Feline idiopathic cardiomyopathy: A retrospective study of 106 cats (1994–2001) (original) (raw)

Abstract

The case records of 106 cats with idiopathic cardiomyopathy that presented to the Feline Centre of the University of Bristol between September 1994 and September 2001 were reviewed retrospectively. Hypertrophic cardiomyopathy (HCM) was the most common form seen (57.5%), followed by restrictive cardiomyopathy (RCM) (20.7%), dilated cardiomyopathy (DCM) (10.4%) and unclassified cardiomyopathy (UCM) (10.4%). One cat showed echocardiographic changes compatible with a moderator band cardiomyopathy (MBCM). Most affected cats were domestic short hairs (DSH) (57.5%). The mean (±SD, range) age of cats with cardiomyopathy at presentation was 6.8 (4.3, 0.5–16) years, with an equal distribution of males and females. Clinical findings, electrocardiographic changes and radiographic abnormalities were also reviewed. The median survival time for 73 cats for which follow-up data was available was 300 days. A greater survival time was observed for cats with UCM (925 days) when compared with those with HCM (492 days), RCM (132 days) or DCM (11 days).

Introduction

Cardiomyopathy is defined as an acquired cardiac disease characterised by damage to the myocardium (Fuentes 1992) but excluding the pathologies of the myocardium caused by an inflammatory process (myocarditis). Cardiomyopathies for which specific underlying condition cannot currently be identified are classified as idiopathic.

Several different forms of cardiomyopathy are recognised in cats. Idiopathic hypertrophic cardiomyopathy (HCM) is characterised by a variable concentric hypertrophy of the ventricular myocardium in the absence of any other obvious cause of hypertrophy, such as pressure overload or hormonal stimulation. The aetiology of primary HCM in cats is not fully understood, though familial HCM has been identified in Maine Coon cats (Kittleson et al 1999). Possible inheritance has also been suspected in American Shorthairs (Meurs et al 1997) and in a litter of mixed-breed cats (Kraus et al 1999).

Restrictive cardiomyopathy (RCM) is an idiopathic myocardial disease characterised by a left ventricle that has normal to near normal echocardiographic appearance and left atrial dilation (Kienle 1998), often accompanied by endocardial fibrotic lesions (Bonagura 1994).

Dilated cardiomyopathy (DCM) is characterised by a dilated left ventricular chamber and hypocontractile ventricular myocardium. Previously, DCM had represented the second most common form of feline heart disease (Fox 1999). However, since the association between taurine deficiency and DCM was reported (Pion et al 1987) and the subsequent recognition of the importance of including adequate taurine in feline diets, there has been a dramatic reduction in the prevalence of feline DCM. Taurine deficiency may also cause central retinal degeneration in cats that seems to persist even when plasma taurine level is restored (Pion et al 1987). The rare cases of taurine-associated feline DCM observed nowadays are generally the consequence of anon-traditional diet (ie, vegetarian diet, dog diet)(Kittleson 1998a), although evidence of genetic involvement has also been reported (Lawler et al 1993).

A significant number of cardiomyopathies show echocardiographic changes that are not typical of any other commonly recognisedcardiomyopathy. These cases are considered as ‘unclassified’ cardiomyopathy (UCM).

The aim of this retrospective study was to assess the relative frequency of these different forms of cardiomyopathies and to review their clinical features, diagnostic findings and prognosis.

Materials and methods

The case records of cats that underwent a full cardiac investigation at the Feline Centre of the University of Bristol between September 1994 and September 2001 were reviewed retrospectively and those cases affected by an idiopathic cardiomyopathy (_n_=106) were selected for the present study. Cases in which clinical investigation indicated a primary underlying cause of concentric ventricular hypertrophy, such as aortic stenosis, hyperthyroidism, acromegaly, primary or secondary systemic hypertension (systolic blood pressure higher than 180mmHg), were excluded. Signalment (age, breed and sex), clinical findings, electrocardiographic (ECG) changes, radiographic and echocardiographic abnormalities were investigated. In all patients, systolic blood pressure (BP) was measured using a Doppler technique (Parks Doppler 811-BTS, Perimed UK Ltd, Bury St Edmonds, Suffolk, UK). A standard six-lead ECG (Cardiofax, Nihon Kohden, Tokyo, Japan) was recorded with the patient in right lateral or sternal recumbency and ECG traces were examined by analysis of the rhythm and the wave morphology according to Tilley (1992). All cats were sedated prior to radiographic examination (right lateral and dorso-ventral view of thethorax) and echocardiographic study. The dose of sedation used was based on a standard protocol (ketamine 5mg/kg and midazolam 0.25mg/kg) modifiable according to the cat's presentation and given intramuscularly (i.m.).

