EDITORIAL COMMENT
Hemodynamic Assessment of Aortic Stenosis
Are There Still Lessons to Learn?*
Helmut Baumgartner, MD, FACC, FESC*
Department of Cardiology Medical University of Vienna, Vienna, Austria
* Reprint requests and correspondence: Dr. Helmut Baumgartner, Department of Cardiology, Medical University of Vienna, Vienna General Hospital, Wahringer Gurtel 18-20, A-1090 Wien, Austria (Email: helmut.baumgartner{at}meduniwien.ac.at).
Doppler echocardiography with estimation of pressure gradients and valve area has become the mainstay for assessing the hemodynamic severity of aortic stenosis (AS). The method has been validated extensively, showing its strength. Nevertheless, it has also been recognized that a number of sources of error must be considered to provide data solid enough for guiding appropriate patient management. Although well known, in particular an inappropriate recording angle and less frequently recording of the wrong velocity (i.e., proximal velocity or mitral regurgitation velocity), failure to account for an increased subvalvular velocity and selection of nonrepresentative velocity data in the presence of arrhythmias remain major reasons for miscalculations of Doppler-derived gradients in daily practice when high technical expertise is lacking (1). Over the years we have also learned that more complex fluid dynamic phenomena such as pressure recovery need to be considered in certain subsets of patients. Although aortic diameters <30 mm—the cut-off point at which pressure recovery may become clinically relevant—are present in a minority of patients, Doppler-derived gradients may be largely misleading in this subset of AS patients (2). Doppler gradients measure the conversion of pressure to kinetic energy induced by the stenosis. As soon as significant pressure recovery occurs, the head loss of energy (i.e., net pressure decrease measured after pressure recovery), which determines the left ventricular pressure required to maintain a given systemic pressure and therefore the actual hemodynamic burden, is significantly overestimated by the Doppler measurement.
Because pressure gradients are highly flow dependent, it has generally been accepted that reliable assessment of AS requires estimates of the aortic valve area (AVA), particularly in the presence of low flow rates. Again, catheterization is no longer considered the gold standard. Although the hemodynamic principle may be valid, difficulties in accurately estimating transvalvular flow rates and the questionable constant used in the Gorlin equation limit its precision (a number of simplifying assumptions and an error in unit conversion have brought up the generally used "discharge coefficient" of 44.3) (3). Direct visualization of the stenotic orifice with planimetry of AVA has been considered a theoretically ideal way for assessment of AS severity. Current available imaging techniques such as transesophageal echocardiography, magnetic resonance imaging, and multislice computed tomography have been shown to enable visualization of AVA. However, in the vast majority of patients AS is of calcific etiology. In this case proper delineation of the orifice circumference has been found to be difficult (1). Thus, calculation of the AVA using the continuity equation has become the most frequently used method. According to the law of conservation of mass, flow, which is given by velocity times cross-sectional flow area, must be identical at left ventricular outflow tract (LVOT) and AVA. Thus, AVA can be calculated by dividing the flow measured in the LVOT by transvalvular velocity. Again, the hemodynamic principle is solid. In clinical practice, however, difficulties in measuring LVOT diameter and velocity precisely at the same level as well as the simplifying assumption of a flat flow profile and circular shape for the LVOT may cause inaccuracies. Indeed LVOT has been shown to be more oval in most patients, causing LVOT area underestimation, resulting in flow and eventually valve area underestimation (4). Even more importantly, it has largely been neglected that the continuity equation does not provide the anatomic (i.e., geometric) orifice area (GOA) as it is intended by direct imaging and also by invasive calculation but gives the effective orifice area (EOA). This is the smallest cross section of the flow across the stenosis at the so-called vena contracta. As flow exits a stenotic orifice, the streamlines continue to converge for a short distance. This causes the EOA to be only 70% to 90% of the GOA, depending on stenosis morphology (5). This should actually be taken into account when grading AS severity by AVA measurements.
