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Re: [FH] Introducing Tabby Jean..and question about commercial pet food

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  • Susan
    ... Atenolol is doing several things for Tabby Jean that are so important. For me understanding how it works was important. There are andergenic receptors
    Message 1 of 2 , Jun 2, 2004
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      --- sandworm90292 <erosla77@...> wrote:
      > Folks,
      >
      > My beautiful, sweet as sugar and SUPER SMART female
      > short-haired tabby, Tabbatha Jean
      > was diagnosed last week with cardio-myopathy. 40%
      > enlarged left ventricle, arrhythmia,
      > and two of her valves are slightly thickened.
      >
      > The vet has her on Atenolol, which seems to be
      > having zero side-effects; she was totally
      > asymptomatic when a routine yearly physical spotted
      > the problem

      Atenolol is doing several things for Tabby Jean that
      are so important. For me understanding how it works
      was important. There are andergenic receptors which
      certain substances secreted by the adrenal gland fit
      into. These receptors occur in the heart and the
      lungs. Atenolol is a selective beta-blocker, meaning
      it is like a key that fits into a certain lock. In the
      case of atenolol it fits into the andergenic receptors
      on the heart unlike propanolol which is not specific
      and also fits into receptors on the lungs. When these
      receptors on the heart are filled they are unavailable
      to the substances secreted by the adrenal gland that
      increase heart rate. So atenolol slows the heart rate
      giving our cat's left ventricle a longer time to fill
      up. Atenolol also reduces the oxygen demand of the
      heart. When the heart has an increased demand due to a
      fast heart rate that is not being adequately supplied
      the heart muscle suffers damage. So atenolol helps to
      prevent that damage. You also mentioned arrhythmia,
      atenolol helps with this also.

      > Question: can switching her food make a difference?

      You do not want to initiate severe sodium restriction
      until your cardiologist or internist tells you to.
      However extremely salty people snacks are not a good
      idea.

      >
      > I am wondering, once Tabby's arrhythmia is under
      > control, if there is ANY kind of
      > supplement to retard the myopathy so her heart does
      > not continue to enlarge.

      The short answer is that veterinary cardiologists are
      not sure yet, but there have been intriquing reports.

      According to Clarke Atkins:
      http://www.vetlatranquera.com.ar/pages/wild/small_animal_2.htm


      "A recent report by Rush, et al. demonstrated a
      reduction in wall thickness with the administration of
      enalapril to cats with HCM. This suggests a potential
      role for ACE-inhibitors in the treatment of HCM.
      These drugs are generally safe and do play a role in
      cases which are refractory or in which pleural
      effusion is present. In asymptomatic patients, it is
      logical that the renin-angiotensin-aldosterone system
      is not pathologically activated, and hence
      ACE-inhibitors would not be useful. The study
      referred to argues that they may play a role, however.
      Further studies are being planned. Enalapril is used
      at .5 mg/kg daily."


      Other therapies, including oxygen, aspirin, home
      confinement, and moderate salt restriction should be
      instituted as needed. Taurine supplementation is not
      necessary in the treatment of HC. In asymptomatic
      cats with HC, the author advises home confinement,
      moderate salt restriction, Beta- and/or calcium
      channel blockade, and aspirin indefinitely."

      According to Dr. O'Grady of VetGo Cardiology Concepts:
      http://www.vetgo.com/cardio/concepts/concindx.php

      "Growth hormone excess is being investigated, however
      it is too early to suggest if or how common this
      abnormality is involved in feline HCM.

      Work in people with the identical disorder suggests
      that Angiotensin II or aldosterone excess, likely at
      the myocardial tissue level without elevated
      circulating blood levels of angio II or aldosterone,
      may activate gene expression resulting in myocyte
      hypertrophy. If this also occurs in the cat, then ACE
      Inhibitor therapy may reduce the local tissue levels
      of Angio II or aldosterone aborting this process.

      Alpha adrenoreceptor blockers may also reduce left
      ventricular concentric hypertrophy.

      As described above, the first prospective, randomized,
      placebo-controlled clinical trial investigating the
      treatment of feline HCM and CHF is underway. This
      trial is investigating four treatments groups (all
      groups receive furosemide as they are CHF patients):
      placebo, ACE-inhibitior, atenolol (beta blocker), and
      diltiazem (calcium channel blocker). We await the
      results of this trial to determine the appropriateness
      of these therapeutic modalities to treat feline HCM."

      Susan






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