Patent Ductus Arteriosus

Introduction

Patent ductus arteriosus (PDA) is a common defect in young animals. The reported incidence of this congenital defect in dogs varies from 11–32% (2,54–58). This defect has been seen in most breeds but Poodles, Keeshonds, cocker spaniels, German shepherds, Pomeranians, collies, Shetland sheepdogs, Cavalier King Charles spaniels, and Springer spaniels all have an increased risk for maintaining a patent ductus (18,59). The defect is also common in calves and cats but is rare in the horse (10,60,61). Since its other clinical and radiographic features are usually very diagnostic and clear cut, echocardiography is not necessary to make the diagnosis of PDA. Echocardiography however does confirm the diagnosis, especially if there are any conflicting clinical or physical sings, and it identifies the presence of other coexisting defects. Currently echocardiography plays a role in measurement of ductal diameter and definition of ampulla morphology when planning for catheterbased occlusion of a ductus.

Two-Dimensional and M-mode Evaluation

Structural Changes

Patent ductus arteriosus includes the following in its shunt pathway: the main pulmonary artery, lungs, left atrium, left ventricle, and back to the ascending aorta up to the level of the ductus. Echocardiographic images show volume overload of all of these structures (Figure 9.15). The larger the shunt, the larger the volume overload. The right atrium and ventricle are not part of the pathway and should not be enlarged if there are no other defects or complications. Long-axis images show bowing of the interventricular and atrial septums toward the right side of the heart. Left ventricular outflow and transverse views typically show a large left atrium, and the left atrial to aortic root ratio will be large (21,54,62).

PDA—shunt pathway descending aorta → pulmonary artery → lungs →

left atrium → left ventricle → aorta →

Figure 9.15 Patent ductus arteriosus results in left ventricular and left atrial volume overload since these chambers are involved in the shunt pathway. (A) The long-axis outflow views in this cat and in this dog (B) show large left ventricular and atrial chambers. RV = right ventricle, LV = left ventricle, LA = left atrium, AO = aorta, VS = ventricular septum, PA = pulmonary artery.

A large pulmonary artery is seen on both right and left parasternal transverse images of the heart base. The dilation includes the artery at the level of the pulmonary valve and the right and left main pulmonary artery branches (Figure 9.16). Differentiation of the dilated pulmonary artery seen with PDA and the artery dilation seen with pulmonary hypertension or pulmonary stenosis is usually possible. Pulmonic stenosis rarely causes dilation of the artery at the level of the valves and the poststenotic dilation is evident by vessel walls diverging away from each other beyond the stenotic lesion. An artery dilated secondary to pulmonary hypertension will have a large diameter at the level of the pulmonary valve but may also show concurrent right ventricular changes of hypertrophy and possibly dilation if the pulmonary vascular pressures are high enough.

Figure 9.16 Pulmonary artery dilation occurs with a patent ductus arteriosus. The dilation involves the entire artery from the valve to and including the bifurcation. Plane = right parasternal transverse heart base, RV = right ventricle, AO = aorta, PA = pulmonary artery, RA = right atrium.

The ductus is oriented from the aorta to the pulmonary artery in a way that directs flow up toward the pulmonary valve. One or more of the pulmonary valve cusps often prolapse as ductal flow strikes them. They may prolapse significantly but can remain competent. Dilation of the pulmonary artery may also prevent cusps from coapting properly causing regurgitation (63).

Left Ventricular Function

Systolic function is depressed in dogs with PDA with typical fractional shortenings of less than 25%, systolic time intervals (PEP/ET) greater than .44, and two-dimensional measurement of ejection fraction using Simpson’s Rule of less than 40% (Figure 9.17) (59,64,65). These parameters are all preload and afterload dependent and are not necessarily a good indicator of myocardial contractility (66). Despite significant dilation of the left ventricular chamber in most dogs, there is often inadequate hypertrophy of the wall and septum (59,67). This and the fact that the shunt is beyond the ventricular chamber elevate the systolic wall stress. As a result fractional shortening in hearts with a PDA are often low or within the normal range. A preload independent and heart rate corrected myocardial fiber shortening (VCFc) may be a better indicator of myocardial contractility than fractional shortening or ejection fraction. VCFc is inversely and linearly correlated with myocardial wall stress. In other words, as wall stress increases the velocity of myocardial fiber shortening decreases (66). In children with PDA, contractility has been shown to be normal despite abnormalities in fractional shortening and ejection fraction when these load independent and afterload corrected parameters are used for assessment (66).

