"yngver" wrote in message
...
On Dec 7, 11:37 am, "Phil P." wrote:
"yngver" wrote in message
...
We just had our six month follow up echo for our cat who was diagnosed
with very mild HCM in May. I'm having trouble understanding the
results and I hope you can shed some light while I wait to hear back
from the cardiologist to clarify.
Our cat was diagnosed with mild HCM with mild LV outflow tract
obstruction and secondary mitral regurgitation, also mild thickening
of the anterior mitral valve leaflet. She had a grade 2 murmur. She
has been on atenolol, 1/4 tablet twice a day which lowered heart rate
to 140-150 (goal range) and eliminated the murmur.
These latest echo results show no progression of the HCM, no SAM, no
LVOT obstruction, no heart murmur. However, what I don't understand is
that the cardiologist said the mitral valve is thicker (moderate now
vs. mild) and there is still mild mitral regurgitation. I was told
this is separate from the HCM. The conclusion was "Stable disease.
Potential for progression of mitral insufficiency. Recheck echo in one
year."
I'm having trouble understanding what is causing the mitral
insufficiency if it isn't from HCM. My vet just said the cardiologist
didn't explain it so he will have to talk to her. She did write "there
has been no significant change in the degree of LV hypertrophy or any
other cardiac size measurements" so I thought at first that meant
nothing had gotten worse.
I hope Phil reads this and can comment, or anyone else who has any
ideas on what this means. I haven't been able to find anything about
this kind of valve problem in cats. Thanks for any advice.
-yngver
Mitral insufficiency can occur as a primary condition or secondary to
HCM.
Mitral insufficiency in cats is almost always caused by thickening of
the
valve leaflets which prevents the valve from closing properly. This
allows
blood to leak through the valve from the left ventricle to the left
atrium
during systole (regurgitation). Thickening of the valve leaflets can be
independent of HCM and is usually caused by myxomatous degeneration
(myxomatous atrioventricular valvular degeneration) which is usually
progressive-- however, the rate of progression can be very slow. I don't
know of any drug that slows the progression of mitral valve
degeneration.
I'm sorry I can't be more helpful.
Best of luck,
Phil
Thanks, Phil. Since posting I did hear back from the cardiologist. She
explained that whether the mitral valve leaflet is mildly or
moderately thickened is just her visual impression at the moment and
didn't necessarily mean anything had changed over time. She felt that
whether the thickening is mild or moderate is insignificant. She said,
just as you have, that the thickening could be an independent process
or could be caused by the HCM, due to the outflow obstruction. She and
my vet seemed to think that it's far more likely with a cat to be
caused by HCM than independent valve disease. Myxomatous degeneration,
as you mention, seems to also be called endocarditis
Endocardiosis - not endocarditis. Endocarditis is inflammation of the valve
leaflets.
and I couldn't
find anything about it in cats, except that it's very rare or some
sources say it is non-existent in cats. My vet says he's never seen a
case of it in a cat.
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.
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.
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)
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.
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.
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.
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?
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