More About
Hypertrophic Cardiomyopathy (HCM)

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[ANIM: Neko]
Hypertrophic
Cardiomyopathy (HCM)


The following retransciption is gleaned from the Cornell Book of Cats, 1989, Mordecai Siegal and Cornell University, Chapter 20 - The Internal Cat, pp. 192-3...which book I, unfortunately, have had on my bookshelf since 1995 - two years after Raisen and Bran were born. Had I noticed the signs, and then searched the book for those very signs, maybe Raisen might still be alive today, under medication and at least stabilized from becoming any worse. 8-(

MYOCARDIAL DISEASES:
  Cardiomyopathy.  Cardiomyopathies are primary diseases that affect the heart muscle. The ultimate result is an inability of the heart to compensate for stress, and heart failure may occur. Inheritance, viral infections, autoimmune mechanisms, biochemical disorders, and diet deficiencies (e.g., insufficient taurine) are factors that may contribute to the development of cardiomyopathies.
  Cardiomyopathies are subdivided into hypertrophic, dilated, and restrictive. However, an increaseing number of cats is being recognized with cardiac disease that cannot be classified into just these three categories. Middle-aged male cats and certain breeds seem more predisposed to cardiomyopathies. Generally, the observed signs of labored breathing, lameness, or paralysis, lethargy, and ascites (accumulation of fluid in the abdomen) are a result of cardiac arrythmias, congestive heart failure, or blood clots. In advanced stages collapse may occur. This occurs when a partial or complete temporary suspension of respiration or circulation results from obstructed arterial blood flow.
  Hypertrophic Cardiomyopathy  (HCM).  HCM is the most common form of acquired heart disease in the cat, and it predominantly affects young to middle-aged male cats. It is the enlargement of the left ventricular wall, papillary muscles, and septum, which limits the size of the left ventricular chamber. This type of enlargement prevents the heart from expanding (to receive blood) adequately, thus decreasing cardiac output. The incidence of blood clots is somewhat greater than in other forms of cardiomyopathy. The dynamics of this clotting directly relate to the restricted ventricular filling, which allows the blood to remain for a longer period of time in the left atrium, therby having a greater chance of forming blood clots.
  Signs indicative of HCM include labored and noisy breathing, lethargy, loss of appetite, and possible lameness or paralysis of the hind legs due to arterial blood clots.
  Prognosis is fair if arrythmias and clots can be controlled medically. Treatment by the veterinarian consists of dosages of negative inotropes (substances that affect the force of muscle contractions), diuretics, and carefully controlled doses of aspirin.

[...]

DIAGNOSIS OF CARDIOMYOPATHIES.  Diagnostic tests that may be performed by a veterinerian include electrocardiogram, radiography, serum chemistries, and hemogram (includes blood counts, packed cell volume, percent of hemoglobin). These tests do not necessarily help in differentiating between the various types of cardiomyopathies; however, they can provide vital information on the function of other organs. This information is important in determining appropriate methods of treatment.
  Sophisticated tests that can be performed at progressive small-animal clinics or at veterinary college clinics are echocardiography and angiocardiography. These tests can differentiate between the various types of cardiomyopathy.

DRUGS USED IN TREATMENT.  Treatment is directed at reducing the workload on the heart and improving oxygenation of blood. Therapy regimen varies according to the type and severity of the cardiomyopathy. Also, a low-sodium diet can be beneficial to the patient by preventing fluid retention. some of the drugs used by the veterinerian follow:
  Furosemide  is a diuretic that is prescribed for feline patients experiencing pulmonary edema (lungs filling up with fluid). Diuretics act primarily by blocking reabsorption of sodium.
  Digitalis  increases the strength of contractions by the heart and reduces the heart rate. Therefore, this drug is used to control atrial tachyarrythmias (rapid, irregular heart beat rhythm) and improve cardiac performance. The veterinerian must maintain close supervision of dosage since toxicity can easily occur. An acute onset of vomiting, loss of appetite, and diarrhea are signs of toxicity.
  Vasodilators  (e.g., nitroglycerin, hydralazine, and captopril) influence blood vessels, usually by decreasing peripheral vascular resistance (restricted blood circulation in the extremeties). This effect is particularly important in counteracting the vasoconstriction that occurs in heart failure. Vasodilators help in preventing the onset of pulmonary edema by reducing pulmonary venous pressure.
  Propranolol  improves the filling of the ventricles by prolonging the atrioventricular conduction time. When combined with Digoxin, it will decrease the ventricular rate in atrial fibrillation. Propranolol should not be used in cats with asthma, bradycardia, and some types of heart failure.
  Dubutamine  (i.e., Dobutex) is used for acute heart failure and is given intravenously by the veterinerian.

[...]

I know. I know. Don't tell me. I'm just killing myself, you say. But still, I can't help but feel like I let her down by not catching this. To find out that there were available methods of prevention like this after the fact... It just...it hurts. I wish I had caught the signs. There were some, but the way in which those signs were presented to me themselves seemed trivial, unrelated, and so dissimilar to this untrained eye.

