Liz Bode
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Hi Nathalie,
Interesting case, happy for you to email me a video if you would like (liz@vtx-cpd.com).
It sounds like you have done a comprehensive cardio work-up and, if the heart does not show a large right side on echo, then I think you can exclude a R-L PDA at this point. An MEA shift does usually occur with a R-L PDA, but I wouldn’t rely on this finding. Interesting that the HR was 90bpm, have you done a Holter? I would if there is the money to do one, just to make sure you have excluded (as much as you can at the moment) an underlying arrhythmia.Liz
Hi everyone,
SO, I was going to post a case this week for you to think about. However, I closed a PDA today and we got a really cool anaesthesia record (I might do a SM post on it at some point as the physiology is cool). Hopefully this will work and you will be able to see a picture. The purple arrow represents device deployment in the PDA with occlusion. The red line is the systolic BP, green line the diastolic BP and the blue the heart rate.
Can any body explain what is happening here? How might the pulses change if you were feeling them during this time, from just before device deployment to just after?
It might not be very useful clinically (sorry) but I love physiology and think this is cool…Plenty more time for cases over the coming weeks.
Liz 🙂
Hi Francois,
Another good question, and you raise a good point. Why is it that we can hear a gallop sound in an aged cat, but I have never heard one (or seen it documented) in an old dog? Their ventricles will age the same and become stiffer over time? I wonder if it is more to do with heart rate – the faster the rate the more likely we are to hear a gallop sound (hence why we hear them more commonly in cats)? I can’t find the answer though. In dogs gallop sounds are mostly associated with the presence of DCM.
Sorry I am not much more help!
LizPatterson, many years ago, bred a colony of dogs that had PDAs and reversed PDAs. He found that the ones that reversed generally did so within the first 6 months of life. There will be a spectrum of disease – some animals will be born with the PDA and it will be shunting R to L due to abnormal pulmonary vasculature that they are born with, some will have a L-R shunting PDA for weeks or months but if the ductus is large (and they may also have concurrently abnormal pulmonary vasculature) then Eisenmenger’s develops and the shunt reverses (this usually occurs in the first 6 months as I mentioned) and there will be a few (but this is very much the minority) that will have a L-R PDA in to adulthood but then they develop lung disease that causes pulmonary hypertension and then they get shunt reversal. If the shunt is not reversed at birth, or shortly after birth, then a continuous murmur will be heard which will then diminish as the shunt reverses. If the dog develops a R-L shunting PDA at birth or shortly after then it will have a quiet or no murmur.
In terms of echo – you can have pulmonary hypertension and not have TR – the new consensus statement from ACVIM has a table that gives you info on how to diagnose PHT in the absence of TR or pulmonic regurgitation. In my experience it is very unusual for a dog with marked pulmonary hypertension not to have elevated TR (apart from those dogs with polycythaemia where the blood flow is too slow). Acceleration of pulmonic flow is very easy to over interpret and I would not rely on it at all. Dogs with chronic PHT should all have RV remodelling.
You can still see the PDA in these reversed dogs, it is just harder to spot as you can’t rely on colour as much. I was involved in a study that was published recently in rPDA:Reverse PDA in dogs – outcomes
and the consensus statement is here:
Hope that is helpful.
Liz
I am not aware of the use of sotalol in such cases, and I wouldn’t use it for this, personally. It is mainly a potassium channel blocker although it does have some non-selective beta blocking effects too – it has two isomers l and d and the l isomer is the beta blocker (at lower doses) and the d is the potassium channel antagonist (at higher doses). I think the main point here would be that it is non-selective, whereas atenolol is a selective B1 blocking agent and there is no reason to block any channels that are involved with generation of the action potential as you are not targeting an arrhythmia (unless the dog had a concurrent arrhythmia, but atenolol could also be trialled in this case).
Other brachycepahlic breeds have been shown to have them too, especially French bulldogs. There are other forms of coronary anomalies too that have been reported in all sorts of breeds, not necessarily causing pulmonic stenosis though. Brian Scansen has done a very nice review of these in JVC.
Eisenmenger syndrome suggests a group of signs and symptoms, and is most commonly used. Eisenmenger complex is a subset of ES where there is a VSD with severe pulmonary hypertension and shunt reversal with cyanosis. Eisenmenger physiology is synonymous with syndrome (I believ).
