Liz Bode
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Hi 🙂
Some great questions! I’ve used rivoraxaban for longer, it’s not licensed in cats and these cats are on borrowed time so as long as the owner is happy I’d continue with it.
Yes, furosemide can be antagonised by NSAIDs and it can, therefore, contribute to resistance. They see it in humans. I’m not aware of any reports in the veterinary literature and although it is a consideration it is not something I worry about too much. If his renal function is fine on bloods and BP ok then it’s one of the only analgesics that will make a difference in this case. I’d just advise the owner to monitor RRR carefully. You can always stop the NSAID if needed. Hopefully, if he has just hurt his paw a little he might only need a couple days treatment. Other thing you could do is give a slightly lower dose.
Liz
This is a very good question. There are several problems with this test (or what I think could be problems):
This is a new test looking for HCM in Sphynx cats run by NC state – so first thing is they are the only centre so you have to get the kits from them or at least post the samples to the USA.
They have only just published this paper (in February) – I have not read it yet, but it is very odd that a test would be commercially available PRIOR to the publication being released.
It is in American Sphynx cats and we know, for example, that the Boxer ARVC genetics seem slightly different between USA and UK.
It only detects 60% of cats with HCM – so in the Sphynx there must be other genes that cause it.
If an owner really wanted to go ahead with the test then they could go ahead but I am not sure at the present time I would be advocating it for screening. I would want more validation form other countries first.Liz
Hi Nathalie,
I have never seen a normal left atrium in a cat in CHF, even with large volumes of pleural effusion – the only time I might expect to see this is with endocarditis of the aortic valve where the pressures have risen so suddenly that the LA has not had chance to dilate.
If the pleural effusion was that large as to cause left atrial tamponade I would expect the cat to die fairly quickly. It is thought to be possible to get left sided heart failure with a very large pericardial effusion due to LA tamponade, but again I think the animal would be very near death if this were to happen and I have never seen it or heard of my colleagues having seen it. So, theoretically a large pleural or pericardial effusion could cause tamponade of the LA and then the LA might look a more normal size (if the LA was squashed by the effusion), but I think this would be extremely rare.
Liz
Hi Nathalie,
I always give it twice a day as it has a half life of approximately 3.5 hours (although heart rate was still reduced in normal cats 12 hours post-pill in one study). I will give the liquid version to cats and small dogs too. Always up-titrate and down-titrate atenolol over a week or so – you can’t start and stop these drugs suddenly as you need to give the heart time to acclimatise to them or without them. I would usually start or stop them over 5-7days.
Absolutely, use the gelatin capsules to give more than one tablet – clopidogrel and furosemide or clopidogrel and atenolol, whatever works best for the client 🙂
Liz
Hi Nathalie,
Here is the original paper that describes this technique:
I use the oblique left-parasternal view to get it – the paper has images and described the techniques nicely.
Liz
Hi Ewelina,
Hope you are finding this useful and glad you got to see this surgery a little last week. Hopefully there will be more!
It is indeed a great example of the Branham reflex. When we have a PDA, there is an overall increase in cardiac output to account for the run off of blood across the PDA. When we close the PDA there is a momentary increase in systemic blood pressure which stimulates the baroreceptors (thought to be the ones in the left ventricle) and causes activation of the parasympathetic nervous system. This then slows the heart rate.
Meanwhile diastolic pressure will increase and mean arterial blood pressure will elevate slightly. This is because we have closed the PDA and there is now more blood within the arteries during diastole, elevating diastolic blood pressure (there is no run-off through the PDA – having a PDA is like pumping a bike tyre up that has a hole in it – there is a constant leak, close the hole and the pressure within the tyre is maintained). We can see the effect here on the record.
If you were to feel the femoral pulse before the procedure it would be hyperdynamic. A PDA causes a greater pulse pressure (the difference between the systolic and diastolic blood pressure), mainly because the diastolic blood pressure is lower. Close the PDA and the pulses will get weaker to feel (they will actually be normal) as the diastolic pressure increases, reducing the pulse pressure.
Hope that makes sense!
Liz
Yes, that is right OAVRT is the same as Wolf-Parkinsosn-White or an accessory pathway 🙂
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 🙂
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