Lifespan and Causes of Death in the Irish Wolfhound - Vetsuisse ...

there are marked individual differences in sensitivity to this class of drugs, the initial
dose should be low and then be raised gradually until the desired effect is achieved.
The effect on overall survival has not been studied in dogs (Fox, Sisson et al. 1999).
On a side note, the author is aware of several cases where electrical atrial
defibrillation was attempted in Wolfhounds with varying success. The technique has
also been described in the literature (Osswald, Trouton et al. 1998).
Solatol and other class III antiarrhythmic drugs are an additional possibility for the
treatment of ventricular arrhythmias in canine DCM, but there are no studies on its
effects in dogs as of now. There is anecdotal evidence of its benefits where other
antiarrhythmic drugs had failed (Fox, Sisson et al. 1999).
A relatively recent development is the addition of the calcium-sensitising inodilator
pimobendan to standard treatment with furosemide, enalapril and digoxin, which was
shown to increase survival in Doberman Pinschers, but not in English Cocker
Spaniels (Fuentes, Corcoran et al. 2002). Pimobendan was also reported to increase
survival in a hamster model of hereditary Cardiomyopathy (van Meel, Mauz et al.
1989). However, some results from human medicine suggest that there may be an
increased mortality in the long term (Mathew and Katz 1998; Fox, Sisson et al. 1999).
While thrombosis is not a usual complication of DCM in dogs, left atrial thrombi have
been identified at autopsy in Wolfhounds with DCM, and it might therefore be
indicated to add anticoagulants (e.g. aspirin or warfarin) to the treatment regimen
(Brownlie and Cobb 1999).
Surgical treatment techniques have also been described. While in humans, the
treatment of choice is a heart transplant, such operations are not usually performed
in dogs. Successful dynamic cardiomyoplasty, the covering of both ventricles with an
envelope of skeletal muscle (usually the right M. latissimus dorsi) which is then
connected to a pacemaker, has been used in humans since 1985 and is also
described as a clinical therapy for canine DCM (Aklog, Murphy et al. 1994; Monnet
and Orton 1994; Orton, Monnet et al. 1994). Prosthetic cardiac binding and adynamic
(no pacemaking of the muscle graft) cardiomyoplasty have also shown a positive
effect in the treatment of experimentally induced canine DCM (Oh, Badhwar et al.
1998). However, these techniques are not currently in wide clinical use.
Cellular cardiomyoplasty is another experimental technique that involves the injection
of previously cultured autologous skeletal muscle cells into the heart muscle. While
there have been promising results so far in hamsters, only very limited data are
available for dogs with DCM (Borenstein, Chetboul et al. 2002).
3.3.1.5 Prognosis
Survival time is highly variable from one individual to the next, which makes it
basically impossible to predict how long a dog is going to survive on treatment. At
least in cases presenting with advanced heart failure, it is recommended to observe
the animal’s individual reaction to therapy before making a tentative prognosis based
on these observations (Fox, Sisson et al. 1999). An early initiation of treatment with
ACE inhibitors and (where indicated) digoxin or antiarrhythmic drugs seems to
influence the course of the disease in a positive way (Vollmar 2000).
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