewed 74 consecutive patients weighing < 10 kg (median 8.1 kg, range 3.98 to 10) and aged 4 to 30 months (median 13 months) who underwent patent ductus arteriosus occlusion between June 1986 and November 1992. A modification of the delivery system to facilitate application in small children is described. RESULTS: A 12-mm device was implanted in 50 patients and a 17-mm device in 24. Three device embolizations occurred early in the experience, and one required removal because of hemolysis associated with a moderate residual shunt. One 17-mm device was removed at catheterization because of acute compromise to left pulmonary artery flow after implantation. Prevalence of residual shunting was 33% at 6 months, 20% at 12 to 18 months and 17% at 2-year follow-up and was not related to device, age, weight or size of the patent ductus. Altered flow to the left pulmonary artery was noted in seven patients (9.9%), with more significant compromise associated with the 17-mm device. CONCLUSIONS: Transcatheter patent ductus arteriosus occlusion is feasible in the small child < 10 kg, particularly with the use of a modified delivery system. However, implantation of a 17-mm device in this patient population may impair flow to the left lung and should be reserved for the symptomatic child.
BACKGROUND: We wished to determine the nature and incidence of changes in the iliofemoral arteries after balloon dilation angioplasty (BDA) for aortic arch obstruction in children and to determine the reliability of gradient magnetic resonance imaging (MRI) in their detection. METHODS AND RESULTS: Sixty-three children, including 62 with and 1 without arch obstruction, underwent MRI of the iliofemoral vessels. Of these, 36 patients had undergone transfemoral BDA (7 after previous transfemoral diagnostic catheterization), 12 had undergone diagnostic transfemoral catheterization but not BDA, and 15 had no history of femoral arterial catheterization. The iliofemoral arteries were normal on MRI in all 15 children without catheterization. Among the 36 children who had undergone BDA, the ipsilateral iliofemoral artery was normal in 15, mildly narrowing in 7, and severely stenotic or occluded in 14 (39%), including 6 of 9 patients treated for acute femoral artery thrombosis and 8 with no history of femoral artery thrombosis. Two patients had documentation of progressive obstruction. Six patients had concordant conventional angiography. There was a significant correlation between the number of balloon catheters used for the angioplasty and severe occlusive changes. Nine of 19 patients who had undergone diagnostic transfemoral catheterization had severe obstructive changes on MRI; 8 of 9 weighed < 10 kg at catheterization. CONCLUSIONS: Obstructive lesions of the iliofemoral arteries are common after transfemoral BDA of arch obstructions (58%) and can be reliably evaluated with gradient MRI. Catheter size and manipulation are the main contributing factors.
The antagonistic effects of magnesium ion as a calcium ion blocker may decrease calcium influx associated with ischemia. However, the effect of magnesium on the preischemic neonatal myocardium has not been investigated previously. The purpose of this study was to investigate the effects of the administration of increasing doses of magnesium on left ventricular performance in the neonate. We assessed left ventricular function (pressure-volume data obtained by the conductance catheter/micromanometer technique) in three groups (n = 6 in each) of newborn pigs (3 to 5 days old) differing with respect to magnesium concentrations. End-systolic elastance did not change during infusion in group A (magnesium = 1.2 mmol/L), whereas in groups B (magnesium = 8 mmol/L) and C (magnesium = 16 mmol/L) it decreased significantly (P < .05) to 67 +/- 6% and 44 +/- 8% of baseline, respectively. The decrease in end-systolic elastance was associated with a significant reduction in cardiac output (P < .05) and stroke work (P < .05) in group C. After administration of magnesium, end-systolic elastance returned to baseline in group B in contrast to group C (78 +/- 3% of baseline value, P < .05). The slope constant of the end-diastolic pressure-volume relation decreased significantly (P < .05) from the preinfusion baseline values of 0.42 +/- 0.08 mL-1 in group B and 0.46 +/- 0.05 mL-1 in group C to 0.3 +/- 0.04 and 0.26 +/- 0.03 mL-1, respectively, versus no change in group A.(ABSTRACT TRUNCATED AT 250 WORDS)
