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J Am Coll Cardiol, 2006; 47:138-140, doi:10.1016/j.jacc.2005.10.001
(Published online 13 December 2005). © 2006 by the American College of Cardiology Foundation |
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).
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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  K. K. Poh, R. A. Levine, J. Solis, L. Shen, M. Flaherty, Y.-J. Kang, J. L. Guerrero, and J. Hung Assessing aortic valve area in aortic stenosis by continuity equation: a novel approach using real-time three-dimensional echocardiography Eur. Heart J., February 9, 2008; (2008) ehn022v1. [Abstract] [Full Text] [PDF]
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 A. N. DeMaria, O. Ben-Yehuda, G. K. Feld, G. S. Ginsburg, B. H. Greenberg, W. Y.W. Lew, J. A.C. Lima, A. S. Maisel, J. Narula, D. J. Sahn, et al. Highlights of the Year in JACC 2006 J. Am. Coll. Cardiol., January 30, 2007; 49(4): 509 - 527. [Full Text] [PDF]
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