OK, this starts off about valves...but then isn't really about valves...but it's the broader educational point (which is relevant to valves) that I want to make this week...no poll I'm afraid, but as always, comments encouraged! 😁
In my office doing Admin, lot to get through & a very busy morning ahead. Asked to r/v a TTE for helping determine AS severity. Pt admitted with heart failure, clinically severe AS is all I know at this point. Now, the golden rule in this situation is *review the whole study*...
Not just one or two images.
But I was super-busy, I BROKE MY OWN RULE and just looked at the relevant images. Here's the PW and CW Doppler tracings (Pt in AF)...
Here's a PSAX view. Images were challenging...
With low velocities and AVA 1.36 I wasn't too worried about severe AS, although did note very low LVOT VTI...but tracing could have been an underestimate due to image quality.
So I said quickly not severe AS, moderate at worst.
Next day asked to look again. Colleague convinced clinically AS was severe. So, this time, with more time dedicated to this, I look at the *whole* study, from the beginning, and now something else starts going through my mind! See what you think...here's the PLAX view...
Anything catch your eye? Apart from the monumental LA? Well, I was curious about something so checked out Ap4Ch...👇
What do you think? No BBB on the ECG...
Septum looking a bit funky, right?!
So, next stop...IVC!
IVC measured 25mm with minimal collapse with breathing / sniff...
So, remembering that "a bouncy septum and a dilated IVC is xxx until proven otherwise"....now I decided to check out the other parameters. Some of you know where this is going...
MV Doppler shows tall E wave with rapid deceleration time. And check out the TDIs...lateral E' velocity is 13.7! Medial E' is 14.9! They're not normal, they're supranormal! And... they're the wrong way round... that's annulus inversus!!
So, actually, we've got:
-Septal bounce
-Dilated IVC
-Tall MV E wave with short DT
-Supranormal LV E' velocities
-TDI annulus inversus
-Dilated atria (albeit AF)
So now, I'm less worried about AV and I'm wondering...why are there multiple features of constrictive physiology?!
Turns out a CT scan has commented on unusual thickening of the pericardium!! Cardiac cath awaited.
So, by looking at the *whole* scan, you see the *whole* picture! Sounds so simple, but in the daily hustle of work it's so easy to be tempted into looking at 1 or 2 images only...!
Take home message 1: if you're scanning, always think about the numbers you're measuring and images you're seeing...the echo request can't tell you what you may unexpectedly find, so you've got to be alert to expect the unexpected!
Take home message 2: For those asked to review
echocardiograms, if it's a "what's the severity of xxx?" question remember to take the time to check all the images...you never know what you may find! 😁
This week's case dedicated to our friend Nicolas @NMerke...hope all is well & look forward to seeing your posts again soon👊
Another nice example recently of the importance of a systematic approach to assessment of mitral regurgitation during TOE
Indication was known MR, assess suitability for TEER
Mid oesophageal 4Ch & 5Ch views...wondering if we have the right patient! No real MR to see...
The segmentation approach in the bicommisural view is a very reliable and easy-to-do method
Start at the lateral side of the valve with X-plane (Philips) / MultiD (GE) and you have A1-P1 coaptation on the right side...do this with 2D only & then with colour Doppler too
Then move to the middle of the valve with your cursor, cutting through A2 in bicomm view so you see A2-P2 coaptation on the right side
It takes time to read the paper, read the supplementary appendix, analyse the results, think about them etc!
Some thoughts...🧵
On Sunday I wrote a thread about asymptomatic severe AS and what we knew already from RECOVERY & AVATAR RCTs and what the guidelines currently advocate
Transthoracic echocardiography (TTE), when performed with care and diligence, can reveal a lot about the valve. TOE isn't necessary in all cases to determine leaflet pathology.
A worked example below:
In the PLAX view, you can assess the scallops of the leaflets
In a true PLAX view with aortic valve clearly visible, you mostly see the A2-P2 interface. Here, you can see a clear & large prolapse of the posterior leaflet
If you tilt upwards towards the PLAX RV outflow (pulmonary valve) view you see mostly the A1-P1 interface
Here, you can see the valve looks slightly different & no prolapse is seen
PE has garnered a reputation for huge profits as they typically buy into a company, aggressively ⬇️ costs whilst ⬆️ profit margins, leverage debt if needed, and then sell, often at a large profit
Does this matter when it comes to delivering healthcare services?