Fractional shortening is typically not elevated in hearts with PDA secondary to high afterload.

Figure 9.17 Fractional shortening is typically not elevated despite significant volume overload in hearts with patent ductus arteriosus. The fractional shortening here is approximately 36% in a significantly dilated left ventricle. LV = left ventricle, VS = ventricular septum, LVW = left ventricular wall.

Poorer systolic function is a common finding in hearts after PDA closure (59,64,68,69). The immediate decrease in left ventricular function in dogs and people after PDA closure is the result of a decrease in left ventricular diastolic dimension but an unchanged left ventricular systolic dimension compared to preclosure values (67,70). Left ventricular function may take from 6 months to 1 year to return to preclosure levels, and function may never return to normal after closure of the ductus in older animals and people (64,67,70).

Diastolic dysfunction has been documented in hearts with PDA both before occlusion and in longterm follow-up evaluation. Parameters of diastolic function that were evaluated include transmitral flow E : A (abnormal if <1) isovolumic relaxation time (abnormal if >80 msec), mitral valve slow deceleration time (abnormal if >98 msec), and abnormal pulmonary venous flow (normal = PVs .25 −

.53m/sec, PVd − .42 − .70 m/sec, PVar − .12 − .28 m/sec) (64,71).

PDA

Diastolic function abnormal when

MV E : A <1

IVRT >80 msec

MV dec time >98 msec

Pulmonary venous flow abnormal

Changes in the heart after either surgical or device closure of a ductus include decreases in left ventricular diastolic dimensions, decreases in left atrial size, and decreases in fractional shortening (67). The decrease in left atrial to aortic root ratio was seen on M-mode imaging but was not seen in two-dimensional measurements of left atrial and aortic roots size until approximately 1 month after ductal closure (67).

There is a report of aneurysmal dilation of the aortic portion of the ductus arteriosus after surgical ligation. This is a rare occurrence but is thought to be the result of hematoma development in the wall of the ductus after using hemoclips, progressive dilation of the aortic portion of the ductus after closure at the pulmonary artery side, or from incomplete closure of the ductus with high velocity flow moving through a very narrow orifice creating increased stress on already potentially weak walls. This

aneurysmal dilation can be seen on right parasternal transverse imaging planes of the heart base at the level of the main pulmonary artery segment. A large anechoic circular structure will be seen to the right side of the pulmonary artery and the proximal portion of the descending aorta (72).

Spectral and Color-Flow Doppler Evaluation

Color-flow Doppler shows turbulence within the main pulmonary artery when a patent ductus is present. The aliased signal will usually fill the artery and extend from the bifurcation up to the pulmonary valve (Figure 9.18). This can be seen on any of the view that shows the main pulmonary artery segment. The turbulence in some animals completely fills the artery, and although the direction of flow from the descending aorta into the main pulmonary artery segment can be discerned, no specific jet related to ductal flow can be identified. When smaller shunts are present however a welldefined jet is usually seen on right parasternal transverse images even if the ductus is not actually seen (Figure 9.19).

Figure 9.18 The entire pulmonary artery fills with a turbulent color-flow signal in most hearts with patent ductus arteriosus. The turbulence stops at the level of the pulmonic valves and extends to the bifurcation. Here the color-flow signal outlines a prolapsing pulmonic valve (arrow) and a small red jet of pulmonic insufficiency. Plane = right parasternal transverse heart base, RV = right ventricle, RMPA = right main pulmonary artery, AO = aorta, RA = right atrium.

Figure 9.19 A well-defined jet representing ductal flow is seen within the pulmonary artery (arrow). Plane = right parasternal transverse heart base, RV = right ventricle, RMPA = right main pulmonary artery, AO = aorta.

