The stress in a dispersion of mutually polarizable spheres.

Dispersions of dielectric and paramagnetic nanoparticles polarize in response to an external electric or magnetic field and can form chains or other ordered structures depending on the strength of the applied field. The mechanical properties of these materials are of interest for a variety of applications; however, computational studies in this area have so far been limited. In this work, we derive expressions for two important properties for dispersions of polarizable spherical particles with dipoles induced by a uniform external field-the isothermal stress tensor and the pressure. Numerical calculations of these quantities, evaluated using a spectrally accurate Ewald summation method, are validated using thermodynamic integration. We also compare the stress obtained using the mutual dipole model, which accounts for the mutual polarization of particles, to the stress expected from calculations using a fixed dipole model, which neglects mutual polarization. We find that as the conductivity of the particles increases relative to the surrounding medium, the fixed dipole model does not accurately describe the dipolar contribution to the stress. The thermodynamic pressure, calculated from the trace of the stress tensor, is compared to the virial expression for the pressure, which is simpler to calculate but inexact. We find that the virial pressure and the thermodynamic pressure differ, especially in suspensions with a high volume fraction of particles.

Anisotropic diffusion of concentrated hard-sphere colloids near a hard wall studied by evanescent wave dynamic light scattering.

Evanescent wave dynamic light scattering and Stokesian dynamics simulations were employed to study the dynamics of hard-sphere colloidal particles near a hard wall in concentrated suspensions. The evanescent wave averaged short-time diffusion coefficients were determined from experimental correlation functions over a range of scattering wave vectors and penetration depths. Stokesian dynamics simulations performed for similar conditions allow a direct comparison of both the short-time self- and collective diffusivity. As seen earlier [V. N. Michailidou, G. Petekidis, J. W. Swan, and J. F. Brady, Phys. Rev. Lett. 102, 068302 (2009)] while the near wall dynamics in the dilute regime slow down compared to the free bulk diffusion, the reduction is negligible at higher volume fractions due to an interplay between the particle-wall and particle-particle hydrodynamic interactions. Here, we provide a comprehensive comparison between experiments and simulations and discuss the interplay of particle-wall and particle-particle hydrodynamics in the self- and cooperative dynamics determined at different scattering wave vectors and penetration depths.

Measuring thermal rupture force distributions from an ensemble of trajectories.

Rupture, bond breaking, or extraction from a deep and narrow potential well requires considerable force while producing minimal displacement. In thermally fluctuating systems, there is not a single force required to achieve rupture, but a spectrum, as thermal forces can both augment and inhibit the bond breaking. We demonstrate measurement and interpretation of the distribution of rupture forces between pairs of colloidal particles bonded via the van der Waals attraction. The otherwise irreversible bond is broken by pulling the particles apart with optical tweezers. We show that an ensemble of the particle trajectories before, during and after the rupture event may be used to produce a high fidelity description of the distribution of rupture forces. This analysis is equally suitable for describing rupture forces in molecular and biomolecular contexts with a number of measurement techniques.

Dynamics of concentrated hard-sphere colloids near a wall.

We investigate the Brownian motion of hard-sphere colloids near a solid wall by Evanescent Wave Dynamic Light Scattering (EWDLS). We carried out measurements for various volume fractions of sterically stabilized poly(methyl methacrylate) (PMMA) particles over a range of scattering wave vectors, q. While in the dilute regime, the near wall short-time diffusion is significantly slowed down due to particle-wall hydrodynamic interactions (HI); as volume fraction increases, the wall effect is progressively diminished at all q's. We present a new analysis for the EWDLS short-time self- and collective diffusivities applicable to all volume fractions and a simple model for the self-diffusion describing the interplay between particle-wall and particle-particle HI. Moreover, a weaker decay of the near-wall self-diffusion coefficient with volume fraction is predicted by Stokesian dynamics simulations.

Insulin resistance in chronic heart failure: relation to severity and etiology of heart failure.

