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yngver
December 5th 07, 08:38 PM
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

Phil P.
December 7th 07, 05:37 PM
"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

yngver
December 7th 07, 10:41 PM
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 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.

Do you know whether there is any way to tell whether the valve problem
is caused by the HCM or not? 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. No SAM or LVOT
obstruction." (initial echo showed mild SAM with mild LV outflow tract
obstruction <50 mm Hg, 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? 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.

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. 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.

Your comments are most appreciated--thanks so much, Phil.
-yngver

Phil P.
December 10th 07, 05:43 AM
"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/mitral_valve-septal_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

yngver
December 10th 07, 04:55 PM
On Dec 9, 11:43 pm, "Phil P." > wrote:
> "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.

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 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.
>
> 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/mitral_valve-septal_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.
>
>
>
> > 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? Don't cardiologists normally
look at the papillary muscles when diagnosing HCM, so am I right in
assuming she must have done so?
>
>
>
> > 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

Phil P.
December 18th 07, 09:59 AM
"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_atrioventricular_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/mitral_valve-septal_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

yngver
December 18th 07, 07:49 PM
On Dec 18, 3:59 am, "Phil P." > wrote:
> "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.

That's terrible, worse even than the cat we rescued who was shot with
a bbgun. I'm glad to her she will 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."
>
I suppose it depends on whether the HCM diagnosis is clearcut.
>
>
>
> > > > 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?

No, I didn't get a photo printout or video, just a copy of the
cardiologist's report.

Here is the first report:
Repost--

Here is the summary:
Overall left ventricle systolic function is normal with FS% greater
than 35%. The left ventricle size is normal. Left ventricular free
wall thickness is normal. Mild asymmetric septal hypertrophy with
bulge of basal IVS into the LV outflow tract. Mild SAM with mild LV
outflow tract obstruction (<50 mm hg).

The left atrium, right ventricle, right atrium all normal in size and
function. Aortic valve normal. No aortic stenosis or regurgitation.
Tricuspid valve, pulmonic valve, pericardium, aorta, pulmonary aorta
all normal.

Mild thickening of the anterior mitral valve leaflet. Mild mitral
regurgitation present, predominately a posteriorly directed jet.

Values:
2D
IVSd .55 cm
LVPWd .54 cm
(aren't these normal values? They are less than .6 cm.)
Ao diam 1.05 cm
LA diam 1.25 cm
LA/Ao 1.19

M-Mode
IVSd .51 cm
LVIDd 1.44 cm
LVPWd .47 cm
IVSs .71 cm
LVIDs .60 cm
LVPWs .90 cm
EDV(Teich) 5.46 ml
ESV (Teich) .51 ml
EF (Teich) 90.67%
%FS 58.23%
SV (Teich) 4.95 ml

Doppler
AV Vmax 2.67 m/s
AV maxPG 28.47mmHg
PV Vmax 1.27 m/s
PV maxPG 6.48 mmHG

Grade 2/6 systolic murmur L apex, gallop; mm pink; normal pulses.

ECG rhythm: Sinus rhythm.

Cardiac size wnl. Pulm vasc. wnl. Lungs wnl. (rads)
Diagnosis: Mild hypertrophic cardiomyopathy with LV outflow tract
obstruction and secondary mitral regurgitation. Normal LA size so low
risk of CHF/LA clot at this time. Recommend Tx with beta-blocker
Atenolol (6.25 mg BID) to decrease LVOT obstruction and secondary
mitral regurgitation.
********************************************
Second report, at six months:

2D
IVSd .61cm
LVPWd .48 cm
Ao diam 1.19 cm
LA diam 1.37 cm
LA/Ao 1.15

M-Mode
IVSd .59 cm
LVIDd 1.34 cm
LVPWd .49 cm
IVSs .78 cm
LVIDs .57 cm
LVPWs .87cm
EDV(Teich) 4.47 ml
ESV (Teich) .45 ml
EF (Teich) 89.99%
%FS 56.97%
SV (Teich) 4.02 ml
Ao Diam 1.12 cm
LA Diam 1.29 cm
LA/Ao 1.16
RVIDd .79 cm
RVIDs .61 cm
HR 151.68 bpm

Doppler
MR Vmax 3.94 m/s
MR maxPG 61.99 mmHg
AV Vmax .70 m/s
AV maxPG 1.96 mmHg
PV Vmax .51 m/s
PV maxPG 1.06 mmHG

(these last values have diminished quite a bit, which I assume is
good, right? Or is this just due to a slower heart rate?)

