Feline hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is the most common cardiac disease in the cat (Ferasin et al, 2003). Generally speaking, it tends to be diagnosed in the middle age to older cat, but can be present in both very young and very old cats (Atkins et al, 1992; Rush et al, 2002; Ferasin et al, 2003; Payne et al, 2010). Clinical signs range from the asymptomatic cat with a heart murmur detected at Atkins et al, 1992; Rush et al, 2002; Ferasin et al, 2003; Payne et al, 2010). Cats seem to be incredibly good at hiding any signs of heart failure, therefore, when they do present with signs of distress, they must be dealt with using extreme care. The severity of the disease, which is exacerbated by stress, at this point can be life threatening.

What is HCM?

HCM is a primary (idiopathic) cardiomyopathy (chronic disease of the heart muscle), and it is believed to have a genetic cause in most cases (Kittleson et al, 1997; Meurs et al, 1997). In Maine Coons and Ragdolls a genetic mutation has been discovered, which is the cardiac myosin binding protein C gene (Meurs et al, 2005; Meurs et al, 2007). The form of HCM found in Ragdolls seems to cause severe disease, often with an early age of onset (Lefbom et al, 2001) and with a very poor prognosis (Payne et al, 2010). Other breeds that seem predisposed are Persian, British Shorthair, Sphynx, Norwegian Forest Cat and Bengal cats. However, HCM is often seen in mixed breed cats also. It is a disease characterized by a thickening (hypertrophy) of the left ventricle (Maron et al, 2006). This can also occur secondary to other diseases, such as systemic hypertension, hyperthyroidism, and acromegaly (Si-kwang et al, 1984; Bond et a, 1988; Peterson et al, 1990; Nelson et al, 2002). Left ventricular hypertrophy causes stiffness of the heart muscle meaning that the ventricle cannot relax as it should. The increased thickness of the heart muscle may also exceed the myocardial blood supply, causing localized areas of ischaemia. This further exacerbates stiffness and inefficiency of the ventricle. Some parts of the ventricle get thicker than others, and if the increased thickness occurs on the interventricular septum, it can cause an obstruction to blood flow out of the left ventricle into the aorta (sometimes referred to as hypertrophic ‘obstructive’ cardiomyopathy). This compromises cardiac output further, because the ventricle has to counter increased resistance. With either form of HCM, the left atrium may increase in size to try and accommodate the increased pressure in the ventricle. Sometimes this can lead to left sided CHF. The pattern of hypertrophy can be variable and this may be related to prognosis. Many cats present with focal hypertrophy on just the septal wall, which is often well tolerated. However, severe, generalized or free wall hypertrophy is often associated with left ventricular dysfunction (Bonagura, 2010).

What is CHF?

The most important function of the circulatory system is to maintain adequate blood pressure to the vital organs (the heart, brain, and kidneys). When the heart starts to fail, the body initiates compensatory mechanisms to increase cardiac output, such as increasing heart rate and retention of fluid via the kidneys. If excessive fluid accumulates, pulmonary oedema, pleural effusion, or ascites (uncommonly) occur, and it can be said that clinical CHF is present (Luis Fuentes, 2010). CHF can be either left sided or right sided, and some severe cases can have both. Sometimes mild compensation is enough to normalize arterial pressure without causing CHF, then affected patients will not have clinical signs, or only develop signs if they undergo excessive exertion or stress, such as a visit to the veterinary practice.

Clinical signs of CHF

Cats often hide clinical signs of heart failure very well. Exercise intolerance and lethargy in the dog can be easily recognized, but who can honestly say that they notice when their cat is exercise intolerant? Therefore, when cats are seen in the practice, it is often not possible to know how severe their underlying heart disease is at that time. The visit to the practice alone is sometimes enough to be a trigger event for some cats to develop heart failure (Box 1).

Box 1.Risk factors for cats for the development of CHF

• Stress
• Intravenous fluid therapy
• Anaesthesia

In most cases of HCM, CHF develops from increased left ventricular stiffness, which causes elevated left atrium and venous pressures, which ultimately manifests as pulmonary congestion and oedema (Bonagura, 2010). Pleural effusion, which is usually associated with right-sided CHF (R-CHF), can occur in cats with left-sided CHF since the visceral pleurae (blood supply to the lungs) drains into the left atrium. Sometimes chylothorax (a milky white, sometimes blood tinged effusion that leaks into the pleural cavity from the thoracic duct) can develop, which is a result of R-CHF. This is because the thoracic duct drains into the right atrium via the cranial vena cava. Another complication that often occurs in cats with HCM is the formation of thromboemboli, and subsequent systemic dislodgement to the arteries supplying blood to the limbs or major organs, known as aortic thromboembolism (ATE) (Figure 1). Cats that have suffered an ATE event are usually presented to the practice with a sudden onset of paresis or lameness. More commonly, this affects the hindlimbs, but can also occur in the forelimb. The affected limbs are cold to touch, very painful and have no pulse. ATE occurs as a consequence of an enlarged left atrium and the presence of slow moving blood due to left ventricular dysfunction. This slow blood can form a clot that will sit in the left atrium until some or all of it is dislodged into the systemic circulation via the aorta.

