Jet eccentricity: a misleading source of agreement between Doppler/catheter pressure gradients in aortic stenosis.

Characterization of the severity of aortic stenosis relies on accurate measurement of the pressure gradient across the valve and the valve area. Pressure gradients measured by Doppler ultrasound based on the clinical form of the Bernoulli equation often overestimate pressure gradients by catheter as the result of pressure recovery. Doppler techniques measure the velocity of the vena contracta of the stenotic jet. This corresponds to the maximal pressure gradient and the minimal effective valve area. Pressure recovery can be characterized by analysis of the spread of the stenotic jet downstream of the valve as it fills the aorta and should be influenced by the shape of the velocity profile of the decaying jet. In this study, we addressed the hypothesis that the site of complete pressure recovery (the point at which the jet fully expands to the size of the aorta), the effective valve area, and the maximal pressure gradient are affected by jet eccentricity. To accomplish this, we developed a computational model of aortic stenosis that provides detailed velocity and pressure information in the vicinity of the valve. The results show that the width of the eccentric wall jet decreased and maximal velocity increased with greater jet eccentricity. Furthermore, for a constant anatomic area, the effective valve area decreased, the distance to complete pressure recovery increased, and the maximal pressure gradient increased with the degree of eccentricity. Failure to take this into account could fortuitously drive Doppler and catheter measurements toward agreement because the distal pressure sensor will not record the fully recovered pressure. Therefore the pressure gradient across a stenotic valve depends on jet eccentricity. The spread of the wall jet after attachment must be characterized to develop a robust method for the prediction of pressure recovery.

Simultaneous Doppler/catheter measurements of pressure gradients in aortic valve disease: a correction to the Bernoulli equation based on velocity decay in the stenotic jet.

BACKGROUND AND AIM OF THE STUDY: Characterization of the severity of a stenotic aortic valve relies on accurate measurement of the pressure drop across the valve. A simplified form of the Bernoulli equation has been used to estimate pressure drops using Doppler ultrasound, but these measurements often overestimate gold standard measurements performed during cardiac catheterization. Sources of discrepancy between the Doppler and catheter measurements have been identified, but no method has been developed to fully reconcile the two techniques. METHODS: In this study we developed a correction to the clinical form of the Bernoulli equation based on receiving chamber geometry and turbulent jet profiles. The theoretical treatment of the mechanical energy balance, assuming a shape to the stenotic jet profile is described, and the assumptions in our model are discussed. The use of the model was then demonstrated in an in vivo clinical study in which simultaneous Doppler and catheter data were obtained. RESULTS: Discrepancies between Doppler and catheter are shown to be a function of the predicted pressure recovery location based on our assumed profile. There exists a distance of about 8.67 valve radii downstream where agreement in peak pressure gradients is theoretically achieved. CONCLUSION: The results demonstrate the ability to characterize pressure recovery distal to the valve. Our approach, to substitute a more appropriate velocity profile into the mechanical energy balance, unifies geometric parameters and the physics of turbulent jet flow in an equation involving quantities already routinely measured in an echocardiographic examination of aortic stenosis. This allows for both the maximal and recovered pressure gradient to be obtained from the Doppler data. These results have implications for optimal pressure sensor placement for the assessment of aortic stenosis and also for the evaluation of prosthetic heart valves in vitro.

Inter-laboratory comparisons: approaching a new standard for prosthetic heart valve testing in vitro.

Current standards governing the evaluation of prosthetic heart valve designs have come under scrutiny. Generally, standards require measurements of pressure drops and regurgitant flow. While this information is important in the characterization of valve performance, these standards are both insufficient and ambiguous. Their insufficiency is due to the fact that they do not cover issues related to thrombosis and structural damage, and their ambiguity is demonstrated by the fact that different pulse duplicators will produce different results for nominally the same set of conditions. While the insufficiency of the current standards has recently been addressed, the ambiguity has not been addressed in a systematic way except for one particular study involving two pulse duplicator systems. This paper explores physical sources for disagreement in pressure and flow measurements between pulse duplicators, and suggests ways to account for them. By considering these physical phenomena, standards can be developed for testing chambers that improve similarity between systems. This should not compromise innovation in the design of new pulse duplicators, which may be necessary to address additional concerns besides the pressure and flow characteristics of the valve.

Potential role of mechanical stress in the etiology of pediatric heart disease: septal shear stress in subaortic stenosis.