ECG and Radiographic findings:
PE: no murmur or gallop. MM pink, pulses wnl. Lung sounds wnl.

Findings:
Sinus rhythm.
Left ventricle: 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. No SAM or
LVOT obstruction.
Mitral valve: The mitral valve is thickened. Moderate thickening of
the anterior mitral valve leaflet. Mild mitral regurgitation is
present, predominately a centrally directed jet.
(does it mean anything that in the previous echo it was a posterior
directed jet?)
All other findings normal: left atrium, right ventricle, right atrium,
aortic valve, tricuspid valve, pulmonic valve, pericardium, aorta,
pulmonary artery.

Diagnosis: compared with the findings of the previous study, there has
been no significant change in the degree of LV hypertrophy or in any
other cardiac size measurements. There is no LV outflow turbulence or
obstruction on the Atenolol. There is still mitral thickening and mild
secondary mitral regurgitation. Recommend continue Tx with Beta-
blocker Atenolol (6.25 mg BID) to keep the HR lowered which will
decrease LV obstruction and secondary mitral regurgitation. Stable
disease since 5/07. Potential for progression of mitral insufficiency
due to mitral valve thickening. No apparent cardiac contraindications
for anesthesia at this time. Recheck ECHO in one year to assess
progression; sooner if problems.
************************************************** *******************************
>
>
> > > 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_atrioventricular_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?

The cardiologist travels among several cat clinics (and I guess "dog
and cat" clinics too) and brings her ultrasound equipment with her.
They don't let the owner come in the room but from what I could see
through the window, she did the echo herself while an assistant holds
the cat down. Unfortunately this means the owner doesn't get to talk
to the cardiologist directly. The vet comes out and tells you the
report. Then when I had question, he called her to discuss it with her
and let me know what she said. I assume the way the report is written,
the diagnosis is based on what she is calling mild focal hypertrophy
of the basal LVS with small bulge into the LVOT.
>
>
>
> > > 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/mitral_valve-septal_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.
>
My vet said there isn't any way to make the mitral valve leaflet get
thinner, so my assumption is the goal of treatment is to prevent
further thickening. Of course he is not a cardiologist.
>
>
>
> > > > 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.

I will ask. I'm surprised she didn't mention this then. I have a
suspicion, however, that the written reports she gives the vet (which
is he gives me when I ask for a copy) is just a summary of her
complete findings. I've seen considerably briefer reports than this
one posted on the feline heart group.
>
> > > > 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

Thanks, Phil. I've posted both reports for your comparison. When you
have a chance to take a look, I'd appreciate your impression.

I was thinking of trying a different cardiologist, but I've been told
by several other owners of HCM cats that this one is good, and
recommended by the nearest veterinary school. There is only one other
veterinary cardiologist in the area that I could find, and I don't
know if he is any better.
-yngver

Phil P.
December 19th 07, 03:02 PM
"yngver" > wrote in message
...
> On Dec 18, 3:59 am, "Phil P." > wrote:
> > "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.
>
> That's terrible, worse even than the cat we rescued who was shot with
> a bbgun. I'm glad to her she will be alright.

She's doing really well. I think she'll be ready to go into foster next
week- that's if I don't fall in love with her!

The bullet my vet took out looks like a .22 or .25. I really want to find
the shooter so I can return his bullet to him....



> > 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?
>
> No, I didn't get a photo printout or video, just a copy of the
> cardiologist's report.

At the next check up, ask the vet if she can make a video or photo printout.
You can use them to get second opinions without having to get you cat
scanned. You can also send them to some of the top guns like Kittleson.