Neonates undergoing heart surgery are exposed to high levels of circulating catecholamines. Our objective was to determine to what extent epinephrine (E)-related cardiotoxicity can be attributed to induced tachycardia. We assessed left ventricle function by pressure-volume data obtained by conductance catheter/micromanometer technique and correlated it with ultrastructure in newborn piglets (3 to 7 d old). Group A (n = 6) received E (1 microgram/kg/min) for 2 h, whereas group B piglets (n = 6) were atrially paced at a rate (220/min) matched to group A. Left ventricle peak systolic pressure and stroke work were significantly higher (p < 0.05) in group A. End-systolic elastance increased during E infusion (70%) versus no significant change in group B. After 2 h of E infusion, end-systolic elastance was significantly reduced in group A from 9.8 +/- 3.5 to 5 +/- 2.4 mm Hg/mL (p < 0.05). Chamber stiffness index increased during E infusion from 0.36 +/- 0.2 to 0.6 +/- 0.3 mL-1 (p < 0.05) and remained elevated (0.58 +/- 0.2 mL-1) after E infusion was discontinued versus no change in group B. E-induced left ventricle dysfunction was associated with scattered but irreversible ultrastructural changes consisting of sarcolemmal rupture and loss of mitochondrial architecture, whereas only minor reversible changes such as microvesicular lipid accumulation and mitochondrial swelling were seen in group B. We conclude that E cardiotoxicity in the neonate is independent of induced tachycardia.
A model of in utero ventilation was used to elucidate the mechanisms by which left ventricular (LV) output increases with the transition from a fetal to a neonatal circulation. Using a conductance catheter, LV volumes were measured in seven anesthetized, near-term fetal sheep. Pressure-volume data was recorded before and with oxygen ventilation and again after occlusion of the umbilical cord. Ventilation caused increases in LV end-diastolic volume measured in seven anesthetized, near-term fetal sheep. Pressure-volume data was recorded before and with oxygen ventilation and again after occlusion of the umbilical cord. Ventilation caused increases in LV end-diastolic volume (2.3 +/- 0.9 to 2.9 +/- 0.6 mL/kg; p < 0.05), stroke volume (1.2 +/- 0.3 to 1.9 +2- 0.2 mL/kg; p < 0.001), and ejection fraction (52.8 +/- 11.1 to 66.4 +/- 8.8%; p < 0.001). Contractile state, as assessed by end-systolic elastance, did not change during the transition. Heart rate also remained constant. Afterload, as assessed by effective arterial elastance, decreased from 1.80 +/- 0.37 to 1.04 +/- 0.33 kPa/mL (p < 0.01). Occlusion of the umbilical cord did not result in any further change in hemodynamic parameters. Pressure-volume analysis revealed that a decrease in effective LV afterload and an increased LV end-diastolic volume are the major determinants of, and contribute comparably to, the profound increase in LV output with in utero ventilation. Enhanced contractility is not required for the increase in LV output to occur.
To define the influence of ventriculo-coronary (VC) arterial connections on ventricular performance and late outcome, and associated wall motion abnormalities in patients with pulmonary atresia and intact ventricular septum, 21 patients aged > or = 6 months (mean 4.3 +/- 3.3 years, range 0.5 to 11.8) were reviewed. Ventricular volumes, mass, systolic functional variables and regional wall motion were measured using biplane ventricular cineangiography. Fourteen patients had VC connections, 11 of whom had coronary artery abnormalities. In comparing patients with VC connections and coronary abnormalities (group I) with those without coronary abnormalities (group II), no hemodynamic differences were observed, except the expected increased right-to-left ventricular systolic pressure ratio in group I (1.33 +/- 0.24 vs 0.72 +/- 0.50). Wall motion abnormalities were observed in 8 patients (7 in group I, and only 1 in group II [p < 0.05]). Ejection fraction in patients with abnormal wall motion was significantly lower (50 +/- 6% vs 57 +/- 7%; p < 0.05) and ventricular systolic pressure ratio significantly higher (1.46 +/- 0.16 vs 0.80 +/- 0.45; p < 0.05) than in those with normal wall motion. Five patients died during follow-up, all of whom had wall motion abnormalities. The findings suggest that patients with VC connections and coronary abnormalities have a higher incidence of wall motion abnormalities, which may reflect ongoing ischemia, and are at risk for late death.
