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16658Re: [FH] Understanding HCM

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  • William Draper
    May 30, 2004
      i'm very sorry for your loss. it's always hard to lose a family member, especially when the circumstances are hard to explain or reconcile. i'm no specialist, but i'll see if i can help:

      - "I wonder if positive changes in the morphology of the could cause cell damage and thus clots as easily as negative changes (thickening)-change is change--but I'm not a doctor and this is just an
      intuitive question"
      -- the change in the heart that usually causes a thrombus is left atrial dilation secondary to the left ventricular hypertrophy. as the lumen in the left ventricle gets smaller, less blood goes from the atrium to the ventricle, and this can cause the atrium to dilate. when the atrium gets bigger, that can cause the blood inside it to stay for longer than it should (the atrium kind of acts as a storage vat), and this "stagnation" can cause the blood to coagulate (blood does NOT like to stand still). if the coagulation is severe enough, then a clot can form. this clot can then be released and sent out to the body. it generally travels down to the end of the aorta and sticks there (it "saddles" the terminal branches of the aorta). this can cause decreased blood flow to the pelvic limbs. the point of atenolol is to decrease the number and strength of contractions of the ventricle, allowing it to fill properly. this prohibits the blood from remaining in the atrium for longer than it should. there are a few other things that atenolol does, but this is the "major" effect.

      - "I keep thinking I would have seen some sign that something was wrong and could have stopped it"
      -- cats are notorious for "hiding" cardiac disease states. they are smarter than dogs about reducing their activity level in order to try to stave off terminal heart conditions. thus, most cat owners don't even know that their cat has a heart condition until it is in the emergency stage. this case is very atypical in that you, as a very cognizant owner, discovered the HCM before it presented clinically; and that it progressed in a very strange fashion. the only thing i can say as a comfort is that you did everything you could have to help your kitty get better. it is unfortunate that, even with all of your forward thinking, your cat still passed away.

      dvm in 2005
      ----- Original Message -----
      From: Kelly Tyler Lewis
      To: feline-heart@yahoogroups.com
      Sent: Sunday, May 30, 2004 6:07 PM
      Subject: [FH] Understanding HCM

      My beloved Facie, a doll-faced Persian, died at 14 1/2 on May 9. She was
      just diagnosed with HCM on April 12. I am grieving and also in shock because
      the vets have told me her case is mysterious and I'm not getting answers to
      help resolve this loss. I am hoping someone, particularly a specialist vet
      or cardiologist, can help me understand this better to come to grips with

      Facie had annual exams with full blood profiles, plus in-between
      appointments for any minor issues that might crop up. She was in prime
      condition, kidneys et al just great, only a bit of arthritis in the shoulder
      that made her limp now and then. She looked so great that even the folks at
      the vet's office thought she was only 4 or 5 year old. We had an annual
      visit May '03, everything great. Nov. 29 she had a visit for chin acne and
      vitals checked (weight and heart OK). Her appetite is always great, and she
      keeps herself in good trim--between 8-9 pounds since she was young. We took
      her in early for her big exam on Mar. 30 and discovered she had lost 6.5
      ounces, had a heart rate of 210, and a gallop rhythm (irregularly
      irregular). No breathing trouble, she had not seemed lethargic--she does
      sleep more in the winter months, but she always got sporty on sunny days in
      our enclosed garden. My husband and I both have home offices so we've been
      able to watch her closely through her senior years and she is an
      affectionate mate during the day, perched on our desks or laps. We were
      referred to a cardiologist who made the diagnosis of HCM with ultrasound and
      ECG. He said it was so mild (patchy thickening, 35% at most, most of the
      chamber normal) that he felt she had another 2 years of quality life with
      regular treatment. He prescribed 1/4 tab atenolol per day and bring her for
      a check-up in 4 weeks, when he would consider adding aspirin to her regimen.
      I was due for medical treatment in the US which could not be postponed (we
      are British). I was torn about leaving and also about starting her meds
      without being here, but he assured us that beta blockers do not have a
      downside and she did *not* need close observation to adjust the dose. My
      in-laws care for her regularly, at our house or theirs, and she has an
      immensely fun time at their house (we're always afraid she's going to resent
      going home when we take her down for holidays together), so my husband and I
      decided to take her there during our absence. They are also retired and one
      of them is home 24 hrs a day. We sent records to the local vet and set up
      the contact so he would take instructions from the cardiologists, and in an
      emergency, she would be taken to the Bristol University feline center, one
      of the two top feline cardio research units in the UK. My husband stayed at
      his parents' for the first 5 days of her atenolol, and she seemed great. She
      was springtime frisky, playing and enjoying herself and appetite increasing
      above normal (which happens when she's physically really active in the
      spring and summer). All reports from my in-laws were great. They took photos
      for us, and she looks great. Then, 3 weeks to the day from starting the
      meds, she walked across the kitchen and collapsed. The local vet diagnosed a
      saddle thrombosis and recommended euthanasia. We had a system in place to
      alert our cardiologist, who was on the phone and evaluating her condition.
      She was not in pain (no crying, no , and he said to get her to Bristol , 2
      hours away, which is. She was up and walking before they arrived, and
      strolled out of her carrier in such good shape that the specialist there was
      concerned that it might not have been a clot. Ultrasound & ECG, also blood
      screen for enzymes confirmed that it had been, but her body was clearing it
      effectively. Her heart condition had actually improved since she started the
      meds too. She was seen by a top feline cardiac researcher the next day, and
      her own cardiologist came to see her. He said he was shocked to see her,
      that with her mild HCM he would not have believed a clot was possible. I
      arrived and saw her for an hour each day for the next two days--she was
      clearly dopey from the analgesics, but walking, responsive, and eating well.
      The hospital wanted to keep her for observation for several days before
      releasing her. I will hold off on detailing the rest of her treatment in
      intensive care, but I will tell you that 84 hours after her collapse, she
      had another embolism and died instantly in her sleep. We decided against a
      post-mortem when the vet told us that clots often dissipate before they can
      have a look and leave no evidence. Given that poor outlook, we decided
      against it as it was all too traumatic.

      What is most distressing is that all of the vets and cardiologists who
      treated her say they are mystified by her first embolism episode, her fast
      almost "miraculous" recovery from it, and her death. They say they have
      never encountered a case where an asymptomatic, mild HCM patient turned up
      with a clot this early in the progression of the disease. It just seems too
      coincidental that this happens 3 weeks after the atenolol is started, but I
      can't find any data that suggests that it is risky. Nor did I before we
      started the treatment. I wonder if positive changes in the morphology of the
      could cause cell damage and thus clots as easily as negative changes
      (thickening)-change is change--but I'm not a doctor and this is just an
      intuitive question.

      I was deeply anxious about leaving her and would have put my own medical
      treatment behind her own, but for the assurance of the vet who said she did
      not need constant observation. I am not blaming the vet, but myself, and
      finding it hard to live with this. If her case is so atypical, I can't help
      wondering if we did something or could have done something different. She
      was not stressed going to or at my in-laws (she is the rare cat who likes
      car trips and doesn't cry in the car). I keep thinking I would have seen
      some sign that something was wrong and could have stopped it. Does anyone
      have any knowledge of the disease that it can be this capricious and
      unpredictable? She was healthy and beautiful and a wonderful friend for 14
      1/2 years and her loss is unbearable.

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