Liz Bode
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Hi Camilla,
Thank you for the positive feedback. I am glad you are enjoying it so far.
I didn’t go into to detail with regards these definitions as they are either echo based or flow based and there was quite a lot to cover already. In terms of SAS and PS mild/moderate/severe is based on the pressure gradient across the valve on echo. Both conditions are classified as follows:
mild is 20-50 mmHg
moderate is 50-80mmHg
severe is >80 mmHg
You need Doppler echocardiography in order to grade them as above. Murmur grade does tally, as I think I mentioned, but treatment with atenolol or intervention should only be done based on echo findings.In terms of the VSDs a restrictive VSD is very small, such that there is only a low volume of blood crossing it. This means that there is not a significant degree of volume loading as the volume of blood crossing the VSD is small. This VSD is restrictive to flow and so doesn’t cause issues. An unrestrictive VSD is a large defect that does volume load the heart (usually the left side of the heart as the VSD is high in the septum and so the right side of the heart does not ‘see’ this extra blood). We base our decisions a little on size, but also ratios of flow across the aortic and pulmonic valve, which can be done on echo (although in humans they do it in the catheter lab, which is much more accurate) and also how the heart looks on echo.
Hope that makes sense?
Liz
Hi Nathalie,
Interesting case. This dog is a B1 until it reaches the criteria for both LA and LV. That being said if it has a flail leaflet then it needs very close monitoring and I would probably see it back in 3 months.
In terms of LA size it could be either or both possibilities you mention. If it is hypertensive then this will worsen the mitral regurgitation and you might find the LA gets smaller once it is normotensive as the LA pressure will decrease. The flail leaflet will also worsen MR and cause LA dilation and it might be that the LV has not caught up yet in terms of remodelling. Pimobendan would help reduce the mitral annulus size and amount of MR but this is only temporary and the heart will get bigger again so I’d wait until stage B2 to start it.
Liz
Hi Nathalie,
The screening of CKCS in the UK using MV prolapse is in its infancy. I haven’t been on the course yet as only a few people can go each time and it wasn’t run last year due to Covid. You can find more information on the kennel club website but the screening process is loosely based on the Danish screening which has been published – Lisbeth Olsen is the first author. Decision to breed isn’t based on age just on degree of prolapse and the UK use a traffic light system, which is different to Denmark. It is quite difficult to measure the prolapse repeatedly according to my colleagues, hence why the KC insist on cardiologists going on training days. In Denmark, Lisbeth Olsen is the only person that measures the prolapse! She must be a busy lady.
Liz
Hi Thita,
Good question! I think an acceptable heart rate in a dog or cat on atenolol would be less than 150bpm in a cat and equal to or less than 120bpm in a dog. Depending on the age of the dog, and severity of the SAS, I would not follow up a mild case (if adult) but I would follow up a moderate every year and a severe every 6 months. If the dog isn’t adult then I would recheck around 18 months of age to evaluate the severity again.
In terms of the PDA, I am not sure where you are, but some cardiologists are closing very small dogs (<2kg) and PDAs with either coils (old fashioned technique that can still be useful) or with a new device called an AVP II, which you place via the femoral/ jugular vein as that vessel is bigger. If neither of these are a possibility, some surgeons will ligate very small puppies so if the owner can afford to, and you have potential access to a surgeon that is happy to do this, then that would also be an option. If not, then there is nothing pre-heart failure that you can do other than ask the owner to monitor resting respiratory rate. I would probably monitor this dog every 6 months until CHF and every 3 months thereafter.
I hope that is helpful 🙂
Liz
This is a very good question. There is a paper on troponin I in doxo treated patients, published in mid-2000s and they showed that it wasn’t an effective marker for myocardial injury following doxorubicin. It does go up, but in dogs where it is increased there was no correlation with those that suffered clinically significant myocardial damage. However, it did go up prior to the echo findings of DCM-phenotype. We don’t routinely track it in patients receiving doxo, but I would measure it in a dog where I was worried about the possibility, probably more of an academic exercise though.
Hi Nathalie,
I am not aware of this product nor any literature that has validated it. I assume we can get it in the UK. I have just read the promotional literature and I would have a couple of concerns/ things to consider if I were to use it:
1. an abnormal result is >900 so this could not be used in Doberman to look for occult disease
2. some animals, like the Labrador, can have hugely increased NT-proBNP (in the 1000’s) and this is normal for them so not all cases would have CHF at this level (obviously any abnormal result would need following up anyway)
3. I think we are in a position where we need some sort of breed reference ranges for Nt-proBNP in the dog, although this is not a criticism of this test but something to think about for all of them.I would be interested to know if anyone is using this test and if they are there experiences with it and if anybody knows of any supporting literature?
