Author + information
- Shahbudin H. Rahimtoola, MB, FRCP, DSc (Hon)⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. S. H. Rahimtoola, University of Southern California, 1200 N. State Street, Old GNH, Room 7131, Los Angeles, California 90033
How can you know the future, If you don't know the past.—Adapted from John W. Kirklin, MD
Severe calcific aortic stenosis (AS) is the most common cause for aortic valve replacement, especially in the developed world. Initially, assessment of severity of AS was largely based on physical examination.
In 1960, valve replacement became a clinical reality and documentation that AS was severe became essential.
Normal Cardiovascular Physiology
In the normal heart, in the earliest part of systole, the dynamics of left ventricular (LV) ejection are determined by the phenomenon of mass acceleration (1). As a result, early there is a small gradient between the LV and ascending aorta (AA) (1,2). This gradient can be increased with administration of an inotropic agent such as isoproterenol (2). Subsequently, AA pressure is imperceptibly delayed; however, LV and AA pressures are almost identical. From the AA to peripheral vessels there is: 1) an increase of systolic pressure and reductions of diastolic and mean pressures; and 2) decrease of the amount of blood flow (3).
Energy loss is an established engineering concept that has been well understood and has been applied to obstruction to flow in the circulation (4). Mechanical energy in the circulatory system exists in 3 forms (4): 1) static pressure is energy per unit volume. It represents force that performs work to move a mass over a distance. 2) Acceleration due to gravity is mechanical energy in which force moves the mass over a vertical distance. 3) Kinetic energy or energy of movement. These 3 forms of energy occur in the normal heart during LV ejection and can be converted from one form to another without energy loss (4).
Aortic Stenosis: Pathophysiology
As blood passes across an obstruction, such as in AS, the total energy loss is the loss of static pressure, and there is no loss of kinetic energy. In the area beyond the obstruction, a proportion of the energy loss is recovered and is called “conservation of energy” (Fig. 1) and is converted to pressure, which is called “pressure recovery phenomenon.” Thus, not all of the energy is truly lost; some of it is added back to the energy in the AA and measurement of energy/pressure at this level determines the actual energy lost in the circulation to overcome the AS. This combined energy in the AA is the energy that is available and is required to perfuse the body and is called “effective energy requirement” (Fig. 1). The delay between the peak LV and peak AA pressures is very short (5) (Fig. 2).
Akins et al. (4) explain, “the primary source of mechanical energy in the circulation is work performed by the left ventricle. Ventricular contraction generates mechanical energy in blood in the form of static pressure.” Conversion of pressure to kinetic energy leads to movement of a volume of blood. Thus, there are at least a couple of ways of examining energy developed in the LV: 1) for myocardial shortening to occur, the LV has to overcome afterload (6). Braunwald et al. (6) stated, “afterload may be defined as tension, force, or stress (force per unit cross-sectional area) in the ventricular wall during ventricular ejection (i.e., after the onset of shortening).” Thus, afterload is an integral of LV pressure, volume, and mass during systolic ejection (6). 2) Pressure-volume work (“stroke work”) is equivalent to the integral of the LV pressure and volume during ejection. This forms the basis of examining LV stroke work loss to assess severity of AS (7,8).
Assessing That AS is Severe
Clinically, 2 parameters have been used: 1) aortic valve gradient (AVG); and 2) aortic valve area (AVA). These determinations should be made considering “energy” (pressure) that is required and is available to perfuse the body beyond the AS.
AVG represents energy lost and is not available to perfuse the body. Very early, Braunwald et al. (9) determined that AVG obtained at cardiac catheterization, which is measured after pressure recovery, should be greater than 50 mm Hg in severe AS. Subsequent data have confirmed that mean AVG greater than 50 mm Hg has a high specificity for severe AS (10). Mean AVG obtained by echocardiography/Doppler at this site can be expected to be similar to that obtained by cardiac catheterization. Gradients are not fixed but are influenced by several factors (11) (Table 1). Mean AVG ≤50 mm Hg may be present in nonsevere and severe AS (10).
