A Cat Cardiology case to discuss :)

RE: A Cat Cardiology case to discuss :)

Dave Dickson — Tue, 19 Mar 2019 12:55:54 GMT

[quote user="Beats"] I share your curiosity as to whether these values would have stayed similar, decreased or increased over last year.[/quote]

I don't think a proBNP will change much know - in cats, proBNP tells us whether the animal is likely to have significant disease, with the emphasis on the negative test - ie a negative proBNP means the cat probably doesn't have bad heart disease. Not 100%, but pretty good. A positive proBNP means the cat needs an echo to know more. More false positives than false negatives as a rule.

However, once the cat is on a diuretic, proBNP will add nothing really. Also proBNP is not a marker of myocyte damage (it's a marker of LV stress/stretch) - troponin is the marker for myocyte damage.

Troponin tells us if there is ongoing myocardial damage but again, probably doesn't add much unless you suspect an active myocarditis or endocarditis.

For me, what I really want to know are the cats SRR, blood pressure, renal values and electrolytes. An echo would be really nice to know what the disease looks like, but given the current medication and provided it is clinically stable, we are unlikely to change anything. I generally don't use beta-blockers for most cat heart disease, particularly when they are in failure, but that is a different discussion!

The only other thing that occurs to me is to check about anti-thrombotic therapy (clopidogrel or aspirin) as they might be of use if the cat's LA is massive. However it is already on a lot of medication so I'd need a good reason to add another drug.

Dave

RE: A Cat Cardiology case to discuss :)

Beats — Sun, 17 Mar 2019 19:16:12 GMT

[quote user="Miriam Lynch"]

Hi,

Out of curiosity did you do any follow up pro BNP samples ? Just to see how much ongoing damage to the cardiac myocytes occurring?

[/quote]

Hi Miriam,

thanks for your curiosity!

no follow-up proBNP (or troponin) I'm afraid, but now you mention it, I share your curiosity as to whether these values would have stayed similar, decreased or increased over last year.

I'll leave it to those more knowledgeable than me to speculate on that (and what it might or might not mean for any change).

RE: A Cat Cardiology case to discuss :)

Christina Smith — Sat, 16 Mar 2019 23:00:45 GMT

[quote user="Miriam Lynch"]

Hi,

Out of curiosity did you do any follow up pro BNP samples ? Just to see how much ongoing damage to the cardiac myocytes occurring?

[/quote]Respectully. Would that change the apparently successful protocol ?

RE: A Cat Cardiology case to discuss :)

Miriam Lynch — Sat, 16 Mar 2019 19:20:12 GMT

Hi,

Out of curiosity did you do any follow up pro BNP samples ? Just to see how much ongoing damage to the cardiac myocytes occurring?

RE: A Cat Cardiology case to discuss :)

Beats — Tue, 19 Feb 2019 22:37:34 GMT

Follow-up:

Other than an increase in felimazole to 5mg morning and 2.5mg evening at some point in the last year, has continued on happily.

Rightly or wrongly, owner has continued to religiously medicate with atenolol, furosemide, pimobendan and benazepril.

RE: A Cat Cardiology case to discuss :)

Beats — Wed, 06 Dec 2017 19:17:20 GMT

Follow-up:

Reported to be doing well at home.

Has continued on same felimazole dose and 6mg atenolol daily and 1mg/kg furosemide orally once daily as well as half a 1.25mg cardisure once daily.

Takes all these medicines very happily and starting on 2.5mg benazepril once daily now also.

RE: A Cat Cardiology case to discuss :)

David Mills — Tue, 28 Nov 2017 14:50:18 GMT

[quote user="Martin Atkinson"]Not such a good case to try out kitty NT-proBNP then [/quote]

Just like most cases vs competent echo examination

[quote user="Martin Atkinson"]Also AFAIA Troponin doesn't rise in simple HCM only when there is significant cardiomyocyte injury which indicates there is an ongoing mycocardial damage[/quote]

All the more reason to echo rather than rely on a lab test. I agree, troponin in long-standing HCM is not often raised, but where there is inflammation, or scarring (likely given this cat's abnormal ECG at presentation) then it could be advanced HCM, RCM, DCM, myocarditis, infarction...

