"yngver" wrote in message
...
On Dec 9, 11:43 pm, "Phil P." wrote:
"yngver" wrote in message
I'm sorry for the delay response- I've been really busy. I'm nursing a cat
whose in pretty bad shape, so I have a little time. She was attacked by a
dog. When we x-rayed and echoed her to look for internal damage, we found a
bullet in he side! That's probably why the dog was able to catch her. I
think she'll be alright.
Its probably underdiagnosed because not many necropsies are preformed on
cats with HCM and/or MR because the COD is already known. Fibrosis of
the
anterior mitral valve leaflet is also common in HCM cats with MR.
I came across this by Neil Harpster- DACVIM-Cardiology- he was director of
cardiology at Angell for many years: "The prevalence of degenerative changes
affecting the left AV valve leaflets in the cat is significant, for
myxomatous degeneration is common in all forms of cardiomyopathy. However,
myxomatous degeneration can also be found in some cats not exhibiting the
classic or clearcut findings of cardiomyopathy."
Do you know whether there is any way to tell whether the valve problem
is caused by the HCM or not?
I don't know if there's a way to distinguish a primary valve disease
from
one that occurs secondary to HCM in a cat with HCM.
I guess that's basically what the cardiologist was saying as well, but
that most likely it's the HCM that caused the mitral valve leaflet to
thicken.
The jet might be smaller in a cat with MR secondary to HCM- But I have an
older human machine with a frame rate that's probably too slow to compare
the differences acurately in cats with warp-speed hearts.
If I remember correctly, her last measurements weren't really that bad-
could you post them again along with the most recent measurements - Did you
happen to get photo printouts or a video of the echo?
The diagnosis of HCM is based on "LV
size, wall thickness, and systolic function are normal, with a normal
FS%, except for a mild focal hypertrophy (.61-.62 cm) of the basal IVS
with a small bulge into the LVOT.
The small buldge in the LVOT could be a fibrous contact plaque. The
white
arrow in the photo:
http://maxshouse.com/Cardiology/LVOT.jpg
See how close the plaque is to the anterior mitral leaflet (AMVL in the
photo)
So there is no way to tell which caused which, the bulge causing the
leaflet to thicken through contact or vice versa.
The septal leaflet is a lot bigger than than the posterior (parietal)
leaflet- this can make the septal cusp *seem* thick.
http://maxshouse.com/Cardiology/left...ular_valve.jpg
Do you know if she did the echo herself or did she just interpret the
results? Is she basing her diagnosis of HCM solely on the septal bulge?
No SAM or LVOT
obstruction." (initial echo showed mild SAM with mild LV outflow tract
obstruction 50 mm Hg,
50 mm Hg is very mild.
That's good to know. It's gone or greatly reduced now, she said.
now eliminated by the atenolol). If I
understood correctly, my vet seemed to be saying that this bulge
interferes with the function of the mitral valve and that could cause
it to thicken. Does that sound plausible?
Yes-- if the mitral valve leaflet keeps hitting the ventricular septum
it
could become fibrotic..
http://maxshouse.com/Cardiology/mitr...al_contact.jpg Follow
the
arrow from SAM
The cardiologist said the
important thing is that the report was good and the atenolol is
improving heart function by decreasing the LVOT and secondary mitral
regurgitation.
That's the important thing! MR produces a feedback loop- "MR begets MR"
and
can lead to CHF.
I thought the atenolol would stop the MR, but it hasn't.
It wouldn't if there's a problem with the leaflets or some other component
of the valve.
This report gives MR Vmax and MR maxPG figures but those were not
reported in the first echo so I can't see how much it's been reduced.
This says MR Vmax 3.94 m/s.
I realize I should probably just be happy that the HCM hasn't
progressed but I'm a bit bewildered by the mention of the valve
problem. The first report mentioned a thickened mitral valve leaflet
and mild MR but it was presented to me as part of the HCM.
That's probably because mitral regurgitation and fibrosis of the
anterior
mitral valve leaflet almost always occur secondary to LVOT obstruction
in
cats with HCM- They're considered part of HCM.
Okay, thanks. That seems to be have a better prognosis than primary
valve disease.
This second
report says "there is still mitral valve thickening and mild secondary
mitral regurgitation" which almost sounds to me as though the
cardiologist expected this to improve or disappear with the atenolol.
I'm not sure why it would, however.
Did she mention anything about the papillary muscles or chordae
tendineae?
No, and I'm assuming if there were something abnormal there she would
have. Everything else in the report is listed as normal: left atrium,
right ventricle, right atrium, aortic valve, tricuspid valve, pulmonic
valve, pericardium, aorta (ascending and arch), pulmonary artery, all
normal. LA/Ao 1.15.
Is this something I should ask her about?
Yes. If the chordae tendineae are short (or long) or thick- or extend into
the cusp, they can prevent the MV from closing properly. Abnormal or
displaced papillary muscles (which anchor the chordae tendineae and MV) that
don't contract properly can also cause MR.
http://maxshouse.com/Cardiology/feline_heart.jpg
Don't cardiologists normally
look at the papillary muscles when diagnosing HCM, so am I right in
assuming she must have done so?
I wouldn't take anything for granted. If they're normal- she should have
said they're normal especially since they are components of the MV apparatus
in a cat with MR.
Your comments are most appreciated--thanks so much, Phil.
-yngver
The report really doesn't sound too bad- I wouldn't be too upset.
Best of luck,
Phil
Thanks, Phil. Your assessment that the report doesn't sound very bad
means a lot to me, since I know you have a lot of experience in this
area. Thanks for helping me feel better about this.
-yngver
Don't forget to post the first echo - if you can.
Best of luck,
Phil