heterogeneous in appearance, containing many small hypoechoic areas. Despite this heterogeneous appearance, they are difficult to differentiate from benign myxomas (Figure 8.27) (135).

Echocardiography cannot identify tumor types. Location and appearance provide information as to the most likely type of tumor, but many tumors look alike and are found in similar places within the heart.

Figure 8.27 Echocardiographically myxosarcomas are usually multilobed and heterogeneous in appearance, containing many small hypoechoic areas. (A) Here a large myxosarcoma (arrows) is seen in the right ventricular chamber on a right parasternal transverse view of the heart base. (B) The same mass seen on apical four-chamber view crosses the tricuspid valve and fills part of the right atrial chamber and most of the right ventricular chamber. AO = aorta, LA = left atrium, RV = right ventricle, LV = left ventricle, MV = mitral valve, RA = right atrium, plane = left apical four chamber.

Pericardial Disease

Introduction

Pericarditis is classified into three broad categories with some overlap: effusive, fibrinous, and constrictive. Large fluid accumulations characterize effusive pericarditis, fibrinous tissue within the pericardial fluid characterizes fibrinous pericarditis, and when the fibrinous tissue matures and consolidates causing fibrosis of the pericardial sac it has advanced to constrictive pericarditis (139,140).

Idiopathic Effusion

The diagnosis of a thickened pericardium is sometimes possible on echocardiographic images, but there are many false positives unless there is pleural effusion to help define both boundaries of the sac (141). Idiopathic pericardial effusion is an uncommon occurrence in dogs, is even rarer in large animals, and is referred to as chronic proliferative pericarditis, benign idiopathic pericardial effusion, idiopathic hemorrhagic pericardial effusion, or idiopathic pericardial hemorrhage (1,27,37,142). The diagnosis of idiopathic pericardial effusion is one of exclusion after neoplasia and infection have been ruled out as causes (142).

There is generally a large amount of pericardial effusion (Figure 8.28). The fluid accumulates slowly, and signs of tamponade are a late sequela. Pleural effusion is usually present as well, and this allows better imaging of the pericardial sac itself (Figure 8.5). The sac is usually thickened and irregular by the chronic accumulation of fibrin on the pleural side of the sac, and undulating fibrin tags may be seen within the pleural space and adhered to the sac. At times the fibrin accumulation may appear to be masses. A thorough exam to rule out masses still does not lead to a definitive diagnosis of idiopathic effusion since small masses may not be seen. Massive effusions however do make it easier to identify neoplasia. Surgical and histological examination is necessary for the definitive diagnosis (10,37).

Idiopathic effusions typically have very large volumes.

Figure 8.28 (A) The effusion is typically very large in animals with idiopathic pericardial effusion. Plane = right parasternal transverse left ventricle. (B) The large echo-free space of pericardial effusion surrounds the heart of this dog with idiopathic pericardial effusion. Notice that the fluid does not extend around the base of the heart, and its boundaries are relatively smooth and circular. PE = pericardial effusion, RV = right ventricle, LV = left ventricle, LA = left atrium, RA = right atrium, plane = right parasternal four chamber.

Pericardial Neoplasia

Pericardial disease may be secondary to metastatic disease involving the sac with lymphosarcoma being the most common of these. Other cancers found to metastasize to the pericardial sac in dogs and cats include melanomas and mammary and pulmonary adenomas, mesothelioma, and rarely hemangiosarcoma (2,5,30,78,81,82,143,144). Pericardial tumors are difficult to diagnosis. When no effusion is present, the pericardial sac cannot be defined well and when pericardial effusion is present, the sac may still appear to be normal in appearance because the tumor is so diffuse in nature (2,11,142,143,145,146). Pericardial effusion is typically present and is usually a significant volume. When the sac is thick and irregular, pericardial neoplasms cannot be differentiated echocardiographically from other pericardial disease or fibrin deposition on the sac.

Infectious Pericarditis

Infectious pericarditis is rare in small animals, but traumatic fibrinous pericarditis is frequently seen

in the bovine and less commonly seen in the horse (1,27,139,147–150). This form of pericarditis is usually the result of foreign body penetration, other trauma such as bite wounds, or systemic infections (27,147, 151–153). It is generally easy to differentiate fibrinous pericarditis from other forms of pericardial disease because of the extensive amount of fibrin adhered to the epicardial surface and moving around within the pericardial space (Figures 8.29, 8.30) (27,150,154,155). The epicardial surface appears irregular because of the fibrin buildup, and the sac is thick. The amount of pericardial fluid varies from a lot to very little. When pleural fluid is also present, the pericardial sac will also appear to be irregular and the thickness of the sac can be determined with greater accuracy.

Figure 8.29 Fibrinous pericarditis presents with varying amounts of pericardial effusion. A small effusion is seen in this cow with traumatic pericarditis. The pericardial space contains many irregular echo densities. PS = pericardial sac, PE = pericardial effusion, F = fibrinous adhesions, RV = right ventricle, LV = left ventricle, PLE = pleural effusion.

Figure 8.30 Fibrinous pericarditis in a dog showing many fibrinous strands attached to the pericardial sac and epicardium floating within the pericardial fluid. PE = pericardial effusion, RV = right ventricle, LV = left ventricle.

