right ventricular compliance and relaxation and may also affect hepatic flow (1,168,169).
Spectral Doppler and TR
RF and RV have much error.
Use for RV pressure calculation.
Systolic flow reversal in hepatic veins is very specific for severe TR.
Overall Assessment of Tricuspid Regurgitation
The evaluation of tricuspid regurgitation is more error prone than the assessment of mitral regurgitation. Table 5.6 lists the parameters that help define the severity of tricuspid regurgitation in man. These parameters, set by the Society of Echocardiography Task Force on the Assessment of Native Valvular Regurgitation in man, include analysis of ventricular and atrial size, jet area, vena contracta, PISA, jet density, regurgitant profile shape, and hepatic vein flow. The more parameters that are in agreement with regard to severity, the more reliable the assessment will be (1).
Table 5.6
Tricuspid Regurgitation: Parameters for the Assessment of Severity in Man
Adapted from: Zoghbi W, Enriquez-Sarano M, Foster E, et al. American Society of Echocardiography. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr 2003;16:777–802.
Pulmonary Regurgitation
Small amounts of pulmonary insufficiency are also a normal finding in most species. Generally nonphysiologic pulmonary insufficiency occurs secondary to infective lesions or in association with other disease such as patent ductus arteriosus, pulmonic stenosis, pulmonary hypertension, or significant volume overload of the right side of the heart where the pulmonary annulus may be dilated.
Pulmonary insufficiency does not have the history of evaluation that insufficiencies at the other valves do. Rarely is pulmonary insufficiency significant enough to be of concern. Severe pulmonary insufficiency may be seen with valvular dysplasia and after interventional procedure. Although trivial to mild pulmonary regurgitation is a common finding in normal animals, it may become severe when pulmonary hypertension is present and even then is rarely life threatening (1).
Two-Dimensional Evaluation
Two-dimensional echocardiography can be used to define the underlying cause of insufficiency. Dilation of the pulmonary artery is consistent with the diagnosis of pulmonary hypertension, in the absence of shunts. In the absence of pulmonary hypertension and significant tricuspid regurgitation, dilation of the right ventricle is a sign that the pulmonary regurgitation is significant (1).
Color-Flow Doppler Imaging
Jet length of pulmonary regurgitation is not very specific for severity because small changes in driving pressure affect it. Jet area correlates better with severity of regurgitation but is still extremely variable with much overlap between the grades of severity (170). Vena contracta has not been studied and validated for pulmonary regurgitation.
Spectral Doppler Imaging
There are no reliable methods to quantify pulmonary regurgitation with CW Doppler. Short pressure half-times are seen with severe regurgitation as they are with aortic regurgitation, but in the presence of low pulmonary artery diastolic pressure, rapid deceleration may be seen without significant regurgitation (1).
Use spectral Doppler to calculate diastolic PA pressure.
No accurate method to assess severity of PR.
Using spectral Doppler to determine end diastolic pulmonary artery pressure is frequently done however. This is discussed more in Chapter 4, but peak early diastolic velocity represents mean pulmonary artery pressure, while end diastolic pressure gradient represents pulmonary end diastolic pressure (Figure 4.90).
Quantification of regurgitant fraction and volume is inaccurate since the pulmonary artery diameter changes throughout the cardiac cycle, and it has not been validated. Use the pulmonary artery diameter early in systole, two to three frames after the beginning of the QRS complex, if regurgitant fractions are measured using a combination of spectral and two-dimensional echocardiography (1,171,172).
Overall Assessment of Pulmonary Regurgitation
There are no well-established parameters to evaluate the severity of pulmonary regurgitation. Using multiple parameters is helpful and is clinically useful if they agree. The Society of Echocardiography Task Force on the Assessment of Native Valvular Regurgitation in man has defined several parameters and their relationship to severity of pulmonary insufficiency. These are listed in Table 5.7.
Table 5.7
Pulmonary Regurgitation: Parameters for the Assessment of Severity in Man
Adapted from: Zoghbi W, Enriquez-Sarano M, Foster E, et al. American Society of Echocardiography. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr 2003;16:777–802.
Endocarditis
The aortic valve is the most common site of vegetative endocarditis in the horse with the mitral and tricuspid valves following in frequency of occurrence (Figure 5.54) (115,118,173). In the dog, the mitral valve is the most susceptible valve for vegetative growth followed by the aortic valve. The pulmonary and tricuspid valves are rarely affected in the dog (Figures 5.55, 5.56, 5.57, 5.85) (174– 176). Cows develop endocarditis lesions more often on the tricuspid and pulmonary valves (Figure 5.86) (177–180). In man the predisposition for development of vegetative growth seems to be related to pressure on the valves while they are closed (174,181). There is a theory that bacterial endocarditis develops secondary to high pressure flow on the respective valves when they are open. Lesions are seen more often on the ventricular side of aortic valves and on the atrial side of mitral valves (174,182,183).