Recently, a case of right isomerism with totally anomalous pulmonary venous connection (TAPVC) to the innominate vein through a vertical vein that ascended in the mediastinum posterior to the left-sided main bronchus was encountered. This retrobronchial vertical vein that has not been described previously in patients with TAPVC to the innominate vein prompted the performance of a retrospective analysis of 44 cases with TAPVC to the innominate vein in which angiography had been performed. The 44 cases consisted of 36 patients with situs solitus, 7 with right isomerism, and 1 with left isomerism. The spatial relation of the vertical vein to the adjacent pulmonary artery and main bronchus could be defined in 41 cases. The vertical vein was retrobronchial in 4 of 5 cases with right isomerism in which the location of the vertical vein could be defined with certainty. No case with situs solitus or left isomerism was associated with a retrobronchial vertical vein. In all 4 patients with a retrobronchial vertical vein, angiographic evidence of obstruction of pulmonary venous drainage was present, and was due to an extrinsic bronchial compression in 2 and to an intrinsic narrowing of the vertical vein in 2.
Between January 1990 and February 1992, 5 asymptomatic patients were identified with hypoplasia of the aortic isthmus at the time of cardiac catheterization for closure of a small patent ductus arteriosus. Isthmal diameters measured from lateral aortograms were 62 +/- 11% of age-matched controls. All patients had a small communication occluded with a 12 mm device and remained asymptomatic at 6-30 months follow up. Residual shunting was demonstrated by color Doppler in 2 patients. No child has developed an arm-leg systolic blood pressure gradient or systemic hypertension. Following device placement, Doppler interrogation across the isthmus in 2 patients demonstrated a velocity shift of 2.1 m/s. Transcatheter occlusion of the patient ductus arteriosus associated with mild isthmal hypoplasia of the aortic arch appears safe and effective and does not result in a clinically significant impairment to isthmal flow in short-term follow-up.
OBJECTIVES: The objectives of this study were to determine the anatomic and physiological factors most responsible for the severe symptoms and poor prognosis of infants with scimitar syndrome. BACKGROUND: Whereas the diagnosis of scimitar syndrome is often made incidentally in older children and adults who undergo chest radiography for diverse reasons, infants in whom the diagnosis is made typically present with severe symptoms and have a poor prognosis. METHODS: The clinical, catheterization and imaging data of 13 consecutive infants with scimitar syndrome who underwent cardiac catheterization in the 1st 6 months of life were reviewed, with emphasis on the pulmonary artery pressure, pulmonary and cardiovascular anatomy, therapeutic interventions and outcome. RESULTS: Twelve of the 13 infants had pulmonary hypertension at the time of diagnosis. Six patients died despite specific treatment. Eleven of 13 infants had associated cardiac malformations and 9 had large systemic arterial collateral channels to the right lung. Seven patients had anomalies involving the left side of the heart, especially varying degrees of hypoplasia of the left heart or aorta, and six of these patients died. Ten patients underwent surgical or transcatheter therapy in the 1st year of life. Systemic arteries to the right lung were ligated in three patients and occluded by transcatheter embolization in four. Balloon angioplasty was carried out in two patients, one with stenosis of the left-sided pulmonary veins and one with stenosis of the anomalous right pulmonary vein. The latter had placement of a balloon-expandable stent. In both patients, pulmonary vein stenosis progressed. Six patients had surgical repair of associated cardiovascular anomalies, and two required repair of extracardiac congenital anomalies. Occlusion of the anomalous systemic arteries was generally associated with clinical improvement, but congestive heart failure and pulmonary hypertension recurred in those patients with associated cardiovascular anomalies, whose condition subsequently responded after correction of the shunt lesions. CONCLUSIONS: The severe symptoms and pulmonary hypertension found in infants with scimitar syndrome have many causes. Anomalous systemic arterial supply, pulmonary vein stenosis and associated cardiovascular anomalies play a significant role, and the ultimate outcome of individual infants depends on the feasibility of treating these anomalies in early infancy.
