Congestive heart failure associated with a large transverse left ventricular moderator band in a cat

Abstract

Cardiomyopathy associated with abnormal trabecular bands of tissue traversing one or both ventricles is reported rarely in cats. The case of a 9-year-old cat which presented in congestive heart failure is reported. Multiple cardiac abnormalities were found, including a large trabecular tissue bridge which bisected the left ventricle. Other findings included arrhythmia, thrombocytopaenia and raised serum creatine kinase. The cat was euthanased due to clinical deterioration. Necropsy findings included increased cardiac weight, the division of the left ventricle by a large trabecular band composed of connective tissue and cardiac myofibres consistent with a moderator band, nodular thickening of the mitral valve, left atrial dilation, and fibroplasia/fibrosis of the left ventricular myocardium associated with widespread myofibre necrosis due to infarction. Pathological findings in this case differ from previous reports of ventricular transverse bridging tissue in cats with cardiac disease.

A 9-year-old female neutered domestic shorthair cat (3.4 kg) presented with a 3-week history of increased respiratory effort and inappetence. From primary vaccination a grade 3/6 early systolic left apical high pitched cardiac murmur had been noted, but further investigation had been declined. Relevant laboratory abnormalities were limited to thrombocytopaenia of 73×10⁹/l (150–550), confirmed by blood smear examination, and elevated creatine kinase of 3027.7 IU/l (20–225). Radiography performed after sedation with 0.85 mg midazolam (Hypnovel; Roche) and 6 mg ketamine hydrochloride (Ketaset; Fort Dodge) intravenously demonstrated generalised left atrial enlargement, a generalised hazy/lacy mixed alveolar/interstitial lung infiltrate and lobar venous dilation and tortuosity, consistent with congestive heart failure. The vertebral heart score was measured to be 9.5 (7.5±0.3) (Lister and Buchanan 2000). A 3-lead ECG recording (Kontron Micromon 7141 ECG monitor) was consistent with a left ‘anterior fascicular’ block-type pattern with a qR pattern in lead I and rS pattern in leads II and III. A 2D echocardiogram (Fig. 1) using a 10 MHz phased-array transducer (GE Ultrasound Vivid 3) demonstrated a prominent ‘bridge’ of tissue, isoechoic to and confluent with the left ventricular free wall, traversing the left ventricle from the midpoint of the free wall to the septum in an apical–basilar direction. Some confluence with the caudodorsal papillary muscle was noted and dysplasia of the posterior mitral valve apparatus was suspected and diastolic excursion of the free wall and septum was subjectively reduced in the left ventricular apex. A diagnosis of congestive heart failure due to unclassified cardiomyopathy associated with multiple cardiac defects was made. The cat was euthanased due to clinical deterioration and necropsy performed. Gross necropsy demonstrated diffusely oedematous lungs which oozed pink-tinged foamy fluid on sectioning. No evidence of thromboembolism was found within the left auricle, pulmonary vessels or aorta. Gross and histological examination of the heart was performed by a pathologist (SS). Cardiac weight was 19.9 g representing a heart (g) to body weight (kg) ratio of 6.14 (3.83±0.20) (Liu et al 1982). Gross examination demonstrated left ventricular and septal thickening, a prominent trabecular band of fibrous connective tissue and muscle diagonally bisecting the left ventricle into a smaller medial chamber and a larger lateral chamber, mild left ventricular outflow tract dilation, left atrial dilation, mild nodular thickening of the mitral valve leaflets, a dense meshwork of associated trabecular fibres on the septal endocardial surface and two discrete large wedge shaped dark brown foci within the left ventricular myocardium (Fig. 2). Microscopic examination (Fig. 3) demonstrated multifocal, well-demarcated areas of myocardial necrosis and degeneration circumscribed and infiltrated by necrotic neutrophils consistent with acute multifocal infarction of myocardium and papillary muscle. Additionally the left ventricular myocardium demonstrated interstitial oedema, and scattered foci of lymphoplasmacytic inflammation interspersed with areas of marked fibroplasia and fibrosis; these latter changes were suspected to be secondary to infarction. The large trabecular band comprised largely dense collagenous connective tissue partially covered with endocardium, in which were cardiac myocytes, loosely spaced bland fibroblasts and clusters of mononuclear cells (predominantly lymphocytes and plasma cells) and occasional neutrophils. Endocardial pathology was limited to endocardial fibrosis within the left atrium; generalised endocardial fibroelastosis was not seen. No evidence of primary vascular disease or intraluminal thrombosis of cardiac vessels was seen. A Steiner stain preparation did not demonstrate bacterial organisms. Mitral valve lesions consisted of increased numbers of bland spindle cells within a myxoid stroma.

Fig 1.

Echocardiographic examination. (A) Right parasternal long-axis view of left atrium and ventricle, early diastole. A dense tissue band isoechoic or slightly hyperechoic to the left ventricular myocardium traverses the left ventricle in an apical–basilar direction. (B) Right parasternal short-axis view of left ventricle at level of tissue band, end diastole. The band of tissue can be seen bisecting the left ventricle.

Fig 2.

Gross appearance of left atrium, ventricle and mitral valve apparatus. The trabecular tissue band can be seen within the left ventricle (a needle is inserted behind it to show communication beyond the tissue band). Mild nodularity of the mitral valve edge can be appreciated and there is a large wedge shaped (dark brown) infarct of the apical left ventricular free wall. Smaller focal infarcts are seen also within the left ventricular free wall.

Fig 3.

