Hypertrophic cardiomyopathy (HCM) is the most common cause of CHF in cats (Goutal et al., 2010). Some cats with HCM may also have systolic anterior motion of the mitral valve (SAM), which should be considered when planning therapy. Other causes of CHF include dilated cardiomyopathy, restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy, congenital heart disease, minoxidil toxicity and systemic diseases such as hyperthyroidism and anaemia. Some therapeutics have also been associated with CHF.
Recently, a new cause of CHF has been described in cats. This disease, called “transient myocardial thickening” (TMT), mimics HCM on echocardiography but is thought to be due to myocardial swelling associated with cate-cholamine toxicity (Novo Matos, 2018). Careful history taking may reveal a stressful event often within two weeks of development of CHF. Cats with TMT are usually critical on presentation and accompanied by cardiogenic shock, but following appropriate support are expected to have an excellent long-term outcome.
Prognosis varies widely with studies showing a broad survival range from days to years. This likely is due to heterogenicity of the underlying cause of CHF. In general, an average survival time is 6 to 12 months. Cats with structural heart disease will likely develop recurrent signs of CHF over time and require lifelong medication.
Stabilisation in hospital
The cornerstone of CHF stabilisation is oxygen and furosemide. Oxygen can be supplemented in a form of oxygen cage, mask or flow by. Whichever option is available, the emphasis should be made to minimise the stress of the cat while providing oxygen supplementation. The preferred route of furosemide administration is intravenous for its rapid onset of action. However, attempting intravenous access using an IV catheter or a needle may be detrimental in cats with severe respiratory distress, as even a minimal handling can result in deterioration and respiratory arrest. Therefore, the intramuscular route is often chosen on initial presentation.
Subcutaneous injection is less preferred as the cat may have poor peripheral perfusion (ie cardiogenic shock) and absorption can be delayed. The furosemide dose should be based on how severely the cat is affected, although a commonly used dose is 1 to 2mg/kg every one to two hours until the respiratory rate improves. In severely affected cats, continuous rate infusion may be required. The frequency can then be decreased to a bolus every four to six hours and then transitioned to oral medication at 1 to 2mg/kg PO q12h. In mildly affected cases, transition to oral medication can be possible even after a single parenteral administration of furosemide.
Cats with respiratory distress often benefit from a light sedation. Commonly used sedation in hospital is butorphanol at 0.1 to 0.2mg/kg intramuscularly. Heavy sedation should not be used, as the resultant marked cardiac and respiratory suppression can be detrimental.
Stabilisation at home
Owners of cats with documented heart disease, particularly with an enlarged left atrium or previous episode of CHF, should be instructed to count sleeping respiratory rate at home. Similar to dogs, a normal count is below 30 breaths per minute (Ljungvall et al., 2013). It is normal to count more than 30 if a cat is purring. Sleeping respiratory rate of 30 to 40 breaths per minute is a grey zone, but should raise suspicion of pulmonary oedema.
If a cat shows signs of CHF at home and is able to be tableted, there is an option of stabilisation at home. An initial or extra dose of furosemide at 1 to 2mg/kg PO q12h may result in an improvement over one to two hours. If no improvement is seen, the owner can be instructed to repeat the dose or bring the cat to the clinic for assessment and stabilisation. If stabilisation at home is successful, cats with first onset of CHF should continue on furosemide at 1 to 2mg/kg PO q12h, and for those cats already receiving furosemide, an increased dose is indicated. These cats should ideally be invited for a routine recheck in one to two weeks for a renal profile including electrolytes and discussion of the ongoing plan.
In contrast to pulmonary oedema, pleural effusion is more challenging to monitor at home. A small to moderate pleural effusion may only result in a mild increase in respiratory effort rather than rate. It is therefore common for these cats to suddenly deteriorate when a significant volume has already developed and require emergency admission and thoracentesis.
Clopidogrel should be started in cats with CHF following stabilisation as the risk of aortic thromboembolism is probably high. If a cat has already developed a thrombus, analgesia and antiplatelet therapy such as clopidogrel and aspirin should be started promptly.
There is some evidence that pimobendan improves survival in cats with HCM and CHF (Gordon et al., 2012). While it is generally well tolerated, a prospective survival analysis showed that cats with SAM have worse outcomes when receiving pimobendan (Schober et al., 2019). This is likely due to the worsening of left ventricular outflow tract obstruction with the pimobendan-induced increase in systolic function. If pimobendan is started, ideally the cat should be referred for echocardiography to determine if it should be continued.
Oral torsemide is a potent diuretic with the same mechanism of action as furosemide. Torsemide also has the benefit of a long duration of effect and can be given once daily in early management of CHF. Torsemide is often reserved for refractory CHF, but can also be used as a first-line diuretic in cats that are difficult to pill to improve compliance. As with any diuretic therapy, regular renal monitoring is advised.
In contrast to dogs, a recent double-blinded placebo control trial showed no survival benefit when benazepril was used in cats with CHF (King et al., 2019). Although a similar study does not yet exist, no known survival benefit has been established for spironolactone.
Significant hypokalaemia (below 3.0mmol/L) may develop with diuretic therapy. Either oral potassium supplementation or spironolactone can be used to conserve potassium and as adjunctive diuretic therapy.
Some cats may have significant arrhythmias (eg atrial fibrillation). Antiarrhythmic therapy should ideally be started after consulting with a cardiologist. However, urgent stabilisation may be needed. For atrial fibrillation or supraventricular tachycardia, diltiazem can be used. For ventricular tachycardia, lidocaine can be used although at a lower dose (0.5mg/kg IV) as cats are more sensitive to lidocaine than dogs.
Due to the silent yet progressive nature of cardiomyopathies in cats, it is unfortunately common for cats to develop fulminant CHF without the owner being aware of the underlying heart disease. While difficult, full information should be provided regarding the prognosis, management and aim of therapy. Some owners may elect for euthanasia with the diagnosis of CHF.
As frequent client communication and medication adjustment may be needed, CHF management should ideally be overseen by one clinician (general practitioner or a cardiologist) to ensure continuity. Maintaining quality of life is the focus in management of CHF, not longevity. Cats with inappetence or that are challenging to medicate unfortunately have a poor prognosis. Various options such as pill pockets or treats can be tried, although in some cases it may be necessary to stop most medication and prioritise diuresis. Such cats are unlikely to live long, but would have a better chance of enjoying their time at home with the owner. Mirtazapine may be tried although the effect has not been consistent.
Azotaemia in CHF
Mild azotaemia can often be ignored in clinically stable cats. Diuretic dose reduction should only be done if the dose was inappropriately high. However, azotaemia should be addressed if the cat is sick, or if the furosemide dose needs to be increased. In cats with significant azotaemia and associated clinical signs, yet concurrent uncontrolled CHF, the prognosis is poor.
Refractory to therapy
Cats with CHF will likely become refractory to therapy over time despite higher doses of diuretics. A routine recheck may be needed to assess for causes of refractory CHF (eg arrhythmia or difficulty medicating at home). Adding additional diuretics may be needed to control clinical signs, although refractory CHF carries a poor prognosis.