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Send to a FriendThe assessment of the severity of native valve disease and the assessment of prosthetic valve performance potentially have much in common. In essence one can divide such assessments into the evaluation of hydrodynamic valve performance and the measurement of valve-related complications.
Taking the latter first, in terms of native valve disease, the cardiology literature is replete with studies that relate the development of symptoms to the severity and natural history of valve disease. In terms of prosthetic valve performance, cardiac surgeons have been very attentive to addressing the late valve-related complications associated with valvular prostheses, to wit the initial publication of the “Guidelines for Reporting Morbidity and Mortality After Cardiac Valvular Operations” in 1988 [1] and the revised Guidelines in 1996 [2], and the recent attention given to actual versus actuarial methodology in assessing nonfatal, late, valve-related complications [3].
The same cannot be said for how we evaluate the hydrodynamics of diseased native valves or valvular prostheses. For example, I am quite certain that all cardiac surgeons frequently have patients with aortic stenosis referred by a cardiologist, who simply implies the severity of the disease by stating something like, “The patient has a 60 mm gradient,” as if that fully defines the situation. We cardiac surgeons are not completely innocent of this superficial approach either!
Despite the fact that the Gorlins published their formula for the determination of valve area from direct pressure measurements in 1951 [4], even today valve area – let alone indexed valve area - is not always included in the presentation of cardiac catheterization or echocardiographic results. Admittedly, the Gorlin formula does have its failings, for it has been known to break down to some degree in the presence of low gradients and low cardiac outputs, and Dutton and his investigators in British Columbia have been able to demonstrate that the Gorlin formula calculation ought to be corrected for regurgitant fraction, when that can be measured [5]. Yet even echocardiographers, who can estimate the aortic valve area from the continuity equation, often settle for presenting only valve gradient and may not even mention aortic regurgitation.
Further complicating the issue is the tendency for prosthesis manufacturers to still present hydrodynamics in terms of gradients, or potentially more misleading, geometric orifice areas, which are merely static in vitro measurements of the “hole” in a valvular prosthesis that has nothing to do with occluder function. Fortunately, there has recently been an effort to compare different valvular prostheses using effective orifice areas, namely the clinically measured functional valve areas of prostheses implanted into patients. Even better, some groups have now made us cognizant of indexed effective orifice areas, namely in vivo valve areas adjusted for patient size, as they draw our attention to the problem of patient-prosthesis mismatch.
Yet all of these assessments to a greater or lesser degree miss the point. First, they focus solely on systolic valvular hydrodynamic performance and ignore the impact of any valvular regurgitation, as if we are only interested in the third of the time that the ventricle is in systole! Second, they ignore the importance of the well-described issues of pressure recovery and turbulence. Evidence even exists that the geometry of the outflow portion of the left ventricle and the size of the aorta above the annulus can impact the performance of an aortic valvular prosthesis.
Even worse, all of these assessments focus on the valve, not on the ventricle. This “lesion concentration” is similar to how some interventional cardiologists see coronary artery disease; they focus only on the lesion in the artery and ignore the muscle it serves. As cardiac surgeons have tried to focus on myocardial viability and performance in coronary artery disease, we need to refocus our attention on the impact of valvular lesions on ventricular function. Thus, the concept of energy loss. Cardiac surgeons, and cardiologists, need to consider the impact of native valvular disease and prosthetic valves on the work of the left ventricle. We have at least begun that effort indirectly with our controversy over the impact of various aortic valvular prostheses on left ventricular mass regression.
Biomechanical engineers have understood and measured energy loss for decades. My first introduction to the concept came from some of the outstanding in vitro research published by Ajit Yoganathan’s group from Georgia Tech. In one study they demonstrated that as one went progressively down from a size 23 to a size 21 to a size 19 bileaflet valve, there was a 30-35% increase in energy loss for their in vitro ventricle with each decrement in valve size [6,7]. Yoganathan’s group has continued to demonstrate the importance of energy loss as a method of evaluating the severity of aortic stenosis [8]. More recently a study from the excellent laboratory of Dumesnil and Pibarot in Quebec presented the concept of an energy loss index to assess aortic valve severity [9].
I do not pretend to be a biomechanical engineer nor to fully understand the mathematics and measurement of energy loss, but the focus of the assessment of valve performance on left ventricular work seems to finally bring our attention to the place where it always should have been.
Cardiac surgeons want to know how both stenosis and regurgitation of native and prosthetic valves affect the left ventricle. If we could, we would like to know how lesions of both aortic and mitral valves affect the left ventricle. Maybe then we would know if it is necessary to correct mild to moderate mitral regurgitation at the same time we are repairing or replacing the aortic valve, if mild to moderate aortic valve disease is better corrected or left alone during coronary artery bypass grafting or mitral valve operations, or if we can reliably achieve left ventricular mass regression in patients with left ventricular hypertrophy.
Cardiac surgeons also want to know how to evaluate new valvular prostheses as they come on the market. We may have to wait months or years to evaluate their late valve-related complications, but we ought to immediately know their true hydrodynamic performance. Just as a manufacturer’s designated prosthesis size often bears little relationship to which valve will actually fit into a given annulus, raw gradients and geometric orifice areas tell us little of any real value about hydrodynamic prosthesis performance. Let us see systolic and diastolic performance together and how this performance impacts left ventricular work.
The time is past due for cardiologists, cardiac surgeons and prosthesis manufacturers to focus on the impact of native and prosthetic valve function on the work of the left ventricle and consistently utilize energy loss as an index of valve performance.