Constrictive Pericarditis

Two-Dimensional Findings

Not all pericarditis is fibrinous in nature, and there are no specific echocardiographic changes to help differentiate idiopathic effusions from infectious pericarditis. Constrictive pericarditis however involves a thickened scarred pericardium, which limits diastolic filling of the heart (28). Constrictive pericarditis is typically not effusive, but can be, and there are usually no visible adhesions connecting the sac to the epicardium (156,157). When effusion is present, the term effusive-constrictive pericarditis is used (157). Constrictive pericarditis is thought to start with an episode of acute pericarditis. This usually goes undetected, and fluid is resorbed. The pericardial sac then becomes thick and fibrotic during a chronic phase. Causes of the acute subclinical phase may be idiopathic effusion, mycotic infections, neoplasia, and foreign bodies (147,157,158). Differentiating effusive constrictive pericarditis from acute cardiac tamponade is sometimes only possible after a centesis. Cardiac pressures do not return to normal in constrictive pericarditis (159).

The pericardium may appear normal in thickness echocardiographically, during surgery and with histological examination (28,160). The diagnosis of a thick pericardium is tricky using echocardiography. When a small amount of effusion is present, parallel motion of the parietal pericardium and epicardium can be seen with a thick sac (28). Transthoracic imaging however is very insensitive to increases in pericardial thickness, and both false positives and negatives are common. Pericardial thickness assessed by transesophageal echocardiography in man however correlates well with thicknesses obtained from computed tomography (28,161). When the pericarditis leads to constrictive physiology, the cardiac chambers are typically smaller than normal as the pericardial sac constricts the heart and prevents adequate ventricular filling (Figure 8.31). Both sides of the heart are affected by the increased pressures applied to it by the thickened sac, but the signs of right-sided heart failure predominates because of the thinner right ventricular wall.

Figure 8.31 Constrictive pericarditis typically has very little pericardial effusion. Fibrin is seen attached to the outside of the pericardial sac. The heart is small and volume contracted secondary to the constriction. PLE = pleural effusion, PS = pericardial sac, PE = pericardial effusion. RV = right

ventricle, LV = left ventricle, LA = left atrium, RA = right atrium.

Two-dimensional imaging will show biatrial dilation, increased mitral and tricuspid valve excursions, and an abnormal contour to the junction between the ventricular and atrial chambers. The atrial chamber appears to balloon out this junction as opposed to the smooth transition usually seen when the atrium and ventricular chamber both dilate (28,162,163). Echogenic areas within the myocardium may be seen after resolution of the pericarditis on follow-up exams. These areas are thought to be areas of fibrosis secondary to myocarditis, which was probably present in addition to the pericarditis (164).

M-mode Findings

When constrictive pericarditis exists, the ventricles stop filling early in diastole, typically by the end of the first third of diastole (28). This is sometimes seen on M-mode images as a decrease in the normal gradual downward motion seen on the left ventricular free wall throughout diastole. Left atrial dilation is commonly seen with constrictive pericarditis secondary to increased left ventricular filling pressures. M-mode images of the left ventricle may also show early diastolic notching on the left side of the interventricular septum or later in diastole with atrial contraction. These are not specific, and even the presence of all of these M-mode findings does not confirm the diagnosis of constrictive pericarditis, the lack of any of them definitely rules out the diagnosis (28,165).

Spectral Doppler Findings

Inspiration decreases intrathoracic pressure, which normally increases flow into the right side of the heart. There is enhanced ventricular interaction with constrictive pericarditis however, and expansion of the right heart during inspiration reduces left ventricular filling. Pulmonary venous pressure decreases during inspiration as a result, but there is no decrease in left ventricular pressure, which additionally limits left ventricular filling. The reverse occurs during expiration with constrictive physiology (28,163).

The decrease in pulmonary venous pressure during inspiration decreases pulmonary vein diastolic

flow velocity, and with expiration there is a very pronounced increase in diastolic flow into the left atrial chamber. Expiration also decreases the pulmonary venous S : D ratio since diastolic flow into the left atrial chamber is enhanced. The enhanced interdependence between the right and left ventricular chambers and the changes in pulmonary venous flow cause exaggerated respiratory changes in flow through the atrioventricular valves. During the beat just after inspiration while there is negative intrathoracic pressure, trans tricuspid flow velocity increases while transmitral flow velocity is decreased by 25–40% and the reverse happens during expiration (Figure 8.32). In the normal heart, there will be variation in trans tricuspid flow velocities with respiration, but there is little ventricular interdependence, and respiratory changes are not noted during left ventricular filling. Lower left atrial pressure during inspiration will increase isovolumic relaxation time, while increased pulmonary venous return and higher left atrial pressure with expiration decreases isovolumic relaxation. Since expiration results in poor flow into the right side of the heart, there is also increased hepatic flow reversal during this respiratory time period (28,163,166,167).

Constrictive Pericarditis

Trans tricuspid flow

Increases with inspiration

Decreases with expiration

Transmitral flow

Decreases with inspiration

Increases with expiration

Figure 8.32 During the beat just after inspiration while there is negative intrathoracic pressure (A) trans tricuspid flow velocity increases while (B) transmitral flow velocity is decreased by 25 to 40% and the reverse happens during expiration. In the normal heart, there will be variation in trans tricuspid flow velocities with respiration, but there is little ventricular interdependence, and respiratory changes are not noted during left ventricular filling. TV = tricuspid valve flow, MV = mitral valve, INS = inspiration, EXP = expiration.