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Re: [FH] How common is Feline Heart Disease?

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  • Susan
    ... It is not known how common HCM is because there have been no long term studies following a large group of cats. It is more common in males. It is seen more
    Message 1 of 2 , Jul 30, 2003
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      --- 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:

      "Dr. Friedlander,

      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."

      His answer:

      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
      "catecholamine cardiomyopathy"
      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
      start somewhere.

      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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