Experimental and clinical studies have shown when AVA is ≤1.0 cm2 the gradient increases rapidly (8,12). Patients with AVA of ≤1.0 cm2 have a poorer outcome (11). Because many of the patients studied in the very early era were children, AVA ≤1.0 cm2 was corrected for body size by normalizing it to an average adult, which yielded an AVA index (AVAI) of ≤0.6 cm2/m2 (7). There is a range of AVA in normal adults that is related to their cardiac output (CO) needs and, therefore, to body size. Braunwald et al. (13) from the National Institutes of Health recommended that AVA should be corrected for body surface area and that AVAI of <0.7 cm2/m2 represented severe AS. A subsequent natural history study (14) from the same institution (National Institutes of Health) using this criteria showed poor patient prognosis; however, in that study, all patients had AVAI of ≤0.63 cm2/m2. The precision of all techniques to measure AVA and AVAI do not allow their calculation to hundredths of a centimeter. Severe AS is AVA ≤1.0 cm2 and AVAI of ≤0.6 cm2/m2. AVAI ≤0.6 cm2/m2 correlates with LV stroke work loss of ≥30% (7).
The aortic valve area of even calcified valves is not totally fixed, that is, the valve can open to a greater degree with increased flow. The larger the AVA beyond 1.0 cm2, the more it is able to increase with increasing flow, and thus the LV in patients with mild/moderate AS can easily accommodate increased blood flow (15). Even for AVA of ≤1.0 cm2, a change of ±10% can be expected due to changes in flow and for variability of the reproducibility of the calculation; for AVA of ≤1.0 cm2, this would mean AVA ranges from ≤0.9 to 1.1 cm2 (11). An experimental study showed that at a certain degree of calcific AV stenosis, the valve could not open to a greater degree to accommodate an increase of blood flow (12). This level represents “critical obstruction to left ventricular outflow,” which Braunwald recommended in patients was AVAI “less than about 0.4 cm2/m2” (16).
Convergence of the criteria
In this issue of iJACC, Bahlmann et al. (17) present data from a large number of patients in the SEAS (Simvastatin and Ezetimibe in Aortic Stenosis) study in whom they have investigated the magnitude of pressure recovery in asymptomatic patients with AS using echocardiographic/Doppler data. They have shown that for accurate assessment of AS severity by echocardiography/Doppler, AVA must be adjusted for energy recovery and calculated as energy loss index (18). This is best done at the sinotubular junction. The calculated appropriate energy loss index for severe AS was ≤0.6 cm2/m2, a value identical to that obtained by cardiac catheterization. The investigators' conclusion that evaluation of energy/pressure recovery is important for proper assessment of severity of AS needs to be emphasized. Their data shows that such evaluation using echocardiography/Doppler is best done at the sinotubular junction.
Pitfalls to be aware of
The following pitfalls may affect the accuracy of AS assessment:
1. A normal left ventricular ejection fraction (LVEF) may not mean CO is normal. There is no direct relationship between a certain level of LVEF and CO. For example, a normal LVEF may be associated with reduced CO; a reduced LVEF may be associated with a normal CO.
2. For quantification of gradient and AVA, an important determinant is stroke volume. In 2 studies of normal people (19,20), the cardiac indexes were 3.5 ± 0.7 and 3.6 ± 0.9 l/min/m2 and stroke indexes were 46 ± 8 and 44 ± 13 ml/m2 (mean ± SD).
3. Criteria obtained from surrogates. Be wary of and cautious about their use.
4. Lack of meticulous attention to technical details and to comprehensive assessment increases the risk of error in the assessment of severity.
5. Errors in the assessment of severe AS may have important deleterious effects in patient outcomes.
6. A multitude of criteria, several of which have been enshrined in guidelines, have been recommended for determining that AS is severe (21). In clinical practice, this can cause confusion and not clarity; it also leads to dilemmas in patient management.
Clinical decision making that AS is severe
Severity of AS is judged by: 1) proper assessment of the physical signs; and 2) at effective energy requirement, energy loss index and/or AVAI is ≤0.6 cm2/m2 for severe AS and is ≤0.4 cm2/m2 for “critical” (very severe) AS (22).
Dr. Rahimtoola has received Honoraria for educational lectures from the American College of Cardiology Foundation; American College of Physicians; University of California Los Angeles; University of California Irvine; Cornell University; Creighton University; Thomas Jefferson University; Cedars-Sinai Medical Center; Harvard Medical School; University of Wisconsin; University of Hawaii; Cardiologists Association of Hong Kong, China; San Bernardino Medical Center; ATS; St. Jude Medical; Carbomedics; Edwards Lifesciences; Merck; and Pfizer.
↵⁎ Editorials published in JACC: Cardiovascular Imaging reflect the views of the authors and do not necessarily represent the views of JACC: Cardiovascular Imaging or the American College of Cardiology.
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