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56° Congresso Internazionale Multisala SCIVAC
241
Management of feline heart failure
Virginia Luis Fuentes
MA, VetMB, PhD, CertVR, DVC, MRCVS, Dipl ACVIM Dipl ECVIM-CA (Cardiology), North Mymms, Hatfield, (UK)
Although congestive heart failure may be caused by many
different types of cardiac disease, the therapeutic approach
may be dictated more by clinical signs and stage of disease
than by aetiology.
Dobutamine should be started at lower doses than in dogs
(1.25mcg/kg/min) and an attempt should be made to wean cats
off sooner: seizures may occur on the 2nd day of treatment. No
data are available on the acute use of pimobendan in cats.
MONITOR EFFECTS OF THERAPY
Stage A- at risk
Maine coons may be at increased risk of developing
hypertrophic cardiomyopathy (HCM), so may be presented
for screening. Obviously no treatment is indicated.
Stage B- asymptomatic heart disease
There are few studies of treatment in asymptomatic cats to
help guide therapy. Beta-blockers and diltiazem have been
suggested.
Stage C- the acutely-decompensated cat
It is rarely possible to carry out a detailed Doppler-echo
exam on a dyspnoeic cat to confirm the type of myocardial
disease, although when the diagnosis of congestive heart
failure is in question, it may be less stressful to perform an
ultra-rapid echo exam than to obtain thoracic radiographs.
If left atrial enlargement present → aggressive management of congestive failure
If large pleural effusion present → thoracocentesis
Note: more care required than in dogs with avoiding prerenal azotaemia.
Administer O2: cats are small enough for oxygen cages
to be practical.
Sedation: It may be even more important to sedate cats
than dogs, as dyspnoeic cats often become very distressed
(eg, butorphanol 0.25mg/kg IM)
IV furosemide: initial dose should be no more than 2
mg/kg, thereafter 1-2mg/kg every 60 mins until respiratory
rate decreases.
Thoracocentesis: Significant pleural effusions are more
common than in dogs with congestive heart failure, and
these should be drained with a butterfly cannula.
Cats with low-output failure
Consider dobutamine, despite the theoretical contraindications of positive inotropes causing increased myocardial
oxygen consumption and increased toxicity in cats
• Monitor respiratory rate and effort in congestive failure
• Monitor attitude, body temperature, heart rate and arterial
pressure in low output failure.
• Monitor renal function and electrolytes
Stage C- moderate congestive failure and
maintenance therapy
The aims of chronic therapy are to eliminate abnormal
fluid retention, modulate neurohormonal activation and optimize haemodynamic function. In addition, prevention of
thromboembolism is important. There are fewer studies
available to guide treatment options, although the initial
results of a large-scale blinded study of feline diastolic heart
failure suggested that furosemide remains the most important part of treatment.1 In this study, treatment with atenolol
hastened the recurrence of congestive failure or death,
whereas ACE inhibitors and diltiazem were neutral.
Furosemide: (1-5 mg/kg q12-24h PO) oral furosemide is
used at doses sufficient to eliminate pulmonary oedema, or
until unacceptable azotaemia develops.
ACE inhibitors: although not proven to help with control
of congestive signs, ACE inhibitors have not been shown to
cause harm, even in cats with hypertrophic obstructive cardiomyopathy.2 A target dose of benazepril would be 0.5
mg/kg q24h, but dosing should be started at half this dose.
There has been considerable interest in the concept that ACE
inhibitors might be able to affect progression of hypertrophy in
HCM, or even reverse hypertrophic changes.3 While angiotensin
converting enzyme genotypes have been shown to influence
the expression of hypertrophy in human HCM, there are no
human studies as yet documenting regression of hypertrophy
with ACE inhibitor use. One study has shown regression of
hypertrophy with losartan in a rabbit model of HCM.4
DECREASE HEART RATE?
Traditionally, diastolic heart failure has been treated with
atenolol or diltiazem to slow heart rate. In view of the preliminary results of the multicentre study by Fox et al.,
atenolol should only be used with caution in cats with a
history of congestive failure, and not at all in cats with current signs of congestive failure.1
Proceedings of the SCIVAC Congress, Rimini, Italy, 2007
56° Congresso Internazionale Multisala SCIVAC
Negative inotropes for dynamic obstruction: human
HCM patients with LVOTO have a worse outcome, although
the same may not be true in cats.5;6 Negative inotropes can
decrease LVOTO gradients, and beta-blockers are more effective at this than diltiazem in cats.7 The importance of controlling LVOTO gradients in cats with HOCM is uncertain.
Positive inotropes for cats with systolic dysfunction:
digoxin is relatively difficult to use in cats because of the high
incidence of toxicity. Although there are no published data on
the use of pimobendan in cats, it may be better tolerated.
Stage D- refractory congestive failure
Furosemide: increase dose to effect (monitor renal function)
Spironolactone: add to furosemide therapy (1 mg/kg q24h).
Potassium levels should be monitored.
Thiazides: in very refractory cases where furosemide is
no longer effective, a thiazide can be added at low doses.
