Case Study — Hypertrophic Cardiomyopathy and Congestive Heart Failure in a Cat

Bailey, a 14 year old female cat was presented for assessment of laboured breathing and decreased appetite. Bailey’s Vet was suspicious that Bailey was in congestive heart failure (CHF) and decided to schedule a VVS real-time cardiac work-up with one of our cardiology Specialists, to help guide her through the diagnostic and treatment options.

On physical examination, Bailey’s heart rate was 180 bpm and her heart rhythm was regular. No heart murmur was audible but there was an obvious gallop sound (third heart sound). Her respiratory rate was increased at 50 breaths per minute and there was a noticeable abdominal component to her breathing.

Many cats with heart disease do not have a heart murmur, but the presence of a gallop sound is highly suspicious for significant underlying heart disease. The gallop sound indicates that the heart muscle is not relaxing normally.

Diagnosis

Thoracic x-rays were taken which showed an enlarged cardiac silhouette and a moderate volume of pleural effusion.

ECG revealed a sinus rhythm. No arrhythmias were seen.
Echocardiography revealed mild, irregular hypertrophy of the left ventricle. The myocardium appeared stiff with decreased systolic and diastolic function. The left ventricular chamber size was moderately increased. The left atrium was markedly dilated and spontaneous echo-contrast (“smoke”) was present. There was moderate bilateral pleural effusion.

Our findings were consistent with end-stage Hypertrophic Cardiomyopathy (HCM) and left sided CHF with pleural effusion. The fact that Bailey was in congestive heart failure explained her increased respiratory rate and effort and her decreased appetite.

 

HCM is typically characterised by thickening of the left ventricular walls. However, the end-stage of the disease frequently results in ventricular wall thinning, as well as decreased myocardial contractility and severe left atrial enlargement.

In middle aged and older cats with HCM, secondary systemic causes of left ventricular wall thickening should be excluded such as systemic hypertension and hyperthyroidism.

Bailey’s thyroid status was confirmed to be normal. Her Doppler systolic blood pressure was slightly low, with average readings of 110 mmHg.

Bailey’s owners were very dedicated and understood that her underlying heart disease was already advanced and incurable. However, they were keen to start medical therapy to try to improve her quality of life.

Treatment

Initially the pleural effusion was drained and Bailey was treated with intravenous furosemide and oxygen therapy until her respiratory rate and effort were stable on room air. The following day Bailey was discharged on oral furosemide therapy to treat her CHF, pimobendan to improve her myocardial systolic function (pimobendan is not licensed for use in cats but appears safe and well tolerated) and clopidogrel, an anti-platelet drug used to try to minimise the risk of left atrial thrombus formation.

Unlike pulmonary oedema which responds rapidly to furosemide therapy, pleural effusion does not. Therefore the initial treatment for pleural effusion is thoracentesis to remove the fluid from the chest cavity to allow the lungs to re-expand. Following thoracocentesis, furosemide therapy can then be started to try to prevent re-accumulation of the pleural effusion.

Follow-up

Bailey’s respiratory rate and effort remained normal at home for the next week, but then started to gradually increase again despite increases in her daily furosemide dose. She was presented for a follow-up with her vet and the VVS Cardiologist two weeks after initial presentation. A moderate volume of pleural effusion had re-accumulated and required drainage. A follow-up blood test revealed a mild azotemia and borderline hypokalemia.

The increased renal values were most likely due to impaired renal perfusion secondary to poor cardiac output, potentially combined with some primary renal insufficiency due to her age. It was felt that Bailey’s lack of response to the furosemide was due to a phenomenon called diuretic resistance.

Diuretic resistance is defined as persistent congestion despite adequate and escalating loop diuretic doses. Diuretic resistance can be caused by many factors. One of the causes is decreased glomerular filtration rate (GFR), which results in decreased delivery of the furosemide to its site of action in the kidney nephron. Therefore the furosemide is less effective, despite increasing doses. Causes of decreased GFR in patients with advanced heart disease can be multifactorial: decreased cardiac output due to poor heart muscle function, renal insufficiency, systemic hypotension and hypovolaemia secondary to the use of high doses of loop diuretics.

Fortunately, Bailey was a very compliant patient and her owners were able to medicate her easily at home. The VVS Cardiologist was able to suggest some alternative cardiac medication protocols in an effort to control Bailey’s recurrent pleural effusion. The following new drugs were added, in addition to the pimobendan and clopidogrel:

Torsemide was substituted for furosemide.

Torsemide is a loop diuretic that is better absorbed than furosemide with a longer half-life. When substituted for furosemide, it should be dosed at approximately 1/10th of the dose of furosemide, since it is at least 10 times stronger. It is not licensed for cats but appears to be well tolerated and effective in this species.

Benazepril and spironolactone were added.

Benazepril is an ACE-inhibitor and spironolactone is a potassium-sparing diuretic. These two drugs have renin-angiotensin-aldosterone system (RAAS) blocking properties, which should help to control the CHF and prevent hypokalaemia (potassium loss is a side-effect of loop diuretic usage). Spironolactone is not licensed for cats but appears to be well tolerated and effective in this species. If the renal values increase or systemic blood pressure decreases, the ACE-Inhibitor may need to be stopped.

Bailey’s owners were asked to continue to count her sleeping respiratory rate (SRR) at home and since making these adjustments to her medication regime, her SRR has remained normal. Follow-up Doppler systolic BP and renal blood work/electrolytes have all improved after starting this new medication regime.

It is important that owners are shown how to count sleeping respiratory rate (SRR) at home as this is a simple way to monitor response to medical treatment for CHF and to detect if the patient is starting to redevelop pulmonary oedema and/or pleural effusion. Normal SRR in a cat is typically less than 30-35 breaths per minute.

Bailey’s owners are delighted that their commitment and dedication has paid off, as more than 3 months on Bailey is still doing great with no further episodes of pleural effusion. She is eating well, energetic and playful and is even climbing trees again!

Bailey’s case emphasises the importance of obtaining an accurate diagnosis in order to guide therapy appropriately. It also shows how a cardiac medication regime specifically tailored to the individual patient’s needs, can result in excellent quality of life and improved outcomes, even in those patients with advanced heart disease.

If you would like help with a case like Bailey, please contact VVS today.