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A report by Andre Hess MRCVS
on the The Joan Read Lecture on 4th February 2007
which was entitled:
‘Heart Disease and the Norfolk Terrier’
by Dr David Connolly
BSc., BVetMed., PhD., Cert SAM., CertVC.,
DipECVIM-CA(Cardiology)., MRCVS
The Club had the unique pleasure of having Dr David Connolly from the Royal Veterinary
College deliver a lecture on Heart Disease in the Norfolk Terrier. From the start it was very
clear that Dr Connolly had prepared an up-to-the-minute talk with the Norfolk Terrier in
particular, in mind, and that it was going to be a rare opportunity for those attending.
He started off with a brief discussion on Congenital Heart Disease (ie. present at birth), which
served mainly to contextualize it in terms of other kinds of heart disease we sometimes see,
including Degenerative Mitral Valve Disease (DMVD) - the one we had come to hear all
about. This he followed with a very interesting an important discussion on whether or not the
disease is as significant in the breed as we think it is. After this he went on to describe and
illustrate, by means of video footage, slides, and Xrays, DMVD and what we as owners are
likely to witness. Dr Connolly ended his lecture with a discussion on treatment options.
We were all anxious to find out how important the disease is in our breed, so we were
particularly interested to hear what Dr Connolly’s experience was. He confirmed that no
existing list of breeds prone to heart disease contains the Norfolk Terrier. He also confirmed
that a study of veterinary literature in general did not reveal that there is a predisposition for
heart disease in our breed. He did, however, go on to remind us that this does not mean that
spontaneous cases cannot occur within the Norfolk Terrier – and occur seemingly frequently
in a breed of such small numbers.
Dr Connolly premised his discussion on the significance of DMVD by alerting the audience
to the fact that all small breeds, and terriers in particular, are very likely to develop heart
disease in later life. That is, if you have a terrier of any sort, do not be surprised that it
acquires a heart condition in its old age. It is in the light of this that we should consider
What is important to us, Dr Connolly noted, is the age of onset and the speed of progress of
heart symptoms. This, he stated, is exemplified by the disease in the Cavalier King Charles
Spaniel, where the age of onset is early and the deterioration rapid. And the Yorkshire
Terrier, where the disease arrives, but hardly ever kills the animal – they die of other reasons
at a ripe old age usually. With this in mind, he revealed that no surveys published here or in
the USA mention the Norfolk Terrier, and that he could not recall seeing Norfolk Terriers
referred to the RVC with heart problems. This sounded like good news, but we needed to
tread carefully, he warned: it could be that the disease prevalence is indeed low; that the
number of Norfolk Terriers in this country is still small; that vets in practice feel confident
about diagnosing and treating DMVD, so do not refer; or that owners of Norfolk Terriers
cannot afford referral fees!
It was important to note, he went on, that even in the USA there have been no papers
published describing the nature of the disease in Norfolk Terriers. What we do have, however,
is some unpublished work by Dr Sunshine Lahmers, a resident in Cardiology at Washington
State University, which looked at the prevalence. This research was sponsored by ANTA,
their equivalent of the Norfolk Terrier Club of Great Britain. It suggested that >60% (!) of the
Norfolk Terriers studied showed evidence of ‘mitral valve regurgitation’ – that is, leakage of
blood back through the mitral valve. Her research also suggested that there appeared to be a
wide age distribution, with two peaks. This, Dr Connolly noted, could indicate the possibility
of an early onset form of the disease – the sort of problem we should be concerned about if it
is true. Dr Lahmers’ study suggested that only half the affected Norfolks (therefore 30% of
the total) had physical signs of the disease (ie. heart murmurs), and that
echocardiography/ultrasound would be needed as a screening tool to identify the early stages
of the disease. She also claimed that all Norfolks used for breeding should be examined by
echocardiography so that ‘silent’ mitral valve degeneration could be identified. That is,
auscultating the heart with a stethoscope was not enough.
Dr Connolly was of the opinion that the interim assertions offered by Dr Lahmers’ research
left a lot of questions unanswered:
Since it is the later onset disease we are interested in, a clear echocardiography
examination at 18 months of age cannot rule out future disease development.
In the light of this, what age should be set for an animal to be declared ‘echo’
clear before it is allowed to breed? Whatever age is chosen, it has no relevance
to the severity of future disease. For example, a soft murmur or ‘echo’ positive
detected at 5 years of age may never develop into severe disease.
If the age is set high, say 6 years, before a dog or bitch is allowed to breed,
what will be the effect on the gene pool?
If the age is set low, at 2 years for example, there is a chance that a large
number of dogs given the clear at the time will go on to develop heart disease.
If at 6 years of age a large number of dogs with ‘silent’ heart disease (ie. ‘echo’
positive) are eliminated from breeding (as the study appears to suggest), the
loss of good genes could prove catastrophic for the breed.