The final diagnosis was based on B-mode, M-mode and colour-Doppler echocardiography in all cases, using an ultrasound machine ATL Apogee 800 and a 7.5MHz transducer. Theexamination was performed with the cat in lateral recumbency over a cut-out in the examination table and images were obtained by scanning from beneath the patient (Boon 1998). Criteria for echocardiographic diagnosis were established as follows:

Hypertrophic cardiomyopathy: cats were diagnosed with HCM when the interventricular septum (IVS) and/or left ventricular free wall (LVFW) thickness in diastole was ≥6mm, in a two-dimensionally guided M-mode scanning obtained from the right parasternal short axis view of the left ventricle just above the papillary muscles (Fox et al 1995).

Restrictive cardiomyopathy: echocardiographic diagnosis of RCM was based on the presence of a marked left atrial or biatrial dilation without a concomitant myocardial hypertrophy (Kienle 1998).

Dilated cardiomyopathy: diagnosis of DCM was based on the echocardiographic observation of left ventricular dilation (end systolic diameter ≥14mm) and a poor fractional shortening (≤28%) in a two-dimensionally guided M-mode scanning (Pion et al 1992).

Unclassified cardiomyopathy: echocardiographic diagnosis of UCM was made by exclusion, on the basis of evidence of myocardial abnormality that did not fit to any of the recognised disease classification (Kienle 1998).

Moderator band cardiomyopathy: diagnosis of moderator band cardiomyopathy (MBCM) was made in the presence of thickened false tendons in the left ventricle on echocardiography (Kienle 1998).

Whole blood taurine concentration was measured using ion exchange chromatography in all cats in which DCM was diagnosed. Cats with a taurine concentration lower than 100nmol/ml were considered taurine deficient.

Management of the cats following diagnosis varied considerably depending largely on the severity of the cardiac disease. The availability of cardioactive drugs changed during the period over which cats were selected for this study and, in addition, cases were managed by a number of different clinicians which influenced the choice of drugs used. Not all cats received treatment initially and treatment was frequently adjusted during the course of management. Most of the cats received diuretics, most commonly frusemide (1–2 mg/kg, intravenously (i.v.)/i.m., every 6h). After stabilisation frusemide was usually administered orally (2mg/kg, bid-tid) alone or in combination with spironolactone(2–4mg/kg, sid, per os). Additional treatments used in occasional cases were glyceryl trinitrate ointment 2% (3–6mm topically, tid) or thiazide diuretics.

Most of the cats with HCM, RCM or UCM received either atenolol (6.25–12.5 mg/cat, sid or bid, per os) or diltiazem (1.75–2.5 mg/kg, tid, per os) or enalapril (0.25mg, bid, per os) or a combination of these different drugs. Cats with DCM were treated with digoxin (10μg/kg, sid, per os) and/or dobutamine (0.5–10μg/kg/min, constant rate of i.v. infusion) and/or enalapril (0.25mg, bid, per os) in combination with taurine supplementation (250–500mg, sid).

Survival time was obtained from the case records and from telephone interviews with the referring veterinary surgeons.

Results

One hundred and six cats were diagnosed with idiopathic cardiomyopathy. The mean (±SD, range) age of these cats at presentation was 6.8 (4.3, 0.5–16) years, with an equal distribution between males and females. Thirteen breeds were represented, the most common of which were domestic shorthaired (DSH, 61) and Persian (14) (Table 1).

Table 1.

