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Background Blood speckle tracking echocardiography allows for direct quantification of interventricular and aortic flow profiles, principally in children. Here, we sought to demonstrate the feasibility and reproducibility of blood speckle tracking echocardiography in the aortas of healthy children. Methods and Results One hundred healthy White children evaluated for the screening of congenital heart disease were prospectively enrolled. Echocardiographic examinations were performed using a Vivid E 95 ultrasound system, with blood speckle tracking from a focused and zoomed view of the aortic root and the ascending aorta. Vortex position, height (mm), width (mm), sphericity index, and area (cm 2 ) were measured and indexed by body surface area. Median (interquartile range) age was 8.2 (5.6–11.0) years, median (interquartile range) weight was 28 (19–35) kg, and median (interquartile range) body surface area was 1.01 (0.79–1.16) m 2 . Vortices were visualized in only a single phase of the cardiac cycle in 25 subjects—14 (56.0%) were evident in early diastole and 11 (44.0%) in late systole. Vortices visualized in diastole had a mean area of 0.27±0.1 cm 2 /m 2 , while those in systole had a mean area of 0.34±0.12 cm 2 /m 2 . In a subset of 20 patients, inter‐ and intraobserver coefficient of variation and intraclass correlation coefficients were determined and showed good reproducibility. Conclusions We demonstrate feasibility and reproducibility of blood speckle tracking and identified vortical flow patterns in the aortic root and ascending aorta in healthy children. These data may serve as a baseline for evaluating aortic flow patterns in children with congenital and acquired heart disease.

BACKGROUND: Ventricular septal flattening, frequently present in pulmonary hypertension (PH), can be quantified using eccentricity index (EI). EI has not been evaluated by concurrent echocardiography and cardiac catheterization, and traditionally does not account for post-systolic septal flattening, often seen in PH. We evaluated left ventricular (LV) shape, including a novel measure of maximal EI (EIM) to account for post-systolic septal flattening, to establish the relationship with concurrent invasive hemodynamics. METHODS: Echocardiography was performed at 2 institutions in 78 pediatric pulmonary hypertension patients during cardiac catheterization, and in 78 matched controls. From mid-papillary parasternal short-axis views, EI and right-to-left ventricular diameter ratio (RV:LV) were assessed. RESULTS: EI and RV:LV measures were significantly increased in PH compared to controls. Shape measures correlated with invasive hemodynamics and PH outcome measures (PH-related hospitalization, functional class, medical therapy escalation, and brain natriuretic peptide). End-systolic EI of 1.16 best identified the presence of PH, while an EIM of 1.42 and 1.94 best identified half-systemic and systemic PH, respectively. An EIM of 1.27 was associated with an odds ratio of 16.16 (95% CI 6.62-39.46) for PH-related hospitalization or escalation of therapy. CONCLUSIONS: Using simultaneous echocardiography and catheterization in the largest study population to date, we demonstrate that EI and RV:LV ratio correlate with invasive hemodynamics and outcomes measures, and EI can accurately define those with clinically important PH. These measures strengthen the ability of echocardiography to identify and follow pediatric PH patients, especially in the absence of methods to quantify RV systolic pressures.

The evaluation of left ventricular (LV) dimensions, area, volumes, and function by 2D echocardiography is challenging. Quantification of LV chamber size and function is an essential and routine part of echocardiographic examination at all ages and in all settings.1,2 However, these fundamental measurements, although often critical for clinical decision making, are often subject to significant variability, especially in the pediatric age group.3–6 If a measurement is not accurate or reproducible, it may be difficult to be sure whether it is normal or not and also hard to follow the trend over time.3–6 Interpretation of an echocardiographic measurement over time should take into account several biases. An incomplete list of these potential biases includes (1) measurement accuracy (ie, Do we measure it in the same way? How much the final result will be affected by different measurement approaches?), (2) measurement reproducibility (how standardized a measurement varies according to different observers, and how standardized imaging collection varies according to different operators/repeated observation by the same operator), (3) physiological variation (How the variation over time is related to growth and age/body size changes?), (4) disease-related variations (How much the variation is pathological?), and (5) environment (patient cooperation/sedation; To what extent variations in basic parameters [ie, heart rate, blood pressure, and loadings conditions] influence our measurements?). See Article by Selamet Tierney et al

Background— Pulsed-wave Doppler determination of the pulmonary artery acceleration time (PAAT) as a surrogate for pulmonary artery pressure was found to be of clinical value for assessment of pulmonary hypertension (PH) with studies to date exclusively performed in adults. This study aims to provide representative, normal reference values for PAAT in children of all ages. Moreover, we validated abnormal PAAT values in 54 children with PH. Methods and Results— We conducted a prospective echocardiographic study in 756 healthy children (aged 1 day to 18 years) and in 54 children with PH. Possible associations of age, body length, body weight, body surface area, and heart rate on PAAT were investigated. The PAAT correlated positively with age ( r =0.848), body length ( r =0.871), body surface area ( r =0.856), and body weight ( r =0.825) and negatively with heart rate ( r =−0.906). PAAT increased with age (neonates: median: 81 ms, range: 53–104; 18th year of life: median: 151 ms, range: 107–187). Receiver operating characteristic analysis for detecting PH patients using age-specific z scores showed an excellent performance of PAAT ( P Conclusions— The PAAT normal reference values and z scores we provide here will be useful to identify children with a shortened PAAT. Abnormal PAAT values with scores

Continuous venovenous hemodiafiltration (CVVHDF) in infants is challenging due to a lack of specific and widely available technology. There is need for high precision of fluid balance and hemodynamic stability. The aim of this study is to report the first experience with the newly developed Prismaflex HF20 disposable set (HF20 set) in infants with CVVHDF. We provided safe treatment in four infants (4-14 kg) suffering from acute renal failure with the HF20 set. Treatment monitoring included patients' blood pressure, patients' weight change, and fluid balance. The anticoagulation was performed with unfractionated heparin. We used commercially available bicarbonate-buffered solutions as dialysate fluid and substitution fluid. At start and during the treatment, the patients showed hemodynamic stability. Desired fluid balance was achieved in all patients during the treatment periods of 49-102 hours. No complications occurred. This report presents CVVHDF experience on the feasibility and safety of the HF20 set in infants. It can be used in CVVHDF or hemodialysis mode. Treatments were well tolerated in all patients, and flow rate adaptability to infants' needs was very acceptable, and the usage of this device was easy and safe.

Measurements of anti-FXa or anti-FIIa (thrombin) activities are conventional tests for biological monitoring of low molecular weight heparin (LMWH) or unfractionated heparin treatment. It was the aim of our study to assess the anticoagulant efficacy of the LMWHs nadroparin and enoxaparin and that of unfractionated heparin not by the above-mentioned isolated measurements but in the physiological environment of clotting plasma or whole blood. The effects of increasing amounts of nadroparin, enoxaparin, or unfractionated heparin on the time-course of FXa or FIIa formation were investigated in tissue factor activated platelet-poor plasma using a subsampling technique and chromogenic substrates. Moreover, the anticoagulant efficacy of these drugs was also investigated in whole blood triggered by the physiological relevant activator collagen/endogenous thrombin using thrombelastometry. Nadroparin is as efficient as enoxaparin concerning suppression of endogenous FXa or FIIa formation. The two LMWHs are capable of suppressing the formation of FIIa as efficient as that of FXa. Compared with equivalent anti-FXa activity, unfractionated heparin is markedly more efficient in suppressing the formation of FXa and FIIa than the LMWHs. Corresponding results were obtained in whole blood. The anticoagulant efficacy of nadroparin was comparable with that of enoxaparin and the influence of unfractionated heparin on thrombelastometry parameters was markedly stronger than that of the two LMWHs. We conclude that LMWHs are efficient inhibitors not only of endogenous FXa formation but also of endogenous FIIa formation. Under our experimental conditions, the anticoagulant efficacy of nadroparin was comparable with that of enoxaparin but markedly lower than that of unfractionated heparin.

OBJECTIVE: To evaluate the clot strength in cord versus adult blood. METHOD: Thrombelastometry (TEM) was the method of choice as it provides information on the clot strength in terms of the maximum clot firmness (MCF) and on the fibrin polymerization process in terms of the clot formation time and the alpha angle. RESULTS: The MCFs were significantly lower in cord versus adult platelet rich plasma (PRP, 63.0+/-3.8 vs. 67.0+/-3.9 mm, P=0.006) and in cord versus adult whole blood (WB, 55.3+/-3.8 vs. 59.3+/-3.6 mm, P=0.001) employing the thrombelastometry with extrinsic activator assay. We suggest that the diminished clot strength in cord versus adult blood and plasma samples is attributable to an impaired polymerization of neonatal fibrin: (i) the thrombelastometry with extrinsic activator and inactivated platelets (FIBTEM) assay revealed significantly lower MCFs in cord versus adult PRP (23.0+/-3.1 mm vs. 27.3+/-3.9 mm, P=0.002) and in cord versus adult WB (11.6+/-2.3 mm vs. 15.3+/-3.3 mm, P

In the present study, we compared the levels of intravascular tissue factor (TF) present in cord versus adult whole blood (WB) prior and after lipopolysaccharide (LPS) stimulation. High levels of intravascular TF might help to explain the clinically observed efficient clotting of cord blood despite low levels of procoagulatory factors. Quantitative reverse transcription-polymerase chain reaction revealed same (basal) TF mRNA expression levels in both native cord and adult WB, and approximately same increase in TF mRNA expression owing to LPS incubation in both cord and adult WB (normalized to the housekeeping gene beta-actin). Flow-cytometric (fluorescence activated cell sorting) analysis revealed significantly higher surface TF antigen exposure on the neonatal monocyte membrane in native WB samples, and approximately same ability of neonatal and adult monocytes to express TF upon LPS-stimulation. Thrombelastography revealed significantly shorter clotting times of native cord versus adult WB (527+/-41 vs. 592+/-23 s, P

The aim of our study was to investigate the combined in vitro effects of melagatran and eptifibatide on platelet aggregation and thrombin generation under low and high coagulant challenge in tissue-factor-activated, platelet-rich plasma. Increasing amounts of melagatran dose-dependently decreased prothrombin fragment 1.2 and activated factor X values, and dose-dependently prolonged the lag phase until the onset of platelet aggregation. Eptifibatide exerted a dose-dependent anti-aggregating effect under both high and low coagulant challenge. The combination of melagatran and eptifibatide resulted in significant additive prolongation of the lag phase until the onset of platelet aggregation, which was more pronounced under low coagulant challenge. Under low, but not under high, coagulant challenge, the combination of melagatran and eptifibatide had a significant additive inhibitory effect on platelet aggregation. No additive effects on decreasing prothrombin fragment 1.2 and activated factor X values were observed with combined administration of the drugs. The present study demonstrates the additive effect of melagatran and eptifibatide on platelet aggregation inhibition and on prolongation of the lag phase until the onset of platelet aggregation.