Hope that clears that up for you.
Liz
Another good question.
So, ideally we would do it in a younger dog, not necessarily size related but before the myocardium remodels and becomes fibrosed. You are right that the cutting balloons are small (8mm maximum). The aortic annulus will be greater than 8mm in many dogs (even young ones), but we are using it across the stenotic region. Therefore, in some animals the stenotic region might be <8mm. The Kleman et al (2012) technique report suggested that they still used the balloon in larger breed dogs with lesions that were >8mm wide. They did conclude though that a wider cutting balloon would be ideal for large dogs.
We have no data about the usefulness or otherwise of this procedure, only that it is feasible. There are only a handful of case reports/ series and one pilot study on pulmonic stenosis. So, braver cardiologists may indeed use this technique in younger dogs. However, given that there is no long term data and the fact that it is a risky procedure (can cut the mitral valve, damage the myocardium, damage the aortic valve or even the aorta) I would not be jumping to do this in an asymptomatic young dog, and I am not sure many owners would if they knew we had no survival data on it. I might suggest it in a young dog that had arrhythmias/ syncope otherwise I would wait for the dog to develop clinical signs such as these (or CHF) before advising it. That being said we probably should mention it as a possibility to owners who have dogs with severe SAS whatever their age.
Liz 🙂
Good question. We can access the tricuspid valve easily enough via the external jugular vein or femoral vein. The left side is slightly trickier as we would have to go via a trans-septal puncture from the right atrium to the left atrium. There are case reports of this in dogs but it would usually need a human interventionalist involved to perform it. The other option is surgical repair with bypass which has been performed successfully. Mitral stenosis is pretty rare – I’ve only seen a couple of cases.
Here are this week’s suggested reading for you. The first three papers cover epidemiology of congenital diseases and how it’s changed in recent years and a closer look at outcomes of dogs that have minimally invasive procedures for pulmonic stenosis and PDAs.
Epidemiology of congenital heart disease
PS and outcomes
PDA and outcomesThe following is an in depth review of the classification of congenital heart diseases in cats (applicable to dogs too). You’ll need several cups of tea though!!!
Classification of congenital heart diseases
Happy reading 🙂
Liz
Hi,
There are a few resources online that I’ve found. The most comprehensive appears to be this one;
You have to sign up to get access but they are free.
Hope that helps.
Liz
Hi!
Lovely to hear from you so far. I really hope that you find this course useful. My plan post-Covid (if there is such a thing!)is to also do some echo courses with a couple of echo practical days. I’m always looking for feedback or suggestions of future topics so please feel free to post here too.
Liz
Hi Nathalie,
This is a good question! I think it comes down to the fact that if there was a murmur due to a VSD it is most likely going to be louder than that associated with relative pulmonic stenosis. As a VSD murmur and PS murmur both occur in systole you wouldn’t be able to hear the relative PS one, only the VSD. Relative PS will be very quiet. You hear a relative PS murmur associated with an ASD because there is no murmur from the ASD itself, the pressure in the atria is too low to cause one. Generally, you can only hear a murmur when velocity of blood flow is >2m/s.
Hope that makes sense!
Liz
Unfortunately, that is something we have to accept. It happens to me all the time too! If stroking the nasal planum does not help, and gabapentin doesn’t either then that is all you can do 🙂
Hi Nathalie,
Yes, that is correct. As the heart ages is gets stiffer and less compliant so you can here a gallop sound due to diastolic dysfunction in this group of cats, and this wouldn’t be pathological. Cats with a cardiomyopathy have stiffer ventricles (and so diastolic dysfunction) but this is pathological.
I don’t know if you perform Doppler echocardiography, but we can appreciate this on echo when we look at relaxation patterns. Cats with HCM and older cats (from around 10yrs) will have grade 1 diastolic dysfunction or an impaired relaxation pattern on E and A waves across the mitral valve. This is the stage of diastolic dysfunction BEFORE left atrial pressure rises.
Therefore, if we hear a gallop sound in an older cat we cannot know, without echo, if this is associated with a normal, aged heart or a heart with a cardiomyopathy.Hope that helps a bit.
Liz
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