Signalment (age, sex and breed) in 106 cats with cardiomyopathy

Hypertrophic cardiomyopathy

Sixty-one (57.5%) cats were diagnosed with HCM. The mean (±SD, range) age of cats with HCM at diagnosis was 5.9 (4.5, 0.5–16) years.

Clinical signs at initial examination were variable. However, a systolic heart murmur was the most common finding (_n_=41, 72.1%), followed by dyspnoea (_n_=22, 36.1%) and tachycardia (_n_=16, 26.2%) (Table 2). Only three cats diagnosed with HCM did not have clinical signs referable to a cardiac condition (4.9%). Two of these cats were referred for gastro-intestinal problems and the third case was referred after the sudden death of one of its littermates. ECG changes were not commonly present (Table 3) and 26 cats with HCM (42.6%) did not show any significant abnormalities. The most frequent findings were represented by a left anterior fascicular block (_n_=17, 27.9%) and a pattern of left ventricular enlargement (QRS complexes >0.04s and R waves >0.9mV) (_n_=15, 24.6%). Arrhythmias were detected only in a few patients and were mainly represented by episodic ventricular premature complexes (VPCs). Signs of congestive heart failure (CHF) were indicated by the presence of pleural effusion and/or pulmonary oedema on thoracic radiographs and/or ascites. Fourteen (23%) cats with HCM showed signs of pulmonary oedema, four (6.6%) had evidence of pleural effusion and only one had radiographic evidence of ascites. Generalised cardiomegaly was found in 36 (59%) patients(Table 4).

Table 2.

Clinical findings in 106 cats with cardiomyopathy

Table 3.

Electrocardiographic (ECG) changes in 106 cats with cardiomyopathy

Table 4.

Radiographic changes in 106 cats with cardiomyopathy

Echocardiographic examination of all cats in the HCM group revealed thickening of the IVS and/or LVFW. In 20 (32.8%) cases, the hypertrophied septum was seen to compromise the left ventricular outflow tract (LVOT) during systole with consequent dynamic LVOT obstruction, causing a turbulent blood flow that was identified using the colour-flow Doppler. Echocardiography revealed the presence of pericardial effusion in four (6.6%) cats, and the presence of a thrombus or ‘smoke’ in the left atrium in seven (11.5%) cats.

Other echocardiographic findings were identified in this group including left atrial dilation, systolic anterior motion (SAM) of the mitral valve, reversed ratio between E wave (early or passive diastolic phase) and A wave (atrial contraction phase) on the Doppler study of the mitral inflow indicating diastolic dysfunction. However, these echocardiographic studies were not always performed and thereby could not be analysedretrospectively.

Restrictive cardiomyopathy

Diagnosis of RCM was made in 22 cats (20.7%). Cats with RCM were predominantly females (72.7%). The mean (±SD, range) age of cats with RCM at presentation was 7.1 (3.1, 3–16) years (Table 1).

The most common clinical findings were dyspnoea (_n_=12, 54.5%), heart murmur (_n_=8, 36.4%) and tachycardia (_n_=7, 31.8%) (Table 2). ECG changes were represented mainly by the presence of VPCs (_n_=3, 13.6%) (Table 3). Radiographic signs of CHF were more frequent in this group when compared to cats with HCM. Pleural effusion was observed in 12 cases (54.5%) and pulmonary oedema and ascites in nine (40.9%) and five (22.7%) cases, respectively. Cardiomegaly was present in 16 (72.7%) cats (Table 4).

The echocardiographic abnormalities in cats with RCM were characterised by a marked left atrial or biatrial dilation without a concomitant myocardial hypertrophy. In some cases, patchy areas of increased echogenicity of the endocardium could also be observed. Transmitral Doppler inflow was performed only in a few cases and was characterised by an increased E:A ratio. Echocardiographic evidence of a thrombus in the left atrium was found in five (22.7%) cats and pericardial effusion in two cats (9.1%).

Dilated cardiomyopathy

DCM was diagnosed in 11 cats (10.4%) with a higher proportion in females (72.7%) and a mean (±SD, range) age at presentation of 9.1 (3.6, 2–15.5) years (Table 1).