Clinical signs

Unlike dogs, cats do not tend to cough with heart failure (Table 1).

A study of 127 cats with HCM conducted at a cardiology referral centre showed that 71% of the cats had a murmur detected on auscultation, and a murmur was more likely in cats that had the obstructive form of HCM (Payne et al, 2010). Gallop rhythms were detected in 18% and only 10% had an arrhythmia. Rather surprisingly, 46% of cats had no clinical signs, 37% presented in CHF, and 11% had an ATE on arrival.

Diagnostic tests

The definitive diagnostic test for HCM is echocardiography. It allows assessment of wall thickness, chamber size, systolic and diastolic function. This provides the most accurate differentiation between HCM and other cardiac diseases. Left atrial size has been proven to be an excellent indicator of clinical signs and thus can be used to assess severity and progression of the disease (Payne et al, 2010). Echocardiography can also detect thrombi within the left atrium.

Other diagnostic tests should include:

• Physical examination, including counting resting respiratory rate
• Measuring systolic blood pressure, to rule out systemic hypertension as an underlying cause for left ventricular hypertrophy, but also to assess for hypotension, which may be present in cats with advanced disease
• Thoracic radiography is most useful to assess for evidence of CHF
• Blood tests should include biochemistry to assess kidney function (another common feline problem), haematology to exclude anaemia or inflammatory disease. Total thyroxine (T4) should also be measured in older cats to rule out underlying hyperthyroidism
• Electrocardiogram (ECG) may be useful if an arrhythmia is suspected
• Thoracocentesis in cats with pleural effusion and respiratory distress is essential to resolve clinical signs. Analysis of the fluid can assist with diagnosis of CHF and rule out any other reason for pleural effusion (Figure 2).

Treatment

Unfortunately, as the underlying cardiac disease cannot be resolved medically, therapy is only palliative. The main treatment aims therefore are to:

• Promote ventricular filling
• Alleviate congestive failure
• Prevent thromboembolism
• Control arrhythmias if present.

Asymptomatic cats

At present there is no consensus on whether therapy is beneficial in asymptomatic cats due to a lack of data. When severe outflow tract obstruction exists, a beta-blocker, such as atenolol, may be used to slow the heart rate and decrease the force of contraction, as this may decrease or abolish the outflow tract obstruction and improve filling time of the ventricle.

Past or present heart failure: chronic management

Cats that have been in heart failure are usually treated with diuretics (furosemide) to remove excess fluid, while an angiotensin-converting enzyme (ACE) inhibitor is commonly used to block the activation of the neurohormonal system. If there is no CHF present, then a beta-blocker might be used, and depending upon left atrial size, anti-platelet drugs (aspirin, clopidogrel) might be added. Client education at this point is very useful, because the owner can count resting respiration rate at home, and if they find that the rate is increased, on the advice of the veterinary surgeon, can administer another dose of diuretic at home. They can also monitor appetite and demeanour of the cat in its own environment.

Acute CHF

Management of cats with acute CHF is particularly challenging. The immediate goal is to improve signs of respiratory distress (Figure 3) by use of diuretics to resolve venous congestion, and oxygen to improve oxygenation of blood. Furosemide is the first line treatment when CHF is diagnosed.

Handling should be minimized, because this is a life-threatening condition that is exacerbated by stress. A prepared kennel with oxygen supplementation is essential, so that from admission the cat can be assessed, given diuretics and then left to recover in its new surroundings.

Case 1. Gina.Gina was a 12-year-old, female neutered domestic short hair cat. On presentation, Gina was tachypneoic, with a respiration rate of 60 breaths/minute. She had increased respiratory effort with paradoxical abdominal movement and was open-mouth breathing. On auscultation, she had dull ventral lung sounds, and a gallop rhythm. Her heart rate was 180 beats/minute and femoral pulses were weak. Her weight was recorded as 4.6 kg, a loss of 0.5 kg in 1 month. No further physical examination was performed due to the level of respiratory distress. Instead she was immediately given 2 mg/kg furosemide intramuscularly (IM) and 60% oxygen supplementation in a ready prepared oxygen kennel.Initial diagnostics and resultsA very brief thoracic ultrasound was performed and a large volume of pleural effusion was seen. Thoracocentesis was performed and 300 ml of fluid was removed. The fluid was slightly milky and blood tinged in appearance. Laboratory analysis was consistent with a chylous effusion. Echocardiography after thoracocentesis revealed enlargement of the left and right atria, focal left ventricular hypertrophy, and areas of myocardial thinning. Systolic function appeared decreased. There was no evidence of outflow tract obstruction. Doppler blood pressure was 100 mmHgDaily notes — day 1Mentation was quiet but alertThe plan for Gina was:

• Initial furosemide bolus of 2 mg/kg IM on presentation and oxygen supplementation
• Thoracocentesis
• Monitor respiration rate and effort remotely
• Intravenous (IV) access, bloods for haematology, biochemistry and thyroid panel when stable
• Echocardiography when stabilized (Figure 4

  Figure 4.Echocardiogram showing hypertrophic cardio myopathy.

