Often, but not always, a heart murmur is evident on auscultation, which may be the first clinical sign of any apparent disorder in affected cats. Other symptoms such as ascites and peripheral oedema may be present if congestive heart failure is present. In other cats, aortic thromboembolism (acute hind-limb paralysis) may be the only presenting sign which leads to a primary diagnosis of cardiomyopathy. The most common cause of symptomatic heart disease is diastolic heart failure. This results from diastolic dysfunction, the principal pathophysiological consequence of a wide range of heart muscle disorders, most prominent of which are hypertrophic cardiomyopathy or restrictive cardiomyopathy
The classification of feline cardiomyopathy, although mirroring human classification of cardiomyopathy, focuses on the predominant pathophysiology involved.
- Hypertrophic cardiomyopathy (HCM) - most common form, inheritable in Maine coon and Ragdoll cats. There appears to be examples of familial hypertrophic cardiomyopathy in other breeds of cats including the British shorthair, Bengal, Norwegian forest cat and Sphinx, although extensive testing has not been done. There is no evidence that any of these breeds share the same mutations as Maine coon or Ragdoll cats, and screening these breeds witht the two genetic tests is not likely to be useful.
- Restrictive cardiomyopathy (RCM) - old cat congestive heart disease
- Dilated cardiomyopathy (DCM) - old cat congestive heart disease
- Arrhythmogenic right ventricular cardiomyopathy (ARVC) - old cat congestive heart disease, often mistaken as tricuspid dysplasia
- Unclassified cardiomyopathy (UCM)
The role of taurine as a causative factor in the development of dilated cardiomyopathy in cats in the 1980s has been well document, and since then largely unseen in recent years due to changes in commercial dietary preparations. Since then, most cases of feline dilated cardiomyopathy have no known etiological agents and therefore attributed as idiopathic in origin.
Aortic thromboembolism is the leading cause of presentation to veterinary clinics, and often, at this stage, prognosis is more guarded. If a murmur or gallop sound is detected on auscultation, HCM is more likely than RCM or DCM, since the latter two often have clinical signs related to concurrent congestive heart disease, such as respiratory distress, weakness, reduced femoral pulses, anorexia and, sometimes, vomiting.
Not all cats with cardiac disease are in a decompensated state if concurrent diseases augment cardiac function, such as is seen in hyperthyroidism and anaemia. Pleural effusion may be evident on auscultation. In HCM with hyperthyroidism, an apical impulse may be prominent with a jugular pulse visible (August, 2006). Symptoms of congestive heart failure (CHF) may or may not be present, and include weakness, weak femoral pulses, mucous membrane pallor, respiratory distress and, sometimes, crackling of auscultation of lung fields.
Diastolic dysfunction is the primary disorder associated with hypertrophic and restrictive cardiomyopathies, manifesting as severe ventricular concentric hypertrophy and left atrial enlargement.
Although radiography is the first diagnostic tool applied in ascertaining a diagnosis, echocardiography is recommended in determining the nature of the cardiomyopathy involved.
|Differential diagnosis of feline heart murmurs|
|Asymptomatic cat with murmur||HCM||Innocent (Functional) murmur (anaemia, high cardiac output, fever, aortic dilation)|
|ARVC||Hyperthyroidism, Systemic hypertension, Congenital heart disease|
|Dyspnoeic cat without murmur||HCM and CHF||Pleural effusions|
|DCM and CHF||Noncardiogenic pulmonary oedema|
|RCM and CHF||Intrapulmonary haemorrhage|
|ARVC and CHF||Asthma, Heartworm disease, Aortic thromboembolism, mediastinal masses, pulmonary neoplasia, etc|
|Dyspnoeic cat with murmur||HCM and CHF||Congenital heart disease|
|DCM and CHF||Hyperthyroidism and CHF|
|RCM and HCF||Anaemia and CHF|
|ARVC and CHF|
Complications of Cardiomyopathy
Recurrent syncope is a risk factor for sudden death in humans with HCM, and retrospective feline studies related syncope and poor outcome. In cats syncope can be associated with tachyarrhythmias, dynamic LV outflow obstruction, and ischemia (infarction). Symptoms can often be managed successfully with beta-blockers to reduce or abolish LV outflow tract obstruction.
