The first day of the American College of Cardiology (ACC) meeting is like the first lap of crit or cross race. It’s a whirlwind. Your head spins. You are trying to get oriented, but as a part-time journalist, you also know that big news happens on the first day.
And oh did it ever.
One of the meeting’s most anticipated trials, was pulled from the program one hour before presentation. The PREVAIL trial was eagerly awaited because it studied a device that stood to change the practice of stroke prevention in patients with atrial fibrillation. The Watchman device is a plug of sorts that is inserted into the left atrial appendage (LAA). The idea is that most (not all) clots in AF come from the LAA. If this could be occluded, stroke risk would be reduced and patients would no longer need to take drugs that increase bleeding risk. There are millions of patients with AF, stroke is a dreaded complication and no one likes anticoagulants.
You can see why this is so big.
But then, the morning of the presentation, there came an announcement that the trial would not be presented because Boston Scientific, the makers of Watchman, breached the embargo. But the slides were still in the program. This created quite a stir. And journalism folks were already inflamed from the argy-bargy in the week leading up to the meeting: It seemed the trial would not be presented, then partially presented, then fully presented, now not presented.
These antics were not the reason why I wrote this decidedly negative opinion piece on the Watchman. I wrote it because the Watchman is not likely going to make it past FDA muster. And if it does, I would be very hesitant to adopt the technology. I gave eight reasons to be doubtful in the piece.
The other news of my day:
I was really happy to see theHeart.org journalism team again. They are a super-professional bunch and they are awfully nice to me. I’m like a Cat 4 in a 1-2 race when it comes to journalism.
I saw this picture in the expo. It’s hard to wrap your head around Coke being heart-healthy. Keep that cynicism about industry sponsorship of medical societies at bay, please.
I went to an interesting session on AF and athletes. (Look for an update later.)
I met Dr. James Beckerman (@jamesbeckerman)
I walked to dinner and ate an entirely vegan meal! It’s heart meeting after all.
Oh, and BTW: it was really nice out here yesterday.
I’ve already written my second piece. It address the issues of over-monitoring and noise pollution in the hospital. Here is Shelley Wood’s recap of the study. My opinion will be published soon.
For breaking news, theHeart.org team has it covered. Their home page looks amazing.
JMM
2 replies on “Notes from ACC – Day 1”
JOHN – It is GREAT that you are at the meeting and actively reporting to us! I’ll look forward to your ongoing accounts.
While perusing theheart.org home page – the link about Dr.JamesFreeman’s presentation, “Another Strike for Digoxin: Mortality Goes Up in Cohort Study” caught my eye. In my opinion – the main point about Digoxin has once again been both missed and misinterpreted. Clearly Digoxin is a drug whose time has come and for the most part gone – and clearly exponential advancemens in your field of electrophysiology are by far the most exciting development in recent years regarding optimal management of the ever increasing numbers of our aging population who develop AFib. But I feel it wrong to “blame the drug” when the true fault I believe lies elsewhere. I’ve therefore taken the liberty of posting below what I just posted on the heartwire page:
REGARDING DR. FREEMAN’s REPORT ON DIGIXIN IN AFIB:
I am not surprised that there may be an increase in mortality among the group of patients receiving Digoxin for rate control. That said – newer trained clinicians no longer gain enough (if any) experience in starting and maintaining patients on this medication (either for heart failure or AFib). Given the drug’s narrow therapeutic window – the potential for iatrogenic adverse outcome is significant, if not downright probable.
I am definitely NOT advocating a return to use of Digoxin as it was used in the past in so many patients with cardiac problems. On the contrary – better drugs have been available for years – and as alluded to, increased availability to skilled EP cardiologists has added an entirely new and exciting dimension to management of AFib. BUT – association (as found in this study) does NOT prove “cause-and-effect” – AND – if prescribed by experienced clinicians well aware of Digoxin pharmacokinetics, drug interactions, indications and dosing – I believe the drug could still have a potential role in a selected number of patients. Having said all of that – the clinical reality is given current lack of expertise in use of this medication with no more than limited opportunity to gain more experience during one’s medical training – use of Digoxin appropriately continues on the wane. But I feel it important to emphasize that this is NOT because Dig per se is the “cause” of increased mortality (really NO evidence to prove this …. ) – but rather the reality that a clinician inexperienced in Dig use is a HUGE risk factor for adverse outcome …
THANKS FOR ALLOWING ME TO VOICE MY OPINION ON THIS ISSUE!
Ken,
Thanks for adding your opinion. Association and causation is always an important topic. As is the notion that drugs are not bad or good–rather they have benefits and harms. Thanks as always.