The Study of the Week stays with the theme of applying trial evidence to patients, once again in the heart failure field. Perhaps GDMT might not always apply?
Who, exactly, are “those measuring how well I practiced evidence-based medicine”? The clipboard nurses? Joint Commission? Insurers? I’m asking honestly—I am not a physician and don’t know how this monitoring works.
Physicians don’t have the full freedom to treat their patients as they see best.
One commenter said it well: it’s these “One size fits all” guidelines. How did we get here? Everyone BUT the patient’s physician is making decisions on how best to treat their patient. I get it that there are quacks doing really crazy things—and I bet they’re still doing them because they aren’t a part of these monitored health settings. There’s a place for oversight, but how do we let doctors be doctors?
I truly don’t know what to think, personally or professionally.
I’ve had atrial fib since my second year of medical school, some (“many” is a relative adjective) decades ago, and for years the mainstays of my treatment were digoxin and quinidine….which at least made me feel part of the gang – seemingly half of my adult patients – AF or no – were taking one or the other drug (mostly digoxin).
Now I see a patient on digoxin about once every six months, and quinidine is a word roughly on a par with bathroom wall graffiti. On the other hand, despite having had no problems with rate controlI I have been taking metoprolol for years, and in my clinics I frequently encounter AF patients on a beta blocker per guidelines but with heart rates <60 and systolic pressures of <110 despite having 85-year-old brains that perhaps need a somewhat higher cardiac output/cerebral perfusion pressure for those brains to work at peak efficiency.
I have spent my career helping to develop evidence-based therapies for stroke and for migraine… and yet the current guidelines in my own medical neck of the woods do not always match up with the ever-changing existing evidence. I suspect the same maybe so for the beta blockers.
Unfortunately, guidelines can act much like the clinical trials that create those guidelines: like steamrollers that seek to flatten a diverse population with diverse needs into one where “one size fits all“.
Combining patient level data across studies allows investigators to construct huge datasets that allow analyses that would not be otherwise possible. These patient-level data meta-analyses (PLDMAs) can show us which types of patients are likely to benefit from a treatment and which types aren’t.
When the difference between sub-populations in a PLDMA is large , as demonstrated by a very low p-value (e.g. 0.002), the statistical power lost by performing a comparison that was not pre-specified by the original investigators becomes moot. We get a large powerful RCT for free!
As we physicians, we are obligated to practice according to our understanding of the data to best benefit the patient in front of us. Go ahead, John: Give your patient HFrEF/AF patients digoxin and not a beta-blocker as you believe you must. “Best” practice alerts be damned. They are written by short-sighted bureaucrats. Educate your colleagues so they join you.
At the end of the day, it is yourself you must answer to.
Just a couple of thoughts off the top of my head, one of the biggest issues in patients with HFrEF and AF is rate control so typically I end up treating with Metoprolol Tartarate +/- Digoxin but I'm really trying to restore SR first. If they have permanent AF rate control is always going to be an issue so I'm looking ultimately at an AV nodal ablation at CRT. I like Dig but a lot of these patients have CKD and/or polypharmacy so Dig toxicity is always a concern. In the end this is definitely a sicker cohort of patients.
Who, exactly, are “those measuring how well I practiced evidence-based medicine”? The clipboard nurses? Joint Commission? Insurers? I’m asking honestly—I am not a physician and don’t know how this monitoring works.
Physicians don’t have the full freedom to treat their patients as they see best.
One commenter said it well: it’s these “One size fits all” guidelines. How did we get here? Everyone BUT the patient’s physician is making decisions on how best to treat their patient. I get it that there are quacks doing really crazy things—and I bet they’re still doing them because they aren’t a part of these monitored health settings. There’s a place for oversight, but how do we let doctors be doctors?
I truly don’t know what to think, personally or professionally.
I’ve had atrial fib since my second year of medical school, some (“many” is a relative adjective) decades ago, and for years the mainstays of my treatment were digoxin and quinidine….which at least made me feel part of the gang – seemingly half of my adult patients – AF or no – were taking one or the other drug (mostly digoxin).
Now I see a patient on digoxin about once every six months, and quinidine is a word roughly on a par with bathroom wall graffiti. On the other hand, despite having had no problems with rate controlI I have been taking metoprolol for years, and in my clinics I frequently encounter AF patients on a beta blocker per guidelines but with heart rates <60 and systolic pressures of <110 despite having 85-year-old brains that perhaps need a somewhat higher cardiac output/cerebral perfusion pressure for those brains to work at peak efficiency.
I have spent my career helping to develop evidence-based therapies for stroke and for migraine… and yet the current guidelines in my own medical neck of the woods do not always match up with the ever-changing existing evidence. I suspect the same maybe so for the beta blockers.
Unfortunately, guidelines can act much like the clinical trials that create those guidelines: like steamrollers that seek to flatten a diverse population with diverse needs into one where “one size fits all“.
Combining patient level data across studies allows investigators to construct huge datasets that allow analyses that would not be otherwise possible. These patient-level data meta-analyses (PLDMAs) can show us which types of patients are likely to benefit from a treatment and which types aren’t.
When the difference between sub-populations in a PLDMA is large , as demonstrated by a very low p-value (e.g. 0.002), the statistical power lost by performing a comparison that was not pre-specified by the original investigators becomes moot. We get a large powerful RCT for free!
As we physicians, we are obligated to practice according to our understanding of the data to best benefit the patient in front of us. Go ahead, John: Give your patient HFrEF/AF patients digoxin and not a beta-blocker as you believe you must. “Best” practice alerts be damned. They are written by short-sighted bureaucrats. Educate your colleagues so they join you.
At the end of the day, it is yourself you must answer to.
Just a couple of thoughts off the top of my head, one of the biggest issues in patients with HFrEF and AF is rate control so typically I end up treating with Metoprolol Tartarate +/- Digoxin but I'm really trying to restore SR first. If they have permanent AF rate control is always going to be an issue so I'm looking ultimately at an AV nodal ablation at CRT. I like Dig but a lot of these patients have CKD and/or polypharmacy so Dig toxicity is always a concern. In the end this is definitely a sicker cohort of patients.