OBJECTIVES: We attempted to assess insulin sensitivity in patients with chronic heart failure (CHF) and its relation to disease severity. BACKGROUND: Peripheral muscular changes influence the progression of heart failure. This effect may be due to chronic disturbances of insulin and glucose metabolism that affect the energy status of skeletal and myocardial muscle. METHODS: We investigated insulin sensitivity in 79 men-38 patients with CHF, 21 patients with angiographic evidence of coronary artery disease without CHF and 20 healthy control subjects-and assessed its relation to disease severity, etiology and hormonal status (all subjects had a similar age and body mass index). Insulin sensitivity was estimated by minimal modeling analysis of the glucose and insulin and profiles during a 0.5 g/kg body weight intravenous glucose tolerance test. RESULTS: Compared with control subjects, patients with CHF had similar mean fasting glucose but increased insulin levels (67 vs. 29 pmol/liter, p < 0.002) and a 58% reduced mean insulin sensitivity (2.01 vs. 4.84 min-1/pmol/ml x 10(5), p < 0.0001). Peak oxygen consumption (VO2) (r = 0.63), fasting triglycerides (r = -0.62) and age (r = -0.46, all p < 0.001) predicted insulin sensitivity independently. Rest norepinephrine and epinephrine levels, left ventricular ejection fraction and heart failure etiology were not related to insulin sensitivity. Patients with coronary artery disease but no CHF had an intermediate mean insulin sensitivity (3.30 min-1/pmol/ml x 10(5) [-32%, p = 0.042 vs. control subjects; +113%, p = 0.0023 vs. patients with CHF due to ischemic heart disease]). In multivariate analyses of all 79 subjects, age (p = 0.0006), triglycerides (p = 0.0023), fasting insulin (p = 0.0037) and the presence of CHF (p = 0.018) were independent predictors of impaired insulin sensitivity (adjusted joint R2 = 0.53, p < 0.0001). CONCLUSIONS: CHF is associated with marked insulin resistance, characterized by both fasting and stimulated hyperinsulinemia. Advanced heart failure (in terms of reduced peak VO2) is related to increased insulin resistance, but this is not directly mediated through ventricular dysfunction or increased catecholamine levels.

Hormonal changes and catabolic/anabolic imbalance in chronic heart failure and their importance for cardiac cachexia.

BACKGROUND: The role of hormonal and cytokine abnormalities in the development of cardiac cachexia remains obscure. METHODS AND RESULTS: Healthy control subjects (n=16) and patients with chronic heart failure (CHF), classified clinically as cachectic (8% to 35% weight loss over > or = 6 months before study, n=16) or noncachectic (n=37), were assessed for markers of disease severity (maximal oxygen consumption, left ventricular ejection fraction, NYHA functional class). These markers were compared with plasma concentrations of potentially important anabolic and catabolic factors. The degree of neurohormonal activation and catabolic/anabolic imbalance was closely related to wasting but not to conventional measures of the severity of heart failure. Compared with control subjects and noncachectic patients, cachectic patients had reduced plasma sodium and increased norepinephrine, epinephrine (all P<.0001), cortisol, tumor necrosis factor (TNF)-alpha (both P<.002), and human growth hormone (P<.05). Insulin-like growth factor-1, testosterone, and estrogen were similar in all groups. Insulin was increased only in the noncachectic patients (P<.005 versus control subjects). Dehydroepiandrosterone was reduced in the cachectic patients (P<.02 versus control subjects). Insulin, cortisol, TNF-alpha, and norepinephrine correlated independently with wasting in CHF (P<.05; multiple regression of these four factors versus percent ideal weight, R2=.50, P<.0001). CONCLUSIONS: Cachexia is more closely associated with hormonal changes in CHF than conventional measures of the severity of CHF. This study suggests that the syndrome of heart failure progresses to cardiac cachexia if the normal metabolic balance between catabolism and anabolism is altered.

Serum uric acid as an index of impaired oxidative metabolism in chronic heart failure.

