JAMA Cardiology featured a strong editorial urging cardiologists to intervene early in patients who have aortic valve stenosis and no symptoms. I do not agree.
What early TAVR needed was sham control. Really pretty egregious for any device trial to not have sham control, after the example from Orbita.
If it had sham control, we wouldn’t need to be incredulous at the huge and immediate curve separation, and early increase in “unplanned hosp” in the control group….right after they had ETT confirming absence of symptoms.
And I’d say it’s not “not nefarious” when writers with conflicts of interest are boosting a procedure on the basis of a very soft endpoint from a trial tilted towards the observed result.
Im almost 71. For 5 years Ive been told I had a heart murmur but that was it--no tests of any kind until a year ago. After echo etc they said I have 'mild aortic stenosis'. They told me not to worry about it and to go about life normally but step up my exercise as Im very sedentary from having polio in the 60s. Im short of breasth even standing up but was told its from eing severly out of shape and also having post polio. So---having no medical background, I cant make heads or tails of this article. It causes me to worry, as Ive read stenosis always becomes worse. Do I have it taken care of now or wait for it to leave the 'mild' category? Im greatly concerned now. Also, I think the article leads more toward open surgery?
The Hutchison quotation resonates broadly, not just in this well explained assessment in the clinical issue under study, but far ranging to many other facets of what should be true medical “practice”…It brings to mind the John Hunter quotation that hung behind my desk for my entire academic surgery career, and one that I tried to live by daily…the reluctant surgeon…
“This last part of surgery, namely, operations, is a reflection on the healing art; it is a tacit acknowledgement of the insufficiency of surgery. It is like an armed savage who attempts to get that by force which a civilised man would get by stratagem.” John Hunter (1728-1793)
You are wrong. This is where there is a decided difference between medical and surgical approach and philosophy. The watch and wait is full of pitfalls. Constant monitoring and testing. What is the cost of that?
If the patient has a bicuspid valve, as one suggested, you will eventually need surgery. It's just a matter of time. Now you consider this. As the patient ages, recover and resilience diminishes. Surgery at age 60 is not the same as surgery at age 80.
I think what's not discussed is the critical point at which symptoms develop can be quite precipitous. What is the critical aortic root diameter at which surgery is mandatory?
It’s not “constant monitoring”. I don’t keep asymptomatic severe AS pts in my guest room, or in the CCU. I educate them on the cardinal symptoms, and ask them to notify me. And I see them periodically.
Bicuspids were only about 8% of the Early TAVR cohort.
I'm speaking as a patient whose consulting physician at the end was Eric Topol, but also as decades-long financial journalist and many would say is known for having a skeptic view on things – so please don't dismiss me!
I have been intrigued with the early trial, but mostly because I was in the watchful/waiting camp with my aortic insufficiency for more than 40 years. And I viewed myself as asymptomatic. (Tho as most asymptomatics will likely tell you, post-surgery they realize they probably were! I exercised regularly and over the decades saw top-notch cardiologists as I moved for my job from coast-to-coast and in between.
But it was my original diagnosis by a member of one of the most prestigious pioneering heart-related families in St. Paul that woke me up to what I'm about to say...
His view when he heard the murmur was, "It's nothing." This was in the early days of HMOs and hearing I had a "murmur" got my attention. After all, it was MY heart and I was learning for the first time in my 20s that it wasn't perfect!
I had no idea what a murmur was, but demanded an ultrasound - and had to fight to get it. From that point on, I watched it annually, with physicians showing varying degrees of interest and concern as I moved from city to city - Chicago, New York, San Francisco, where I was always seen at the top institutions.
As medicine progressed, I received CTs, MRIs - never a TEE, interestingly enough. Every year for a decade one cardiologist did a stress echo. Why a stress echo annually? I don't know. I read and researched to the point that I'm sure my regular cardiologist, in the final few years until surgery, dreaded having to see me and having me ask SO many questions.
All imaging over the past two decades suggested I had a "probable bicuspid valve" with increasingly severe stenosis. This includes imaging in Cleveland pre-surgery.
It wasn't until about six month pre-surgery that I started to have symptoms (it took a suprisingly long time to recovery my breath after walking up a steep hill. On one hand I thought nothing of it, but the more it happened, the more I hoped it wasn't what it turned out to be). By that point, because of also having an aortic aneurism that was edging toward the 5.0 mark, I was on the every 3-month scan plan.
This is where things get interesting...
My cardiologist here in San Diego suggested coming back in yet another three months, but my body suggested I get a second opinion. Thanks to Eric's intro, I had been going back/forth over the years with Lars Svensson at Cleveland. Each year, after reviewing the images, he would suggest I continue to watch it. This time, after seeing the results, he suggested I fly in for further tests and consultations. Within I month I did and his conclusion after reviewing the results, when I suggest we wait maybe eight months until after a grandchild was born was: "I would do this soon." Not because of the aneurism, which was hovering at 4.9, but the valve combined with my symptoms.
A month later I had the full slice-and-dice. I was in good health and the surgery and recovery were surprisingly fantastic.
But here's the kicker: I was 67. When he opened me up, he found I had a unicuspid valve, but that my heart had expanded to an athlete's heart to compensate, which is why I was asymptomatic well beyond when most unicuspid valves would have been replaced. My point: Despite all the great imaging, perhaps because of the way I'm built, they couldn't see that until they got inside.
They also did a bypass of my marginal obtuse artery, but the overall consensus is that it was my valve that was causing my breathlessness after walking up hills, not the blockage.
Moral of my story: I'm among those who watched it like a hawk and educated myself, keeping my fingers crossed at every echo that the measurements of my left ventricle would be stable. I don't believe most people do, and my bigger concern is physicians who discover murmurs and tell the patient, "Don't worry about it," when in the very least they need to get a baseline. In fact, it wasn't until about seven years before surgery, after moving back to San Diego from Connecticut, where I saw a Yale cardioligst, that a doctor even suggested I get a solid baseline on the size of my aorta... which is when we realized IT needed to be watched. That should have been SOP on any bicuspid patient, but nobody ever mentioned it.
I was skeptical of the early trials for the reason you were. I'm a huge fan of Edwards and I and I genuinely think heart failure is a big issue that can be prevented. I'm just dubious that most internists/family med doctors will make the referrals to a cardiologist on discovering a "murmur." And if they do, that most patients will realize WHY they should monitor it going forward. After all, you don't feel aortic insufficiency if it's minor or even moderate – and if like me, you feel (or felt) fine. I simply don't think the risk of heart failure or other ramifications are communicated enough to valve patients.
Again, I speak as a non-med professional but as someone with a keen and very personal interest in the topic.
Thanks1 And re AS/AI - that's a nuance I didn't pick up. I look at it through the eyes of somebody who hit the jackpot by having both so I look at it through those eyes. My bigger concern is that I'm in the minority of folks who keep/kept up on it. I'd like to know I'm wrong. My heart goes out to inner-city and deep rural folks who might not have the time, coverage or medical encouragement to stay with it. Or... insurance.
So happy it worked out for you. However, you really were asymptomatic for a long time and didn't need intervention. What I think is unstated however but the point of the op-ed is the reality of what such a huge change will result in. Directly stated it is massive over adoption for financial personal, institutional and corporate benefit without significant clinical improvement in pt outcome. Most of us "seasoned physicians" see this continually in practice. If we switch to "early asymptomatic" intervention the outcome winner will be the medical industrial complex unless we have better trials truly showing it improves morbidity and mortality.
Thanks for the insight. Again, I'm a big fan of Edwards but then again, I'm biased. But I agree on the early trial concerns, and it has been a concern from an analytical perspective for the reasons you state; in fact, it was my first reaction. Another reaction is how early can you do valve-in-valve, given durability unknowns. (Again, just a patient.)
Well, they should say what symptoms are, especially if valve disease is one of the most untreated out there. And not just symptoms, but implications for untreated. Then again, it's like HBP - if you can't feel it, why worry?
To your bigger point: I actually think that if I hadn't thought about it after that, I might've been one of those folks who landed in the bucket of waking up one day and realizing I had a problem. I can't imagine not wanting to monitor a murmur once you know you have one... and not just that, but try to get clarity on the type of murmur, which valve, etc.
I go back to the relationship between bicuspid and aneurism. Just knowing you're in the 2% with a bicuspid can ultimately save your life. I realize most people who die of aortic dissection probably had normal valves, but I do wonder how many had a bicuspid they didn't know about.
I consider myself very lucky that I found all of it before it found me. I realize there is a big gap between your world and mine, as a patient. But I choose to be as informed as a layman can be. When it was time for surgery, nobody had to twist my arm because
I knew the odds, plus I had a fantastic surgeon. I was actually excited - treating it very much like a first-person journalistic experience. Anyway, thanks for your insight. Cheers!
Congrats, Herb, on your successful outcome! It seems to me that things were handled just the way they should have? You were forewarned and waited (40 years!) for symptoms. When they finally arrived, the surgeons took care of it. Would it have been preferable if, 20 or 30 years ago, you had had prophylactic AV replacement? That’s what these people are advocating. (And I say this as someone whose mother died awaiting a TAVR operation. We just have to recognize that once AS becomes symptomatic, we have to act fast.)
Over the course of the decades I lived in SF, Chicago, NY/NJ/CT and here in San Diego and saw good docs at top medical centers all along. Nobody ever suggested it. In fact, they sometimes seemed puzzled by my situation. Maybe my unicuspid gave off false readings? I have no idea. The good news is that it all worked out. The big question now for folks, of course, is how early is TOO early for asymptomatic? All I know is that I watched it like a hawk and held my breath after every ultrasound on the diameter of my heart chambers.
For nearly 50 years I followed innumerable patients with AS long before TAVR. Some opted for surveillance while others elected surgical intervention. The natural history of AS is typically progression to symptomatic disease.
In your article, and in reference to the EARLY TAVR trial, you state: "The sole driver of the primary endpoint was unplanned hospitalization, mostly for symptoms of AS. Death and stroke were not different."
The key for me in this sentence is your observation that death and stroke were unchanged, so the effective endpoint might have more simply been unplanned hospitalization, resulting in similar conclusions to those of the actual trial. Following this logic, the trial concludes (and the editorial supports) early intervention as a preferable route to the *possibility* of later unplanned hospitalization. Such hospitalization may never occur, or may be for treatment that is less invasive or risky than TAVR.
To me this is a major problem that is in addition to the one you raised.
Well, back in the old days if we had a patient with AS and we weren't sure if they were "asymptomatic" - you put them on the treadmill. If you're sending them home because "they're asymptomatic."- the treadmill should be safe.
The concept of "asymptomatic " I believe is the most flawed term in all of our records for cardiovascular disease.
An asymptomatic 80 year-old man in rural Lampasas who threw hay ( 50 pound bales 30 of them) is a lot different than the asymptomatic 80 year old watching TV.
I would always ask the following question . What is the most strenuous thing you do? Then if they were asymptomatic, I would say the most strenuous thing the patient does is X and they say they are asymptomatic when they are doing it.
If you're evaluating a patient with aortic stenosis and you don't have a understanding of what their functional capacity is, labeling them "asymptomatic" can result in a lethal decision.
And your summary exemplifies why I gave up on MSM medical journal years ago. Bia$ and political pandering have rendered most/all to the downfall in trust in medicine. IMHO.
Excellent counterpoint to the recent JAMA Viewpoint paper. The underlying problem is the proliferation of confusing combined primary endpoints that seem designed to increase chances of getting to a "positive" trial rather than revealing unbiased medical truth. EARLY TAVR was particularly egregious - defining TAVR as a therapeutic procedure in the intervention group and an adverse event in the control arm. Subsets of hospitalizations should not be accepted as an endpoint, as they are clearly biased toward intervention. What good is an intervention that reduces CV or heart failure hospitalization but increases non-CV/HF hospitalization? More in the CV community need to call out this problem, or it will continue.
Unfortunately, some diabetic patients will eventually progress to the point where we will have to amputate their feet. So should we amputate the feet of all upon their initial diabetes diagnosis? It would prevent 100% of any future amputations… That’s the logic these trialists/marketers are using. The same scam is used in PCI trials where they include “unplanned”—or even total—PCIs in the primary endpoint counts of unblinded, non-sham trials. It’s totally bogus and we need to call these scams out.
I agree with you John.however, Jama paper recently put, in the supplemental material, the cases of death in conservative arm, sudden death was present before symptoms …… ? What are your thought about it?
I could not agree more. This is simply about profit for both the manufacturers, the physicians and hospitals involved. Of course no one really has the patients best interests at heart.
Secondly who defines what is symptomatic.
And thirdly and I constantly berate the point the numbers(n) in both trials were just too small( irrespective of whatever statistical methods were employed.)
What early TAVR needed was sham control. Really pretty egregious for any device trial to not have sham control, after the example from Orbita.
If it had sham control, we wouldn’t need to be incredulous at the huge and immediate curve separation, and early increase in “unplanned hosp” in the control group….right after they had ETT confirming absence of symptoms.
And I’d say it’s not “not nefarious” when writers with conflicts of interest are boosting a procedure on the basis of a very soft endpoint from a trial tilted towards the observed result.
Im almost 71. For 5 years Ive been told I had a heart murmur but that was it--no tests of any kind until a year ago. After echo etc they said I have 'mild aortic stenosis'. They told me not to worry about it and to go about life normally but step up my exercise as Im very sedentary from having polio in the 60s. Im short of breasth even standing up but was told its from eing severly out of shape and also having post polio. So---having no medical background, I cant make heads or tails of this article. It causes me to worry, as Ive read stenosis always becomes worse. Do I have it taken care of now or wait for it to leave the 'mild' category? Im greatly concerned now. Also, I think the article leads more toward open surgery?
The Hutchison quotation resonates broadly, not just in this well explained assessment in the clinical issue under study, but far ranging to many other facets of what should be true medical “practice”…It brings to mind the John Hunter quotation that hung behind my desk for my entire academic surgery career, and one that I tried to live by daily…the reluctant surgeon…
“This last part of surgery, namely, operations, is a reflection on the healing art; it is a tacit acknowledgement of the insufficiency of surgery. It is like an armed savage who attempts to get that by force which a civilised man would get by stratagem.” John Hunter (1728-1793)
You are wrong. This is where there is a decided difference between medical and surgical approach and philosophy. The watch and wait is full of pitfalls. Constant monitoring and testing. What is the cost of that?
If the patient has a bicuspid valve, as one suggested, you will eventually need surgery. It's just a matter of time. Now you consider this. As the patient ages, recover and resilience diminishes. Surgery at age 60 is not the same as surgery at age 80.
I think what's not discussed is the critical point at which symptoms develop can be quite precipitous. What is the critical aortic root diameter at which surgery is mandatory?
Critical diameter? 0.75 mm2.
It’s not “constant monitoring”. I don’t keep asymptomatic severe AS pts in my guest room, or in the CCU. I educate them on the cardinal symptoms, and ask them to notify me. And I see them periodically.
Bicuspids were only about 8% of the Early TAVR cohort.
I'm speaking as a patient whose consulting physician at the end was Eric Topol, but also as decades-long financial journalist and many would say is known for having a skeptic view on things – so please don't dismiss me!
I have been intrigued with the early trial, but mostly because I was in the watchful/waiting camp with my aortic insufficiency for more than 40 years. And I viewed myself as asymptomatic. (Tho as most asymptomatics will likely tell you, post-surgery they realize they probably were! I exercised regularly and over the decades saw top-notch cardiologists as I moved for my job from coast-to-coast and in between.
But it was my original diagnosis by a member of one of the most prestigious pioneering heart-related families in St. Paul that woke me up to what I'm about to say...
His view when he heard the murmur was, "It's nothing." This was in the early days of HMOs and hearing I had a "murmur" got my attention. After all, it was MY heart and I was learning for the first time in my 20s that it wasn't perfect!
I had no idea what a murmur was, but demanded an ultrasound - and had to fight to get it. From that point on, I watched it annually, with physicians showing varying degrees of interest and concern as I moved from city to city - Chicago, New York, San Francisco, where I was always seen at the top institutions.
As medicine progressed, I received CTs, MRIs - never a TEE, interestingly enough. Every year for a decade one cardiologist did a stress echo. Why a stress echo annually? I don't know. I read and researched to the point that I'm sure my regular cardiologist, in the final few years until surgery, dreaded having to see me and having me ask SO many questions.
All imaging over the past two decades suggested I had a "probable bicuspid valve" with increasingly severe stenosis. This includes imaging in Cleveland pre-surgery.
It wasn't until about six month pre-surgery that I started to have symptoms (it took a suprisingly long time to recovery my breath after walking up a steep hill. On one hand I thought nothing of it, but the more it happened, the more I hoped it wasn't what it turned out to be). By that point, because of also having an aortic aneurism that was edging toward the 5.0 mark, I was on the every 3-month scan plan.
This is where things get interesting...
My cardiologist here in San Diego suggested coming back in yet another three months, but my body suggested I get a second opinion. Thanks to Eric's intro, I had been going back/forth over the years with Lars Svensson at Cleveland. Each year, after reviewing the images, he would suggest I continue to watch it. This time, after seeing the results, he suggested I fly in for further tests and consultations. Within I month I did and his conclusion after reviewing the results, when I suggest we wait maybe eight months until after a grandchild was born was: "I would do this soon." Not because of the aneurism, which was hovering at 4.9, but the valve combined with my symptoms.
A month later I had the full slice-and-dice. I was in good health and the surgery and recovery were surprisingly fantastic.
But here's the kicker: I was 67. When he opened me up, he found I had a unicuspid valve, but that my heart had expanded to an athlete's heart to compensate, which is why I was asymptomatic well beyond when most unicuspid valves would have been replaced. My point: Despite all the great imaging, perhaps because of the way I'm built, they couldn't see that until they got inside.
They also did a bypass of my marginal obtuse artery, but the overall consensus is that it was my valve that was causing my breathlessness after walking up hills, not the blockage.
Moral of my story: I'm among those who watched it like a hawk and educated myself, keeping my fingers crossed at every echo that the measurements of my left ventricle would be stable. I don't believe most people do, and my bigger concern is physicians who discover murmurs and tell the patient, "Don't worry about it," when in the very least they need to get a baseline. In fact, it wasn't until about seven years before surgery, after moving back to San Diego from Connecticut, where I saw a Yale cardioligst, that a doctor even suggested I get a solid baseline on the size of my aorta... which is when we realized IT needed to be watched. That should have been SOP on any bicuspid patient, but nobody ever mentioned it.
I was skeptical of the early trials for the reason you were. I'm a huge fan of Edwards and I and I genuinely think heart failure is a big issue that can be prevented. I'm just dubious that most internists/family med doctors will make the referrals to a cardiologist on discovering a "murmur." And if they do, that most patients will realize WHY they should monitor it going forward. After all, you don't feel aortic insufficiency if it's minor or even moderate – and if like me, you feel (or felt) fine. I simply don't think the risk of heart failure or other ramifications are communicated enough to valve patients.
Again, I speak as a non-med professional but as someone with a keen and very personal interest in the topic.
Thanks for reading, assuming you got this far!
Big fan of your journalism.
Be aware that the current discussion is about pure aortic stenosis, which is quite different from aortic insufficiency or mixed AS/AI.
Nevertheless, you are living confirmation of the utility of active surveillance--- for 40 years!
Thanks1 And re AS/AI - that's a nuance I didn't pick up. I look at it through the eyes of somebody who hit the jackpot by having both so I look at it through those eyes. My bigger concern is that I'm in the minority of folks who keep/kept up on it. I'd like to know I'm wrong. My heart goes out to inner-city and deep rural folks who might not have the time, coverage or medical encouragement to stay with it. Or... insurance.
Herb,
So happy it worked out for you. However, you really were asymptomatic for a long time and didn't need intervention. What I think is unstated however but the point of the op-ed is the reality of what such a huge change will result in. Directly stated it is massive over adoption for financial personal, institutional and corporate benefit without significant clinical improvement in pt outcome. Most of us "seasoned physicians" see this continually in practice. If we switch to "early asymptomatic" intervention the outcome winner will be the medical industrial complex unless we have better trials truly showing it improves morbidity and mortality.
Thanks for the insight. Again, I'm a big fan of Edwards but then again, I'm biased. But I agree on the early trial concerns, and it has been a concern from an analytical perspective for the reasons you state; in fact, it was my first reaction. Another reaction is how early can you do valve-in-valve, given durability unknowns. (Again, just a patient.)
Well, they should say what symptoms are, especially if valve disease is one of the most untreated out there. And not just symptoms, but implications for untreated. Then again, it's like HBP - if you can't feel it, why worry?
To your bigger point: I actually think that if I hadn't thought about it after that, I might've been one of those folks who landed in the bucket of waking up one day and realizing I had a problem. I can't imagine not wanting to monitor a murmur once you know you have one... and not just that, but try to get clarity on the type of murmur, which valve, etc.
I go back to the relationship between bicuspid and aneurism. Just knowing you're in the 2% with a bicuspid can ultimately save your life. I realize most people who die of aortic dissection probably had normal valves, but I do wonder how many had a bicuspid they didn't know about.
I consider myself very lucky that I found all of it before it found me. I realize there is a big gap between your world and mine, as a patient. But I choose to be as informed as a layman can be. When it was time for surgery, nobody had to twist my arm because
I knew the odds, plus I had a fantastic surgeon. I was actually excited - treating it very much like a first-person journalistic experience. Anyway, thanks for your insight. Cheers!
Congrats, Herb, on your successful outcome! It seems to me that things were handled just the way they should have? You were forewarned and waited (40 years!) for symptoms. When they finally arrived, the surgeons took care of it. Would it have been preferable if, 20 or 30 years ago, you had had prophylactic AV replacement? That’s what these people are advocating. (And I say this as someone whose mother died awaiting a TAVR operation. We just have to recognize that once AS becomes symptomatic, we have to act fast.)
Over the course of the decades I lived in SF, Chicago, NY/NJ/CT and here in San Diego and saw good docs at top medical centers all along. Nobody ever suggested it. In fact, they sometimes seemed puzzled by my situation. Maybe my unicuspid gave off false readings? I have no idea. The good news is that it all worked out. The big question now for folks, of course, is how early is TOO early for asymptomatic? All I know is that I watched it like a hawk and held my breath after every ultrasound on the diameter of my heart chambers.
For nearly 50 years I followed innumerable patients with AS long before TAVR. Some opted for surveillance while others elected surgical intervention. The natural history of AS is typically progression to symptomatic disease.
In your article, and in reference to the EARLY TAVR trial, you state: "The sole driver of the primary endpoint was unplanned hospitalization, mostly for symptoms of AS. Death and stroke were not different."
The key for me in this sentence is your observation that death and stroke were unchanged, so the effective endpoint might have more simply been unplanned hospitalization, resulting in similar conclusions to those of the actual trial. Following this logic, the trial concludes (and the editorial supports) early intervention as a preferable route to the *possibility* of later unplanned hospitalization. Such hospitalization may never occur, or may be for treatment that is less invasive or risky than TAVR.
To me this is a major problem that is in addition to the one you raised.
Thank you for the great article and analysis!
Well, back in the old days if we had a patient with AS and we weren't sure if they were "asymptomatic" - you put them on the treadmill. If you're sending them home because "they're asymptomatic."- the treadmill should be safe.
The concept of "asymptomatic " I believe is the most flawed term in all of our records for cardiovascular disease.
An asymptomatic 80 year-old man in rural Lampasas who threw hay ( 50 pound bales 30 of them) is a lot different than the asymptomatic 80 year old watching TV.
I would always ask the following question . What is the most strenuous thing you do? Then if they were asymptomatic, I would say the most strenuous thing the patient does is X and they say they are asymptomatic when they are doing it.
If you're evaluating a patient with aortic stenosis and you don't have a understanding of what their functional capacity is, labeling them "asymptomatic" can result in a lethal decision.
“Asymptomatic” is free from syncope or a heart failure hospitalization, both hard outcomes.
Angina, a “soft” outcome is more problematic, and, admittedly, requires judgment…
So the pt lives their life at max 3 METS and is asymptomatic.
You put them on a treadmill and elicit symptoms at 5 METS, and herd them off to AVR.
Then they go back to their asymptomatic 3 METS life.
Unless they have a peri-op stroke, wound infection, Afib, bleed, or bacterial endocarditis.
And your summary exemplifies why I gave up on MSM medical journal years ago. Bia$ and political pandering have rendered most/all to the downfall in trust in medicine. IMHO.
Sir Robert Hutchinson, "The Physician's Prayers" sounds spot on. Also wisdom that is clearly missing in many aspects of medicine.
Edit
Hutchison "the physician's prayer"
Excellent counterpoint to the recent JAMA Viewpoint paper. The underlying problem is the proliferation of confusing combined primary endpoints that seem designed to increase chances of getting to a "positive" trial rather than revealing unbiased medical truth. EARLY TAVR was particularly egregious - defining TAVR as a therapeutic procedure in the intervention group and an adverse event in the control arm. Subsets of hospitalizations should not be accepted as an endpoint, as they are clearly biased toward intervention. What good is an intervention that reduces CV or heart failure hospitalization but increases non-CV/HF hospitalization? More in the CV community need to call out this problem, or it will continue.
Unfortunately, some diabetic patients will eventually progress to the point where we will have to amputate their feet. So should we amputate the feet of all upon their initial diabetes diagnosis? It would prevent 100% of any future amputations… That’s the logic these trialists/marketers are using. The same scam is used in PCI trials where they include “unplanned”—or even total—PCIs in the primary endpoint counts of unblinded, non-sham trials. It’s totally bogus and we need to call these scams out.
Exactly.
TAVR in January prevents TAVR in May.
I agree with you John.however, