Theresa A. Tacy

Range of normal valve annulus size in neonates

Abstract In preterm and term infants, weight can be used as a predictor of normal valve annulus dimensions measured by 2-dimensional echocardiography. The relation of weight and annulus size in neonates with-out heart disease may be used as a reference standard for determining adequacy of valve annular dimensions.

In Vitro Analysis of Regurgitant Fraction Using Doppler Power-Weighted Sum of Velocities☆☆☆★

The power-weighted sum of velocities (PWS) is the sum of each velocity component of the Doppler signal multiplied by its power. The purpose of this study was to determine (1) whether PWS is linearly related to volume flow and (2) whether PWS can predict the regurgitant fraction in an in vitro pulsatile flow system simulating aortic regurgitation. Doppler analysis of aortic flow was performed with an intact valve and two regurgitant valves. For each valve a linear relation between the forward flow PWS and forward flow volume was demonstrated, with excellent correlation (r = 0.99). For the valves with regurgitant orifices, the values for the PWS-derived regurgitant fraction were compared with measured regurgitant fraction. A fair correlation was demonstrated (r = 0.59), with low accuracy in prediction (error 44% +/- 24%). The PWS was inaccurate in predicting flow ratios in our in vitro system despite the strong relation with forward flow volume. The error incurred may be due to effects of filters that remove low velocity and low amplitude information.

VESSEL COMPLIANCE MISMATCH CAN INCREASE WORKLOAD OF THE LEFT VENTRICLE IN ABSENCE OF OBSTRUCTION AFTER REPAIR OF AORTIC COARCTATION. † 220

VESSEL COMPLIANCE MISMATCH CAN INCREASE WORKLOAD OF THE LEFT VENTRICLE IN ABSENCE OF OBSTRUCTION AFTER REPAIR OF AORTIC COARCTATION. † 220

Proximal Pulmonary Artery Banding Does Not Simulate a Systemic Afterload for Conditioning a Left Ventricle in Mustard Patients

Proximal Pulmonary Artery Banding Does Not Simulate a Systemic Afterload for Conditioning a Left Ventricle in Mustard Patients

Effect of Suspended Red Blood Cells On Pressure Gradients Across Blalock-Taussig Shunts 151

It is generally assumed that blood behaves strictly as a particle-free fluid and not as a suspension in arterial sized vessels (> 1 mm). However, we have previously demonstrated a biphasic deviation of pressure gradients(PG) of blood from a particle-free fluid of equal viscosity in straight tubes, with the blood PG being greater than the particle-free fluid at low flowrates and lower at high flowrates. Since this behavior may affect velocity-derived PG, we addressed the hypothesis that PG across a BT shunt would show significant deviation from that of a particle-free blood analog fluid (BAF). Methods: The in vitro BT shunt model consisted of two arterial sections connected by a physiologically sized shunt (D = 5 mm, L = 9 cm). PG across the shunt were obtained by measuring pressure 10 cm proximal and distal to the inlet and outlet respectively. For a given flow rate the PG across the shunt was recorded for both blood and an equal viscosity BAF(aqueous glycerin solution, 3.8 cP). PG differences were plotted vs. Reynolds number (Re = ratio of inertial to viscous forces) and divided into laminar and turbulent flow regimes, with a transition Re of 2100 (the approximate transition from laminar to turbulent flow in tubes). Differences in PG between blood and BAF were considered significant at a level of 0.01 using a paired t-test for both the laminar and turbulent regimes. Results: For Re 0.5). However, for Re > 2100, the PG for blood were consistently lower than that of BAF and the differences were significant (mean difference = 9.9 mmHg, p < 0.01). Conclusions: Blood PG across BT shunts deviate from BAF PG. This effect is especially pronounced in the turbulent regime and is consistent with our previous investigations using straight tubes, suggesting Re-dependent phenomena may account for this behavior. These findings may have important implications in the noninvasive assessment of pulmonary artery pressure in patients with BT shunts.

Pulsatile Wall Shear Stress Gradient and Aortoseptal Angle: Implications for Subaortic Stenosis |[dagger]| 147

A better understanding of the etiology of discrete subaortic stenosis (SAS) would be useful in identifying patients at risk and in surgical decision making since the onset, progression, and recurrence of SAS are difficult to predict. Previous studies have shown that congenital defects and morphologic abnormalities associated with SAS (such as steepened aortoseptal angle [AoSA]) cause significant, localized elevations in peak wall shear stress and the wall shear stress gradient (WSSG). High WSSG has been associated with cellular changes in the endothelium. Since the magnitude of wall shear stress varies thoughout the cardiac cycle, we addressed the hypothesis that these morphologic abnormalities have similar effects on the time-averaged shear stress and WSSG. Methods: A finite element model of the left ventricular outflow tract was implemented on the Cray C90 at the Pittsburgh Supercomputing Center for typical pulsatile flow conditions. AoSA was varied between 120 and 150 degrees, maximum aortic velocities from 0.5 to 1 m/s, and aortic diameter from 1 to 1.5 cm. Shear stress and WSSG were directly calculated from the velocity field at discrete points in time. The time-averaged wall shear stress and WSSG at the location of the peak was determined. Results: At an aortic velocity of 1 m/s, the peak and time-averaged shear stress increased with steeper AoSA by 52% and 49.5% respectively. WSSG was more sensitive to changes in AoSA with the peak WSSG increasing by 217%, compared to the time-averaged WSSG which increased by 225%. Conclusions: Geometric variables had similar effects on both the peak and mean shear stress and WSSG. Although the progression and recurrence of SAS may be dependent on time-varying exposure to shear stress, this exposure may be quantified using either a peak or a mean value.

VENTRICULAR SEPTAL DEFECT MODULATES SEPTAL SHEAR STRESS CAUSED BY AORTO-SEPTAL ANGLE: IMPLICATIONS FOR SUBAORTIC STENOSIS. † 219

VENTRICULAR SEPTAL DEFECT MODULATES SEPTAL SHEAR STRESS CAUSED BY AORTO-SEPTAL ANGLE: IMPLICATIONS FOR SUBAORTIC STENOSIS. † 219

NECROTIZING ENTEROCOLITIS IN THE NEWBORN WITH CONGENITAL HEART DISEASE IS A POOR PROGNOSTIC SIGN. 155

NECROTIZING ENTEROCOLITIS IN THE NEWBORN WITH CONGENITAL HEART DISEASE IS A POOR PROGNOSTIC SIGN. 155