BACKGROUND: Elevated serum uric acid concentrations have been observed in clinical conditions associated with hypoxia. Since chronic heart failure is a state of impaired oxidative metabolism, we sought to determine whether serum uric acid concentrations correlate with measures of functional capacity and disease severity. METHODS: Fifty nine patients with a diagnosis of chronic heart failure due to coronary heart disease (n = 34) or idiopathic dilated cardiomyopathy (n = 25) and 20 healthy controls underwent assessment of functional capacity. Maximal oxygen uptake (MVO2) and regression slope relating to minute ventilation to carbon dioxide output (VE-VCO2) were measured during a maximal treadmill exercise test. Metabolic assessment consisted of measuring serum uric acid and fasting lipids, and insulin sensitivity, obtained by minimal modelling analysis of glucose and insulin responses during an intravenous glucose tolerance test. Clustering of indices of functional disease capacity and metabolic factors was explored using factor analysis and multivariate regression analysis. RESULTS: Compared to 20 healthy controls, patients with chronic heart failure had a 52% lower MVO2 (P < 0.001), 56.8% higher serum uric acid concentrations (P < 0.001) as well as a 60.5% lower insulin sensitivity (P < 0.001). Salient univariate correlations in the chronic heart failure group included serum uric acid concentrations with exercise time during the exercise test (r = -0.53), MVO2 (r = -0.50) (both P < 0.001), VE-VCO2 slope (r = 0.45), and NYHA functional class (r = 0.36) (both P < 0.01). In factor analysis of the chronic heart failure group, serum uric acid formed part of a principal cluster of metabolic variables which included MVO2 and VE-VCO2 slope. In multivariate regression analysis, serum uric acid concentrations emerged as a significant predictor of MVO2, exercise time (both P < 0.001,) VE-VCO2 slope and NYHA functional class (both P < 0.02), independent of diuretic dose, age, body mass index, serum creatinine, alcohol intake, plasma insulin levels, and insulin sensitivity index. CONCLUSIONS: There is an inverse relationship between serum uric acid concentrations and measures of functional capacity in patients with cardiac failure. The strong correlation between serum uric acid and MVO2 suggests that in chronic heart failure, serum uric acid concentrations reflect an impairment of oxidative metabolism.

The influence of muscle mass, strength, fatigability and blood flow on exercise capacity in cachectic and non-cachectic patients with chronic heart failure.

BACKGROUND: The influence of age, skeletal muscle function and peripheral blood flow on exercise capacity in chronic heart failure patients is controversial, possibly due to variations in skeletal muscle atrophy. METHODS AND RESULTS: To assess predictors of exercise capacity in patients with clinical cardiac cachexia, we studied 16 cachectic and 39 non-cachectic male chronic heart failure patients of similar age and ejection fraction. All cachectic patients were wasted (% ideal body weight: 81.2 +/- 1.9 vs 105.2 +/- 2.1, P < 0.0001, mean +/- SEM) and had documented weight loss (5-30 kg). Peak oxygen consumption (14.9 +/- 1.4 vs 16.3 +/- 0.6 ml.kg-1, min-1, resting and peak blood flow (plethysmography) and 20 min fatigability (% baseline strength) were all similar between the two groups. Quadriceps strength, muscle size (all P < 0.0001), strength per unit muscle (right: P < 0.05: left: P < 0.001) and 5 min fatigability (P < 0.05) were all lower in cachectic patients. In non-cachectic patients, age (R = 0.48) and quadriceps strength (R = 0.43, all P < 0.01) predicted peak oxygen consumption. Only in cachectic patients did peak blood flow predict peak oxygen consumption significantly (R = 0.72, P = 0.005), whereas age and strength did not. Similar findings were confirmed using other previously published definitions of cardiac cachexia. CONCLUSIONS: The predictors of exercise capacity change with the development of cardiac cachexia from age and strength to peak blood flow. This shift may be caused by additional endocrine or catabolic, abnormalities active in end stage heart failure.

The increased ventilatory response to exercise in chronic heart failure: relation to pulmonary pathology.