Imaging of the ductus from right transverse views is less successful than from left cranial transverses views, which have up to a 96% visualization rate (59,67,73). The ductus is a hypoechoic structure between the main pulmonary artery near its bifurcation and the aorta. The pulmonary artery and its bifurcation should be clearly imaged and then subtle twisting and rocking of the transducer in the area of the ductus while color-flow Doppler is on will allow visualization of the ductus (19,62). The use of color-flow Doppler helps identify the ductus (Figures 9.20, 9.21). The jet originates just proximal to the bifurcation of the pulmonary artery on the right side of the image and flows upward toward the pulmonary valve. Identification of a tapering ductus and measurements of ductal diameter can then be made for possible catheter-based occlusion procedures. The ductus should be measured without color flow as color often bleeds onto the surroundings, and ductal measurements will be overestimated (67,73–75). Low Nyquist limits also create increased aliasing in the area of the ductus and lead to overestimation of size (67,73). A small sector angle helps improve resolution and measurement results (73). Using color-flow Doppler, ductal diameter measurements are within 1 mm of true size in 48% of dogs and within 2 mm in 83% of dogs (73). Using two-dimensional imaging, ductal size is measured within 1 mm of true size in 72% of dogs and within 2 mm in 100% of dogs (67,73). Underestimation of ductal size is rare (67,73). Freeze an image with the ductus identified by color-flow Doppler and then remove the color before measuring ductal diameter. The minimal ductal diameter as it enters the pulmonary artery and the size of the ampulla before it narrows should be measured (Figure 9.22). A larger ampulla confirms the presence of a tapering ductus, which is necessary for catheter-based occlusions of PDAs (67,73). Length of the ampulla and the aortic side of the ductus cannot be seen with transthoracic echocardiography (73). Therefore, becoming more specific about the anatomy of a ductus such as elongated, tubular, or a ductus with several constrictions is difficult without trans esophageal echocardiography (TEE) (67,73,74).

Measure ductal size at the pulmonary artery side from two-dimensional images without color-flow Doppler.

Figure 9.20 The patent ductus is usually seen on left cranial views of the pulmonary artery. It is easier to identify when color-flow Doppler is used. (A) The aliased color-flow jet is seen flowing from the ductus (arrow) into the pulmonary artery in this image. (B) The ideal image for recording a spectral

Doppler signal of ductal flow is when both flow acceleration (arrow) and the jet extending the pulmonary artery are seen. Plane = left cranial modified transverse pulmonary artery, PA = pulmonary artery, AO = aorta, RV = right ventricle, D = ductus.

Figure 9.21 This ductus with a large ampulla is seen on a left cranial transverse view. The ductus (large arrow) enters the pulmonary artery just proximal to the left main pulmonary artery. PA = pulmonary artery, AO = aorta, LMPA = left main pulmonary artery, RMPA = right main pulmonary artery, AMP = ampulla.

Figure 9.22 Measure the ductus (arrow) without color flow as color often bleeds onto the surroundings and ductal measurements will be overestimated. Plane = left cranial transverse view, PA = pulmonary artery, AO = aorta, RMPA = right main pulmonary artery, D = ductus.

Comparison of ductal measurements obtained from right and left transverse images with and without color-flow Doppler as well as TEE with and without color-flow Doppler, showed that TEE without color-flow Doppler was the most accurate (67). Ampulla length and width can only be measured using transesophageal echocardiography and has high correlation with angiographic measurements of ductal size (67). TEE can identify tubular ductal morphology, which typically requires surgical ligation. This is not always possible to identify with transthoracic imaging.

Spectral Doppler shows a very classic flow pattern that is not seen with any other congenital defect. Using any of the pulmonary artery views, place the Doppler beam over the artery with the gate located about halfway between the valves and the bifurcation. Continuous positive flow will be seen on the spectral tracing (Figure 9.23). Negative flow may be either continuous from ductal flow that is swirling back toward the bifurcation or primarily systolic from right ventricular ejection flow. In cases where a distinct jet of ductal flow is present, the gate needs to be moved side to side within the

