Liz Bode
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Hi Julie (and Camilla),
That’s actually a very useful link for me Camilla, thank you.
I’ve no experience with this machine or heard of it. I see that Camilla gives it an excellent review and, for abdomens, it certainly looks like it would do an excellent job.
I have one main concern about using it for heart scans in cats though. It looks like it has a huge footprint which means you won’t get it to sit nicely between the ribs which will make image quality poor and you will probably get quite frustrated.
Camilla, would this be a fair assessment? Please feel free to contradict me as I’ve not used it.
Liz
Hi,
I would expect some improvement in that time frame. It’s not a hard and fast rule but that time gives the heart enough chance to start repairing.
Liz
It was a homemade one. We know that golden retrievers are prone to taurine deficiency even on normal diets, so definitely something to consider. In the USA they are seeing what they think are cases of DCM associated with grain-free or more unusual meats (kangaroo for example) and there is lots of research into the area currently. We don’t seem to see the same in UK or EU but we need to be aware of this too! Always get a good diet history in any cardiac case 🙂 if people are interested there is a questionnaire you can give owners here;
Lots of useful info there.
Liz
Liz
Hi,
Thanks for you comments. The radiographs show marked cardiomegaly with mixed interstitial-alveolar pattern predominantly in the caudodorsal lung fields but also ventrally in cranial lung fields (almost an aspiration type pattern here). The pulmonary veins and arteries are prominent. These findings are consistent with pulmonary oedema secondary to heart failure. In my experience large breed dogs can cough with pulmonary oedema, especially Dobermanns! So this could be the cause of the cough, but the cranial lung lobes do have a very ventral interstitial-alveolar pattern that could be consistent with some aspiration too. However, we treated him for CHF with furosemide, pimobendan and once stable ACE inhibitor (benazepril) and spironolactone and his cough resolved (although this could be coincidence).
This dog was markedly taurine deficient and we supplemented this. When we saw him back 3 months later his heart looked like this:And we actually managed to wean him off furosemide and eventually pimobendan! If they have a truly taurine deficient DCM then we can see this dramatic remodelling. However, sometimes dogs (and cats) will be taurine deficient with DCM and we supplement with taurine and their hearts do not remodel like this. It is very case dependent and needs good follow-up.
Cool case 🙂
Liz
Hi Thita,
Thank you for the questions.
In terms of taurine we usually start at 500mg PO BID but the dose range is wide at 500-1000mg BID to TID. You can recheck taurine blood levels after 3 or so months but the test is expensive to run. I would expect improvement after 3 months but some might respond sooner than this. On echo you would see a smaller heart with improved systolic function.
In terms of anti-thrombotics at the moment I would always choose clopidogrel as that is the drug we have most evidence for. However, if I were to add a drug on top then I would probably choose rivaroxaban as it is cheaper then low molecular weight heparin and is given orally. If the cat was difficult to medicate then I’d stick with the injectable LMWH though.
Hope that helps.
Liz
Hi Nathalie,
It might depend on which assay is being used -it would be interesting to know if they differed between labs (although I assume that whoever taught you on the ESAVA course uses the high-sensitivity assay too). The Idexx assay is highly-sensitive and so I would follow their instructions if that is who you use. If I am not analysing troponin immediately then I will separate the serum and cool, yes. However, that is because I use Idexx for my samples.
I am not aware of any literature on this though. I will have a look!
Liz
Hi Nathalie,
Generally, it has to be severe PHT to cause syncope. I will cover this a little in lesson 6, but in dogs with significant structural heart disease, especially MMVD then syncope is usually preload related, triggering neurocardiogenic syncope. Of course, it could be a combination of things so mild-moderate PHT with high preload, making syncope more likely. I would worry that this dog was in, or very close to CHF and that the PHT was left-heart related. In a syncopal patient such as this I would also do a Holter to evaluate for the possibility of an arrhythmia or to document any bradycardia associated with a syncopal event. If the syncopal events are initiated with coughing etc than it is likely tussive syncope (although I would still Holter these patients too).
Liz
Thanks all for the discussion and questions. My answers are as follows to the case:
The views show:
1. Right parasternal 4 chamber long axis – demonstrates a dilated LV and LA, with a slightly dilated right side (in the normal animal the right side should be 1/3-1/2 the size of the left, in this dog the right side is almost a 1/3 so if the left side is big the right side must also be a little big to maintain the proportions). The LV is round and subjectively hypokinetic and this can be appreciated on the short axis view too. The mitral valve is slightly thickened and appears tethered (doesn’t open properly).
2. Right parasternal 4 chamber long axis with colour over mitral valve – shows a central jet of mitral regurgitation.
3. M-mode at level of papillary muscles shows a hypokinetic septum with relatively normal free wall (posterior wall) motion.
4. Right parasternal short axis view at the level of the left atrium/ aorta demonstrates a markedly dilated LA.The ECG shows sinus rhythm throughout.
I’m not sure I can evaluate PA size on the last view as I can see the body of the left atrium and the auricle, which is dilated. However, there was tricuspid regurgitation at 3.7m/s indicating mild pulmonary hypertension.
There should be relatively normal cardiac output in this case as systolic blood pressure has been maintained and so this can’t explain why the aorta might be a bit smaller (if it is at all – we would need a better view of the pulmonary artery first to evaluate this).
The aortic annulus does look a little bit strange but I think that this is because there is a coronary artery appearing in this view.
Endocarditis lesions do not always produce those nodular/ thickened looking valves that we are used to seeing they can look relatively normal so cannot always exclude based on echo (I don’t particularly like ‘hunt the endocarditis’ in a pyrexia of unknown origin for this reason, unless more obvious things have been excluded first or the animal has a new murmur etc).
My echo diagnosis would be – DCM-phenotype with probable degenerative mitral valve disease. I think it is more likely a DCM-phenotype because of the central jet of MR and the depressed systolic function of the septum. Although it can be difficult in large breed dogs as MMVD can also reduce systolic function.
Our DDx for a DCM-phenotype would be:
Primary DCM
Tachycardia-induced (a dog paced at 180bpm for 4 weeks will develop heart failure. You can also develop this with intermittent tachyarrhythmias as long as they increase your mean heart rate significantly).
Myocarditis – acute or chronic (if chronic and normal troponin then you wouldn’t know this unless you did a biopsy – however the treatment is the same whatever the pathology in this case)
Diet induced (including taurine deficiency).
A shunt is possible, but less likely and I would only do a bubble study if the right side showed changes consistent with pulmonary hypertension).Further tests:
Taurine
Thoracic radiographs
A Holter could also be consideredResults:
Taurine 7umol/l (ref range 50-180 umol/l) measured in this case due to diet AND because we know Golden Retrievers seem to suffer from taurine deficiency that causes DCM.
Thoracic radiographs:How would you interpret these results and radiographs and what treatment would you advise?
I look forward to reading your answers.
Liz
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
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