OBJECTIVE: To assess the exercise limitation of patients with chronic heart failure (CHF) and its relation to possible pulmonary and ventilatory abnormalities. SETTING: A tertiary referral centre for cardiology. METHODS: The metabolic gas exchange responses to maximum incremental treadmill exercise were assessed in 55 patients with CHF (mean (SD) age 57.9 (13.0) years; 5 female, 50 male) and 24 controls (age 53.0 (11.1) years; 4 female, 20 male). Ventilatory response was calculated as the slope of the relation between ventilation and carbon dioxide production (VE/VCO2 slope). RESULTS: Oxygen consumption (VO2) was the same at each stage in each group. Ventilation (VE) was higher in patients at each stage. Patients had a lower peak VO2 and a steeper VE/VCO2 slope than controls. Dead space ventilation as a fraction of tidal volume (VD/VT) was higher in patients at peak exercise, but dead space per breath was greater in controls at peak exercise (0.74 (0.29) v 0.57 (0.17) litres/breath; P = 0.002). End tidal CO2 was lower in patients at all stages, and correlated with peak VO2 (r = 0.58, P < 0.001). Alveolar oxygen tension was higher in patients at each stage than in controls. CONCLUSIONS: Patients with CHF have an increased ventilatory response at all stages of exercise. Although this is accompanied by an increase in VD/VT, there is hyperventilation relative to blood gases. It is more likely that the excessive ventilation is not due to a primary pulmonary pathology, but rather, the increase in dead space is likely to be a response to increased ventilation.

Leg blood flow, metabolism and exercise capacity in chronic stable heart failure.

OBJECTIVES: To assess the metabolic state of skeletal muscle during exercise in patients with chronic heart failure (CHF) and relate this to exercise capacity. BACKGROUND: During exercise in CHF, there is little relation between exercise capacity and central haemodynamic function. Skeletal muscle and limb blood flow are abnormal in CHF. We investigated the relationship between leg blood flow, metabolism and exercise capacity and ventilation in 10 patients (average age 63.3 +/- 6.0 years; 3 female) with stable CHF. METHODS: Patients undertook maximal exercise testing. Peak oxygen consumption (VO2) and the slope of the relationship between ventilation and carbon dioxide production (VE/CO2 slope) were derived. During a supine cycle exercise test, cardiac output (CO) by Doppler echocardiography, femoral blood flow (FBF) by thermodilution, pulse and blood pressure were recorded, and radial arterial and femoral venous blood samples taken for catecholamine, lactate and potassium estimation every 3 min. RESULTS: The average peak VO2 was 19.7 (+/- 5.2; range 11.3-29.0) ml/kg/min. The proportion of CO to the right leg increased from 0.08 (+/- 0.03) to 0.22 (+/- 0.06) (P < 0.001) at 3 min, with no further significant change thereafter. There was a liner increase in leg VO2 reaching a plateau towards peak. At peak, femoral venous saturation was 22.79% +/- 7.20%. Venous lactate and potassium were higher than arterial (P < 0.001 for each comparison). There was no correlation between exercise performance and any of the measured metabolites either in absolute measurements, expressed as change from rest to peak exercise or as arterio-venous difference. The closest correlate of leg VO2 was leg hydrogen ion production, V[H+]. Change in femoral venous lactate from rest to peak exercise correlated with VE/VCO2 slope even when calculated from before the anaerobic threshold (r = -0.80; P = 0.025). CONCLUSIONS: In CHF, exercise capacity is not determined by individual haemodynamic events, and does not seem to be determined by the possible humoral signals we investigated. Ventilation is abnormal before anaerobic threshold, and predicts subsequent lactate rise, suggesting that skeletal muscle is the origin of excessive ventilation.

Ventilation-perfusion matching in chronic heart failure.

