🦀You Can Strike, But We Could Never

Well, paint a placard and call me a scabber — it would seem I’ve made it into work today. Unfortunately, medical news doesn’t seem to respect the rules of industrial action. It’s a very demanding master.

I know i’ve let the team down… but can 3 research articles make up for it?
Yes? Wonderful 🙏

👋 Happy Friday. Here’s what we got:

If you want to read any previous editions of The Handover, you can on our website.

There is an impostor among us… Do you know who it is?

Following a heart attack, secondary prevention is a must. 
Aspirin. Clopidogrel. Atorvastatin. Ramipril. Spiranolactone. Bisoprolol. 

Slap 'em’ all in a blister pack of pills and (hopefully) that’ll keep another infarct at bay 🙏

But you see, that’s the thing about group projects: there’s always one free-loader.
They doomscroll TikTok whilst everyone does the heavy lifting. 

And one of these medications is looking suspiciously….ineffective 😑

Today, it’s Beta-Blockers being accused of being a bum 👀

Quick history lesson:

Back in the 80s, seminal studies like BHAT and ISIS-1(unfortunate name) had launched Beta-Blockers in ACS stardom. The cardiologist just loved that vasodilator.

But we’ve come a long way since then… Advances in cardiac diagnostics, reperfusion and revascularisation have got us questioning – are beta-blockers now a has-been like Britney Spears or Ronaldo?

What better way to figure it out than a meta-analysis? 

Published in NEJM this week, this investigation gathered 5 recent RCTs, including 17,801 patients. 

They all asked the same question: In patients with a preserved ejection fraction(LVEF >= 50%), do beta-blockers actually help morbidity and mortality? 

In these studies, participants were randomised to either:

The primary endpoint was a composite of death from any cause, myocardial infarction, or heart failure. 

What they found was this: 

Beta-blockers did not significantly reduce the composite endpoint compared to no beta blocker therapy (8.1% vs 8.3%) (hazard ratio: 0.97; 95% CI, 0.87 to 1.07; P = 0.54).

Even breaking down to its individual components barely made a dent. Comparing Beta-Blocker vs No-Blocker : 

These results were consistent across subgroups(based on sex, age and type of MI), and the beta-blocker given didn’t seem to have an effect either. 

So it would seem that in patients with preserved ejection fraction, Beta-blockers seem to be as functionally useful as your appendix :/

But in the words of Uncle Ben: “With Great Research Comes Great Limitations” - or something along those lines…

Limitations aside, this study concludes with this:

In those with preserved ejection fraction, Beta-blockers remain on the post-MI team sheet. But their role is looking more like a squad rotator than a first-team starter.

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Anddddd there it is.
That one inevitable question.

The one you prayed wouldn’t surface in clinic 🫣
Or on the ward round.
Or in the seventh circle of hell, known as post-take.

You’re asked a clinical question you absolutely do not know. Not even vaguely. 🥀

Your senior: Missing In Action
The guidelines: 47 clicks deep on the intranet
GPT: Thinks Kawasaki is a Japanese motorbike :/ 

The pressure is on. And you’ve got nothing

If nothing else, remember these wise words:
If Medwise.ai can’t answer your clinical question… you’re f*cked.

Why?

Because Medwise.ai is like ChatGPT… if ChatGPT had been force-fed every NICE guideline, society consensus statement, and Royal College publication until it begged for mercy. 

You type a question and bam:
Evidence-based answers
NICE-aligned. Instantly cited.

No more PDF trawling. No more second-guessing. No more panic-Googling behind a drug chart.

There’s a reason clinicians in 1,000+ NHS organisations already use it.
They stopped winging it. You can too.

So in 99% of clinical scenarios, Medwise.ai has got you covered
For the remaining 1%... I’m sorry.  

Start looking dangerously competent on wards and use Medwise.ai today.

And use your NHS email address to get access completely free 👇

So you’ve got an AKI. Bummer.

Not to worry! A multi-million pound, hospital-grade, expert scientist-engineered haemodialysis machine is here to take over for your two soggy pee beans.

Dialysis = pretty OP.
But also? A massive nuisance.

Imagine sitting through twelve full episodes of Andrew Tate’s podcast every week.
That’s how long a CKD patient spends hooked up to one of those bad boys.
Avoiding it where possible is a no-brainer.

But our poor little kidneys? It doesn’t take much to set them off.
Y’know, the little things…

… and they’re going on strike like [you fill in the blank 😉]

So: kidneys go kaput, dialysis swoops in to save the day.

Easy, right?

Not so fast, keen bean.
Published in JAMA this week, the LIBERATE-D trial asked this:

If we dial back the dialysis, could the kidney actually recover better??

