Liz Bode
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Here is a link to the notes for this lesson too;
Any problems let me know.
Liz
Hi Areti,
In cats with CHF of any cause I would now use furosemide and clopidogrel only. Possibly spironolactone too as we haven’t any good evidence for or against this currently. There was a recent paper by King et al (2019) that showed no benefit of ACE inhibitors either in CHF or pre-clinically.
In pre-clinical HCM I don’t use anything. In severe HOCM I do use atenolol still.
Hope you have a lovely weekend,
Liz
That all sounds good. If they’re normal then it’s likely to be the case and I wouldn’t be too concerned. Fractional shortening is a poor marker of systolic function as it’s affected by so many variables so I’d rely more on chamber dimensions in this case and if the owner wants to pursue it I’d look at other markers of systolic function.
I have in my head (anecdotally) that I get a few advice requests with Labs and cardiac silhouette queries and they generally turn out to be normal. Occasionally we see tricuspid valve dysplasia/ mitral valve dysplasia or degeneration and sometimes DCM but relatively rare for the latter compared to other breeds. Always good to check it out though.
Liz
Hi Emma,
Good question!
It really depends on your premed, induction and inhalational agents. There are many publications on the effects of various sedative agents on heart function. Generally, things like opioids do very little, even ACP and alfaxalone. Obviously, any alpha2 can, especially on systolic function.
Generally, I think that GA does not overly affect heart size but it will have the potential to alter systolic (and perhaps diastolic) function. Therefore, if chamber sizes are normal then they are normal, but you cannot tell anything about systolic function from your echo.
If the dog had increased chamber size then this may be real. However, I would always want to repeat an echo without sedatives/ GA if any abnormalities were present, where possible.
Hope that helps a little.
Liz
Hi Areti,
I can help with your NT-proBNP question 🙂
An abnormal result of >270pmol/l in a cat with signs of dyspnoea (this is an abnormal result on a SNAP test) is highly specific for CHF. The SNAP test will also pick up an abnormal result if levels are 150-270 and again in a cat with clinical signs of CHF this is specific.
A SNAP test should be followed up by a quantitative test where possible.
As a screen for heart disease NT-proBNP is less effective in cats without clinical signs. Specificity and sensitivity are between 80-95% depending on the cut-off used. If you get a high result – >150 in a cat with a murmur (although as you know cats with HCM don’t always have murmurs) a gallop or arrhythmia then the cat probably has heart disease. Although a cat with an arrhythmia almost certainly has heart disease anyway! A result of 50-100pmol/l probably means that it doesn’t have HCM BUT cats with heart disease do occasionally have low results.
If you can perform echo, even just a basic echo, this is superior to NT-proBNP but I’m aware that this isn’t available to everyone.
I wouldn’t advocate using NT-proBNP as a screening tool generally. However, where your suspicion of heart disease is high and owners won’t go for an echo straight away it could be a good tool to use – and if it’s high it might make owners opt for an echo.
Hope that helps!
Liz
Hi Emma,
Some great questions. The best place to look for a protocol when treating dogs and cats with heart worm is the American Heartworm Society – they have very detailed guides, regularly updated and a ‘how to’ protocol. I have also written a webinar which you should have access to 🙂
https://www.heartwormsociety.org
A positive Elisa should be confirmed with additional tests as false positive are found and melarsomine is not a nice drug!
Treatment really depends on the severity (how symptomatic the dog is) of heart worm. Dogs that are symptomatic should get steroids, doxy, macrocyclic lactones and melarsomine (you can get it in UK but needs to be imported). Thromboembolic disease is usually caused by the worms themselves so possibly why clopidogrel/ aspirin aren’t advised.
Hope that is helpful.
Liz
Hi all,
I, obviously, love a heart worm case – although I have only ever seen one case of it in the UK. I have had advice calls about them and seen some cases when I was doing an externship in US. The case I saw was also a rescue from Romania and presented to me OOH as a resident in Edinburgh (where you’d least expect heart worm to be) with 3rd degree AV block. When we imaged it there was endocarditis (unrelated to heart worm, but probably myocarditis as an extension of the endocarditis was the cause of the AV block – the aortic valve is anatomically very close to the AV node). We took bloods and, routinely, did blood smears which a student looked at first for me – they came back to say they could see worms!!! We were so surprised – there were loads of microfilaria squirming around in the dog’s blood! We treated the heart worm, endocarditis and the dog did much better than we thought. The 3rd degree AV block even resolved and so we did not need to place a pacemaker.
Just thought I’d share a case with a more positive outcome ?
Liz
Hi Kerida,
Andy might be able to help with video posting here as I’m not sure. Other option would be to use the clinical advice service and submit them through there. You have advice credits with your membership. If that’s tricky email them to liz@vtx-cpd.com
Let me know if any issues
Liz
Hi Kerida,
Thanks for uploading the history and the radiographs to the discussion forum, what an interesting case!
