Etiology of Valvular Regurgitation

Valvular regurgitation may be due to congenital or acquired abnormalities of the valve leaflets or to abnormalities of the associated supporting structures. For example, dilation of the ascending aorta or sinuses can result in AR even with anatomically normal valve leaflets. Similarly, LV dilation can result in mitral regurgitation (MR) even with normal valve leaflets and chordae. Echocardiographic examinations allow definition of the etiology of valvular regurgitation in most cases. Even when a single definite cause is not evident, the differential diagnosis of the etiology of regurgitation often can be narrowed to the few most likely possibilities. The examination also may provide clues as to whether regurgitation is acute or chronic in duration.

When transthoracic echocardiographic (TTE) images are not diagnostic for the evaluation of aortic or mitral valve anatomy and the etiology of regurgitation, transesophageal echocardiographic (TEE) imaging may be helpful. With diseases of the aorta, visualization of the ascending aorta often is suboptimal on TTE imaging, so TEE imaging typically is needed to fully define the extent and severity of disease.

Fluid Dynamics of Valvular Regurgitation

The fluid dynamics of a regurgitant valve (Fig. 12-1) are, in many ways, similar to the fluid dynamics of a stenotic valve and are characterized by:

Even though the anatomy of inadequate valve closure may be quite complex, the valve can be thought of as having a regurgitant orifice, which in simple physiologic terms is characterized by a high-velocity laminar jet (Table 12-1). The instantaneous velocity in this jet (v) is related to the instantaneous pressure difference (∆P) across the valve, as stated in the simplified Bernoulli equation: ∆P = 4v². Recording this high-velocity jet with continuous-wave (CW) Doppler allows assessment of the time course of the difference in pressure between the two chambers on either side of the valve.

On the upstream side of the regurgitant valve, flow acceleration proximal to the regurgitant orifice is present, and a proximal isovelocity surface area (PISA) can be defined, similar to that seen on the left atrial (LA) side of the stenotic mitral valve. The proximal isovelocity surface area, multiplied by the aliasing velocity, provides a method for quantitative evaluation of regurgitant stroke volume. The narrowest segment of the regurgitant jet, the vena contracta, occurs just distal to the regurgitant orifice, with vena contracta diameter reflecting regurgitant orifice area.

As the high-velocity jet enters the chamber receiving the regurgitant flow, the flow pattern becomes disturbed with nonlaminar flow, multiple blood flow velocities, and multiple blood flow directions. The size of the downstream regurgitant flow disturbance is affected by both physiologic and technical factors and thus is less useful for the quantitation of regurgitant severity (Table 12-2). In addition, the shape and direction of the regurgitant jet are affected by the anatomy and orientation of the regurgitation orifice, the driving force across the valve, and the size and compliance of the receiving chamber. Jets are “pulled” toward adjacent walls (e.g., MR in the LA) if within a critical distance from the wall at the entry site and also are “pulled” toward other flowstreams (e.g., AR and mitral stenosis). Eccentric jets that adhere to the wall of the chamber will have a smaller color jet area on two-dimensional (2D) color flow imaging (and a smaller three-dimensional [3D] volume) because entrainment of additional fluid elements into the jet occurs on only one side, instead of on all sides, as with a central jet.

Volume Overload

In patients with a regurgitant valve, the term total stroke volume refers to the total volume of blood pumped by the ventricle on a single beat. Forward stroke volume is the amount of blood delivered to the peripheral circulation, and regurgitant volume is the amount of backflow across the abnormal valve (Fig. 12-2).

Chronic valvular regurgitation results in progressive volume overload of the ventricle. Volume overload of the LV results in chamber dilation with normal wall thickness so that total LV mass is increased. An important clinical feature of chronic LV volume overload is that an irreversible decrease in systolic function can occur in the absence of symptoms. In fact, an irreversible decrease in contractility can occur despite a normal ejection fraction because of the altered loading conditions of the ventricle when regurgitation is present.

Serial echocardiographic evaluation of LV size and systolic function is a standard method of clinical evaluation, but two factors potentially limit the reliability of this approach. First, suboptimal image quality or recording techniques may result in erroneous measurements. Care is needed to ensure that the dimensions are measured perpendicular to the long and short axes of the LV, and instrument settings must be adjusted for optimal endocardial definition. Accurate tracing of endocardial borders for the calculation of ventricular volumes depends on clear endocardial definition, standard image planes without foreshortening of the long axis of the ventricle, and a trained and experienced individual tracing the borders at end-diastole and end-systole. Three-dimensional echocardiography with semiautomated border detection (see Chapter 6) provides more accurate LV volumes and will become the standard as this instrumentation becomes more widely available.

Second, the reproducibility of LV measurements must be considered. Overall reproducibility includes variation in recording the data, variation in measuring the data, and physiologic variation (such as heart rate and loading conditions) that may affect the measurement. Reproducibility of 2D-guided M-mode measurements of the LV suggests that an interval change of greater than 8 mm in end-systolic or end-diastolic dimensions represents a definite clinical change. Using 2D echocardiography, a change in ventricular volume or a change in ejection fraction greater than 10% on serial studies performed in the same laboratory indicates a significant change. Three-dimensional volumes have lower variability in recording and measuring data but are still subject to physiologic variability.

