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👊
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?
Sixty years ago this month - October 1963 - US cardiologist Dr Robert Bruce published a paper detailing his efforts to devise a multi-stage treadmill test
Little did he know this would go on to become the Bruce protocol the most widely used for exercise testing
A thread...
Prior to this, 'stress testing' to evaluate cardiac function was performed using the Masters 2-step technique, first described in 1935. This crude but simple test involved repeated steps up & down over 90 seconds
Bruce, amongst others, recognized the limitations of this test & set about developing an exercise treadmill test
His initial work focused upon a single stage protocol, but he soon realized this wasn't stressing fitter patients enough & the test was taking too long!
We know now that it is perfectly possible for symptomatic individuals to have abnormal stress tests, with inducible ischaemia, but not have significant epicardial CAD on angiography
So we should stop using epicardial CAD as the arbiter of whether the test is 'right' or 'wrong'
I helped recruit patients for #ISCHEMIA between 2012-13; we saw at least a dozen patients with barn door (core lab verified) abnormal stress tests but normal coronaries on angiography
Here is just one example! Rest on left, stress (exercise) on right...