RE: A Cat Cardiology case to discuss :)

Martin Atkinson — Mon, 27 Nov 2017 16:33:51 GMT

[quote user="Beats"]NT-proBNP 1144pmol/L. [/quote]Wish I'd stuck my neck out and said, I expected it to be very high - many hundreds possibly over 1000!

[quote user="Beats"]

Not such a good case to try out kitty NT-proBNP then

[/quote]It is a very good prognostic indicator though so it is of value - i.e. not a very good prognosis!

Also AFAIA Troponin doesn't rise in simple HCM only when there is significant cardiomyocyte injury which indicates there is an ongoing mycocardial damage and significant cardiac failure so another poor prognostic indicator.

RE: A Cat Cardiology case to discuss :)

Beats — Mon, 27 Nov 2017 14:54:45 GMT

D'oh!

Not such a good case to try out kitty NT-proBNP then if everyone's united that was pointless :-)

Still, for completeness (and comment if worthy of any):

NT-proBNP 1144pmol/L (>270pmol/L - clinically significant cardiomyopathy highly likely)

Troponin I(HS) 1.85ng/ml (ref=<0.04)

RE: A Cat Cardiology case to discuss :)

Martin Atkinson — Fri, 24 Nov 2017 10:57:25 GMT

[quote user="Beats"]I've also been inspired to send off a rare NT-proBNP, the result of which I'm sure the forum will eagerly await[/quote]For once I agree with DM that it will probably not add much to your diagnosis at this stage and will uncharacteristically reserve predictive judgement of the result.

RE: A Cat Cardiology case to discuss :)

Beats — Thu, 23 Nov 2017 20:36:27 GMT

T4 taken yesterday (pre-pill) 12.7nmol/L (10-60) so 2.5mg daily felimazole probably is controlling hyperT4 adequately.

Here are couple more pics and few video attempts of yesterday morning's pre-treatment echo (all done at times of normal rhythm, but playback is in slow-motion)

(I'm not sure the videos will upload in current file format, so will post separately below)

EDIT: 4 videos uploaded to https://www.vetsurgeon.org/members/beats/files/dscf0015.mp4.aspx

let me know if these don't work for everyone. Should be a long axis, 2 x short axis (one of ventricles and one at level of aortic valve) and a somewhat random one of the lungs to prompt a chat about the value or otherwise of identifying "B-lines" and whether pulmonary edema can be suggested ultrasonographically in a cat.

RE: A Cat Cardiology case to discuss :)

Roland Bulkyn-Rackowe — Thu, 23 Nov 2017 18:47:28 GMT

I've seen a few like this both with and without hyperthyroidism. Owner measured heart rates at home can sometimes be dramatically lower (350 in practice, 150 at home). It would be nice to have a holter although I've had little success in cats. If the HR is consistently this high then it would be a massive concern to me! The LA isn't too dramatic on that scan although it would be nice to get an idea of contractility. I would agree a vagal manoevre would be nice to try and I would be reaching for the atenolol (v low dose, titrate upwards!) if there is reasonable general cardiac contractility (atrium and ventricle).

I had one that was a normal HR at home and did no treatment (not hyperthyroid). The cat was fine... for 2 years, then presented with RCM (pleural effusion, myocardial infarcts, massive LA).

Disclaimer: no evidence was used to inform this comment, no flames please.

RE: A Cat Cardiology case to discuss :)

David Mills — Thu, 23 Nov 2017 14:06:24 GMT

[quote user="Robin Grimmer"]This is a case of hyperthyroidism in which you would give a B blocker as well as the thyroid medication which I said on the other cat cardiology thread and Dr Mills poo pooed.[/quote]

What you said was this:

"But HCM secondary to hyperthyroidism is diastolic failure ie the heart is going so fast it doesn't have time to fill properly so a B blocker would be indicated in this case."

And this:

"I've had cases like this that have generally done pretty well". I also used a B blocker as often marked tachycardia".