Masson's trichrome stain, 40× magnification. Anomalous band composed of dense collagen (blue staining) containing loose fibroblasts and several bundles of myocardial fibres (red staining) (A). Haematoxylin and eosin, 40× magnification (B) and 200× magnification (C) of left ventricular papillary muscle. There is a large area of acute necrosis and haemorrhage with an infiltrate of neutrophils indicating a well-demarcated area of infarction. Overlying endocardium demonstrates infiltration with necrotic neutrophils and detail image demonstrated marked subendocardial inflammation and fibrosis. Haematoxylin and eosin, 40× magnification (D) and 200× magnification (E) of mitral valve. The valve leaflets are thickened by bland, loosely spaced fibroblasts in a faintly mucinous stroma.

The finding of traversing bands of tissue within the left ventricle is infrequently described in clinical case reports. Two predominant causes, namely ‘excessive moderator bands’ and endomyocardial fibrosis/endomyocarditis are described (Liu et al 1982, Kienle 1998, Fox 1999, Ferasin et al 2003). Moderator bands have been defined as muscular tendinous bundles of tissue connecting the interventricular septum to the ventricular free wall. It is thought that they may prevent over-distension of the ventricle during diastolic excursion and function to transport Purkinje fibres to extend to the papillary muscle and myocardium of the ventricular free wall (Liu et al 1982). Fine networks of transversing trabecular fibres (referred to as ‘excessive moderator bands’) have been reported as a normal finding in the right ventricle of the monkey, sheep, pig and ox (Truex cited in Liu et al 1982), in the right and left ventricle of dogs (Miller et al 1964), cats (Fox 1999) and humans (Rolleston cited in Liu et al 1982) but have also been reported to be present in cats with congestive heart failure (Liu et al 1982, Ferasin et al 2003). A series of 21 cats is reported in which excessive numbers of left ventricular moderator bands were found at necropsy in cats with ante-mortem signs of congestive heart failure. These cats had left ventricular hypertrophy or dilation, left atrial enlargement and post-mortem heart:body weight ratios which were not significantly different from normal (control) cats and were significantly less than those of cats with heart failure in which the underlying cause appeared to be hypertrophic cardiomyopathy or endocardial fibrosis (Liu et al 1982). Some authors have since questioned the significance of these excessive moderator bands and their relationship to concurrent heart disease (Fox 1999). The excessive moderator bands described in previous reports were found to be largely composed of collagenous connective tissue and bland fibroblasts covered by intact endothelium, similar to the band in the case described. However, unlike in the present case, all cases were found to have multiple small tissue bands rather than one large one. Additionally, widespread ischaemia and associated inflammatory cell infiltrates were not described in the case series published by Liu et al (1982). Fox (1999) similarly describe left ventricular bridging by confluent/adherent endocardial scar tissue in cats with restrictive-type cardiomyopathy caused by endomyocarditis and left ventricular endomyocardial fibrosis. However, whilst focal myocardial fibroplasia, fibrosis and scattered mononuclear focal myocarditis were present in the described case, pathology of the endocardium other than within the left atrium was absent. Mononuclear infiltration was considered to be secondary to infarction and necrosis in this case due to the mild and scattered nature of the mononuclear infiltrate. Myocyte hypertrophy and disarray consistent with hypertrophic cardiomyopathy was not seen in this case. The mitral valve pathology appeared similar to that seen in myxomatous atrioventricular valve degeneration in dogs (ie, endocardiosis) though may have represented another form of valvular degeneration or dysplasia (as endocardiosis is not recognised in cats).

The presence of a loud early systolic high pitched murmur auscultated over the left apical area throughout the cat's life suggests that a congenital malformation was present rather than a purely acquired cardiac disease. However, in the absence of full echocardiographic examinations early in this cat's life, and more complete ante-mortem assessment of diastolic function it is not possible to determine the relative contributions to the congestive heart failure of congenital and acquired disease. Clinical deterioration in this case may have been due to worsening congestive heart failure, progressive pulmonary oedema, arrhythmia or further myocardial infarction. Additional contribution to myocardial dysfunction may have been due to focal inflammatory infiltration and regional fibrosis. The markedly raised level of serum creatine kinase with concurrent thrombocytopaenia (considered consumptive in aetiology), and association of infarcted tissue with an infiltration of degenerate neutrophils suggested that infarction was an event which had occurred prior to presentation. The cause of the myocardial infarction in this case is unclear. Given the increased left ventricular free wall and interventricular septal thickness, it seems likely that reduced myocardial perfusion due to increased left ventricular filling pressure resulting in increased transmural pressure gradient and reduced mural blood flow, combined with increased myocardial oxygen demand, may have contributed. Small vessel luminal obliteration by thrombi or by inflammatory infiltrates was not noted, nor was vasculitis. However, the absence of thrombosis histologically does not categorically exclude its possible involvement, as fibrinolysis may have occurred after death. Regional hypokinesis of the apical left ventricular free wall may have been due to myocardial ischaemia, fibrosis or ‘tethering’ of free wall movement by the tissue band. The left bundle branch block identified in this case on electrocardiography was also considered likely due to myocardial ischaemia and is one of the commonest reported electrocardiographic abnormalities in all cats with cardiomyopathy (Bright et al 1992, Fox 1999, Ferasin et al 2003). Interference with left ventricular outflow tract dynamics and systolic/diastolic left ventricular function was suspected but not confirmed; it is not clear to what degree the anatomical abnormality contributed to cardiac disease in this case.