>
> Here is the first report:
> Repost--
>
> Here is the summary:
> Overall left ventricle systolic function is normal with FS% greater
> than 35%. The left ventricle size is normal. Left ventricular free
> wall thickness is normal. Mild asymmetric septal hypertrophy with
> bulge of basal IVS into the LV outflow tract. Mild SAM with mild LV
> outflow tract obstruction (<50 mm hg).
>
> The left atrium, right ventricle, right atrium all normal in size and
> function. Aortic valve normal. No aortic stenosis or regurgitation.
> Tricuspid valve, pulmonic valve, pericardium, aorta, pulmonary aorta
> all normal.
>
> Mild thickening of the anterior mitral valve leaflet. Mild mitral
> regurgitation present, predominately a posteriorly directed jet.
>
> Values:
> 2D
> IVSd .55 cm
> LVPWd .54 cm
> (aren't these normal values? They are less than .6 cm.)
> Ao diam 1.05 cm
> LA diam 1.25 cm
> LA/Ao 1.19
>
> M-Mode
> IVSd .51 cm
> LVIDd 1.44 cm
> LVPWd .47 cm
> IVSs .71 cm
> LVIDs .60 cm
> LVPWs .90 cm
> EDV(Teich) 5.46 ml
> ESV (Teich) .51 ml
> EF (Teich) 90.67%
> %FS 58.23%
> SV (Teich) 4.95 ml
>
> Doppler
> AV Vmax 2.67 m/s
> AV maxPG 28.47mmHg
> PV Vmax 1.27 m/s
> PV maxPG 6.48 mmHG
>
> Grade 2/6 systolic murmur L apex, gallop; mm pink; normal pulses.
>
> ECG rhythm: Sinus rhythm.
>
> Cardiac size wnl. Pulm vasc. wnl. Lungs wnl. (rads)
> Diagnosis: Mild hypertrophic cardiomyopathy with LV outflow tract
> obstruction and secondary mitral regurgitation. Normal LA size so low
> risk of CHF/LA clot at this time. Recommend Tx with beta-blocker
> Atenolol (6.25 mg BID) to decrease LVOT obstruction and secondary
> mitral regurgitation.
> ********************************************
> Second report, at six months:
>
> 2D
> IVSd .61cm
> LVPWd .48 cm
> Ao diam 1.19 cm
> LA diam 1.37 cm
> LA/Ao 1.15
>
> M-Mode
> IVSd .59 cm
> LVIDd 1.34 cm
> LVPWd .49 cm
> IVSs .78 cm
> LVIDs .57 cm
> LVPWs .87cm
> EDV(Teich) 4.47 ml
> ESV (Teich) .45 ml
> EF (Teich) 89.99%
> %FS 56.97%
> SV (Teich) 4.02 ml
> Ao Diam 1.12 cm
> LA Diam 1.29 cm
> LA/Ao 1.16
> RVIDd .79 cm
> RVIDs .61 cm
> HR 151.68 bpm
>
> Doppler
> MR Vmax 3.94 m/s
> MR maxPG 61.99 mmHg
> AV Vmax .70 m/s
> AV maxPG 1.96 mmHg
> PV Vmax .51 m/s
> PV maxPG 1.06 mmHG
>
> (these last values have diminished quite a bit, which I assume is
> good, right? Or is this just due to a slower heart rate?)

Actually, the IVS and LVFW have increased just a tad.


>
> ECG and Radiographic findings:
> PE: no murmur or gallop. MM pink, pulses wnl. Lung sounds wnl.
>
> Findings:
> Sinus rhythm.
> Left ventricle: 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. No SAM or
> LVOT obstruction.
> Mitral valve: The mitral valve is thickened. Moderate thickening of
> the anterior mitral valve leaflet. Mild mitral regurgitation is
> present, predominately a centrally directed jet.
> (does it mean anything that in the previous echo it was a posterior
> directed jet?)
> All other findings normal: left atrium, right ventricle, right atrium,
> aortic valve, tricuspid valve, pulmonic valve, pericardium, aorta,
> pulmonary artery.
>
> Diagnosis: compared with the findings of the previous study, there has
> been no significant change in the degree of LV hypertrophy or in any
> other cardiac size measurements. There is no LV outflow turbulence or
> obstruction on the Atenolol. There is still mitral thickening and mild
> secondary mitral regurgitation. Recommend continue Tx with Beta-
> blocker Atenolol (6.25 mg BID) to keep the HR lowered which will
> decrease LV obstruction and secondary mitral regurgitation. Stable
> disease since 5/07. Potential for progression of mitral insufficiency
> due to mitral valve thickening. No apparent cardiac contraindications
> for anesthesia at this time. Recheck ECHO in one year to assess
> progression; sooner if problems.
>
************************************************** **************************
*****
> >
> >
> > > > 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_atrioventricular_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?
>
> The cardiologist travels among several cat clinics (and I guess "dog
> and cat" clinics too) and brings her ultrasound equipment with her.
> They don't let the owner come in the room but from what I could see
> through the window, she did the echo herself while an assistant holds
> the cat down. Unfortunately this means the owner doesn't get to talk
> to the cardiologist directly. The vet comes out and tells you the
> report. Then when I had question, he called her to discuss it with her
> and let me know what she said. I assume the way the report is written,
> the diagnosis is based on what she is calling mild focal hypertrophy
> of the basal LVS with small bulge into the LVOT.


