❓Testen Sie Ihre Diagnosefähigkeit in unserem #MedizinQuiz! Hier ein neuer Fall: Echokardiografie in Systole und Diastole bei einem 46- jährigen Patienten mit Belastungsdyspnoe. Was fällt auf? 💬
➡️ herzmedizin.de/fuer-...
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This I interesting. Can you provide a link?
I guess it’s an ok strategy for asymptomatic AS - elective treatment is probably much better than emergency - but EarlyTAVR didn’t quite help answer the question due to bad trial design. If one really believes in the prognostic benefit we should be starting a screening programme.
Substraction anxiety.
Patients in the control group who were asymptomatic but missed out on the fabulous treatment suddenly all had symptoms and got their TAVR anyway within a few months. This drove the end-point and not heart failure or SCD.
Ah this one is tricky because the procedure itself makes the a fib.
But paradoxical embolisation is really Schrodingers‘s cat - I agree
Trigger-substrate-concept. Like in many areas of medicine.
Dr John - likes to voice his opinion in clear words.
I like!
johnmandrola.substack.com/p/industry-v...
This is interesting. For years we assumed that tachycardia/arrhythmia causes EF drops. Now it seems, in some people afib may just be the start into a HF career. Not sure, though genetic testing big scale is feasible. Guess we just have to keep them on a short leash.
www.jacc.org/doi/10.1016/...
Interestingly Packer et al claim that 50% SMR in the disproportionate group are due to dyssynchrony - best treated with CRT. With so many cases, dyssynchronous MR should be its own entity, right?
It can never be proven - unless you find a thrombus in transit. The PASCAL-Score from the paper above help find patients that are likely to benefit from closure.
This graph neatly shows the benefit of PfO-closure in the right ESUS patients.
#cardiosky
Analysis of Pooled Individual Patient Data From RCTs of Device Closure of PFO After Stroke url: jamanetwork.com/journals/jam...
In my department we still fullheartedly recommend open heart surgery for <70 yo with aortic valve disease just like the updated ESC say. Increased re-intervention rates in TAVI patients strengthen that position.
Precisely. Mitral valve surgery used to be a no-go at low EF. Modern MV repair has changed this a bit. But it seems logic that a heart with poor EF may get into trouble when M-TEER is performed.
I think this few years old Packer:Grayburn paper totally makes sense. RVol/LVEDD in my patient is 0,1 - so proportionate MR.
www.jacc.org/doi/10.1016/...
Is it the valve or is it the ventricle? Or does at matter at all, when M-TEER reduces preload?
It wasn't so much out of place. As I said, especially in aortic valve surgery you might find some amyloid. The bigger yield is probably in the TAVI cohort.
A HF patient has an LVEDD of 400 ml is treated with OMT and shows a huge functional MR on Echo. EROA 0,4 - would you consider this patient for M-TEER? (QRS is narrow so CRT not an option).
I have an opinion but curious what others think.
#cardiosky
Sorry for the stupid acronym - I was thinking of carpal tunnel syndrome. But yes, why not a sample of myocardium during aortic valve surgery. The yield must be quite high as well.
Yes same thing with spinal stenosis.
Probably. We just don’t look at pH in a non-intensive patient. Maybe we should.
Interesting thread on contraction alkalosis (or maybe rather chloride-depletion alkalosis) as commonly seen in heart failure patients treated with furosemide.
Serendipitously, I came across a case just today.
#cardiosky
I always wondered: why doesn’t every CTS surgeon send a probe to histology? Many a cardiac Amyloidosis patient could be identified before full-blown heart failure…
#cardiosky
AI is coming closer to replacing your job, doc.
#cardiosky
Design and Architecture of a Generative-AI-Supported, Nonphysician-Delivered Model for GDMT Optimization in HFrEF: The ASSIST-HF Trial | JACC: Advances www.jacc.org/doi/10.1016/...
That's how I see it. Formally, heart failure is defined by symptoms, labs and echo parameters - so here people just look at EF to set the indication.
Ah interesting.
I just read a while ago that small positive trials are often the result of chance - and can't be replicated. (I guess it's because a lot are done, many are underpowerted and just by rules of statistics some will turn out false-positive).
Take home message from the NEJM editorial.
(betablockers post-MI)
www.ovid.com/journals/nej...
In my simplistic concept MI outcome is mostly dependent on early presentation and revasc. If that doesn’t go so well, the patient enters heart failure territory where EF-based OMT is well established. This of course neglects the specifics of ischemic heart disease like pro-arrhythmia/remodeling.
I had to look up the CHAMPION trial. I’d be surprised if non-inferiority can be shown when CLOSURE couldn’t. And if it does, we’ll have more questions than answers. At any rate I listened to too much drjohn to be unbiased on LAAO…
EF has always been a poor surrogate for myocardial damage. So yes: It makes sense to be more precise.
I guess the idea of the EF50% rule is to have a simple rule.
I’m frankly quite unenthusiastic where exactly one sets the threshold.
I understand EF<50% is consensus - which in reality is the same thing.
