Liz Bode
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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
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
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