Liz Bode
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Hi Nathalie,
Interesting case and one of those where there is no clear answer. You can hear flow that is faster than 2m/s and the fact that this is MR means that, in reality, flow must be faster than this to reflect the LV pressure (above 5 m/s as long as normotensive). Therefore, what you are hearing is coming from this regurgitation and it is likely due to a degree of dysplasia given age etc (presuming no other abnormalities).
I think what you have advised is a good option. However, you might not see any progression in such a short timeframe, as you have pointed out. Then it is really up to the breeder – all you can advise is that there is likely a degree of dysplasia, which appears mild and not clinically significant at present. The dog is likely not to progress further unless he develops valve degeneration too (and even then may not progress significantly!). Recommendations would be not to breed from this dog (as he is male and will sire many litters potentially – if he were female you might think otherwise as few litters and could be bred to a male that had been screened too). Ultimately, it is up to the breeder though and all you can do is advise.
This is always a tricky conversation!
Liz
Yes, good point about the hypovolaemia and heart rate. The heart rate is fast side of normal so dehydration rather than hypovolaemia might be possible, but these are low on the Ddx list. I try and list my DDX in order of likelihood as this is good practice when writing case reports etc and when thinking about cases (although I didn’t do that great a job for this case 😉 ).
Francois – a point-of-care ultrasound of the thorax and abdomen are ALWAYS going to be the correct answer for any case! They are some of my most favourite diagnostics. They give you so much information really quickly and then the other tests can follow them as necessary. I didn’t mention them here as the dog appeared pretty stable for further examinations (at present at least…).
I’ll answer everything else once others have had time to look through the videos.
Liz
Hi all,
Great answer!
So the problems were:
Lethargy and exercise intolerance
Coughing
Grade 3/6 left apical systolic murmur
Grade 2/6 right apical systolic murmur
hypodynamic femoral pulsesThe lethargy and exercise intolerance are likely related to the underlying disease process, as Nathalie mentioned.
Coughing – has a long list of differentials. I generally split into upper and lower respiratory tract. Upper respiratory tract: infectious, neoplastic, compression and lower respiratory tract: eosinophilic bronchopneumopathy, chronic bronchitis, cardiogenic pulmonary oedema (although controversial),bronchial compression, infectious (inc parasitic), bronchopneumonia, neoplastic.
Grade 3/6 left apical systolic murmur: MMVD, DCM (yes, a DCM murmur could be a grade 3/6), endocarditis, dysplasia
grade 2/6 right apical: radiation from the left sided murmur, TV degeneration, pulmonary hypertension causing tricuspid regurgitation, TV dysplasia.
hypodynamic pulses: poor systolic function (DCM), hypovolaemia, hypotension due to another cause, shock (although dog does not fit with clinical picture of shock)Further initial diagnostics:
Bloods – haematology, biochemistry, electrolytes, cardiac troponin I and possibly thyroid panel
Blood pressure as possibly hypotensive
ECG
Echocardiography for murmur
Thoracic radiographs given coughingThe results for some of these:
Bloods were all within normal limits including troponin
blood pressure 124 mmHg
ECG – sinus tachycardiaHere is the echocardiography (hopefully this works and they will play when you download them!!)
What is your diagnosis based on the subjective assessment of these videos? What other tests might you consider after these findings?
Liz 🙂
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
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