Rapid tachyarrhythmias can reduce cardiac filling, promote ischemia, and result in hemodynamic instability. Sustained tachyarrhythmias are usually associated with myocardial disease with attendant cardiac remodeling (myocyte necrosis, fibrosis, inflammation, and interstitial matrix changes). Therefore, it is prudent to consider antiarrhythmic therapy in selected cases, particularly when the ventricular rate is rapid.
Pulmonary edema is rapidly progressive and life threatening. Rapid resolution is the goal, and diuretics represent the cornerstone for acute, emergency management. Furosemide administered intravenously causes peak diuresis within 20- 30 minutes. It inhibits renal sodium tubular reabsorption or its accompanying anions; promotes brisk diuresis; and reduces vascular volume decreasing LV filling pressures (i.e., cardiac preload) and pulmonary congestion. Initial dosage is 1- 2 mg/kg IV every 30-60 minutes until dyspnea associated with congestion is reduced. Then, dosage frequency is reduced, typically to every 8-12 hours- or, the animal is changed to furosemide administration via constant rate infusion (ie, based upon estimated dose for 24 hours). Resolution of pulmonary edema may be enhanced by application of trans-dermal 2% nitroglycerin ointment, ¼ to ½ inch q 6hr. To reduce nitrate tolerance, alternate 12 hrs with and 12 hrs without nitroglycerine therapy. Supplemental oxygen (40-60% O2-enriched inspired gas) may improve pulmonary gas exchange. Clinical improvement and resolution of congestion is indicated by reduced respiratory rate and work of breathing, resolved lung crackles, and radiographic clearing of alveolar infiltrates (usually by 24 to 36 hrs). Dehydration, azotemia, and hypokalemia can result from over-diuresis.
- ↑ August, JR (2006) Consultations in feline internal medicine. Vol 5. Elsevier Saunders, Philadelphia. pp:301-310
- ↑ Richardson, P et al (1996) Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the definition and classification of cardiomyopathies. Circulation 93:841
- ↑ Meurs, KM (2010) Genetic screening of familial hypertrophic cardiomyopathy. In August, JR (Ed): Consultations in feline internal medicine. Vol 6. Elsevier Saunders, Philadelphia. pp:406
- ↑ Pion, PD et al (1987) Myocardial failure in cats associated with low plasma taurine: a reversible cardiomyopathy. Science 237:764
- ↑ Atkins, CE et al (1992) Risk factors, clinical signs, and survival in cats with a clinical diagnosis of idiopathic hypertrophic cardiomyopathy: 74 cases. J Am Vet Med Assoc 201:613
- ↑ Cote, E et al (2004) Assessment of the prevalence of heart murmurs in overtly healthy cats. J Am Vet Med Assoc 225:384
- ↑ Bonow, RO (1991) Left ventricular diastolic function in hypertrophic cardiomyopathy. Herz 16:13
- ↑ Fox, PR (1991) Evidence for or against efficacy of beta-blockers and aspirin for management of feline cardiomyopathies. Vet Clin North Am Small Anim Pract 21:1011
- ↑ Fox, PR, Liu, SK & Maron, BJ (1995) Echocardiographic assessment of spontaneously occurring feline hypertrophic cardiomyopathy. An animal model of human disease. Circulation 92:2645
- ↑ Adapted from Fuentes, VL (2006) Cardiomyopathy - establishing a diagnosis. In August, JR (Ed) Consultation in feline internal medicine. Elsevier Saunders, Philadelphia PP:303
- ↑ Fox, PR (2007) Managing feline heart disease - an evidence based approach. Proceedings of the World Small Animal Veterinary Association, Sydney, Australia