Now, if you've have said something along the lines of "In a cat with SVT and hyperthyroidism then I would used a beta blocker" I may have been tended to agree, depending on the particulars of the case. But you didn't.

Now this case, we don't know it has HCM, only SVT and some atrial enlargement.

I also outlined the lack of evidence for using negative chronotropes, including beta blockers, in cases of confirmed HCM as there is often marked systolic dysfunction - diastolic failure is an outdated and incorrect characterisation of the disease process.

It is tiresome when people misquote for the sake of trying to score points.

Regarding this case, I would not have used a beta blocker immediately, but seen the response to frusemide and increased thyroid medication. I may, depending on the type of cardiomyopthy (if it has one) have added pimobendan.

Blanket recommendations to all cases can be at best ineffective and at worst, harmful. If this cat has DCM and you wade in with a big dose of a beta blocker, you could kill it.

God save cardiology from the medics.

RE: A Cat Cardiology case to discuss :)

Robin Grimmer — Thu, 23 Nov 2017 13:50:28 GMT

What was the T4 by the way? I'm guessing uncontrolled. Interesting case

RE: A Cat Cardiology case to discuss :)

Robin Grimmer — Thu, 23 Nov 2017 13:42:57 GMT

SVT - it even says so on the ECG

The complexes are supra ventricular in origin, not ventricular. This is a case of hyperthyroidism in which you would give a B blocker as well as the thyroid medication which I said on the other cat cardiology thread and Dr Mills poo pooed.

Agree re x ray and scan comments.

RE: A Cat Cardiology case to discuss :)

David Mills — Thu, 23 Nov 2017 13:25:43 GMT

[quote user="Beats"]I've also been inspired to send off a rare NT-proBNP, the result of which I'm sure the forum will eagerly await I anticipate this would be most helpful if the result is low enough to make significant cardiac disease causing congestive heart failure appear more unlikely (making it more likely that asthma-like condition responsible for yesterday's dyspnoea) - given that there does appear to be a problem with the heart however, I'm not holding my breath for this![/quote]

I wouldn't bother as it won't tell you more than you already know.

The LA is enlarged (15.9mm on your scan), so the cardiac disease has already caused remodelling, therefore is clinically significant. The proBNP won't tell whether the dyspnoea is cardiac in origin, only the rads can tell you that.

[quote user="Martin Atkinson"]I don't agree, there are no P waves, this is an artifact as the baseline rebounds from the T wave[/quote]

I disagree. The baseline doesn't "rebound".

The QRS are normal width and morphology - they are tall, but this is normally the case - V-tach are almost always wide and bizarre and you will not see T waves in true V-tach (especially if at 350bpm) as the complexes just combine into the sine wine kind of appearance.

There are several P waves visible in the sinus strips, and not all are conducted.

Lidocaine won't touch SVT in most cases.

Another option in this case would be to apply ocular pressure or vagal massage whilst monitoring the ECG.

RE: A Cat Cardiology case to discuss :)

Beats — Thu, 23 Nov 2017 13:03:39 GMT

Thanks for the thoughts

I couldn't decide on whether I thought CHF or not, so went with the give furosemide and rexray plan. Had 2mg/kg furosemide IM thrice with the resp rate increasing over course of morning from average of 50/min pre-anything to 60-80/min.

Got 5mg propranolol (and its usual 2.5mg felimazole - I'm guessing this ain't controlling the T4 ideally) in the afternoon and heart returned to normal rhythm (coincidence or not) and breathing returned to about 30/min. Another 2.5mg propranolol last night and this morning breathing was 20-30/min. Going home on 2.5mg propranolol twice daily and 1mg/kg furosemide twice daily pending further thinking.

Overall, I thought that heart rate of 350/min (I thought SVT rather than VT) probably wasn't allowing sufficient filling to be good (when you echo'd it doing this, it looked more like vibration than beating).