Dr Lahmers’ work infers that heart disease in the Norfolk is a non-sex linked
trait with a Dominant inheritance pattern. In his opinion it is too early to say
and that it is very unlikely that the disease is due to a single genetic mutation
anyway. Dr Connolly reminded us that in the Cavalier King Charles Spaniel,
where the disease was/is much more common and severe, it is considered to be
a polygenetic trait. That is, the disease is not inherited along particular
breeding lines, but exists in the breed as a whole at a particular ‘level’ – and
turns up spontaneously and sporadically. Breeding with affected dogs and
bitches (especially when both are affected) will contribute to this ‘level’.
We should heed, Dr Connolly advises, the experience of other breed schemes in this country.
Care had been taken in the Cavalier King Charles Spaniel not to try and eliminate all traces of
DMVD so as to preserve the gene pool. Fifteen years of work in the Boxer breed to reduce
Sub-Aortic Stenosis (SAS) has had good success despite taking care not to remove all dogs
with SAS from breeding, only those with severe disease. Also, work done in the Boxer with
Degenerative Cardiomyopathy suggested that the genetics of the disease was not the same in
the UK as it was in the USA. This may have implications for DMVD in Norfolks.
Dr Connolly concluded his survey of current and on-going research by making the following
suggestions (and this made the cost of the lecture worth every penny): wait for the full peer
reviewed facts from the USA; do not assume, even then, that the same facts hold true for
Norfolks in the UK; remember that we are dealing with a late onset disease (which must
always be distinguished from the geriatric disease Norfolks get just because they are terriers);
take care not to severely deplete the gene pool in our effort to do good; and not to expect a
single genetic test to give us a nice yes or no answer.
We were then showed slides of Xrays, heart valves collected at post-mortem, video footage of
normal and diseased hearts, and what is seen on echocardiography (ultrasound). Dr Connolly
listed the typical disease symptoms as: rapid breathing requiring effort (not the same as
panting); coughing and retching; weight loss (muscle mass); and some dogs will produce
signs of right heart failure (swollen belly filled with fluid from the enlarged liver, spleen, and
gut). We were even played a recording of what the vet hears when auscultating the heart – ie.
listening with the stethoscope.
The last section of the lecture covered the treatment of dogs with Congestive Heart Failure
produced by DMVD. There is little dispute that ACEi (Ace-Inhibitors, eg. Fortekor and
Enacard) benefit such dogs. Another drug that has shown good results is Pimobendan
(available as Vetmedin; we got the feeling that Dr Connolly liked this one more). Pimobendan
increases the contractility of the heart without requiring more oxygen; it improve the
relaxation phase of the heart, allowing better filling; it induces vasodilation which reduces the
blood pressure; and it has some anti-inflammatory action. Pimobendan can also be used
together with the Ace-Inhibitors. The constant mainstay of disease management is the use of
Diuretics like Lasix. Other drugs used in the treatment of the condition included BetaBlockers and Digoxin. Dr Connolly took care to remind us that the Ace-Inhibitors and
Pimobendan are expensive, even in human medicine.
The lecture was followed by a lively session of questions and answers. It is possible to argue
that the talk as a whole provided us with good news: the disease incidence may not be as high
as we think; the disease must not be confused with other kinds of heart disease in the terrier as
group; any news from the USA must be treated with caution; and it is very unlikely that it is
caused by a single gene. It also became clear, however, that there is work to do: we need to
get a much more accurate idea of the incidence of DMVD in the Norfolk Terrier; and we
must establish a protocol for breeders in the light of that information.
I propose that we start somewhere. I am prepared, as an experienced veterinary surgeon, to
offer myself and my stethoscope for this purpose (remembering how little difference ‘echo’
technology made in Dr Connolly’s opinion). I could, at any gathering of Norfolk Terriers,
auscultate (listen to) all hearts just once, and recording only the age and sex of the dog (so
identities remain anonymous for purpose of the study), produce a set of figures we can offer
to a medical/veterinary statistician for analysis. This will give us a much better idea of the
incidence of early onset heart disease. If by the end of it we find that this is higher than in
terriers in general (and it may not be!), for instance, we could come up with firm proposals.
An example of such a proposal will go along these lines: if a dog or bitch is found to
auscultate positive at five years of age, we stop breeding with it forthwith; there is little we
can do about progeny already produced, but stopping at that point will alone have a massive
impact on the incidence of the disease.
The 2007 Joan Read Lecture represents a significant moment in the breeding of Norfolk
Terriers. We must take advantage of the important work done by Dr David Connolly. It is not
often that we have an expert so sought-after internationally to come and talk to us about our
little demons.
Andre Hess MRCVS
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