This may seem like a funny question-- but does she strike you as more
academic than intuitive? I have a reason for asking.



> >
> >
> >
> > > > 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/mitral_valve-septal_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.
> >
> My vet said there isn't any way to make the mitral valve leaflet get
> thinner, so my assumption is the goal of treatment is to prevent
> further thickening. Of course he is not a cardiologist.
> >
> >
> >
> > > > > 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.
>
> I will ask. I'm surprised she didn't mention this then. I have a
> suspicion, however, that the written reports she gives the vet (which
> is he gives me when I ask for a copy) is just a summary of her
> complete findings. I've seen considerably briefer reports than this
> one posted on the feline heart group.

I don't think she wrote it-- it looks like the computer generated the
report. My machine does the same thing- prints out a canned report based on
the scans. The academic vets let the machines diagnosis the patients. An
intuitive vet uses the machine as a tool.



> >
> > > > > 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
>
> Thanks, Phil. I've posted both reports for your comparison. When you
> have a chance to take a look, I'd appreciate your impression.
>
> I was thinking of trying a different cardiologist, but I've been told
> by several other owners of HCM cats that this one is good, and
> recommended by the nearest veterinary school. There is only one other
> veterinary cardiologist in the area that I could find, and I don't
> know if he is any better.
> -yngver

Thanks for reposting the report. Too bad they didn't give you a photo or
video, I was hoping to see if the bulge in the septum was really due to
focal hypertrophy or if its due to just a sharper-than-average angle in the
septum. In cats, the top of the septum curves towards the RA just about at
the point of the septal cusp of the MV. (See:
http://maxshouse.com/Cardiology/feline_heart.jpg) If the septum curves at a
sharp angle, it can produce a bulge without any actual hypertrophy. I think
this could be the case with your cat because at .55 cm, the septum wasn't
hypertrophied anywhere near enough to cause SAM and LVOT obstruction by
itself- actually, the IVS was and still is practically normal.

The SAM & LVOT obstruction resolved even though the IVS thickness increased
because the atenolol decreased the acceleration of blood ejected from the
LV-- which in turn reduced the pressure that was pushing the MV leaflet into
the LVOT.

I'm not a vet, but if you want my opinion, get a second opinion. Your cat
probably doesn't even have HCM- I think the problem is only in the MV
apparatus- probably just the septal leaflet. Thickening of the valve leaflet
is also a component of mitral dysplasia. Something else to look into.

The cardiologist's machine should have recording capabilities- probably CD.
Get a video copy next time so you can get opinions from top shelf
cardiologists without taking your cat out of the house-- that's assuming the
echoes are halfway decent!

Please keep me posted.

Best of luck,

Phil

yngver
December 19th 07, 05:18 PM
I'm cutting some of this out because it's getting too long to follow.

On Dec 19, 9:02 am, "Phil P." > wrote:
> "yngver" > wrote in message
>
> > That's terrible, worse even than the cat we rescued who was shot with
> > a bbgun. I'm glad to her she will be alright.
>
> She's doing really well. I think she'll be ready to go into foster next
> week- that's if I don't fall in love with her!
>
> The bullet my vet took out looks like a .22 or .25. I really want to find
> the shooter so I can return his bullet to him....

I agree. I take it the bullet didn't hit anything vital. I'm surprised
a cat can survive a gunshot wound.

That's a bit of sore spot with me anyway--when I was a kid one of the
neighbor kids shot my mother's beloved dog. Thought it was funny.
>
>
> At the next check up, ask the vet if she can make a video or photo printout.
> You can use them to get second opinions without having to get you cat
> scanned. You can also send them to some of the top guns like Kittleson.