The main clinical findings at presentation were represented by typical signs of CHF, such as dyspnoea (_n_=9, 81.8%), tachycardia (_n_=6, 54.5%), hypotension (_n_=6, 54.5%), and ascites (_n_=6, 54.5%) (Table 2). None of the DCM diagnosed cats was found to be taurine deficient. However, ophthalmologic examination of the fundus revealed retinal degeneration in two cases (18.2%). ECG changes were not frequently observed and were represented by SVT (_n_=3, 27.3%) and a pattern of four-chamber enlargement (Table 3). All cats with DCM were presented with radiographic changes of CHF characterised by pleural effusion (_n_=10, 90.9%), pulmonary oedema (_n_=4, 36.4%) and ascites (_n_=6, 54.5%). Cardiomegaly was observed in all cases (Table 4).

Cats with DCM showed echocardiographic changes consistent with left ventricular dilation and a poor fractional shortening in a two-dimensionally guided M-mode scanning. In most of the cases, these abnormalities were accompanied by a concomitant dilation of the othercardiac chambers (four-chamber dilation) and a reduced thickness of the IVS and LVFW. Evidence of pericardial effusion and thrombi in the left atrium was found in two cats (18.2%).

Unclassified cardiomyopathy

Eleven cats (10.4%) were diagnosed with a form of cardiomyopathy characterised by echocardiographic changes that did not meet the typical features of the other cardiomyopathies. The mean (±SD, range) age of these cats at presentation was 8.8 (4.8, 0.8–15) years, with a higher proportion of females (63.6%) (Table 1). Clinical findings were represented mainly by dyspnoea (_n_=7, 63.3%) and the presence of a heart murmur (_n_=6, 54.5%) (Table 2). ECG changes were less common and characterised mainly by a pattern of left ventricular enlargement (_n_=3, 27.3%) and atrial standstill (_n_=2, 18.2%) (Table 3). On radiographic examination, five cats (45.5%) showed the presence of pleural effusion and one (9.1%) showed signs of pulmonary oedema. Cardiomegaly was observed in seven patients with UCM (63.6%).

The most common echocardiographic findings were represented by a marked left atrial dilation, mitral regurgitation, focal myocardial hypertrophy and regional wall hypokinesis. Pericardial effusion was observed in one case.

Moderator band cardiomyopathy

A 3.8-year-old male DSH cat was diagnosed with a rare cardiomyopathy characterised by theappearance of thickened false tendons in the left ventricle on echocardiography. The cat was referred for episodic dyspnoea and clinical findings consisted of low systolic blood pressure, tachycardia and the presence of a gallop rhythm on auscultation. ECG showed supraventricular tachycardia and radiographic examination revealed cardiomegaly without signs referable to CHF. At time of publication, this cat was still alive (4.6 years after diagnosis).

Follow-up data were obtained from 73 (68.9%) cats diagnosed with a cardiomyopathy. Median survival time for these 73 cats was 300 days (Table 5). Twenty-seven (37%) cats were still alive at the time of publication, with a median survival time of 1144 days (Fig 1). Substantially greater survival time was observed for cats with UCM when compared with those with RCM or DCM. The survival time of cats that lived for longer than 30 days after diagnosis was noticeably longer for cats with HCM compared to those with DCM.

Table 5.

Survival study in 73 cats with cardiomyopathy

Figure 1.

(a) Survival of 46 cats with cardiomyopathy that died before the time of publication. (b) Survival of 27 cats with cardiomyopathy that were still alive at the time of publication.

Discussion

This study provides information about the relative frequency of the different types of cardiomyopathy in cats presenting to a referral hospital and about the expected survival based on a large series of over 100 cases. There are limitations to a study of this nature. Prospective studies offer some advantages over retrospective studies, particularly for assessing prognosis. However, collection of data from a meaningfully large number of cases for a condition such as this presents some practical difficulties. During the length of time required to collect sufficient cases there are likely to be changes in staff and changes in the way that cases are diagnosed and managed based on advances in knowledge and the availability of treatments. Despite these limitations there are no comparable large studies published from outside the United States and this study provides practical information of value to practitioners, particularly in Europe, in managing cases of feline cardiomyopathy.