BACKGROUND: The exercise limitation of patients with chronic heart failure is associated with an increased ventilatory response during exercise. This is thought to be due, at least in part, to excessive dead space ventilation. METHODS: To assess ventilation perfusion matching, 20 patients with chronic heart failure and eight controls with asymptomatic left ventricular dysfunction underwent symptom limited treadmill exercise with arterial blood sampling. Metabolic gas exchange was determined by expired gas analysis. Fractional dead space ventilation and the alveolar arterial oxygen difference were derived. RESULTS: There was a fall in fractional dead space ventilation (0.43 to 0.28; P < 0.001), more marked in the controls (peak dead space fraction 0.19 (controls), 0.32 (patients); P = 0.002). There was a rise in alveolar arterial difference in all patients (1.59 to 2.55 kPa; P = 0.006) with no difference between patients and controls. Arterial carbon dioxide tension fell during exercise (4.89 to 4.63 kPa; P < 0.001), with no difference between patients and controls. There was no significant change in arterial oxygen tension. CONCLUSIONS: The fall in arterial carbon dioxide was the same in both patients and controls. The modest increase in alveolar-arterial oxygen difference tension was the same in both groups, which, coupled with the stable arterial oxygen tension makes it unlikely that a primary change in ventilation-perfusion matching is the cause of increased ventilatory response to exercise in chronic heart failure.

Relationship between arterial potassium and ventilation during exercise in patients with chronic heart failure.

The mechanisms underlying the increased ventilatory response to exercise seen in patients with chronic heart failure are not clearly understood. Arterial potassium has been suggested as an important ventilatory stimulant. The authors have investigated the arterial potassium response in patients with heart failure. Although arterial potassium rises during exercise, no evidence was found to suggest a greater potassium response in patients with heart failure compared to normal subjects. There was no direct correlation between the rise in ventilation and the rise in arterial potassium. It remains possible that there is an increased sensitivity to arterial potassium in patients with heart failure, but it would need to be three times greater than in normal subjects.

Insulin resistance in chronic heart failure.

The objective of this study was to investigate the existence of abnormalities of insulin sensitivity in patients with chronic heart failure. Glucose metabolism and insulin resistance were assessed in 10 male patients with severe, chronic heart failure and in 10 matched control subjects. Glucose, insulin and C-peptide concentration profiles were measured following a 0.5 g.kg-1 intravenous glucose tolerance test. Insulin sensitivity (inversely related to insulin resistance) was estimated by minimal modelling analysis of the glucose and insulin profiles. Heart failure patients had similar mean fasting plasma glucose concentration to controls but a significantly greater mean fasting plasma insulin concentration (P = 0.002) and C-peptide concentration (P = 0.02). Plasma glucose response profile was similar in the two groups but the incremental plasma insulin response profile of the heart failure group was significantly greater (P = 0.004). Mean insulin sensitivity was 73% lower in the heart failure patients (P = 0.003). These findings show that patients with severe chronic heart failure are hyperinsulinaemic and insulin resistant compared with a matched health group. This insulin resistance and hyperinsulinaemia may contribute to the progressive deterioration in myocardial function and associated clinical features of fatigue and reduced exercise tolerance seen in heart failure. Interventions designed to overcome or reduce insulin resistance warrant further investigation.

Predictors of exercise capacity in chronic heart failure.

Abnormalities of skeletal muscle rather than of haemodynamics may be important determinants of exercise capacity in chronic heart failure. We investigated an array of indicators of central haemodynamics and peripheral muscle function to establish which resting measurements predicted exercise performance. In 20 patients quadriceps strength, resting and peak leg blood flow and leg muscle cross sectional area were measured. In 18 patients average daytime blood pressure and pulse rate, haemodynamic variables at rest and during exercise, and autonomic activity were measured. There were correlations between peak oxygen consumption and quadriceps strength (0.65; P = 0.007), thigh muscle cross sectional area (r = 0.63; P = 0.004), and average daytime systolic blood pressure (r = 0.66; P < 0.01). There were no correlations with indices of peripheral blood flow, measures of haemodynamic function, or autonomic function. Quadriceps strength was the most important individual correlate of exercise tolerance (r = 0.73). With total muscle cross sectional area and left quadriceps strength also taken into consideration, 82% of the variation in peak oxygen consumption was explained. Of the haemodynamic variables, only average daytime systolic blood pressure predicted exercise performance. The resting variables that best predict exercise performance in chronic heart failure are measures of skeletal muscle function and bulk, and average daytime systolic blood pressure. These findings suggest that abnormalities in the periphery largely determine exercise performance in chronic heart failure, and that the ability of the heart to generate an adequate blood pressure response to daily activities is also predictive of functional status.

