CARDIOLOGY
diac myofibrils to calcium. The effect is increased
contractility without any increase in myocardial oxygen consumption. Pimobendan results in a reduction
of pulmonary capillary wedge pressure, an increase in
cardiac output and an increase in stroke volume
Figure 1: Lateral radiographs of dog with dilated cardiomyopathy
L
Figure 2: DV radiograph of dog with dilated cardiomyopathy
Pimobendan requires a special mention as it has
demonstrated a marked increase in survival time
compared to placebo treated groups. A study by Luis
Fuentes and colleagues looking at Dobermans and
Cocker spaniels demonstrated a median survival of
329 days in the Pimobendan groups compared to 50
days in the placebo group. A similar study by O’Grady
and colleagues demonstrated a survival time of 130.5
days in the Pimobendan group compared to 14 days
in the placebo group.
The Bench study looked at the use of Pimobendan to
prevent the onset of congestive heart failure in Dobermans diagnosed with pre-clinical DCM. The Study
found that Pimobendan significantly prolonged (by 9
months) the median time to onset of heart failure or
sudden death in Dobermans with pre-clinical DCM.
This drug has now been registered for this use in Dobermans.
Pimobendan acts by inhibiting phosphodiesterase III
and by increasing the calcium sensitivity of the car-
Beyond standard therapy other therapies addressing
atrial fibrillation such as digoxin can be considered.
Digoxin also has a weak positive inotropic effect to
cause increased cardiac output however its main benefit is from its central effect of promoting vagal tone
and thus slowing SA discharge and AV conduction
rates. This will decrease the heart rate thus reducing
myocardial oxygen consumption. It is vital to initiate
therapy at the appropriate dosage and digitalise the
patient. Digoxin should be dosed on lean body mass
at 0.22mg/m2, po, bid, and the dose reduced in animals with ascites.
Due to the variable half- life in dogs accurate dosing is difficult and serum levels should be checked 5-7
days after initiating treatment. Trough concentrations
(8-12 hrs post-pilling) of 0.8 – 1.2ng/ml (1 – 1.5 nmol/L
being optimal. Beta-blockers can also be considered
as they may have a positive long term effect by reducing the sympathetic drive and thus will protect the
myocardium in the long run. Beta blockers should be
used with care and introduced very slowly and never
used in a patient with decompensated patient with
signs of pulmonary oedema or hypotension.
References:
1. Boswood A. Current use of Pimobendan in canine
patients with Heart disease. Veterinary Clinics of
North America: Small Animals 40 (210) 571-580.
2. Martin M W et al, Canine dilated Cardiomyopathy:
a retrospective study of prognostic findings in 367
clinical cases. Journal of small animal practice
(210) 51, 428-436
3. Borgarelli M et al. 2001 Canine Idiopathic dilated cardiomyopathy. Part II: Pathophysiology and
Therapy. The Veterinary Journal (162):182-195.
4. Dukes-McEwan J Et al. 2003 Proposed guidelines
for the diagnosis of canine idiopathic dilated cardiomyopathy. The ESVC taskforce for canine dilated cardiomyopathy. Journal of Veterinary Cardiology (5) no.2.
5. Summerfield N J et al, 2012 Efficiency of Pimobendan in the prevention of congestive heart
failure or sudden death in Doberman Pinchers
with preclinical dilated cardiomyopathy.(The Protect Study). Journal of Veterinary Internal medicine (26):1337-1349.
6. O’ Grady M et al. Pathophysiology of dilated cardiomyopathy. ACVIM 2012
7. Luis Fuentes V et al. 2002 A double blind, randomized, placebo-controlled study of Pimobendan
in dogs with dilated cardiomyopathy. Journal of
Veterinary Internal medicine (16(:255-61
References available on www.vet360.vetlink.co.za
vet360
Issue 01 | FEBRUARY 2016 | 22
FEB 2016 Vet360 working last.indd 22
2016/01/25 6:18 PM