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Chapter 17: Miscellaneous Myocardial Disease 207
defect. Kittens were evaluated from 2 days to 3 months Radiography
of age at the end-stage of the disease (Paasch and Zook Left atrial and ventricular enlargement has been
1980). Affected cats had an increased heart weight observed, often with evidence of congestive heart failure,
with left ventricular and often left atrial dilation. The including pulmonary edema and/or pleural effusion
endocardium appeared grossly opaque and diffusely (Fox 1999).
thickened, secondary to proliferation of fibrous and
elastic tissue and edema formation (Bonagura &
Lehmkuhl 1999). Histologic abnormalities include a Echocardiography
diffuse hypocellular fibroelastic thickening of the Echocardiography has not been well described for this
endocardium, with thin collagen and elastic fibers, and uncommon defect. Myocardial failure and left ventricu-
marked accumulation of edema. Dilated endocardial lar eccentric hypertrophy may be present. The endocar-
lymphatics are present until the end-stage disease, when dium may appear thickened and hyperechoic due to the
they likely become compressed or obliterated. Purkinje accumulation of fibroelastic tissue.
cells, and often the left bundle branch, become incorpo-
rated into the fibroelastic thickening, and undergo Diagnosis
atrophy or necrosis. Misc. Heart Diseases
Given the uncommon nature of the defect, the diagnosis
is primarily based on pathology findings.
Signalment
Burmese and Siamese kittens were the original breeds Treatment
reported; however, it has been reported in a colony of There is no specific treatment for endocardial fibroelas-
domestic shorthair cats as well (Rozengurt 1994; tosis. Therapy consists of treating congestive heart
Bonagura and Lehmkuhl 1999).
failure when present (see Chapter 19).
History and Chief Complaint Outcome and Prognosis
A family history of the disease is likely, given the heri- The prognosis is grave, and most affected cats die of
table nature of the defect. Clinical signs consistent with heart failure or suddenly at a young age.
congestive heart failure typically develop in cats between
1 and 6 months of age (Bonagura and Lehmkuhl 1999;
Fox 1999). Sudden death may occur (Zook and Paasch EXCESSIVE LEFT VENTRICULAR
1982; Rozengurt 1994). MODERATOR BANDS
Excessive moderator bands (“false tendons”) are promi-
Physical Examination nent muscular bands that cross from the interventricu-
Physical examination findings may include a left apical lar septum to the left ventricular free wall (Liu et al.
holosystolic murmur of mitral regurgitation, tachycar- 1982; Wray et al. 2007). A single one is commonly seen
dia, and a gallop rhythm (Zook and Paasch 1982; Fox in the right ventricle of many species. A single modera-
1999). tor band or a network of small moderator bands has
been reported occasionally in the left ventricle of the cat
(Wray et al. 2007; Fox 1999). Early reports suggested that
Differential Diagnosis
left ventricular moderator bands were typically associ-
Because the disease affects young kittens, the most ated with cardiac disease; however, they have also been
common differential diagnoses include various congeni- found as an incidental finding (Fox 1999). Therefore, the
tal heart defects such as mitral valve dysplasia, ventricu- importance of moderator bands in the left ventricle of
lar septal defect, and endocardial cushion defects, which the normal cat is controversial.
may result in similar clinical presentation.
Etiology, Pathophysiology, and Pathology
Diagnostic Testing Etiology
Electrocardiography The etiology of excessive moderator bands is unknown,
The most common ECG abnormality is increased R and it is unclear if it is caused by a “silent” congenital
wave amplitude suggestive of left ventricular enlarge- anomaly (Liu et al. 1982) or is simply a variant of normal
ment (Fox 1999). in normal cats (Fox 1999).