Although AVA was initially believed to be flow independent, many studies have shown over the years that it may increase with flow (6–10). The changes in AVA vary in previous studies, as do the offered explanations for this observation. Some investigators reported that changes in calculated AVA simply reflect actual changes in GOA caused by incomplete valve opening at low flow rates and by tissue extensibility (6–8), whereas others hypothesized artifacts related to limitations inherent to the Doppler continuity equation measurement at low flow rates (9,11,12). The question of whether flow-dependent changes in Doppler-derived EOA are real or artifact gains particular importance in the setting of low flow–low gradient AS, in which changes of the EOA in response to dobutamine-stimulated flow augmentation are used to differentiate between pseudosevere and truly severe AS (13). Although it is obvious that an increase in GOA with flow is possible, the observation of flow-dependent variation in Doppler-derived EOA for rigid orifices (10,14) supports the idea that additional phenomena must exist. DeGroff et al. (12) suggested that viscous effects may cause a more parabolic flow profile in the vena contracta at low flow rates, resulting in underestimation of the actual EOA by the Doppler method. However, such phenomena can only occur at Reynolds numbers much lower than those present in the clinical setting, even at low cardiac output.
The study by Kadem et al. (15) in this issue of the Journal adds important new information to our understanding of this matter. In an elegant in-vitro study using particle image velocimetry, the investigators were able to show that there is good agreement between Doppler-derived EOA and the measurements obtained by this technique even at low flow rates. More importantly, they were able to show that changes in EOA observed with increasing flow are real and not caused by artifact. Furthermore, they were able to provide an explanation of why EOA may increase with flow even in a rigid orifice: they hypothesized that these flow-related changes in EOA are caused by the predominance of unsteady effects at low flow rates. Using an equation that takes this phenomenon into account, they were indeed able to predict changes in EOA observed in their study as well as in a study previously published by Voelker et al. (10). The results suggest that the predominance of the unsteady effects at low flow rates has significant impact on the flow configuration downstream from a stenotic lesion. At normal flow rates, the kinetic energy of the fluid crossing the obstruction is sufficient to break down the vortex structures generated downstream from the stenosis and thus enables the formation of a large and well-established flow jet. However, at low flow rates, the reduction in kinetic energy may predispose to the formation of vortices, which tend then to squeeze the flow jet and thus the vena contracta, resulting in a smaller EOA. The phenomenon is apparently less important in the presence of very small orifices, but may become clinically relevant in moderately severe AS. The fact that flow-dependent changes in EOA may occur in the absence of changes of the geometric orifice would have important clinical consequences. It can no longer be considered an ideal measure of AS severity to visualize the valve orifice and calculate the GOA even if this were possible with high precision, not only because such measurements concentrate on the peak valve area rather than the mean orifice area (the relation between these two may obviously vary depending on valve extensibility). If it is true that the EOA for a given GOA can vary more than 50% depending on the flow rate, then estimation of the GOA would indeed be of limited value for characterizing the hemodynamic burden imposed on the ventricle by a stenotic valve. Again, it must be taken into account that such changes may not reach clinical relevance in patients with definitely small or large orifices. However, in those with moderate disease and particularly at low flow rates, consideration of such phenomena may result in different judgment of stenosis severity and therefore imply changes in patient management.
In conclusion, Doppler echocardiography has become the gold standard for the assessment of AS. Despite a number of simplifying assumptions in the generally used way of generating pressure gradients and valve areas, the method can provide reliable measurements in the majority of patients as long as the echocardiographer is well trained and the study is carefully performed to avoid any technical reasons for measurement errors. However, in certain subsets of patients, more sophisticated approaches considering increased LVOT velocity, pressure recovery, or flow-dependent variation of EOA due to either valve extensibility, the predominance of unsteady effects at low flow rates, or both may be necessary to provide measurements precise enough to guide appropriate clinical management. This seems to be of particular importance for EOA in the range between 0.8 and 1.0 cm2 and in patients with reduced cardiac output.
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Footnotes
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* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily reflect the views of JACC or the American College of Cardiology. 
