Due to their nature as prey species, most exotic mammals initially only show very subtle signs of cardiac disease and often do not present until late into the progression of the disease. Cardiac disease has been described in a number of species with a brief overview described below.
Cardiac disease in ferrets can range from asymptomatic to fulminant heart failure. Clinical signs can include lethargy, exercise intolerance, weight loss, pale mucous membranes with increased capillary refill time, dyspnoea and/or tachypnoea, hindlimb weakness or a “pot-bellied” appearance (Orcutt and Malakoff, 2006). Heart murmurs can be heard with valvular disease and dilated cardiomyopathy (Wagner, 2009).
If there is a clinical suspicion of cardiac disease, thoracic radiography is an excellent diagnostic starting point (Figure 1). Contralateral thoracic views under appropriate sedation can show evidence of cardiac disease such as an enlarged cardiac silhouette, tracheal elevation (Figure 2) and increased sternal contact on the lateral view (Morrisey and Kraus, 2012). Ferrets have a more globoid cardiac silhouette compared to dogs and cats (Figure 3); however, heart size can be evaluated with a modified vertebral heart score as described by Stepien et al. (1999).
Echocardiography is useful to assess the structure of the heart, diagnose pericardial effusion and evaluate for valvular disease (Figure 4). Multiple echocardiographic values for ferrets have been described (Stepien et al., 2000). Electrocardiography can be utilised to assess for conduction disturbances and rhythm abnormalities (Morrisey and Kraus, 2012).
Valvular disease is common in ferrets, usually affecting the aortic and mitral valves (Orcutt and Malakoff, 2006). Dilated cardiomyopathy and hypertrophic cardiomyopathy have also been described, with definitive diagnosis based on echocardiography findings (Morrisey and Kraus, 2012).
Although not endemic in the United Kingdom, heartworm disease with Dirofilaria immitis should be considered a differential for any ferret with travel history to endemic areas. Diagnostic work-up should be as for any other cardiac presentation with specific ELISA-based antigen snap tests or polymerase chain reaction (PCR) tests available for diagnosis (Wagner, 2009). Antigen tests are only positive five to six months after onset of infection and can produce false negative results in cases of low worm burdens; however, PCR testing is highly sensitive for D. immitis DNA (Wagner, 2009).
Treatment for cardiac disease and congestive heart failure in ferrets follows the same principles as companion animal medicine. Treatment of congestive heart failure involves providing oxygenation and reducing preload and afterload (Morrisey and Kraus, 2012). Diuretics, most commonly frusemide, are used to reduce preload by reducing blood volume, as well as reducing the volume of body cavity effusions (Orcutt and Malakoff, 2006). Angiotensin converting enzyme (ACE) inhibitors are used to reduce afterload by causing peripheral vasodilation. Ferrets are sensitive to the hypotensive side effects of these drugs (Orcutt and Malakoff, 2006) and so should be closely monitored for signs of lethargy when newly started on therapy or an existing dose is increased.
Pimobendan is useful with dilated cardiomyopathy or valvular disease due to its positive ionotropic effects (Wagner, 2009). Drugs described in treatment of arrhythmic cardiac disease in ferrets include beta-blockers, calcium channel blockers and digoxin (Orcutt and Malakoff, 2006).
Anecdotally, cardiac disease is more common in larger-breed rabbits compared to smaller breeds (Orcutt, 2012). Rabbits have a small thorax compared to the rest of the body, so cardiomegaly can lead to compromised respiration (Orcutt, 2014) (Figure 5). Cardiac disease in rabbits often presents with dyspnoea, tachypnoea, exercise intolerance, lethargy, anorexia and sometimes oedematous extremities (Vennen and Mitchell, 2009). Clinical signs in rabbits can be quite subtle, with changes in head and neck position to extend the neck or slight elbow abduction (Orcutt, 2014). Rabbits are obligate nasal breathers and so any rabbit showing signs of open-mouth breathing is in severe respiratory distress.
A full clinical examination should be performed, first with a distance examination of the breathing pattern and effort, followed by auscultation of the thorax before any other stressful examinations are performed (for example intra-oral exam). The mucous membranes, especially the tongue, should be assessed for evidence of cyanosis and peripheral pulses can be assessed using the femoral arteries, the medial metatarsal artery or the central ear artery (Orcutt, 2014).
Cardiac work-up is similar to that described above for ferrets, including with thoracic radiography under appropriate sedation to assess at least two contralateral views. Common radiographic findings can include cardiomegaly, tracheal elevation, pulmonary oedema characterised by a pulmonary interstitial pattern, enlarged pulmonary vessels or pleural effusion (Orcutt, 2012).
Rabbits have a large mediastinum which can make the cranial cardiac border difficult to distinguish on a lateral view (Pariaut, 2009), so obtaining at least two well-positioned views is essential. Anterior mediastinal masses or increased mediastinal fat can have a similar appearance to cardiomegaly (Orcutt, 2012) and in this case ultrasound can be used to determine the difference. Echocardiography can give a wealth of information, with a number of studies recording echocardiographic values in a range of rabbit breeds (Huston et al., 2012).
As rabbits are a prey species, patients may not present until they are in congestive heart failure. Presenting patients often have a severe cardiomegaly with pulmonary oedema caused by left-sided heart failure and pleural effusion caused by right-sided heart failure (Orcutt, 2012). Oxygen therapy (Figure 6) and minimal handling should be instituted, with any significant pleural effusion drained via thoracentesis (Huston et al., 2012). Similar to treatment of cardiac disease in ferrets, drugs and dosages are extrapolated from companion animal practice. The use of diuretics along with drug therapy appropriate to the underlying cause should be instituted, usually including the use of an ACE inhibitor for long-term therapy (Pariaut, 2009).
Hypertrophic cardiomyopathy and dilated cardiomyopathy have been reported in domestic rabbits (Huston et al., 2012); however, dilated cardiomyopathy appears to be more common (Orcutt, 2012). Pimobendan has been used in the treatment of dilated cardiomyopathy; however, no medication has been shown to improve patient outcomes before the onset of congestive heart failure (Pariaut, 2009).
Little information is available for cardiac disease in other small mammal species, although anecdotally it has been seen in a range of different species. Cardiac disease has been described in chinchillas following the onset of syncope, collapse or what appears to the owner to be seizure-like episodes (Goodman, 2011). Atrial thrombosis is commonly reported in hamsters secondary to heart failure, with patients usually presenting with cyanosis, tachypnoea and cold extremities (Brown and Donnelly, 2012) (Figure 7). Diagnostic work-up for small rodents is similar to above, ideally with assessment with radiography and echocardiography. Treatment is symptomatic and usually involves a combination of diuretics, ACE inhibitors and, in the case of hamsters, can include prophylactic anticoagulants (Brown and Donnelly, 2012).
It is important to remember when treating cardiac disease in small exotic mammals that all drugs are off licence and most dosages have been extrapolated from companion animal medicine. Ensuring owners are fully informed of this and choosing appropriate dosing regimens is the responsibility of the clinician. Close monitoring should follow any dose alterations or the start of a new cardiac medication to assess for any inadvertent side effects.