There is no universally accepted classification for cardiomyopathies in cats. The term idiopathic cardiomyopathy has been used in this paper to describe a clinical diagnosis and is commonly used in other publications. It includes primary cardiomyopathies and cardiomyopathies that may be secondary to some other disease process but which cannot be identified. The definitive diagnosis of cardiomyopathy and the assessment of the type of cardiomyopathy were based on echocardiographic criteria. Myocardial histopathology is an alternative approach to diagnosis and classification of cardiomyopathy but this is less relevant to practical clinical considerations.

All our patients were sedated before echocardiography and sedation can affect the measurement of left ventricular parameters. Sedation can decrease the fractional shortening and the left ventricular diameter in diastole (Dummel et al 1996). However, these were not critical measurements used to establish diagnoses in this study. Sedation of feline patients for diagnostic imaging is a standard procedure in many veterinary practices.

In the present study, HCM represented the most common form of feline cardiomyopathy (57.5%), which is in accordance with previous published studies (Atkins et al 1992, Kittleson 1998b, Rush 1998). The age of cats diagnosed with a cardiomyopathy was extremely variable, as previously observed by Bright et al (1992) in cats affected by HCM. In the overall evaluation of the different cardiomyopathies, the disease appeared equally distributed between males and females. However, males seemed more affected by HCM, while females were over represented in RCM, DCM and UCM. Bright et al (1992) also reported a higher proportion of male cats with HCM.

Cats with cardiomyopathies were presented with a wide variety of clinical signs. A heart murmur was the most common finding in patients with HCM, while dyspnoea was the major complaint in all the other cardiomyopathies (Table 2). Cats with RCM or DCM were presented with more severe clinical signs (tachycardia, hypotension, ascites, collapse). Hindlimb paresisassociated with arterial thromboembolism was observed only in cats affected by HCM or RCM. A characteristic taurine-deficient retinal degeneration was observed in two cats with DCM. However, none of the cats in this group was found with a low-plasma taurine concentration, as previously observed in some cases of DCM by Pion et al (1992).

Electrocardiography was an insensitive diagnostic test in cats with cardiomyopathies. The most common finding was represented by a left anterior fascicular block in cats with HCM, as previously reported by Bright et al (1992) and Rush (1998). Morphological changes of the ECG waves that could be related to chamber enlargement were not commonly observed.

The presence of CHF was confirmed on thoracic radiographs by observing signs of pulmonary oedema, pleural effusion and ascites. CHF was more frequently encountered in cats with RCM, DCM and UCM, explaining the higher incidence of dyspnoea in these cases. DCM, in particular, seemed to present more frequently with severe radiographic changes associated with CHF. Generalised enlargement of the cardiac silhouette (cardiomegaly) was more commonly observed in cats with RCM and UCM and present in all cats with DCM.

Echocardiography was the definitive test to diagnose and differentiate feline cardiomyopathies. Diagnosis of HCM was based on the presence of ventricular hypertrophy, that was often accompanied by other abnormalities, such as hyperdynamic ventricular function, left atrial (or biatrial) dilation, and obstruction of the LVOT. SAM and reversed E:A ratio of the mitral inflow were also observed in some cases. These additional findings might be useful to assess the severity of the condition and to give a more accurate prognosis. However, in many of the cases reviewed in this study, diagnosis was achieved only on the basis of ventricular hypertrophy and it was not possible to evaluate the prevalence and significance of changes in other echocardiographic parameters. Cats with RCM showed echocardiographic abnormalities characterised by marked left atrial (or biatrial) dilation and normal thickness and dynamic of the left ventricular myocardium. In many cases, focal hyperechoic areas were observed in the endocardium, possibly indicating fibrotic lesions or endomyocardial plaques (Bonagura 1994). Increased left ventricular end-systolic diameter and reduced fractional shortening were typical echocardiographic features of cats with DCM. Reduced LVFW thickening and mitral and/or tricuspid regurgitation were also frequently observed. A significant number of cardiomyopathies showed echocardiographic changes that were not typical of any other commonly recognised cardiomyopathy. These cases were considered as UCM, according to the classification proposed by Kienle (1998). Echocardiographic evidence of pericardial effusion was occasionally observed in all forms of cardiomyopathy and was often accompanied by clinical signs of right-sided heart failure (jugular distension and ascites). In some patients, echocardiography also allowed the identification of thrombi in the left atrium. This finding was interpreted as the cause of arterial embolism in cats presented with hindlimb paresis and absence of the femoral pulse or as a ‘marker’ of increased risk of thromboembolic lesions in the remaining cats (Rush 1998).