I could ask at the next heart recheck, which is in three months, but
that's just when our vet checks heart rate and blood pressure. He
could find out whether the cardiologist made a video. Otherwise our
cat is not due for another echo for a year, and I'm not sure I want to
wait that long.
>

>
> > Here is the first report:
> > Repost--
>
> > Here is the summary:
> > Overall left ventricle systolic function is normal with FS% greater
> > than 35%. The left ventricle size is normal. Left ventricular free
> > wall thickness is normal. Mild asymmetric septal hypertrophy with
> > bulge of basal IVS into the LV outflow tract. Mild SAM with mild LV
> > outflow tract obstruction (<50 mm hg).
>
> > The left atrium, right ventricle, right atrium all normal in size and
> > function. Aortic valve normal. No aortic stenosis or regurgitation.
> > Tricuspid valve, pulmonic valve, pericardium, aorta, pulmonary aorta
> > all normal.
>
> > Mild thickening of the anterior mitral valve leaflet. Mild mitral
> > regurgitation present, predominately a posteriorly directed jet.
>
> > Values:
> > 2D
> > IVSd .55 cm
> > LVPWd .54 cm
> > (aren't these normal values? They are less than .6 cm.)
> > Ao diam 1.05 cm
> > LA diam 1.25 cm
> > LA/Ao 1.19
>
> > M-Mode
> > IVSd .51 cm
> > LVIDd 1.44 cm
> > LVPWd .47 cm
> > IVSs .71 cm
> > LVIDs .60 cm
> > LVPWs .90 cm
> > EDV(Teich) 5.46 ml
> > ESV (Teich) .51 ml
> > EF (Teich) 90.67%
> > %FS 58.23%
> > SV (Teich) 4.95 ml
>
> > Doppler
> > AV Vmax 2.67 m/s
> > AV maxPG 28.47mmHg
> > PV Vmax 1.27 m/s
> > PV maxPG 6.48 mmHG
>
> > Grade 2/6 systolic murmur L apex, gallop; mm pink; normal pulses.
>
> > ECG rhythm: Sinus rhythm.
>
> > Cardiac size wnl. Pulm vasc. wnl. Lungs wnl. (rads)
> > Diagnosis: Mild hypertrophic cardiomyopathy with LV outflow tract
> > obstruction and secondary mitral regurgitation. Normal LA size so low
> > risk of CHF/LA clot at this time. Recommend Tx with beta-blocker
> > Atenolol (6.25 mg BID) to decrease LVOT obstruction and secondary
> > mitral regurgitation.
> > ********************************************
> > Second report, at six months:
>
> > 2D
> > IVSd .61cm
> > LVPWd .48 cm
> > Ao diam 1.19 cm
> > LA diam 1.37 cm
> > LA/Ao 1.15
>
> > M-Mode
> > IVSd .59 cm
> > LVIDd 1.34 cm
> > LVPWd .49 cm
> > IVSs .78 cm
> > LVIDs .57 cm
> > LVPWs .87cm
> > EDV(Teich) 4.47 ml
> > ESV (Teich) .45 ml
> > EF (Teich) 89.99%
> > %FS 56.97%
> > SV (Teich) 4.02 ml
> > Ao Diam 1.12 cm
> > LA Diam 1.29 cm
> > LA/Ao 1.16
> > RVIDd .79 cm
> > RVIDs .61 cm
> > HR 151.68 bpm
>
> > Doppler
> > MR Vmax 3.94 m/s
> > MR maxPG 61.99 mmHg
> > AV Vmax .70 m/s
> > AV maxPG 1.96 mmHg
> > PV Vmax .51 m/s
> > PV maxPG 1.06 mmHG
>
> > (these last values have diminished quite a bit, which I assume is
> > good, right? Or is this just due to a slower heart rate?)
>
> Actually, the IVS and LVFW have increased just a tad.

Well, I noticed that, but the cardiologist said no significant change.
I meant the AV Vmax, PV Vmax--these decreased significantly from the
first echo.
>
>
(snipped the conclusions in the echo)
>
> ************************************************** **************************
> *****

>
> > > 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?
>
> > The cardiologist travels among several cat clinics (and I guess "dog
> > and cat" clinics too) and brings her ultrasound equipment with her.
> > They don't let the owner come in the room but from what I could see
> > through the window, she did the echo herself while an assistant holds
> > the cat down. Unfortunately this means the owner doesn't get to talk
> > to the cardiologist directly. The vet comes out and tells you the
> > report. Then when I had question, he called her to discuss it with her
> > and let me know what she said. I assume the way the report is written,
> > the diagnosis is based on what she is calling mild focal hypertrophy
> > of the basal LVS with small bulge into the LVOT.
>
> This may seem like a funny question-- but does she strike you as more
> academic than intuitive? I have a reason for asking.