I think there is evidence of some cardiomegaly, particularly at the base on the laterals. You can’t really see the right atrium on these as it is buried in the middle of the cardiac silhouette (unless v severe tricuspid dysplasia, which cats do not often get and this is the wrong age). It is hard to confirm specific chamber enlargement on the DV as the silhouette is effaced by the lung pattern. I see what you mean on the left lateral, there looks like there is some sort of mass cranio-dorsal to the heart. I can’t see this on the Dv, but the slight rotation makes it hard to look at the right-cranial thorax. The heart is rounder on the left lateral, but I think we tend to see this so can’t read too much into that.
The lung pattern is diffuse broncho-interstitial with a greater interstitial component in the caudo-dorsal lung fields.
You don’t mention any murmur/ arrhythmia/ gallop so I assume that these are not present?My DDx would be:
Oedema – cardiogenic vs non-cardiogenic superimposed on feline asthma type pathology
Infection – bronchopneumonia
Possible mass in cranial thoraxIs there any way this cat could have a FAST scan of the thorax to rule in/out cardiomegaly and a mass? I think that would be the single most useful test here?
What did you decide to do with the cat in the end? Interesting that the brother died of resp issues too…
I would be very interested to see what others thought 🙂
Liz
Hi Scott,
The medics are behind the curve 😉 Cardiologist’s have been using gabapentin in cats for ages pre-echo. It works for some and not for others (although always worth a try) and we tend to use a dose of 50-100mg/cat 1-2 hours pre-appointment. I think we also need to be careful in cats with renal disease as it is exclusively. excreted via the kidneys. I thought there had been an abstract on echo parameters and gabapentin, but I can’t find one. There has, however, been one on trazadone and they found that it worked in some cases and avoided the need for other sedatives. However, it did significantly lower BP (although BP was taken in cats prior to use so it makes sense that BP would be lower after trazadone if they are less stressed!). I’ve never used trazadone in cats though.
Liz 🙂No problem 🙂 That sounds like a cool case. I always think comparing what you find to the human literature is super interesting, so you would want to do that. If there are any case reports/ case series of similar things in the veterinary literature you would want to compare your case to those too (if there aren’t you might consider writing this up!). If there was anything unusual about this case or things you didn’t do due to financial limitations then talk about this in the discussion too.
Hope that helps.
Liz
Hi Annette,
Case report writing can be really tricky. You have to do a few for your Cert. Here are some of my tips;
– make sure it has some structure – signalment, history, clinical exam (thoroughly reported and if something was normal state that), problems, differentials, diagnostics, treatment, discussion etc
– structure your differential list as you point out and highlight the most likely differentials for the problem. Put them in order of likelihood.
– during the case report state why certain differentials are excluded by your findings
– you can group differentials together or state that things like anorexia are due to the underlying condition.
– don’t reference apart from in the discussion (only very rarely do you need to reference elsewhere)
– state facts and only discuss aspects of the case in the discussion
– stick to the word count
– follow the guidelines that they provide you (you’ll be amazed how often people don’t do this)
– it doesn’t have to be a perfect case but where there are gaps due to e.g. financial limitations make sure you point these outHope that is helpful 🙂 good luck and remember you can post any interesting cases you have one here.
Best wishes
Liz
Well done Scott, definitely something to be proud of. Danielle is a legend and I learnt so much from her as a resident.
Liz
Hi Sophie,
Excellent questions. The individual variability in dogs with DCM wasn’t tested but I’d imagine it would be the same as the healthy dog. You could serial sample in dogs where you were suspicious of heart disease (generally speaking this is where a dog has a murmur – it is rare to see heart disease without a murmur in a dog, unlike a cat). NT-proBNP has been used to track changes in dogs with mitral valve disease for example and I believe the RVC is looking at this currently. So if a client can’t afford repeated echo then you could consider doing this, but I’d always advise echo for monitoring if you can just to avoid false positives and false negatives with NT-proBNP.
In the ACVIM discussion one of the authors of the Lab paper said the following; “I think more breed-specific information on NT-proBNP would be very useful – although a low index of individuality for NT-proBNP has been reported (as we also found in Labradors – see above), meaning that the individual variability is low compared to the group and individual changes over time may be masked by the background “noise” of the wider population.
That suggests that we should probably track individual changes rather than compare one dog to a population reference. However, I think that’s rather impractical in most cases where people use NT-proBNP for disease screening (certainly common in UK practitioners), so a reference interval should be a guide that is considered less useful than tracking a trend in one dog if they are considered high risk (family history, equivocal echo, etc).”
Hope that’s helpful.
Liz
I think both theories are in their infancy, but there appears to be growing evidence for a role of both these theories. The cardioprotective theory involves the intralipid being able to improve myocardial metabolic function, even reversing some of the effects of ischaemia, which will provide more energy for the heart. It also enhances some calcium handling within the heart which improves inotropy and repairs any lost function present that may have been caused by cardiotoxic drugs. Most evidence appears to be in the use of anaesthetics in people.
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