OBJECTIVES: The purpose of this study was to determine whether wall motion abnormalities are present before or after the Fontan procedure in patients with a univentricular heart of the left ventricular type with an absent right atrioventricular valve connection (tricuspid atresia) and to assess the impact of such abnormalities on ventricular performance and clinical outcome. BACKGROUND: Normal systolic and diastolic ventricular function is critical for a successful Fontan repair. However, there have been no previous studies addressing the relation between regional ventricular function and hemodynamic factors. METHODS: Thirty-seven pediatric patients were studied with biplane ventricular cineangiography. There were 20 male and 17 female patients whose mean age at the time of the Fontan operation was 6.5 +/- 3.5 years (range 2.5 to 15.6). Eighteen patients were studied preoperatively, 25 at > 1 year postoperatively and 6 serially. Wall motion was assessed by a centerline method. Normal ranges for wall motion and other variables were established from 25 normal subjects. RESULTS: Wall motion abnormalities were observed in 2 of 18 patients preoperatively and in 11 of 25 patients postoperatively. Age at operation and ventricular volumes did not differ between postoperative patients who had normal (group I, 14 patients) or abnormal (group II, 11 patients) wall motion. However, ventricular mass and the mass/volume ratio were significantly greater and systolic variables and cardiac index were significantly lower in group II versus group I. Two patients in group I were considered to have a clinically poor outcome (persistent heart failure), and five in group II had heart failure, including one who died late. CONCLUSIONS: These observations suggest that postoperative regional wall motion abnormalities in this setting are not rare, may be related to excessive hypertrophy and may contribute to cardiac dysfunction and a poor clinical outcome.
OBJECTIVES: The purpose of this study was to define the influence of dominant chamber morphology on ventricular performance after the Fontan procedure in patients with double-inlet ventricle. BACKGROUND: Previous studies have reported the impact of ventricular morphology on preoperative ventricular performance and surgical outcome. However, the influence on postoperative ventricular performance has not been addressed. METHODS: Twenty-six clinically asymptomatic patients > 1 year after repair (mean age at procedure 6.1 +/- 3.7 years) were evaluated with ventricular cineangiography and radionuclide blood pool studies (18 with a dominant left ventricular morphology [LV group], 8 with a dominant right ventricular morphology [RV group]) and compared with normal control subjects. RESULTS: Ventricular volume, mass and systolic variables were similar between patient groups. In the LV group, however, the mass/volume ratio was significantly elevated compared with values in control subjects (1.11 +/- 0.28, 0.97 +/- 0.19, p < 0.05), whereas this ratio in the RV group (0.90 +/- 0.11) was within the normal range and significantly lower than that in the LV group (p < 0.05). Mean right atrial and pulmonary artery pressures in the RV group were significantly higher than those in the LV group (p < 0.05). Peak filling rates (2.87 +/- 0.70, 2.41 +/- 1.15 and 3.84 +/- 0.51 end-diastolic volume/s [LV and RV groups and control subjects, respectively]) were significantly lower in both groups than in control subjects (p < 0.001), without intergroup difference. CONCLUSIONS: Ventricular filling abnormalities after atrial to pulmonary anastomosis are common regardless of the type of dominant ventricular morphology, and these abnormalities in patients with dominant right ventricular morphology do not coexist with ventricular hypertrophy. Such diastolic abnormalities may be related to either intrinsic myocardial or acquired factors, not to excessive hypertrophy alone. Those differences may become clinically more apparent with longer follow-up and may raise concerns over the long-term course.