Detection of Valvular Regurgitation

Valvular regurgitation can be detected with:

While anatomic imaging provides detailed information about the valve apparatus and ventricular function, it provides only indirect evidence for the presence or absence of valvular incompetence. The finding of an anatomically abnormal mitral valve in the presence of LA and LV dilation suggests that MR may be present, but Doppler examination is necessary for direct confirmation or exclusion of the diagnosis. Although a few M-mode findings have been shown to be specific for diagnosing valvular regurgitation (e.g., high-frequency fluttering of the anterior mitral leaflet in AR), these findings are not sensitive enough to reliably exclude regurgitation when suspected on clinical grounds.

With color flow imaging, detection of regurgitation is based on identification of the flow disturbance downstream from the regurgitant orifice. When instrument settings and examination technique are optimal, color flow imaging is extremely sensitive (>90%) and specific (nearly 100%) for the detection of valvular regurgitation as compared to angiography. In fact, color flow imaging is so sensitive that regurgitation often is detected that is not audible by auscultation. These cases most often are true positives, as evidenced by angiographic confirmation. False-positive results can occur with color flow imaging when the origin or timing of the flow signal is mistaken. For example, normal pulmonary venous inflow into the LA may be mistaken for MR. False-negative results occur when signal strength is low because of poor acoustic access or attenuation due to the depth of interrogation. False-negative results also occur if color flow processing parameters are set incorrectly or if the examiner fails to evaluate the valve in more than one tomographic plane. Additional parameters important in the detection of valvular regurgitation with color flow imaging include frame rate, Nyquist limit, color gain, and the color velocity-variance display.

CW Doppler detection of valvular regurgitation is based on the identification of the high-velocity jet through the regurgitant orifice. An advantage of CW Doppler is that beam width is broad at the level of the valves when studied from an apical approach. Identification of the regurgitant signal uses the velocity, shape, timing, and associated antegrade flow signal to correctly identify the origin of the signal (Fig. 12-3).

Valvular Regurgitation in Normal Individuals

A small degree of regurgitation, often termed physiologic, is present in a high percentage of otherwise normal individuals (Fig. 12-4). Typically, physiologic regurgitation is:

When meticulously searched for, MR can be detected in 70% to 80%, tricuspid regurgitation in 80% to 90%, and pulmonic regurgitation in 70% to 80% of normal individuals. This small degree of regurgitation is normal and has no adverse clinical implications. AR is found in only a small percentage (5%) of young individuals with an otherwise normal echocardiographic study, but the prevalence of detectable AR increases with age. The clinical significance of a small amount of AR is unknown.

 Vena contracta width

 CW Doppler signal strength compared to antegrade flow

 Pressure half-time (for AR)

 Distal flow reversals

 Regurgitant volume

 Regurgitant fraction

 Regurgitant orifice area

 Proximal isovelocity surface area (PISA) flow rate

 Antegrade volume flow across the regurgitant valve minus the flow across a competent valve

 Total LV stroke volume measured from LV volumes minus Doppler forward stroke volume

Color Doppler Imaging

CW Doppler Approach

Several types of information regarding the severity of valvular regurgitation can be derived from the spectral display of the CW Doppler signal:

First, signal intensity is proportional to the number of blood cells contributing to the regurgitant signal. Because the ultrasound beam is relatively broad and signals from the entire length of the beam are recorded, much of the regurgitant jet can be encompassed in the beam with appropriate adjustment of beam direction. It is particularly helpful to compare the intensity of the regurgitant signal to antegrade flow across the same valve as a qualitative estimate of regurgitant severity (see Fig. 12-11). A weak signal reflects mild regurgitation, whereas a signal nearly equal in intensity to antegrade flow reflects severe regurgitation. Moderate regurgitation has intermediate signal strength relative to antegrade flow.

Second, the associated antegrade velocity across the regurgitant valve provides useful information. Regurgitation results in an increase in the antegrade volume flow rate across the valve, which is reflected in an increase in the antegrade velocity across the valve. The greater the severity of regurgitation, the higher is the antegrade velocity. Of course, the possibility of coexisting valvular stenosis also must be considered.

Third, the shape of the velocity curve depends on the time-varying pressure gradient across the regurgitant valve. Each instantaneous velocity is related to the instantaneous pressure gradient across the valve, as stated in the Bernoulli equation. Normal LV systolic pressure is 100 to 140 mm Hg, and normal LA pressure is 5 to 15 mm Hg, so the LV to LA pressure difference in systole is 85 to 135 mm Hg. Thus, the MR velocity curve typically shows a maximum velocity of 5 to 6 m/s. When ventricular function is normal, there is rapid acceleration to peak velocity, with a maintained high velocity in systole and with rapid deceleration before diastolic opening of the mitral valve. An increase in end-systolic LA pressure (v-wave) results in a late-systolic decline in the instantaneous pressure gradient and in the instantaneous velocity (Fig. 12-12).

Similarly, the shape of the AR velocity curve depends on the time course of the diastolic pressure difference across the aortic valve. When LV end-diastolic pressure is low and aortic end-diastolic pressure is normal or mildly reduced, a large pressure difference (and high velocity) across the valve is present throughout diastole with a slow rate of pressure decline (Fig. 12-13). Acute or severe regurgitation results in more rapid equalization of LV and aortic pressures with a more rapid velocity decline in diastole.

The utility of the CW Doppler curve depends, in large part, on technical factors in data recording in addition to correct data interpretation. The high-velocity regurgitant signal is optimized by:

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