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References
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1. Weyman AE. Principles and Practice of Echocardiography2nd edition. Malvern, PA: Lea and Febiger; 1994514–27.2. Baumgartner H, Stefenelli TH, Niederberger J, Schima H, Maurer G. "Overestimation" of catheter gradients by Doppler ultrasound in patients with aortic stenosis—a predictable manifestation of pressure recovery J Am Coll Cardiol 1999;33:1655-1661.[Abstract/Free Full Text] 3. Dumesnil JG, Yoganathan AP. Theoretical and practical differences between the Gorlin formula and the continuity equation for calculating aortic and mitral valve areas Am J Cardiol 1991;67:1268-1272.[CrossRef][Web of Science][Medline] 4. Baumgartner H, Kratzer H, Helmreich G, Kühn P. Determination of aortic valve area by Doppler echocardiography using the continuity equation: a critical evaluation Cardiology 1990;77:101-111.[Web of Science][Medline] 5. Gilon D, Cape EG, Handschumacher MD, et al. Effect of three-dimensional valve shape on the hemodynamics of aortic stenosis: three-dimensional echocardiographic stereolithography and patient studies J Am Coll Cardiol 2002;40:1479-1486.[Abstract/Free Full Text] 6. Burwash IG, Thomas DD, Sadahiro M, et al. Dependence of Gorlin formula and continuity equation valve areas on transvalvular volume flow rate in valvular aortic stenosis Circulation 1994;89:827-835.[Abstract/Free Full Text] 7. Chambers JB, Sprigings DC, Cochrane TH, Allen J, Morris R, Black MM, Jackson G. Continuity equation and Gorlin formula compared with directly observed orifice area in native and prosthetic aortic valves Br Heart J 1992;67:193-199.[Abstract/Free Full Text] 8. Burwash IG, Pearlman AS, Kraft CD, Miyake-Hull C, Healy NL, Otto CM. Flow dependence of measures of aortic stenosis severity during exercise J Am Coll Cardiol 1994;24:1342-1350.[Abstract] 9. Burwash IG, Dickinson A, Teskey RJ, Tam JW, Chan KL. Aortic valve area discrepancy by Gorlin equation and Doppler echocardiography continuity equation: relationship to flow in patients with valvular aortic stenosis Can J Cardiol 2000;16:985-992.[Web of Science][Medline] 10. Voelker W, Reul H, Nienhaus G, et al. Comparison of valvular resistance, stroke work loss, and Gorlin valve area for quantification of aortic stenosisAn in vitro study in a pulsatile aortic flow model. Circulation 1995;91:1196-1204.[Abstract/Free Full Text] 11. Dumesnil JG, Yoganathan AP. Theoretical and practical differences between the Gorlin formula and the continuity equation for calculating aortic and mitral valve areas Am J Cardiol 1991;67:1268-1272.[CrossRef][Web of Science][Medline] 12. DeGroff CG, Shandas R, Valdes-Cruz L. Analysis of the effect of flow rate on the Doppler continuity equation for stenotic orifice area calculationA numerical study. Circulation 1998;97:1597-1605.[Abstract/Free Full Text] 13. deFilippi CR, Willet DL, Brickner E, et al. Usefulness of dobutamine echocardiography in distinguishing severe from nonsevere valvular aortic stenosis in patients with depressed left ventricular function and low transvalvular gradients Am J Cardiol 1995;75:191-194.[CrossRef][Web of Science][Medline] 14. Mascherbauer J, Noori N, Grimm M, Schima H, Maurer G, Baumgartner H. Flow dependence of continuity equation and Gorlin aortic valve area is caused by both, actual changes of orifice area and intrinsic problems of the equations Circulation 1998;98:I-786. 15. Kadem L, Rieu R, Dumesnil JG, Durand L-G, Pibarot P. Flow-dependent changes in Doppler-derived aortic valve effective orifice area are real and not due to artifact. J Am Coll Cardiol 2005;47:131–7..
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