I can't really answer that because I never talked to her. My vet
conveys to me what she says. And that part bothers me, because I'd
rather talk to the cardiologist face to face. I couldn't find an
office listing for her, so I think she only sees cats and dogs by
referral traveling to the various clinics. I will send you her name by
email rather than post it, in case you or anyone you've worked with
has heard of her. She seems to come highly recommended on the feline
heart group, from what I could find.
>
>
>(more about the echo snipped)
>
> > > > > 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.
>
> > I will ask. I'm surprised she didn't mention this then. I have a
> > suspicion, however, that the written reports she gives the vet (which
> > is he gives me when I ask for a copy) is just a summary of her
> > complete findings. I've seen considerably briefer reports than this
> > one posted on the feline heart group.
>
> I don't think she wrote it-- it looks like the computer generated the
> report. My machine does the same thing- prints out a canned report based on
> the scans. The academic vets let the machines diagnosis the patients. An
> intuitive vet uses the machine as a tool.

Okay, that's interesting to me. I didn't know the computer could
generate a canned report. At least at our clinic, she did echoes on
five cats in one afternoon, so maybe to produce reports on that many
cats, she has to let the computer do it. I could tell some of the
language was picked up from the last report, but I glimpsed her in the
exam room doing what I thought was writing up a report. My vet told me
the cardiologist said she she didn't look at the previous scan when
she wrote up her impression of the mitral valve leaflet, which I also
thought was curious.
>
>
>
> > > > > > 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
>
> > Thanks, Phil. I've posted both reports for your comparison. When you
> > have a chance to take a look, I'd appreciate your impression.
>
> > I was thinking of trying a different cardiologist, but I've been told
> > by several other owners of HCM cats that this one is good, and
> > recommended by the nearest veterinary school. There is only one other
> > veterinary cardiologist in the area that I could find, and I don't
> > know if he is any better.
> > -yngver
>
> Thanks for reposting the report. Too bad they didn't give you a photo or
> video, I was hoping to see if the bulge in the septum was really due to
> focal hypertrophy or if its due to just a sharper-than-average angle in the
> septum. In cats, the top of the septum curves towards the RA just about at
> the point of the septal cusp of the MV. (See:http://maxshouse.com/Cardiology/feline_heart.jpg)

I looked at the jpg, but I couldn't really tell much myself.

If the septum curves at a
> sharp angle, it can produce a bulge without any actual hypertrophy. I think
> this could be the case with your cat because at .55 cm, the septum wasn't
> hypertrophied anywhere near enough to cause SAM and LVOT obstruction by
> itself- actually, the IVS was and still is practically normal.
>
> The SAM & LVOT obstruction resolved even though the IVS thickness increased
> because the atenolol decreased the acceleration of blood ejected from the
> LV-- which in turn reduced the pressure that was pushing the MV leaflet into
> the LVOT.
>
> I'm not a vet, but if you want my opinion, get a second opinion. Your cat
> probably doesn't even have HCM- I think the problem is only in the MV
> apparatus- probably just the septal leaflet. Thickening of the valve leaflet
> is also a component of mitral dysplasia. Something else to look into.
>
> The cardiologist's machine should have recording capabilities- probably CD.
> Get a video copy next time so you can get opinions from top shelf
> cardiologists without taking your cat out of the house-- that's assuming the
> echoes are halfway decent!
>
> Please keep me posted.
>
> Best of luck,
>
> Phil

Thanks, Phil. Now I have to think about what to do. I looked up mitral
dysplasia and read this is a common congenital abnormality in cats,
but it seems to me it's unlikely it would first show up in a cat at
age nine if she was born with it.
Also, if it is the mitral valve problem alone, wouldn't treatment be
pretty much the same--atenolol to reduce the MR and eliminate the SAM?
I am wondering if changing the diagnosis will make a difference in the
treatment plan. In other words, is this something I need to find out
right away to get proper treatment, or is it a case in which whether
it is HCM or mitral dysplasia, the course of the disease might be
about the same?