The theory is this:
Frequent dialysis masks recovery signals and can injure kidneys via transient hypoperfusion and inflammatory activation from blood contacting the extracorporeal circuit. – in other words… You shouldn’t baby the kidneys into recovery. You gotta throw them back into action and work for themselves.

So what did they do?

And what did they find?

In the conservative group 64% (70/109) achieved kidney recovery at discharge (alive and dialysis-free for ≥14 days) versus just 50% (55/109) in the conventional dialysis group.

That’s an absolute difference of 13.8% (95% CI; p=0.04)

Other wins for the conservative :

But there are, as always, caveats:

All in all: More studies are needed to confirm this conclusion.

So do your part as a research-committed medic:
Grab your mates, get absolutely smashed and don’t drink a single drop of water.
Time to see just how much cowabunga your little buddies can handle … in the name of science!*

* The Handover does not endorse self-induced AKIs, binge drinking or any attempt to provoke organ injury for the sake of curiosity. There are easier ways to get portfolio points, I promise.

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Cardiologists love to sing the gospel.
To their patients. To clueless non-specialists.
To whisper it down the phone while rejecting your referral at 3 a.m.

“We’re not an ECG interpretation service”
“It’s not cardiac”
“Are you sure they don’t smoke. With these coronaries?”
“No. Obviously, they shouldn’t drink coffee with AF”

Ok, we made that last one up. But here’s a question:

If you’ve got a history of AF, what do you think loads of coffee does? 

Here’s what you might have been taught. Caffeine = AF recurrence risk factor.

Zero to Finals even says it, so it’s basically scripture.

The physiology checks out, too:

So? Case closed: Caffeine No Good. 

But observational studies couldn’t make up their mind…
A 2022 meta-analysis even concluded caffeine might reduce AF risk. 

What was missing was trial evidence. Until now…hold my mug.

Enter the DECAF trial - Does Eliminating Coffee Avoid Fibrillation? Yes, that’s the actual study name.

This multicentre RCT, published this week in JAMA, randomised 200 regular coffee drinkers who’d just been successfully cardioverted after an episode of AF (or flutter with a history of AF).

Two arms:

The result? 

Those who kept sipping their morning brew had a lower recurrence of AF. 

After 6 months:

A 37% hazard reduction for AF recurrence if you kept drinking the beans.

And no extra strokes, heart failure, or admissions.

So coffee is protective? We’ll drink to that ☕

But hold on. Spill the (limitation) beans

This doesn’t prove caffeine is protective. It just suggests that continued moderate intake might be better than an abrupt caffeine break-up.

The final sip?

When your AF patient asks: “Should I stop drinking coffee?” You can say going cold turkey probably isn’t going to do their atria any favours.

And next time cardiology goes off at you at 3 am 

Smile, don’t stress.
Sip your coffee confidently.
Your rhythm could be more stable than theirs.

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MIT Creates a Sweet Injectable Brain Chip

We’ve seen some many injectable brainchips by now. But this one’s a lil different. Forget the invasive and tedious craniotomy. A simple IV injection lets these chips travel through the blood, past the blood-brain barrier(much to the jealousy of dopamine, ifykyk) and directly into the brain. It can then be used to treat Alzheimer’s, Multiple Sclerosis and tumours.

The Desolate and Decrepit GPland

According to a poll conducted by the RCGP, nearly a 1/3 of GPs are unlikely to be working in general practice in 5 years… yikes. What’s the reason for this mass GP exodus? Stress, of course! Interesting stats include: 44% think of alternative careers, 39% plan to retire and 28% report they feel so stressed, it’s difficult to cope. It’s okay though. I’m sure adding GP Online to 100% helped this stress burden. Great shout from Wes…

Remote Thrombectomy from Scotland to The States

Trump won’t be pleased with this. We can now do surgeries in America without a Visa! A world first was completed this last week, with a surgeon in Dundee conducting a thrombectomy for a patient in Florida. Completely remotely, via a robot. This can be a complete game-changer for people in remote areas without access to specialist stroke facilities. H1-B Visa who?

Dr TikTok and Dr Instagram are on the Rise

Last week, we reported that OpenAI would do a better job at referring patient enquiries to real doctors. However, hasn’t stopped AI from being an increasing force in self-diagnosis. An estimated 9% of men and 7% of women in England use AI chatbots for health advice and information. Another 21% of women and 18% of men are using TikTok, Insta and YouTube for health advice. When you have people like Dr Berg(not an MD, actually a chiropractor) with 14 million followers dishing out health advice, at least we know our patients are in safe hands.

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