To that end, let me herein list those signs as they appeared to me, so that others may recognize them in their own cats, and hopefully, prevent what happened to my cat from happening to your own. At the same time, researching this as much as I can, somehow, makes me feel better. With this knowledge, it's that much less likely to happen again. And, as much as it hurts finding out all that I might have been able to do towards prevention and care, it also helps to understand it, and to know just what, exactly, happened to my cat.

Additional - 10/31/00: I now realize that what was going to happen to Raisen was going to happen no matter what. Unless this had perhaps been caught early on - like in her kittenhood - and actions taken back then, there was really nothing I could towards making her better. To what length would never be known. You see, the above medications only go so far - and that is to stabilize at best what is already happening. It does not prevent. It does not eliminate the disease. The disease always stays, being genetically pre-programmed. The best I could every hope to do would only to prolong her life by some amount. Still, I would have taken that. In all of Raisen's life, I don't think this disease caused her any physical pain or discomfort. At least, nothing that was noticeable in this cat-so-perky.

In the last couple months before her death, some slightly odd things were occuring that I never really picked up on. I hope they help you. They were:

  1. Regarding `labored breathing.' This was not directly indicated. I mean, she wasn't panting, or lying on her side wheezing, or showing any signs of a struggle breathing, or like that. However, in looking back, it was...indirectly. In the last few months before Raisen died, I did notice that she was starting this season to come in more often, when she usually wanted to stay outside for as long as possible. First, it was only once every few days. Then, it became two or three times a day, wanting in and out of the house. And when she'd come in, she'd simply walk into the kitchen and lie down upon the cool linoleum floor, there. Minutes later, I supposed after she'd "cooled down," she'd want back out again. This should have been my first clue. But, I get short of breath on hot days when I exert myself. I'm a little older and I'm not the same. I understand it and what I do when it hits. However, I should have recognized it. She was probably going through the same thing, only because her heart wasn't working right and wasn't getting enough oxygen around her system. I made the mistake of "generalizing" this into the category of "just getting older, and not being able to do the same things as you could when you were 13." As well, it did not seem to be affecting her all that greatly. And she kept wanting back out again...

  2. Regarding `lethargy and lameness.' No, there were no direct signs of lethargy or inability to get around in this cat. She remained just as playful, just as energetic, and in fact she often challenged me to chase her about, just as always. And even without me involved, she'd still get those `weird' momentary, halted, devillish stares, with those mischievous, backward-pointing ears, just before darting off to places in the house chasing ghosts as she always did. She still romped, ran, and played with Muffin about the house. Even an hour before she died, she still jumped up on that kitchen sink and then waited for me to turn on the faucet for her. Then jumped down again. However, there were certain very low-key `odd' things that I'd notice. When Raisen would come up to the table and give me that look, liking the smell of what was on the table, I'd sometimes pick her up and put her on the table. She knows she's not supposed to be up there, and the idea was to start an instinctive pattern of thought in her brain. "I'm not supposed to be up here, I'd better get down" - and that she'd always do. Begging period over. 8^) However, a few days before she died, instead of hopping off of the table, she did something she never did before. She instead just laid down on the table. But, at the same time, she gave me that "I'm not playing this game, stupid" look. So there we ate, this cat lying on the table. On another occasion, the night she died, I was sitting in a particular recliner, near the kitchen. After I sat down, she came over and sat down in front of me just a few feet from my feet, in a place she never usually rested before. Maybe normal. Maybe not. On the other hand, five minutes before she died, I play-chased her down the hall into my room, too. (I now realize that this very act may have been the one which started her on her way. I increased her body effort, but the heart in it's current state would not have been able to compensate for that `stress.')

  3. Regarding `wheezing.' No obvious wheezing noises noted - that you could hear from, say, standing up right above your cat, or something. However, when sleeping very close to my face at night, in bed, I would notice a barely perceptable wheezing noise from the nose. I attributed this to the same sound I make sometimes, which often goes away and depends upon whether you need to blow your nose or not. As well, with her, this also went away, and would come back randomly, but never sounded really bad.

  4. Regarding `paralysis.' No obviously interpretable signs of paralysis. But in the last couple weeks before her death, another strange thing. She'd suddenly rush out of the litter pan scraping her buttucks across the floor. To me, while tempted to yell at her for that, a second thought made me think perhaps she just had a bit of hard feces that just didn't quite "exit" just the right way, causing her minor irritation that she was trying to fix the only way an animal could think of to fix, not being in the habit of toilet paper as we. I also thought "perhaps I need to change the litter pan." So, I changed the litter pan. Then it happened again about a week later. And again a week after that. Perhaps what I was actually witnessing might be a paralysis of her hind legs brought on by the strain of going? I have no idea. I've also discovered recently that it could also mean something else much less serious - but still probably requiring a visit to the vet for fecal examination and some minor medication. I should probably take Muffin to the vet to have her feces examined, too, since it could be transferrable by common use of the litter pan.


More About `Hypertrophic Cardiomyopathy (HCM)'
c/o Todd L. Sherman/KB4MHH
Gainesville, Alachua Co., Fla.
E-mail: afn09444@afn.org
Page created: October 24, 2000.
Last updated: October 31, 2000.

© Copyright 2000 by Todd L. Sherman. All Rights Reserved.


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