artery toward the left main pulmonary artery segment before the continuous flow pattern is seen (19,62,76). The continuous upward flow is seen regardless of which imaging plane is used and regardless of whether the Doppler cursor is positioned exactly parallel with flow. In order to obtain accurate flow velocities and pressure gradients across the ductus, the Doppler beam must line up along the shunting jet. This is usually obtained from cranial left transverse imaging planes (Figure 9.24). The ductal flow is highest during systole since the largest gradient in pressure between the aorta (over 100 mm Hg) and the pulmonary artery (approximately 20 mm Hg) occurs during systole. During diastole, aortic pressure drops to around 60–80 mm Hg or lower while diastolic pressure in the pulmonary artery drops to about 10 mm Hg creating a lower pressure differential and lower flow velocity during diastole on the spectral Doppler flow profile of a PDA. The result is a spectral Doppler flow profile that is continuous but that increases and decreases in velocity with systole and diastole (74). Since systolic pulmonary artery pressures should be approximately 20 and systolic aortic pressure should be above 100 mm Hg, a gradient close to 100 mm Hg is expected. A lower pressure gradient is seen if the ductus is very large or if pulmonary hypertension is present. Pressure gradients in congenital heart disease provide information that is useful in the assessment of hemodynamic significance and prognosis. Since most PDAs are corrected, obtaining a pressure gradient in PDA is not as important as it is with other defects.

Figure 9.23 Using any of the pulmonary artery views, placing the Doppler beam over the artery will show continuous positive flow. A right parasternal image as is used here will usually not yield the highest flow velocity.

Figure 9.24 Maximal velocity for ductal flow is usually obtained from the left cranial view of the pulmonary artery. Here a classic flow profile is seen and a maximum gradient of 84 is obtained from pulmonary artery to aorta, reflecting fairly normal aortic and pulmonary artery pressures.

Stroke volume is high in a significantly shunting ductus because there is increased venous return to the left side of the heart. Stroke volumes can double and even triple in the presence of a large ductus. This is manifested on echo Doppler examination by an elevated aortic flow velocity (Figure 9.25) (59,67,77). High aortic flow velocity therefore suggests the presence of significant ducal shunting.

Aortic flow velocities are usually elevated with PDA. The higher the velocity the more significant the shunt in the absence of aortic stenosis.

Figure 9.25 Stroke volume is high in a significantly shunting ductus as there is increased venous return to the left side of the heart. High aortic flow velocity will be recorded with large volume shunts. This aortic flow velocity is 2.46 m/sec.

Pulmonary to systemic flow ratios can be calculated. This is covered in Chapter 4 but involves recording both aortic and pulmonary flow profiles, measuring the flow velocity integral of each of these flows to derive the area under the curve and multiplying these areas by the diameter of the

respective vessel. To calculate the pulmonary to systemic shunt ratio in the case of patent ductus arteriosus, it is important to remember that systemic flow is calculated from pulmonary artery velocity, while pulmonary flow is calculated from the aorta since the shunted volume enters the pulmonary circulation after passing through the ascending aorta (64).

PDA—Qp : Qs

Qp measured from aortic flow

Qs measured from pulmonary artery flow

Mitral insufficiency is a common finding in most hearts with a PDA (Figure 9.26) (59,64,67,77,78). This diminishes significantly as ventricular and atrial dimensions decrease after ductal closure (67,68,79,80). A long-term study (9 to 121 months) showed a high percentage of dogs with mitral insufficiency after ductal closure via catheter-based devices or surgical ligation. Several of these dogs showed signs of degenerative valve disease, and the regurgitation may not have the same underlying cause as when the ductus was present (64). These degenerative changes were present in older dogs that are not normally predisposed to degenerative changes and also occurred at younger ages than expected (64,69). Van Israël hypothesized that perhaps the turbulence associated with high volume and velocity flow across the mitral valve leaflets contributed to the development of degenerative changes on these valve leaflets (64). Mitral regurgitation may be secondary to myocardial dysfunction before and sometimes after ductal closure, mitral valvular annular dilation, or papillary muscle displacement as the heart dilates (69,77,81,82). Aortic insufficiency can be present as well, and the incidence of this insufficiency remained unchanged after ductal closure via any method. Damage to the cusps and dilation of the aorta are hypothesized to be the cause of this commonly seen insufficiency in hearts with PDA (64,67).

Figure 9.26 Aortic velocities are elevated in patent ductus arteriosus since the shunted blood must flow through the ascending aorta. Color-flow images will show aliasing within the aorta secondary to the increased velocities. A small jet of mitral insufficiency is also seen (arrow). Plane = right parasternal long-axis left ventricular outflow view, LV = left ventricle, AO = aorta, LA = left atrium, RV = right ventricle.