I want to mention one more thing to you--our cat has longstanding
asthma, well controlled with Flovent. One vet in the clinic, not my
regular vet, mentioned that asthma over many years can affect the
heart. Could there be a connection?

Thanks again for all your help, Phil.
-yngver

Phil P.
December 24th 07, 11:44 AM
"yngver" > wrote in message
...
> I'm cutting some of this out because it's getting too long to follow.
>
> On Dec 19, 9:02 am, "Phil P." > wrote:
> > "yngver" > wrote in message
> >


> > Actually, the IVS and LVFW have increased just a tad.


I probably wouldn't have said that if I knew she didn't look at the previous
echo. She probably didn't measure the same area as in the first echo.

>
> I can't really answer that because I never talked to her. My vet
> conveys to me what she says. And that part bothers me,


That would bother me too. I think you and your cat would be better off if
you consulted a specialist with whom you can communicate and ask questions
and
who can educate you about your cat's illness. The "traveling show vets"
don't talk to you because you're not paying them- your vet is. She bills him
for the
echo and he just marks it up. You cat isn't her patient- your vet is her
client. I don't like arraignments like that.


because I'd
> rather talk to the cardiologist face to face. I couldn't find an
> office listing for her, so I think she only sees cats and dogs by
> referral traveling to the various clinics. I will send you her name by
> email rather than post it, in case you or anyone you've worked with
> has heard of her.

I didn't get your email. Try it again: topcatATmaxshouseDOTcom


She seems to come highly recommended on the feline
> heart group, from what I could find.


How could anyone recommend her? She doesn't have any actual patients.



> > I don't think she wrote it-- it looks like the computer generated the
> > report. My machine does the same thing- prints out a canned report
based on
> > the scans. The academic vets let the machines diagnosis the patients. An
> > intuitive vet uses the machine as a tool.
>
> Okay, that's interesting to me. I didn't know the computer could
> generate a canned report. At least at our clinic, she did echoes on
> five cats in one afternoon, so maybe to produce reports on that many
> cats, she has to let the computer do it. I could tell some of the
> language was picked up from the last report, but I glimpsed her in the
> exam room doing what I thought was writing up a report. My vet told me
> the cardiologist said she she didn't look at the previous scan when
> she wrote up her impression of the mitral valve leaflet, which I also
> thought was curious.

So how could she make a comparison?



I was hoping to see if the bulge in the septum was really due to
> > focal hypertrophy or if its due to just a sharper-than-average angle in
the
> > septum. In cats, the top of the septum curves towards the RA just about
at
> > the point of the septal cusp of the MV.
(See:http://maxshouse.com/Cardiology/feline_heart.jpg)
>
> I looked at the jpg, but I couldn't really tell much myself.

Try this-- I outlined the curve in the septum in white:

http://maxshouse.com/Cardiology/angulated_septum%20copy.jpg


>
> Thanks, Phil. Now I have to think about what to do. I looked up mitral
> dysplasia and read this is a common congenital abnormality in cats,
> but it seems to me it's unlikely it would first show up in a cat at
> age nine if she was born with it.

Mitral dysplasia can be congenital or aquired. A cat could be asymptomatic
for years- or even life- depends on the severity.


> Also, if it is the mitral valve problem alone, wouldn't treatment be
> pretty much the same--atenolol to reduce the MR and eliminate the SAM?

There's more to HCM than MR & SAM.


> I am wondering if changing the diagnosis will make a difference in the
> treatment plan. In other words, is this something I need to find out
> right away to get proper treatment, or is it a case in which whether
> it is HCM or mitral dysplasia, the course of the disease might be
> about the same?


The course of the disease would not be the same.



>
> I want to mention one more thing to you--our cat has longstanding
> asthma, well controlled with Flovent. One vet in the clinic, not my
> regular vet, mentioned that asthma over many years can affect the
> heart. Could there be a connection?

I don't think there's any connection. Untreated asthma could lead to cor
pulmonale- but that involves the right side of the heart. There's no
evidence in echo report.


>
> Thanks again for all your help, Phil.
> -yngver

I wish you and your cat a happy holiday

Best of luck,

Phil