This study aimed to determine whether cancer risk was elevated among patients exposed to radiation from diagnostic cardiac catheterization during childhood. The study cohort included 3915 children who underwent at least one cardiac catheterization at a major children's hospital in Toronto, Canada, between 1950 and 1965, were < or = 18 years at the time of the procedure, and were residents of Ontario. Follow-up of the cohort was done by linkage to the Ontario Cancer Registry up to 1986. A total of seven cancer deaths were observed (O), compared with 5.7 expected (E) based on provincial cancer rates (mortality ratio [O/E] = 1.2; 90% confidence interval [CI] : 0.6-2.3). In the analysis of cancer incidence, 13 cancers were detected, compared with 17.3 expected (O/E = 0.75; 90% CI : 0.4-1.2). These mortality and incidence ratios were not statistically significantly elevated. Detailed analyses were conducted according to age at exposure, age at diagnosis, sex, number of procedures, year of first catheterization, and latent period. Detected deviations in risk were confined to an early period of exposure, indicating that later practices of cardiac catheterization were not associated with increased risk. In general, there was no statistically significant excess risk of cancer among the cohort.
Transcatheter occlusion of Blalock-Taussig shunts was successfully performed in three children with the Rashkind double umbrella occluding device. Complete occlusion was confirmed angiographically in two patients and echocardiographically in the third. The delivery system was adapted for use through smaller sheaths making it more suitable for small children or arterial access.
BACKGROUND: Transcatheter device occlusion of atrial septal defects is an attractive approach, but its efficacy and place in patient management remain to be determined. METHODS AND RESULTS: To evaluate the medium-term results of atrial septal defect device occlusion and factors influencing residual shunting, transesophageal and transthoracic echocardiograms of 49 patients were reviewed. Transesophageal echocardiograms on 48 patients immediately following surgical closure revealed residual shunting in 2% compared with 91% after device occlusion; this proportion decreased to 53% after a mean follow-up of 10 months. The actuarial analysis suggests a progressive resolution of shunting with time. One patient had residual shunting by transesophageal echocardiography immediately after surgical closure compared with 29 after a mean follow-up of 10 months after device occlusion. Residual shunting was not influenced by (1) dimension, location, or position with relation to the device as assessed by transesophageal echocardiography; (2) location of the defect; or (3) device size relative to the stretched dimension of the defect. In 15 patients, a poor correlation existed between transesophageal and transthoracic echocardiographic findings. Variability in serial transthoracic echocardiographic findings was observed in 14. Right ventricular dimension, heart size, and presence of a murmur at follow-up did not correlate with the presence or size of residual shunting after device occlusion. CONCLUSIONS: These results suggest that ongoing spontaneous resolution of residual shunting occurs after device insertion. Factors related to the defect or device could not predict eventual resolution of residual shunting. Transthoracic echocardiography in the follow-up of these patients may not be reliable in determining presence of residual shunting.
Using the conductance catheter technique, we measured the effects of hypoxic acidemia on left ventricular end-systolic elastance in anesthetized, 133-d gestation, in utero fetal sheep (n = 7). Conductance and Millar catheters were introduced into the left ventricle through a carotid artery cutdown. Fetuses were rendered progressively hypoxic and acidemic by placental embolization with repeated injections of 5 x 10(5) 50-microns plastic spheres every 15 min via a catheter placed in the fetal abdominal aorta. We recorded pressure-volume data and arterial blood gases at 15-min intervals. End-systolic elastance was computed using a single-beat method of extrapolating maximum isovolumic pressure. A mean of five boluses was required to cause fetal death. Placental embolization caused progressive fetal acidemia. Mean baseline fetal arterial pH was 7.32 +/- 0.06 (mean +/- SD) and gradually decreased with embolization (p < 0.0001). A linear relationship was found to exist between elastance and pH with a mean decrease of 0.46 kPa/mL per 0.1-unit drop in pH (r = 0.96; p < 0.0001). Despite the decrease in end-systolic elastance, stroke volume and left-ventricular output were maintained due to a parallel decrease in afterload. The decrease in end-systolic elastance was gradual and extended over the entire clinically important range of pH, rather than being a terminal event. This study, which, to our knowledge, is the first to use the conductance catheter to measure fetal left ventricular function demonstrates that hypoxic acidemia adversely affects myocardial contractility assessed by end-systolic elastance.
