Customize Consent Preferences

We use cookies to help you navigate efficiently and perform certain functions. You will find detailed information about all cookies under each consent category below.

The cookies that are categorized as "Necessary" are stored on your browser as they are essential for enabling the basic functionalities of the site. ... 

Always Active

Necessary cookies are required to enable the basic features of this site, such as providing secure log-in or adjusting your consent preferences. These cookies do not store any personally identifiable data.

No cookies to display.

Functional cookies help perform certain functionalities like sharing the content of the website on social media platforms, collecting feedback, and other third-party features.

No cookies to display.

Analytical cookies are used to understand how visitors interact with the website. These cookies help provide information on metrics such as the number of visitors, bounce rate, traffic source, etc.

No cookies to display.

Performance cookies are used to understand and analyze the key performance indexes of the website which helps in delivering a better user experience for the visitors.

No cookies to display.

Advertisement cookies are used to provide visitors with customized advertisements based on the pages you visited previously and to analyze the effectiveness of the ad campaigns.

No cookies to display.

Right sided DCM or PHT ?

Sonopath Forum

Right sided DCM or PHT ?

Hi everyone,

I’d love to hear your opinion on this case.

10 yo, female Staffy with ascites. 

Abdominal ultrasound normal appart from ascites and passive hepatic congestion.

Echo: marked RV and RA dilation with eccentric hypertrophy. RV looks hypokinetic. How do we assess RV function? Do we use EF or FS as in the LV?

There is significant TR without gross TV changes or PV insufficiency . 

Hi everyone,

I’d love to hear your opinion on this case.

10 yo, female Staffy with ascites. 

Abdominal ultrasound normal appart from ascites and passive hepatic congestion.

Echo: marked RV and RA dilation with eccentric hypertrophy. RV looks hypokinetic. How do we assess RV function? Do we use EF or FS as in the LV?

There is significant TR without gross TV changes or PV insufficiency . 

The flattening of the IVS ( unfortunately I didn’t have a ECG in place to tell if systolic or diastolic) , does that represent volume or pressure overload or both? 

Any input is welcomed. 

Cheers 

Comments

Peter

Hi!
Looks like acute

Hi!

Looks like acute pulmonary hypertension to me. DDx are decompensated pulmonic stenosis (relatively unlikely) or right sided cardiomyopathy (also relatively unlikely). Did you get a pressure gradient along the TI?

Re assessment of RV function: As you are posting, RV dysfunction is obvious here. FS is not used conventionally. TAPSE (Tricuspid anular plane systolic excursion) based on apical M-Modes of the tricuspid anulus are a modern way (at least in Vet Med) to assess RV function.

If you find a high PG along the TI (as I would assume), I would try and get a minimum data base to look for possible causes of PHT: Abdominal sonogram, chest Rx, Urine sampling (proteinuria?), CBC, heart worm and lung worm testing, D-Dimers, etc.

 

I hope I could help!

Thanks for posting!

Peter

SCultrasounds

Thanks Peter,
Yes ,the

Thanks Peter,

Yes ,the highest velocity I got was 3.7 m/sec.  So I thought could be PHT but the dilated RV confused me. So, over time ( providing she lives long enough) , do we expect to see RV concentric hypertrophy? 

Will request some further testing. 

At the moment the dog is already on Pimobendan and Furosemide, the ascites still not quite controlled. 

Should I add syldenafil ? They don’t have the founds to see a cardiologist btw. 

Thanks again 

 

 

EL

Holy Paradoxical Septal

Holy Paradoxical Septal Motion Batman!

Peter that posterior TV leaflet looks long to me and the septal looks a bit short and teathered…but i may have my imaginoscope on high this morning the espresso is flowing well here in Rome:)  Any chance of TV dysplasia here? I know she is 10 years but milder/moderate TVD forms can live a long life.

Peter

Yes, Eric, this could of

Yes, Eric, this could of course be, but systolic function appears too low for me for a TD case and the valvular changes appear to me not severe enough for this degree of enlargement. In the typical TD case, the septal leaflet usually attaches directly to the papillary muscle (this is something I learned through cardiac surgery but might as well be a European phenotype for genetic reasons) – a finding that I don’t see here. 3.7 m/s  is not very high, though. This could be explained by the right ventricle not being strong enough anymore to develop a high pressure. 

What would be very helpful is a short axis view of the RVOT and pulmonary artery including the bifurcation. If it is PHT, the PA will be widened and the RPA will not change diameters in systole/diastole.

Yet, sildenafil is a good choice given the pressure gradient, Pimobendan as well. in my experience some of these dogs respond to Torsemide better than to Furosemide. Unfortunately, high doses can lead to syncope in cases of pressure overload (like PHT). The case looks end-stage anyway…

Re concentric and eccentric hypertrophy: You see concentric hypertrophy in dogs who develop PHT over a long time, starting at low pressures (like Westies with lung fibrosis). In cases where the heart doesn’t have time to compensate (like acute thrombembolism) only dilation and reduced systolic function is seen. These patient will never develop concentric hypertrophy. 

And: I agree:fulminant TD decompensates in dogs <1yr, severe forms decompensate at 4-6 years, moderate TD usually decompensates when dogs get old – this is as well my experience

 

Peter

 

Peter

SCultrasounds

Thank you both for your

Thank you both for your comments.