The role of right and left ventricular function in the ventilatory response to exercise in chronic heart failure.

BACKGROUND: Right ventricular function may be an important determinant of exercise capacity, peak oxygen consumption (VO2), and the ventilatory response to carbon dioxide production (VE/VCO2 relation) in patients with chronic heart failure (CHF). METHODS AND RESULTS: We studied the role of right ventricular function in CHF and also investigated the effects of absent right ventricular reserve in patients previously operated on with Fontan's procedure by measuring metabolic gas exchange during exercise in five groups of patients: (1) 10 patients who had previously undergone Fontan's procedure for congenital heart disease in whom the right ventricle is not functional; (2) 11 age-matched control subjects with dilated cardiomyopathy (DCM); (3) 15 age-matched normal subjects; (4) 42 patients with CHF; and (5) 16 age-matched control subjects. Left and right ventricular ejection fractions (LVEF and RVEF) were measured by radionuclide ventriculography in group 4. In the young subjects, the VE/VCO2 slope was lower in the control subjects than in the other two groups, being 24.4 +/- 4.3 against 33.3 +/- 6.6 in group 1 (P < .001) and 29.6 +/- 8.1 in group 2 (P < .05). The correlation between peak VO2 and VE/VCO2 was -0.80 (P = .005) in group 1 and -0.76 (P = .007) in group 2. In the older age groups, the VE/VCO2 slope was significantly greater (38.0 +/- 14.9 versus 25.4 +/- 3.7; P < .001) in the heart failure group (group 4). In neither control group was there a significant relation between peak VO2 and VE/VCO2 slope. In group 4, the relation between peak VO2 and VE/VCO2 was similar to that seen for groups 1 and 2. LVEF was 24.3 +/- 14.1%, and RVEF was 32.5 +/- 13.1%. There was no correlation between either RVEF or LVEF and peak VO2 or VE/VCO2 slope in the heart failure group. CONCLUSIONS: The relation between excessive ventilation and reduction in peak oxygen consumption is present in patients with no functioning right ventricle. RVEF is not a determining feature of either exercise capacity or the excessive ventilatory response in CHF.

Assessment of insulin sensitivity in man: a comparison of minimal model- and euglycaemic clamp-derived measures in health and heart failure.

1. Simplified protocols for the measurement of insulin resistance will facilitate studies of this potentially important variable. 2. Using the euglycaemic clamp as the reference technique, we have assessed the validity of the insulin sensitivity index (inversely related to insulin resistance) obtained using a high-dose (500 mg/kg), unmodified intravenous glucose tolerance test with a 16 point sampling schedule and analysis using the minimal model of glucose disappearance. The two methods were compared in 10 clinically normal subjects and five patients with severe heart failure secondary to coronary heart disease. 3. The insulin sensitivity index of the minimal model was compared with four clamp-derived measures. Correlation coefficients of 0.72-0.92 (P < 0.01-P < 0.001) were obtained between the two methods over a wide range of insulin sensitivity [model values 1.03-14.63 min-1/(pmol/l) x 10(-5)]. Patients with heart failure had the lowest measures of insulin sensitivity. 4. The high-dose, unmodified intravenous glucose tolerance test with minimal model analysis is a straightforward and economical clinical procedure and provides a valid measure of insulin sensitivity, in health and disease.

Insulin resistance syndrome as a feature of cardiological syndrome X in non-obese men.

OBJECTIVE: To assess the features of the insulin resistance syndrome in patients presenting with cardiological syndrome X, who experience angina despite angiographically normal coronary arteries. PATIENTS AND METHODS: 14 Non-obese male patients with syndrome X and 38 symptom free, apparently healthy, male volunteers were studied. Insulin sensitivity (inversely related to insulin resistance) was measured by minimal modelling analysis of glucose and insulin concentrations during an intravenous glucose tolerance test. Serum lipids, lipoproteins, and apolipoproteins were also measured. RESULTS: Insulin sensitivity was 31% lower in the men with syndrome X (p < 0.05) and fasting insulin concentration was 30% higher (p < 0.05). The patient group also had 64% higher mean triglycerides (p < 0.001) and 20% lower mean high density lipoprotein cholesterol concentration (p < 0.01). Systolic blood pressure was also 10% higher in the syndrome X group (p < 0.01). There were no differences in total cholesterol, low density lipoprotein cholesterol or lipoprotein (a). CONCLUSION: These findings show that non-obese male patients with anginal chest pain but normal coronary arteries (syndrome X) are insulin resistant, hyperinsulinaemic, and have higher concentrations of triglycerides and lower high density lipoprotein cholesterol than healthy men. The insulin resistance syndrome may predispose to a spectrum of arterial disease capable of causing myocardial ischaemia.