Preliminary assessment of the survival times suggested that, in many cases, cats with cardiomyopathy either died soon after diagnosis has been made or survived for a considerable time.

The cases were therefore compared according to short term or long term survival chosen arbitrarily as 30 days based on the preliminary assessment of the survival data. This concurs with the findings of previous reports.

In 1992 Atkins et al found a median survival time of 732 days in cats with HCM that were not euthanased on day 1. In our study, the median survival for cats with HCM was 492 days. However, when cats euthanased on day 1 were removed from the analysis, the survival time was nearer to that reported in the above mentioned study (596 days). Cats with DCM showed a much shorter median survival time (11 days). A similar survival time in cats with DCM was previously observed by Pion et al (1992). Survival time was noticeably better for cases of UCM when compared with those affected by RCM or DCM. These data might suggest that unclassified cardiomyopathies carry the best prognosis, while DCM and RCM have a poorer outcome. To provide accurate information on prognosis it would be necessary to follow all cats until they died in a prospective study. Although this was not performed in the current study, nevertheless it does provide useful information about outcome for cats with cardiomyopathy for the practitioner and little information on this important question is available. The prognosis for DCM was clearly poor. In the case of RCM the median follow-up periods indicated that in some cats the short-term prognosis is poor but, for those that survive beyond the short term, long term prognosis is better.

Analysis of survival times carries some limitations and care should be taken when interpreting these data. For example, more cats with HCM were presented with a heart murmur in the absence of other clinical evidence of cardiac disease. This may have selected them for cardiac assessment at an earlier stage in the disease process, thus affecting the survival times.

The presence and severity of CHF at presentation would also be an important parameter to consider for the survival time analysis. It was not feasible to assess the correlation of survival time with the absence or presence of CHF in this study because some cats were already on diuretic treatment when referred to our hospital and this may have masked or altered changes indicative of CHF.

Conclusions

Feline cardiomyopathy is often suspected when cats are presented with clinical signs referable to a cardiac disease. However, a cardiomyopathy cannot be confirmed and classified without a thorough cardiac investigation particularly based on echocardiographic examination. Furthermore, some forms of cardiomyopathy do not show characteristic features, often making the classification very difficult. HCM occurs with a wide spectrum of clinical and echocardiographic findings (Bright et al 1992). The pathogenesis of ‘unclassified’ cardiomyopathy is unclear but could represent a variation of another recognised form of cardiomyopathy. As knowledge of feline cardiomyopathies increases different classification may be introduced and some questions regarding the aetiology and pathophysiology of these conditions may be answered.

Acknowledgments

We would like to thank the Feline Advisory Bureau (FAB) for supporting a number of the clinicians involved in this work, the Diagnostic Imaging Service at Langford, the laboratories, our clinical colleagues at Langford, and the referring veterinary surgeons. A particular thank to Mrs Rebecca Giles for obtaining the survival data.