Administration of catecholamines to newborn infants may potentiate reperfusion injury because of increased transsarcolemmal Ca2+ influx and the presence of less developed sarcoplasmic reticulum in the immature hearts. We investigated the effect of administration of epinephrine (1.5 micrograms/kg per minute for 120 minutes) before ischemia and modified serum ionized Ca2+ concentrations in the cardioplegic solution and perfusate on postischemic left ventricular systolic and diastolic function in 25 piglets (5 to 7 days old) undergoing 90 minutes of cold blood cardioplegic arrest. The piglets were divided into four groups; Ca2+ 1.2 mmol/L, group A (n = 6), Ca2+ 0.25 mmol/L, group B (n = 6), Ca2+ 1.2 mmol/L and epinephrine, group C (n = 6), Ca2+ 0.25 mmol/L and epinephrine, group D (n = 7). Left ventricular function was assessed by a conductance catheter in the left ventricle measuring end-systolic and end-diastolic pressure-volume relationships during transient vena caval occlusion. By analysis of covariance, only Ca2+ concentration was important in predicting ventricular function recovery after ischemia (p < 0.01). End-systolic elastance decreased in all groups after ischemia; the magnitude was significantly greater in the normal groups (51% versus 35%, p < 0.01). There was a significant increase in the chamber stiffness index after administration of epinephrine before ischemia (p < 0.05). Groups with low Ca2+ perfusate (B and D) had no change in chamber stiffness index after ischemia. In contrast, there was a significant increase in chamber stiffness in the normal Ca2+ groups with (C) or without (A) epinephrine after ischemia (p < 0.05). Adenosine triphosphate stores declined significantly in the normal Ca2+ groups--48% versus 18% in the low Ca2+ groups (p < 0.01). We conclude that low Ca2+ concentrations in the perfusate and cardioplegic solutions better preserve left ventricular function in the normal and in epinephrine-stressed neonatal heart after ischemia.
Neonates undergoing heart surgery are exposed to high levels of circulating catecholamines. Our objective was to determine to what extent administration of magnesium counters epinephrine-induced cardiotoxicity. We assessed left ventricular function (pressure-volume data obtained by the conductance catheter/micromanometer technique) and ultrastructure in newborn pigs 3 to 5 days of age before and after administration of epinephrine alone (2 micrograms/kg/min, group A, n = 6) and simultaneously with magnesium sulfate (8 mmol/L, 5 ml/hr, group B, n = 6). Plasma levels of magnesium were maintained at 200% to 250% of control, and ionized calcium was maintained at normal levels. During administration of epinephrine, there was a significant increase in end-systolic elastance from 8.9 +/- 2 to 15 +/- 3 mm Hg/ml in group A and from 7.8 +/- 2 to 16 +/- 3 mm Hg/ml in group B (p < 0.05). This increase was accompanied by an increase in chamber stiffness index (p < 0.05) and shortening of the time constant of isovolumic relaxation (p < 0.05; group A, 19 +/- 3 to 13 +/- 3 msec; Group B, 20 +/- 2 to 15 +/- 2 msec). After epinephrine was discontinued, however, systolic and diastolic indexes returned to baseline levels in group B, whereas group A exhibited a significant reduction in end-systolic elastance (5 +/- 1 mm Hg/ml; p < 0.05) and an increase in chamber stiffness index (0.7 +/- 0.08 versus 0.4 +/- 0.1 ml-1; p < 0.05) and time constant (25 +/- 1 versus 19 +/- 3 msec). Left ventricular dysfunction in group A was associated with focal sarcolemmal rupture and mitochondrial swelling, whereas only minor reversible changes (microvesicular lipid accumulation) were seen in group B. We conclude that magnesium has a protective effect against epinephrine-induced cardiotoxicity because of its blocking action on calcium influx of ionized calcium and could be of therapeutic benefit in the perioperative period.