OBJECTIVES: The objective of this study was to show elevations in septal shear stress in response to morphologic abnormalities that have been associated with discrete subaortic stenosis (SAS) in children. Combined with the published data, this critical connection supports a four-stage etiology of SAS that is advanced in this report. BACKGROUND: Subaortic stenosis constitutes up to 20% of left ventricular outflow obstruction in children and frequently requires surgical removal, and the lesions may reappear unpredictably after the operation. The etiology of SAS is unknown. This study proposes a four-stage etiology for SAS that I) combines morphologic abnormalities, II) elevation of septal shear stress, III) genetic predisposition and IV) cellular proliferation in response to shear stress. METHODS: Morphologic structures of a left ventricular outflow tract were modeled based on measurements in patients with and without SAS. Septal shear stress was studied in response to changes in aortoseptal angle (AoSA) (120 degrees to 150 degrees), outflow tract convergence angle (45 degrees, 22.5 degrees and 0 degree), presence/location of a ventricular septal defect (VSD) (3-mm VSD; 2 and 6 mm from annulus) and shunt velocity (3 and 5 m/s). RESULTS: Variations in AoSA produced marked elevations in septal shear stress (from 103 dynes/cm2 for 150 degrees angle to 150 dynes/cm2 for 120 degrees angle for baseline conditions). This effect was not dependent on the convergence angle in the outflow tract (150 to 132 dynes/cm2 over full range of angles including extreme case of 0 degree). A VSD enhanced this effect (150 to 220 dynes/cm2 at steep angle of 120 degrees and 3 m/s shunt velocity), consistent with the high incidence of VSDs in patients with SAS. The position of the VSD was also important, with a reduction of the distance between the VSD and the aortic annulus causing further increases in septal shear stress (220 and 266 dynes/cm2 for distances of 6 and 2 mm from the annulus, respectively). CONCLUSIONS: Small changes in AoSA produce important changes in septal shear stress. The levels of stress increase are consistent with cellular flow studies showing stimulation of growth factors and cellular proliferation. Steepened AoSA may be a risk factor for the development of SAS. Evidence exists for all four stages of the proposed etiology of SAS.

Abnormalities of the left ventricular outflow tract associated with discrete subaortic stenosis in children: an echocardiographic study.

OBJECTIVES: The purpose of this study was to examine the echocardiographic abnormalities of the left ventricular outflow tract associated with subaortic stenosis in children. BACKGROUND: Considerable evidence suggests that subaortic stenosis is an acquired and progressive lesion, but the etiology remains unknown. We have proposed a four-stage etiologic process for the development of subaortic stenosis. This report addresses the first stage by defining the morphologic abnormalities of the left ventricular outflow tract present in patients who develop subaortic stenosis. METHODS: Two study groups were evaluated-33 patients with isolated subaortic stenosis and 12 patients with perimembranous ventricular septal defect and subaortic stenosis-and were compared with a size- and lesion-matched control group. Subjects ranged in age from 0.05 to 23 years, and body surface area ranged from 0.17 to 2.3 m2. Two independent observers measured aortoseptal angle, aortic annulus diameter and mitral-aortic separation from previously recorded echocardiographic studies. RESULTS: The aortoseptal angle was steeper in patients with isolated subaortic stenosis than in control subjects (p < 0.001). This pattern was also true for patients with ventricular septal defect and subaortic stenosis compared with control subjects (p < 0.001). Neither age nor body surface area was correlated with aortoseptal angle. A trend toward smaller aortic annulus diameter indexed to patient size was seen between patients and control subjects but failed to achieve statistical significance (p = 0.08). There was an excellent interrater correlation in aortoseptal angle and aortic annulus measurement. The mitral-aortic separation measurement was unreliable. Our results, specifically relating steep aortoseptal angle to subaortic stenosis, confirm the results of other investigators. CONCLUSIONS: This study demonstrates that subaortic stenosis is associated with a steepened aortoseptal angle, as defined by two-dimensional echocardiography, and this association holds in patients with and without a ventricular septal defect. A steepened aortoseptal angle may be a risk factor for the development of subaortic stenosis.

Turbulent/viscous interactions control Doppler/catheter pressure discrepancies in aortic stenosis. The role of the Reynolds number.

BACKGROUND: Despite good correlation between Doppler and catheter pressure drops in numerous reports, it is well known that Doppler tends to apparently overestimate pressure drops obtained by cardiac catheterization. Neither (1) simplification of the Bernoulli equation nor (2) pressure recovery effects can explain this dilemma when taken alone. This study addressed the hypothesis that a Reynolds number-based approach, which characterizes (1) and (2), provides a first step toward better agreement of catheter and Doppler assessments of pressure drops. METHODS AND RESULTS: Doppler and catheter pressure drops were studied in an in vitro model designed to isolate the proposed Reynolds number effect and in a sheep model with varying degrees of stenosis. Doppler pressure drops in vitro correlated with the directly measured pressure drop for individual valves (r = .935, .960, .985, .984, .989, and .975) but with markedly different slopes and intercepts. A Bland-Altman type plot showed no useful pattern of discrepancy. The Reynolds number was successful in collapsing the data into the profile proposed in the hypothesis. Parallel results were found in the animal model. CONCLUSIONS: Apparent overestimation of net pressure drop by Doppler is due to pressure recovery effects, and these effects are countered by both viscous effects and inertial/turbulent effects. Only by reconciliation of discrepancies by use of a quantity such as Reynolds number that embodies the relative importance of competing factors can the noninvasive and invasive methods be connected. This study shows that a Reynolds number-based approach accomplishes this goal both in the idealized in vitro setting and in a biological system.