Liz
Hello,
I tend to use >6.5mm for all breeds (at least that is the reference point I have in my head, but really rely on other measurements for confirmation of DCM), but I would use breed reference ranges where at all possible.
I measure it from the short axis, but no reason why you can’t do it from the long axis. I only use this method as that is how I was trained, and for no better reason than that. As long as you are repeatable within your own method (so you always do the measurement from the same view) then this is fine. It becomes more of an issue when you change between views. I also do not use anatomic m-mode – if I can’t get a good view then I don’t measure it. Occasionally, I might use anatomic m-mode to give me an impression, but I have never taken my measurements from it, although other cardiologists I know will.
Hope that helps,
Liz
Thanks Nathalie,
BAR means bright, alert and responsive – sorry, forgot to replace that abbreviation!
Liz
It’s entirely up to you, I’m happy with either. If no posts arrive here in next 24-48hours I’ll release the next details of the case 🙂
Hi Francois,
Don’t worry, we recorded it and just need to edit etc so will be available for everyone soon 🙂
Liz
Hi Nathalie,
False tendons are tricky! Generally I think if a cat has HCM we see a more widely distributed HCM rather than a very focal thickening as would be associated with a false tendon. However, there are instances were the false tendon inserts more towards the base of septum and that region can be focally thickened – this is tricky as it could be associated with the false tendon or be true focal HCM.
I am not sure how much thickening a false tendon can cause as such, I would imagine only a mm or less really. I think in these cases, before calling it focal HCM we need to do serial follow-up examinations over a period of months-years. I would see a cat back with query HCM every 6-9 months for repeat examinations (as long as it wasn’t too stressed). This obviously does not help if you are breed screening as then the breeder can’t breed from that cat, but this is all we can do! We can never be 100% sure on the first examination either way.
Hope that answers your question, it is definitely a difficult one.
Liz
Hi Magda,
Thank you for your questions. Yes, generally I would advise IV antibiotics 30 mins pre-dental and then every 90 mins. I actually found these really nice guidelines (which are really nice for dental procedures generally) that talk about using antibiotics with different grades of peridontal disease:
There has only been a link with endocarditis in dogs with sub-aortic stenosis and not any other valve disease, which is good to know. This is different to people where they tend to get endocarditis of the mitral valve!
In terms of systemic hypertension, my first go to drug in both dogs and cats is amlodipine. Although, it does depend on the underlying cause of hypertension and the severity. An ACE inhibitor might be used if the dog was hypertensive due to CKD with PLN, for example. I find ACE inhibitors do not do very much (although they can be added to amlodipine if that isn’t effective). The ACVIM have a very nice consensus statement on this:
Hope that is helpful 🙂
Liz
Hi 🙂
Some great questions! I’ve used rivoraxaban for longer, it’s not licensed in cats and these cats are on borrowed time so as long as the owner is happy I’d continue with it.
Yes, furosemide can be antagonised by NSAIDs and it can, therefore, contribute to resistance. They see it in humans. I’m not aware of any reports in the veterinary literature and although it is a consideration it is not something I worry about too much. If his renal function is fine on bloods and BP ok then it’s one of the only analgesics that will make a difference in this case. I’d just advise the owner to monitor RRR carefully. You can always stop the NSAID if needed. Hopefully, if he has just hurt his paw a little he might only need a couple days treatment. Other thing you could do is give a slightly lower dose.
Liz
This is a very good question. There are several problems with this test (or what I think could be problems):
This is a new test looking for HCM in Sphynx cats run by NC state – so first thing is they are the only centre so you have to get the kits from them or at least post the samples to the USA.
They have only just published this paper (in February) – I have not read it yet, but it is very odd that a test would be commercially available PRIOR to the publication being released.
It is in American Sphynx cats and we know, for example, that the Boxer ARVC genetics seem slightly different between USA and UK.
It only detects 60% of cats with HCM – so in the Sphynx there must be other genes that cause it.
If an owner really wanted to go ahead with the test then they could go ahead but I am not sure at the present time I would be advocating it for screening. I would want more validation form other countries first.Liz
Hi Nathalie,
I have never seen a normal left atrium in a cat in CHF, even with large volumes of pleural effusion – the only time I might expect to see this is with endocarditis of the aortic valve where the pressures have risen so suddenly that the LA has not had chance to dilate.
If the pleural effusion was that large as to cause left atrial tamponade I would expect the cat to die fairly quickly. It is thought to be possible to get left sided heart failure with a very large pericardial effusion due to LA tamponade, but again I think the animal would be very near death if this were to happen and I have never seen it or heard of my colleagues having seen it. So, theoretically a large pleural or pericardial effusion could cause tamponade of the LA and then the LA might look a more normal size (if the LA was squashed by the effusion), but I think this would be extremely rare.
Liz
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