Re: [FH] How common is Feline Heart Disease?
- --- kfmcshane <kfmcshane@...> wrote:
> I can't find any info on how common this disease is.It is not known how common HCM is because there have
been no long term studies following a large group of
It is more common in males. It is seen more on the
East Coast. It is considered to be familial in Maine
Coon for sure, probably American Shorthair, Ragdoll
and Persian as well.
I never thought after my first young HCM kitty died
that I would adopt another from the same place
(PetsMart) placed by the same group who are also
involved in feral rescue. But with my previous
experience and knowlege Rudy was diagnosed at a very
early stage by some very subtle symptoms that I
observed when he ran outside.
My unproven hypothesus is that there is some
connection to the heart being damaged by an
exaggerated flight reflex (sympathetic overactivation
or sustained sympathetic activation) that would be
more of an issue in ferals and may affect males
disproportionately because males fight. I found a
reference to this process and the damage it can do to
the myocyte and I posed the question to a pathologist
who had a refernce to sympathetic overactivation on
his website. I have pasted my question below:
I am just a layperson but I have done a lot of reading
and I stumbled on a reference to sustained sympathetic
activation being deleterious to the myocyte from:
Beta blockade in patients with congestive heart
"In patients with LV dysfunction, a cauldron of
dangerous sympathetic activation smolders beneath the
surface. ACE inhibitors will not fix that. Sympathetic
activation, with increased release and diminished
reuptake of norepinephrine from myocardial sympathetic
nerve terminals, is an acute response to circulatory
stress. In a teleological sense, an acute increase in
sympathetic drive was advantageous for our ancestors.
When they were being pursued by a tiger or bleeding
from a wound, increasing heart rate, peripheral tone,
and myocardial contractility allowed them to reach
safety or maintain central perfusion.
However, sustained sympathetic activation, as occurs
in LV dysfunction, is a maladaptation of what was
intended as an acute response. Chronic sympathetic
activation is ultimately a highly deleterious process.
Excessive norepinephrine is directly toxic to the
myocyte. It also causes down-regulation of the
beta-adrenergic receptor and uncoupling of it from the
post-receptor pathway, resulting in progressive
deterioration in contractility.
My interest in this possibility stems from my own
experience of having two young unrelated cats with
hypertrophic cardiomyopathy who were born to
feral mothers and who both were extremely
skittish/fearful. I am also a member of
a Yahoo group called feline heart and there are others
with young ferals who dropped dead suddenly with an
HCM diagnosis at necropsy. Current feline
HCM research has focused on a familial model seen in
certain breeds, some of which is initiated by breeders
and I wonder if vet cardiologists have ever
thought about a nonfamilial cause specific to ferals
who have been captured."
Hypertrophic cardiomyopathy is an unfortunately-named
illness that is primarily genetic; athletic training
makes the obstructive component worse.
Catecholamine cardiomyopathy results directly from
sympathetic overstimulation, usually from
pheochromocytoma or in torture victims.
Athletic hypertrophy and hypertensive hypertrophy have
been suspected as having to do with sympathetic
stimulation, at least in part.
Perhaps "hypertrophic cardiomyopathy" and
are being conflated. Not really my area. It doesn't
surprise me that you'd see serious anatomic and
physiologic pathology in a caged animal. Thanks for
I suspect that one explanation for higher HCM
incidence on the East Coast could be more cities and
more feral rescue groups. I also suspect that many
shelter adopted cats are feral rescues that we may not
know about. My hypothesus may not pan out but if all
of us brought this idea up to our vet cardiologists it
may get some vets thinking and we may end up with new
treatments to suppress noripinephrine. Afterall if it
were not for one Maine Coon breeder contacting a
cardiologist and donating a line of cats for study we
would not know that HCM may be familial with an
autosomal dominant heritability. New ideas have to
If you think about it our cats are not as domesticated
as dogs and the experience of being confined in our
homes may actually be responsible for a type of
catecholamine cardiomyopathy, which would be even more
acute in a feral rescue no matter how young the feral
was when captured.
Rudy: Male DSH brown tabby, feral mom, diagnosed 09-2002 at 19 months of age with idiopathic HCM: grade 2 murmur, hyperkinetic heart, borderline normal thickening, considered asymptomatic, 12.5 mg Atenolol 1x day, 1/2 baby aspirin 2x week administered via pilling
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