Liz Bode
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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
Hi Nathalie,
I always give it twice a day as it has a half life of approximately 3.5 hours (although heart rate was still reduced in normal cats 12 hours post-pill in one study). I will give the liquid version to cats and small dogs too. Always up-titrate and down-titrate atenolol over a week or so – you can’t start and stop these drugs suddenly as you need to give the heart time to acclimatise to them or without them. I would usually start or stop them over 5-7days.
Absolutely, use the gelatin capsules to give more than one tablet – clopidogrel and furosemide or clopidogrel and atenolol, whatever works best for the client 🙂
Liz
Hi Nathalie,
Here is the original paper that describes this technique:
I use the oblique left-parasternal view to get it – the paper has images and described the techniques nicely.
Liz
Hi Ewelina,
Hope you are finding this useful and glad you got to see this surgery a little last week. Hopefully there will be more!
It is indeed a great example of the Branham reflex. When we have a PDA, there is an overall increase in cardiac output to account for the run off of blood across the PDA. When we close the PDA there is a momentary increase in systemic blood pressure which stimulates the baroreceptors (thought to be the ones in the left ventricle) and causes activation of the parasympathetic nervous system. This then slows the heart rate.
Meanwhile diastolic pressure will increase and mean arterial blood pressure will elevate slightly. This is because we have closed the PDA and there is now more blood within the arteries during diastole, elevating diastolic blood pressure (there is no run-off through the PDA – having a PDA is like pumping a bike tyre up that has a hole in it – there is a constant leak, close the hole and the pressure within the tyre is maintained). We can see the effect here on the record.
If you were to feel the femoral pulse before the procedure it would be hyperdynamic. A PDA causes a greater pulse pressure (the difference between the systolic and diastolic blood pressure), mainly because the diastolic blood pressure is lower. Close the PDA and the pulses will get weaker to feel (they will actually be normal) as the diastolic pressure increases, reducing the pulse pressure.
Hope that makes sense!
Liz
Yes, that is right OAVRT is the same as Wolf-Parkinsosn-White or an accessory pathway 🙂
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