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Staging and management of canine mitral valve disease

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01 November 2013, at 12:00am

Heart failure refers to a clinical syndrome of symptoms and signs caused by impairment of the heart so, if there are no clinical signs, then the dog does not have heart failure. 

In 2009, the ACVIM produced a staging system for canine mitral valve disease, and these stages will now be reviewed in turn.1 It is important to consider, however, that heart disease is a continuous process and doesn’t always jump nicely from one stage to the other (see Figure 1). 

  • Stage A: these dogs do not have evidence of heart disease, but are at risk from a genetic point of view; dogs that are predisposed to mitral valve disease are in stage A, for example any Cavalier King Charles Spaniel. 
  • Stage B1: this refers to dogs that have heart disease (characterised by a typical mitral regurgitation murmur) but do not have an enlarged heart on radiography/echocardiography or clinical signs of the disease. 
  • Stage B2: mitral valve disease patients should be considered at this stage when evidence of cardiac enlargement on echocardiography/radiography is present but still no clinical signs of the disease are apparent. 

No treatment has yet been shown to delay the onset of heart failure in these patients but this is still being actively researched. The main focus at this stage is therefore monitoring to ensure that intervention is provided as soon as possible to avoid, for example, a sudden jump from being stable to requiring hospitalisation. 

Monitoring of the resting or sleeping respiratory rate at home can be very useful. Most dogs have a respiratory rate at home that is <30 breaths per minute.2 If the respiratory rate starts to increase above what is normal for that dog, in particular if it exceeds 40 breaths per minute, then this may be a sign that heart failure is starting to develop.3 

  • Stage C: this refers to the onset of heart failure and the development of clinical signs, such as rapid and/or laboured breathing, that characterises pulmonary oedema. The stage can be further subdivided as follows: 1. Acute (hospital based) therapy. In these life-threatening cases, a high dose bolus of furosemide (2-4mg/kg IV) is usually indicated initially, followed by 1-2mg/kg every hour (or 0.71mg/kg/hour as a constant rate infusion) until the respiratory rate and effort start to decrease. 

If intravenous administration is not possible or c ontraindicated because of the unstable condition of the patient, furosemide can alternatively be administered IM or SC. It is important to monitor urine production to ensure that adequate diuretic therapy is being delivered. 

Oxygen can be beneficial 

In addition to furosemide, oxygen can be beneficial for the initial stabilisation of these patients. Cautious sedation may also be considered to control the patient’s stress (for example with 0.20.4mg/kg butorphanol) and pimobendan (either IV or oral) can help improve the acute haemodynamic status of the dog. Oral drug therapy should be avoided or used very cautiously in any patients with respiratory distress.  

Once these cases have been stabilised, then oral therapies can be started (see below). 2. Chronic (home based) therapy. Many dogs with heart failure present in this stage and treatment involves a combination of oral therapies: 

(a) Furosemide – there is a wide dose range (2-5mg/kg BID to TID) but most patients are prescribed a dose of 1-2mg/kg BID in the initial stages. This should be re-evaluated in 1 and 2 weeks and adjusted according to the individual response. (b) ACE inhibitors/spironolactone – ACE inhibitors reduce the production of angiotensin II whereas spironolactone blocks the harmful effects of aldosterone (see Figure 2). Clinical trials have shown decreased mortality when ACE inhibitors are used alongside furosemide4, and that patients receiving spironolactone in addition to an ACE inhibitor have a substantially longer life.5 The ACE inhibitor benazepril and spironolactone are now available in a combined tablet (Cardalis, Ceva Animal Health), which helps to reduce costs and improve patient compliance. (c) Pimobendan – clinical trials have shown that the outcomes are superior when dogs received the inodilator pimobendan and furosemide compared with an ACE inhibitor and furosemide.6 

All four drugs have therefore independently shown a benefit for the management of canine heart failure, so it is recommended to use them together in chronic stage C heart failure cases. 

  • Stage D: this refers to cases that are refractory (have stopped responding) to the standard therapies. 

Over time, furosemide resistance can develop with chronic administration. In these cases, increasing the furosemide dose may be necessary. However, once a dog is receiving high doses of furosemide (e.g. 4mg/kg TID) then you get the law of diminishing returns, where further dose increases result in a less potent effect. 

Different diuretics, however, are synergistic (termed sequential nephron blockade) so in these cases it may be better to add another diuretic such as hydrochlorthiazide (available in the UK only in a combined formulation with another diuretic, amiloride), starting at 0.5mg/kg SID/BID and then titrating upwards if necessary. 

Another alternative to furosemide in late stages is torasemide. Torasemide is also a loop diuretic with 10 times more potency as a diuretic than furosemide, but produces less electrolyte disturbances. However, it is very expensive, not licensed and should currently only be used in cases which have become refractory to furosemide. 

Prescribe a lower dose 

When changing from furosemide to torasemide, it is recommended to prescribe a dose that is 10 times lower than the current furosemide dose – i.e. if the dog was receiving 10mg/kg furosemide total dose per day, then switch to 1mg/kg torasemide total dose per day. 

Because very limited data are still available with this drug, the patient’s condition should be closely monitored during this process. 

When administering diuretics, in particular high dose/combination diuretics, it is important to monitor urea/creatinine and electrolytes. It is not always a concern to observe mild pre-renal azotaemia with diuretic therapy – but if this starts to increase rapidly or causes uraemia (reduced appetite/vomiting) then this suggests that the diuretic dose may be too high. 

Hypokalaemia is often present when high diuretic doses or sequential nephron blockade are used and supplementation should therefore be considered in these cases. 

In patients with progressive weight loss, omega-3 fatty acids may also be beneficial to improve the patient’s caloric intake and potentially minimise the deleterious effect of chronic inflammatory cytokine activation, involved in the complex process of cardiac cachexia.

Anti-tussives

In patients with chronic cough despite adequate control of congestive heart failure (particularly if the cough impacts significantly in the patient’s or owner’s quality of life) then anti-tussives such as codeine or butorphanol may also be indicated, as long as it has been established that pulmonary oedema is not present. 

Other causes of refractory heart failure discussed during the webinar (which need specific treatment) include atrial fibrillation and pulmonary hypertension. 

Overall the webinar was a fascinating overview, highlighting the key therapies involved in the management of mitral valve disease. 

  • To find out more and watch the full recording of this webinar, visit www.cardioacademy.cevalearn.com.

1. Atkins, C. et al (2009) Guidelines for the Diagnosis and Treatment of Canine Chronic Valvular Heart Disease. Journal of Veterinary Internal Medicine 23: 1,1421,150.

2. Rishniw, M. et al (2012) Sleeping respiratory rates in apparently healthy dogs. Research in Veterinary Science 93: 965-969. 

3. Schober, K. E. et al (2010) Detection of Congestive Heart Failure in Dogs by Doppler Echocardiography Journal of Veterinary Internal Medicine 24: 1,3581,368. 

4. The BENCH Study Group (1999) The effect of benazepril on survival times and clinical signs of dogs with congestive heart failure: results of a multicenter, prospective, randomized, double-blinded, placebo-controlled, long-term clinical trial. Journal of Veterinary Cardiology 1: 7-18. 

5. Bernay, F. et al (2010) Efficacy of spironolactone on survival in dogs with naturally occurring mitral regurgitation caused by myxomatous mitral valve disease. Journal of Veterinary Internal Medicine 24: 331-341. 

6. Häggström, J. et al (2008) Effect of pimobendan or benazepril hydrochloride on survival times in dogs with congestive heart failure caused by naturally occurring myxomatous mitral valve disease: the QUEST study. Journal of Veteriny Internal Medicine 22 (1): 124-135.