Endocarditis
Canine = MV and AV
Equine = AV
Bovine = TV and PV
Figure 5.85 Pulmonary valve vegetative lesions are uncommon in a dog, but here a large growth is seen on right parasternal transverse images of the heart base (cursers). RV = right ventricle, PA = pulmonary artery, AO = aorta, LA = left atrium.
Figure 5.86 The large echogenic irregular mass on the tricuspid valve of this cow is a vegetative growth (arrow). The right-sided valves are the most common places for endocarditis in the bovine. The right side of the heart is dilated secondary to tricuspid insufficiency. The septum bows downward as a result of the right ventricular volume overload. RV = right ventricle, RA = right atrium, AO = aorta, LV = left ventricle, Plane = right parasternal left ventricular outflow view.
Most dogs are older and are medium to large breeds (174). There are no documented predisposing factors for the development of bacterial endocarditis except for the presence of subaortic stenosis (174,184,185). In the cow, endocarditis is most frequently associated with hardware disease.
The lesions of bacterial endocarditis are usually smooth and nodular when small but become irregular as they grow (120,179). Large lesions are echogenic, heterogeneous, irregular, pedunculated, and often mobile (174). Large vegetative lesions often contain a heterogeneous appearance with hypoechoic areas within the lesion (Figure 5.87). When the growth involves the AV valves, they may
extend onto the chordae tendineae. The lesions may cause valvular insufficiency when the growth prevents proper closure of the cusps. Even large lesions however may only create small insufficiencies.
Figure 5.87 The hypoechoic area within this aortic valve growth is common in endocarditis lesions (arrow). LV = left ventricle, AO = aorta, LA = left atrium, View = right parasternal left ventricular outflow view.
It is almost impossible to differentiate between degenerative and vegetative lesion on mitral valves, and this is the most common cause of false positives. The clinical picture and history must be used in conjunction with echocardiographic findings (174,182). The lesions typically will get somewhat smaller as the infective process resolves and only scar tissue remains. They will never completely disappear however, and insufficiencies when present, often remain and may even become worse (118,121). Although valve lesions most commonly cause insufficiencies, obstruction to flow may also occur (123). This can be determined with Doppler echocardiography and applying the Bernoulli equation to the velocity of inflow or outflow through the affected valve. Remember that when insufficiency and obstruction are both present, flow velocity will be elevated secondary to both problems.
Endocarditis lesions never disappear.
May become smaller as they scar.
Insufficiency or stenosis persists.
Cardiac chamber sizes will be normal unless hemodynamically significant insufficiencies develop (118,121). Acute endocarditis results in rapid development of heart failure whereas chronic endocarditis may take months to progress before signs of failure occur (186–188). Chamber enlargement will be accompanied by compensatory hypertrophy, increased cardiac function, and excessive wall motion secondary to the volume overload unless myocardial failure is present (120,123,179,189). Tricuspid and pulmonary insufficiencies create right-sided volume overload while mitral and aortic insufficiencies will cause left-sided changes. The hemodynamic effects on the heart
with chronic endocarditis are the same as those seen with chronic degenerative lesions resulting in insufficiency.
Endocarditis may cause abscesses and secondary rupture of the ventricular, atrial, or great vessel walls adjacent to the infective lesion (121,123). Other complications of infective endocarditis include myocardial infarction secondary to embolism into the coronary arteries, pulmonary thromboembolism secondary to right-sided lesions, or congestive heart failure secondary to significant valvular insufficiency (64,72). Studies in man have shown that aortic valve endocarditis embolizes less often than mitral valve endocarditis but that aortic valve lesions are more often associated with abscess formation (190). Myocardial infarction will create localized or widespread myocardial dysfunction visible on real-time images. M-mode images obtained over the infracted area show hypokinetic or akinetic myocardium (118,191–193). Lesions approaching the 1-cm size are associated with embolization and high complication and mortality rates (190). Many cases of vegetative endocarditis are undetected until necropsy examination or until an echocardiogram is obtained for other unrelated reasons. These lesions are small and create no significant hemodynamic alterations.
Endocarditis lesions larger than 1 cm are associated with high incidence of embolization and mortality.
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