• Thoracic radiographs when stable
• Subsequent furosemide at 1 mg/kg IV three times daily.

Nursing notes: Gina was notably distressed when she arrived, so was handled carefully to avoid further stress. At the end of every examination or diagnostic test, she was given time to rest and recover. Thoracic radiographs were not performed, as she developed worsening respiratory distress when out of the oxygen kennel. She was encouraged to eat, but showed no interest.Daily notes — day 2Gina was markedly brighter and coping well without oxygen supplementation.Temperature 38.3°C; pulse 200 beats/minute; respiration rate 36 breaths/minute. Auscultation confirmed a gallop rhythm and no heart murmur. Lung sounds were normal. Doppler blood pressure was 125 mmHg.Plan:

• Change to oral medication
• Continue to monitor respiratory
• Echocardiography.

Nursing notes: Gina started to show a slight interest in food.Daily notes — day 3Gina was bright and alert. She was starting to get annoyed when handled.Temperature was not attempted due to her temperament; pulse was 190 beats/minute; respiration rate 30 breaths/minute.Nursing notes: Gina was starting to get agitated when handled, so she was sedated for radiographs and blood was taken under sedation (butorphanol 0.2 mg/kg IV). Radiographs showed cardiomegaly and an interstitial terstitial pattern. Biochemistry showed an elevation in urea and creatinine. This was consistent with prerenal azotaemia due to furosemide therapy and poor cardiac output from her cardiomyopathy. However, concurrent intrinsic renal disease could not be excluded. As a result the furosemide dose was decreased with instructions for the owner to give an additional dose in the evening if her respiration rate or effort increased during the day.Case discussionGina's case is an example of how difficult it can be to monitor and care for cats in congestive heart failure. On every visit, Gina let everybody know that she did not like being at the vets, and so she had to be handled in a very delicate and brief manner. She had exhibited signs of concurrent renal problems, so the diuretic dose needed to be titrated very carefully and blood tests taken routinely to monitor her azotaemia. Due to the low blood pressure recorded initially, her blood pressure was also recorded regularly. Owner education and calm management of this case ensured that Gina has enjoyed a good quality of life despite a poor prognosis.

Observation of respiratory rate and respiratory effort is a good way of monitoring without having to handle the cat unnecessarily. Full records should be kept so that patterns can be identified, this should also include demeanour, appetite, drinking and urination.

Diagnostic tests should be done in a calm and prepared environment. Opioid sedation may be useful to calm cats that are very distressed.

Management of ATE

The cat that presents with ATE is also a challenge to the veterinary nurse. Therapy demands high quality critical care. Reports have shown that even with good nursing care, there is only a 40–50% chance of limb function returning (Smith et al, 2003). If limb function does not return, quality of life should be assessed and discussed with the owner. Recommendations for treatment are as follows:

• Analgesia (buprenorphine) for the first 24–48 hours
• Heparin to prevent further thrombosis
• Anti-platelet drugs (aspirin, clopidogrel)
• Treat CHF if present (cats have a worse prognosis if they have concurrent CHF)
• Chronic management could include gentle physiotherapy and passive warming of the affected limbs
• General nursing such as monitoring appetite, demeanour, urination and defecation should be applied as required.

Conclusion

Cats with HCM can live for years with a heart murmur and have no progression of the disease. However, the disease can be life threatening, and stressed cats are even more likely to die suddenly. For those that present in respiratory distress, the best approach is to provide oxygen and diuretics and let the cat settle in its new surroundings before attempting diagnostic tests. Counting respiratory rate and effort is as good as any method to see if the cat is responding to treatment. Education of the owner is also important be because the owner can be monitoring the cat at home, when it should be more relaxed.

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Key Points

• Hypertrophic cardiomyopathy (HCM) is the most common cardiac disease in the cat.
• HCM is not always a progressive disease.
• Frequently cats do not exhibit obvious clinical signs of heart failure, therefore they need to be handled calmly and competently.
• Environment should be kept calm and stress free.
• If a cat presents in respiratory distress — provide oxygen, administer a diuretic, and allow it to recover in its new surroundings.