I wasn't sure on the rads. Pulmonary vein looked OK to me, but I've been caught out placing too much emphasis on this before. I've never been very convinced of the benefits of deciding if alveolar or bronchial etc, so tend to go more with distribution (Nykamp, S., Scrivani, P.V., Dykes, N.L. Radiographic signs of pulmonary disease: an alternative approach. Compendium on Continuing Education for the Practicing Veterinarian. 2002;24:25–36.). That said, I've never been confident that anything other that seeing if responds to furosemide has a high enough sensitivity to hang my hat on when not obvious and clear-cut given that "pattern" and distribution can be pretty variable apparently in clinical cases (https://www.ncbi.nlm.nih.gov/pubmed/19037891).

I thought the left atrium looked enlarged, but whether it was definitely big enough to be causing dyspnoea via CHF again debatable. Still, I thought it big enough that a little furosemide going home while head-scratch further seemed sensible.

I attempted some videos of amateur echo attempt with my oversized probe and grumpy dyspnoeic cat in twisted sternal. I'll see if I can figure how to post them (feel free to mock or constructively criticise them if I do!)

I've also been inspired to send off a rare NT-proBNP, the result of which I'm sure the forum will eagerly await I anticipate this would be most helpful if the result is low enough to make significant cardiac disease causing congestive heart failure appear more unlikely (making it more likely that asthma-like condition responsible for yesterday's dyspnoea) - given that there does appear to be a problem with the heart however, I'm not holding my breath for this!

There is some more extensive sections of "normal" rhythm just prior to the parts posted - I'll try to look that out as I thought the p-waves were synchronised fine in it with the supraventricular complexes that followed.

RE: A Cat Cardiology case to discuss :)

Martin Atkinson — Thu, 23 Nov 2017 11:58:43 GMT

[quote user="David Mills"]This is SVT as the complexes are normal looking, and there appear to be P waves present. There appear to be ectopic P waves present in the short stretches of sinus rhythm, and there is some association of P waves with the QRS.[/quote]I don't agree, there are no P waves, this is an artifact as the baseline rebounds from the T wave which just gives that impression as it goes straight into the Q wave, there is no PQ interval. In the few brief interludes of 'sinus rhythm' there is one discernible P wave otherwise it is in AF and the QRS complexes are different from the ones in VT.

Agreed on the interpretation of the X-ray though.

RE: A Cat Cardiology case to discuss :)

David Mills — Thu, 23 Nov 2017 11:14:54 GMT

[quote user="Martin Atkinson"]

Ventricular tachycardia.

[/quote]

Disagree. This is SVT as the complexes are normal looking, and there appear to be P waves present. There appear to be ectopic P waves present in the short stretches of sinus rhythm, and there is some association of P waves with the QRS.

The x-ray is a mixed bag. There is some bronchointerstitial patterning in the caudal lung fields, which could be asthma-related or the start of pulmonary oedema. Immediately cranioventral to the heart is suggestive of alveolar pattern, and the cranial lung fields are similarly affected, taking into account overlying tissue, difficult to see on my screen. I can't see obvious pulmonary vein congestion. The heart is too tall and there is LA enlargement. There may be a small pleural effusion caudally, there is some leafleting of the lung lobes.

The scan shows an enlarged LA, although I don't like short axis measurements for LA as they are prone to errors. It doesn't quite hit the 16mm magic number.

Dx? Open. There is not a totally convincing CHF in my eyes, although the heart is not normal. Status asthmaticus is possible. Thyroid storm can cause similar dyspnoea, but less likely.

Tx? I would give frusemide IV at a decent dose (4mg/kg) and pill pop with a good slug of felimazole and monitor response, probably re-xray in 6h. The SVT may be due to hypert4 or underlying cardiomyopathy. If no improvement with frusemide, add in IV dex.

Interesting case.

RE: A Cat Cardiology case to discuss :)

Martin Atkinson — Thu, 23 Nov 2017 10:47:36 GMT

Ventricular tachycardia. If this cat is symptomatic it needs urgent medication or it will likely go into VF and die. I would give Lidocaine at 0.25-1mg/kg slowly over 5 minutes. It will then need a B blocker, atenolol at 2mg /kg q 24hrs. Obviously you need to review its thyroid medication and then treat the underlying heart disease but after the 'discussion' on the parallel thread I'm loathe to suggest how you do that!