References

1. Atkins C.E., Gallo A.M., Kurzman I.D., Cowen P. Risk factors, clinical signs, and survival in cats with a clinical diagnosis of idiopathic hypertrophic cardiomyopathy: 74 cases (1985–1989), Journal of the American Veterinary Medical Association, 4, 1992, 613–618. [PubMed] [Google Scholar]
2. Bonagura JD. (1994) Feline restrictive cardiomyopathy. In: Proceedings of 12th ACVIM forum, San Francisco, CA, 1994, pp. 205–208.
3. Boon J.A. The echocardiographic examination. In: Manual of Veterinary Echocardiography, 1998, Williams and Wilkins: Baltimore, pp. 35–150. [Google Scholar]
4. Bright J.M., Golden A.L., Daniel G.B. Feline hypertrophic cardiomyopathy: variations on a theme, Journal of Small Animal Practice, 32, 1992, 266–274. [Google Scholar]
5. Dummel C., Neu H., Huttig A., Failing K. Echocardiographic reference ranges of sedated cats (Abstr.), Tierarztliche Praxis, Suppl 24, 1996, 190–196. [PubMed]
6. Fox P.R. Feline cardiomyopathies. Fox, Sisson, Moise Textbook of Canine and Feline Cardiology. Principle and Clinical Practice, 2nd edn, 1999, WB Saunders: Philadelphia, 621–678. [Google Scholar]
7. Fox P.R., Liu S.K., Maron B.J. Echocardiographic assessment of spontaneously occurring feline hypertrophiccardiomyopathy: an animal model of human disease, Circulation, 92, 1995, 2645–2651. [DOI] [PubMed] [Google Scholar]
8. Fuentes V.L. Feline heart disease: an update, Journal of Small Animal Practice, 33, 1992, 130–137. [Google Scholar]
9. Kienle R.D. Feline unclassified and restrictive cardiomyopathy. In: Small Animal Cardiovascular Medicine, 1998, Mosby: St Louis, pp. 363–369. [Google Scholar]
10. Kittleson M.D. Primary myocardial disease leading to chronic myocardial failure (dilated cardiomyopathy and related diseases). In: Small Animal Cardiovascular Medicine, 1998a, Mosby: St Louis, pp. 319–346. [Google Scholar]
11. Kittleson M.D. Hypertrophic cardiomyopathy. In: Small Animal Cardiovascular Medicine, 1998b, Mosby: St Louis, pp. 347–362. [Google Scholar]
12. Kittleson M.D., Meurs K.M., Munro M.J., Kittleson J.A., Liu S.K., Pion P.D., Towbin J.A. Familial hypertrophic cardiomyopathy in Maine Coon cats. An animal model of human disease, Circulation, 99, 1999, 3172–3180. [DOI] [PubMed] [Google Scholar]
13. Kraus M.S., Calvert C.A., Jacobs G.J. Hypertrophic cardiomyopathy in a litter of five mixed-breed cats, Journal of the American Animal Hospital Association, 35, 1999, 293–296. [DOI] [PubMed] [Google Scholar]
14. Lawler D.F., Templeton A.J., Monti K.L. Evidence for genetic involvement in feline dilated cardiomyopathy, Journal of Veterinary Internal Medicine, 7, 1993, 383–387. [DOI] [PubMed] [Google Scholar]
15. Meurs K., Kittleson M.D., Towbin J., Ware W. Familial systolic anterior motion of the mitral valve and/or hypertrophic cardiomyopathy is apparently inherited as an autosomal dominant trait in a family of American shorthair cats (Abstr.), Journal of Veterinary Internal Medicine, 11, 1997, 138. [Google Scholar]
16. Pion P.D., Kittleson M.D., Rogers Q.R., Morris J.G. Myocardial failure in cats associated with low plasma taurine: a reversible cardiomyopathy, Science, 237, 1987, 764–768. [DOI] [PubMed] [Google Scholar]
17. Pion P.D., Kittleson M.D., Thomas W.P., Skiles M.L., Rogers Q.R. Clinical findings in cats with dilated cardiomyopathy and relationship of findings to taurine deficiency, Journal of American Veterinary Medical Association, 15, 1992, 267–285. [PubMed] [Google Scholar]
18. Rush J.E. Therapy of feline hypertrophic cardiomyopathy, Veterinary Clinics of North America. Small Animal Practice, 28, 1998, 1459–1479. [DOI] [PubMed] [Google Scholar]
19. Tilley L.P. Essentials of canine and feline electrocardiography. Interpretation and management, 3rd edn, 1992, Lea and Febiger: Philadelphia: [Google Scholar]