Liz Bode

Hi Nathalie,

Here is the original paper that describes this technique:

Schober LAu velocity

I use the oblique left-parasternal view to get it – the paper has images and described the techniques nicely.

Liz

Yes, that is right OAVRT is the same as Wolf-Parkinsosn-White or an accessory pathway 🙂

Patterson, 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:

Consensus statement

Hope that is helpful.

Liz

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.

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 🙂