16671Re: [FH] Understanding HCM
- Jun 1, 2004Re: [FH] Understanding HCM- "I notice online that many other vets prescribe diuretics with the atenolol and low-salt diets. Is that only when the disease is severe and has advanced to congestive heart failure or some kind of fluid build-up in the lungs?"
-- yes. we only give drugs if they are indicated. furosemide (a diuretic) can be hard on the kidneys, so there is no use to give it unless you have a volume problem.
- "The cardio decided to consider adding aspirin later. He told us the results are equivocal and it can be harmful. I see that many vets prescribe the two together. Is it pretty routine with mild HCM not to jump right into home-dosed aspirin?"
-- aspirin has a narrow safety margin in cats. it is another drug that we don't like to give if we don't have to.
if you want to give a contribution, then contact dr. kittleson at uc-davis and ask him for some ideas. he will know best how you should give your money. it sounds like everything that could have been done was. it is unfortunate that we sometimes lose patients that we fell we can cure.
dvm in 2005
----- Original Message -----
From: Kelly Tyler Lewis
To: William Draper
Sent: Tuesday, June 01, 2004 9:03 AM
Subject: Re: [FH] Understanding HCM
Thanks so much for writing. That helps so much. I'm having trouble with the fact that the cardiologist said that her ultrasound showed that the thickening had actually reduced and the shape of heart was becoming more normal in the 3.5 weeks since he had seen her (3 weeks on the atenolol). As you explained that the clots form from stagnation from improper filling--he also said irregular flow or irregular surface of the heart that damages red blood cells and thus signals the clotting system to come fix what it perceives as "damage". I wonder if changes could create an odd surface or odd flow any time the heart changes shape, even for the better. He described clots that originate on irregular surface that become hair-like chains that cling tenuously to the heart, then break off and enter the circulation.
Since you have veterinary expertise, could I ask you a couple of other questions that I'm struggling with--please rest assured that I'm not looking to blame anyone, just trying to understand the treatment. There were many fast decisions happening:
I notice online that many other vets prescribe diuretics with the atenolol and low-salt diets. Is that only when the disease is severe and has advanced to congestive heart failure or some kind of fluid build-up in the lungs? She didn't seem to have either. As far as diet, she was on a religious diet of Iams Senior dry and 1/2 or full 3 oz. can of Iams per day. She was a great free feeder who self-regulated and didn't overeat. However, tidbits were irresistible, and I always struggled with my in-laws on this one. They were giving her treats of ham, which suddenly got me alarmed when I read about low-salt diets. I imagine this relates more to blood volume than clots though--more salt consumption equals more drinking and higher blood volume.
The cardio decided to consider adding aspirin later. He told us the results are equivocal and it can be harmful. I see that many vets prescribe the two together. Is it pretty routine with mild HCM not to jump right into home-dosed aspirin?
When she went to the hospital after her embolism crisis on Thurs., the vets opted not to give her any anti-clotting agents. They said there was a relatively new, powerful drug that they would have to have administered in the first 4-6 hours (maybe it was TPA?), and she only arrived there 8 hours after her collapse. (The local vet in rural Wales recommended euthanasia and had no specialist expertise or drugs. Then we couldn't reach her cardio by phone, he was in surgery. When we finally did--3 hours after he collapse, when she was standing and walking again--he said get her to the Bristol feline cardio center. It was a long drive from Wales to Bristol.) Also, they barely saw the last traces of the suspected clot in the aorta, and blood flow had resumed. Her leg pulses returned on Fri. In the next two days, the vet also resisted giving her Heperin. She said Facie's anti-clotting cascade was working efficiently and it would be dangerous to interfere and could cause complications. They just had her on aspirin, painkillers, and small supplement of fluids later. She was eating normally through all this so they felt pretty good about her condition.
When she was diagnosed in April '04, she was also tested for thyroid disease and the lab came back negative. Then the vet's office came and left a message on our machine while we were away that the lab was wrong--no explanation, they either confused results or re-tested her blood--she actually tested slightly hyperthyroid at 59 (when the top end of the lab's normal range was 50). It wasn't noted on palpation in November or March. The cardiologist said that he didn't consider that causal, but a parallel condition developing with her HCM because that slight increase couldn't have caused a heart issue. I am taking some comfort in the fact that I read that atenolol is often prescribed short-term to address both thyroid and heart problems all at once. I don't like to think we could have followed a different regimen with a happier outcome, now that we've lost her.
Admittedly, Bill, I am feeling bad that we didn't opt for blood screening every 6 mos., instead of bloods & physical once a year with a physical exam only in between. I worried about antagonizing her with vet visits that were too traumatic. She had an arthritis exam a year ago (May '03) that included an x-ray and some painful manipulation of her shoulder, sedation, blood testing, and a trial on a medication which upset her stomach. She was always a kitty who was very nonchalant about the vet, just sweaty paws, and that visit upset her so much she hissed at everyone and me when I came to get her and cried pitifully in the car (never a car crier before, she loved car rides and going on vacation). I thought: we really need to keep these visits low-key and relaxed since she will need the vet more in her senior years. Is the blood panel really for her or is it for my peace of mind? So I didn't want to do a jab for tests in Nov., just make it a relaxed physical and exam of her acne.
Sorry I can't remember the arthritis med name and other technical details--I know that sounds stupid, but I am American & just moved to the UK two years ago. Unlike my American vet, British vets don't give you itemized invoices after the appt. that show a weight, vaccination and medication record. It drives me crazy. It's all verbal and you have to take notes, which I've misplaced.
Also-we'd like to memorialize her with a contribution to HCM research. It seems that the Winn Foundation or Mark Kittleson at UC Davis would be good places. Do you have any ideas?
From: "William Draper" <wedraper@...>
Date: Sun, 30 May 2004 21:22:03 -0300
To: "Kelly Tyler Lewis" <ktyler.uk@...>
Cc: "FH" <email@example.com>
Subject: Re: [FH] Understanding HCM
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
-- 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 <mailto:ktyler.uk@...>
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
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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