Long-term growth following neonatal anatomic repair of transposition of the great arteries.

Despite generally normal prenatal growth, surviving infants with transposition of the great arteries (TGA) frequently develop severe and progressive growth impairment which is not always fully reversed by elective atrial repair within the first year of life. This study was undertaken to determine the effect of neonatal anatomic repair of TGA on long-term growth. Twenty-three children with uncomplicated TGA were followed for a mean of 60 (12-90) months after anatomic repair at a mean age of 11 (1-40) days. Standardized measurements of weight, height, and head circumference for both patients and normal siblings were expressed as percentiles as well as in Z scores (in standard deviations from the mean for age and sex) based on internationally recognized standards. At latest follow-up, 22 (96%) of the patients were above the 3rd percentile for weight and 21 (91%) for both height and head circumference, with 13 (57%), 11 (48%), and 13 (57%) above the 50th percentile for each respective parameter. The mean Z scores (+/- SD) for weight, height, and head circumference for the patient group were -0.1 +/- 1.2, -0.2 +/- 1.3, and -0.1 +/- 1.1, respectively, and did not differ significantly from those of the reference population (p > 0.05 for each comparison). Paired comparisons of mean Z scores for each growth parameter with those of 35 normal siblings demonstrated no significant difference for weight or height and a small but significant difference for head circumference. Age at surgical repair (within the first 6 weeks of life), duration of follow-up and the development of moderate supravalvar pulmonary stenosis were not statistically related to long-term growth.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary angioplasty in cardiac transplant recipients.

Accelerated coronary artery disease following cardiac transplantation remains an important obstacle to long-term survival and the correct management strategy remains unclear. This observational, prospective study was designed to examine the feasibility of using percutaneous transluminal coronary angioplasty (PTCA) in the treatment of post-transplant coronary disease. Thirteen consecutive patients were selected from the total population of 276 transplant recipients who underwent routine coronary angiography between 1987 and 1990. Selection of patients was on angiographic criteria alone and PTCA was performed to all accessible stenoses with more than 80% luminal narrowing. PTCA was performed using standard angioplasty equipment and procedure as considered appropriate for the individual lesion. A successful PTCA was defined as more than 30% reduction in luminal narrowing and a residual narrowing of less than 50%. Restenosis was defined as a loss of 50% or more of the gain achieved at the time of successful PTCA or more than a 30% increase in narrowing at the site of stenosis. A total of 31 lesions were dilated in this group and a successful result was achieved in 29 of these (93%) and in 12 of the 13 patients. The one patient with failed PTCA underwent later successful coronary artery bypass grafting to complete revascularization. Four of the 13 patients have had two angioplasty procedures, two for restenosis and two for disease progression in other sites. One patient died 15 months after the initial PTCA and the remaining 12 were asymptomatic with good exercise tolerance and ventricular function at a mean of 19 months (range 1-39 months) following first PTCA.(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiographic appearance of pulmonary artery stenosis.

Colour flow Doppler mapping can show abnormalities of flow even when the echocardiographic image is equivocal. Routine echocardiography in two patients who were thought to have pulmonary valve stenosis and a ventricular septal defect initially appeared to be normal. Colour flow Doppler mapping, however, showed multiple flow aliasing within the pulmonary artery, approximately 1.5 cm downstream from the pulmonary valve. More detailed examination by cross sectional echocardiography showed a membrane at this level in both patients. It is possible that more cases of this uncommon anomaly will come to light with increasing use of Doppler techniques.