CONSIDERATIONS IN SPECIFIC CARDIAC
DISEASES
DCM
Although nowadays most cases of feline dilated cardiomyopathy are not related to taurine deficiency, it is still
worth measuring plasma taurine levels. Taurine supplementation (250-500 mg q12h PO)should be started until the
results are received, and can be discontinued if taurine levels
prove to be normal.
ARVC
242
myocardial disease predisposing to thromboembolism cannot usually be resolved. Principles of treatment include analgesia, management of electrolyte and acid-base abnormalities, and prevention of thrombus extension. Thrombolytic
therapy is still controversial.
• Analgesia (butorphanol 0.2 mg/kg q8h SQ combined with
acepromazine) or epidural anaesthesia.
• Fluid therapy to maintain urinary output (unless there is
concurrent pulmonary oedema).
• Antibiotic therapy effective vs. anaerobic infection (e.g.
ampicillin, amoxicillin).
• Heparin (200 to 300 IU/ kg IV, then SQ q8h for 48-72
hours)
Pulses often return within 72 hours, though use of the
limb usually takes longer.
Prevention of thromboembolism
Antithrombotic options include aspirin, warfarin, lowmolecular weight heparins and clopidogrel. Different doses of
aspirin have been recommended (high dose: 40mg /cat q72h,
or low dose: 5mg/cat q72h).(8) Warfarin is extremely difficult
to use, as there are substantial risks of haemorrhage even with
careful monitoring.(9) Low-molecular weight heparins must
be administered by subcutaneous injection, and are associated
with more risk of haemorrhage than aspirin, but less than warfarin. Their efficacy remains to be demonstrated in cats. Studies of clopidogrel are currently underway in cats.
Reference List
1.
Management of right-sided heart failure in ARVC can be
frustrating, and the same approach is used as in other causes
of feline congestive heart failure. Sotalol has been used for
management of ventricular arrhythmias (2-4 mg/kg q12h PO).
2.
Systemic hypertension
4.
Although hypertension is not a common cause of congestive heart failure in cats, it should be treated when present.
Amlodipine (1.25 mg/cat q12-24h PO) is the first choice
treatment.
5.
3.
6.
Hyperthyroidism
Hyperthyroidism should also be treated when present with
congestive heart failure. If euthyroidism cannot be achieved
(eg. when renal failure is present), diuretics and ACE inhibitors
should be used to resolve congestive signs, and beta-blockers
used for maintenance to minimize thryotoxicosis.
7.
8.
9.
Management of systemic
thromboembolism
Arterial thromboembolism is a frustrating condition to
treat, with more than 50% of cats before leaving the hospital. Cats that survive an acute episode are likely to suffer
repeats bouts of thromboembolism, as the underlying
Prospective, double-blinded, multicenter evaluation of chronic therapies for feline diastolic heart failure: interim analysis. Lakewood,
CO: American College of Veterinary Internal Medicine, 2003.
Oyama MA, Gidlewski J, Sisson DD. Effect of ACE-inhibition on
dynamic left-ventricular obstruction in cats with hypertrophic
obstructive cardiomyopathy. J Vet Intern Med 2003; 17(3).
Amberger CN, Glardon O, Glaus T, Hörauf A, King JN, Schmidli H
et al. Effects of benazepril in the treatment of feline hypertrophic cardiomyopathy. Results of a prospective, open-label, multicenter clinical trial. Journal of Veterinary Cardiology 1999; 1(1):19-26.
Lim DS, Lutucuta S, Bachireddy P, Youker K, Evans A, Entman M et
al. Angiotensin II blockade reverses myocardial fibrosis in a transgenic mouse model of human hypertrophic cardiomyopathy. Circulation 2001; 103(6):789-791.
Maron MS, Olivotto I, Betocchi S, Casey SA, Lesser JR, Losi MA et
al. Effect of Left Ventricular Outflow Tract Obstruction on Clinical
Outcome in Hypertrophic Cardiomyopathy. The New England Journal of Medicine 2003; 348(4):295-303.
Fox PR, Liu SK, Maron BJ. Echocardiographic assessment of spontaneously occurring feline hypertrophic cardiomyopathy. An animal
model of human disease. Circulation 1995; 92(9):2645-2651.
Bonagura JD, Stepien RL, Lehmkuhl LB. Acute effects of esmolol on
left ventricular outflow obstruction in cats with hypertrophic cardiomyopathy. Journal of Veterinary Internal Medicine 5, 123. 1991.
Smith SA, Tobias AH, Jacob KA, Fine DM, Grumbles PL. Arterial
thromboembolism in cats: Acute crisis in 127 cases (1992-2001) and
long-term management with low-dose aspirin in 24 cases. J Vet Intern
Med 2003; 17(1):73-83.
Harpster NK, Baty CJ. Warfarin therapy of the cat at risk of thromboembolism. In: Bonagura JD, Kirk RW, editors. Kirk’s Current Veterinary Therapy. Philadelphic: W.B. Saunders Company, 1995: 868-873.
Author’s Address for Correspondence:
Virginia Luis Fuentes Senior Lecturer - Department of Veterinary
Clinical Sciences, Royal Veterinary College - Hawkshead Lane,
North Mymms, Hatfield AL9 7TA, United Kingdom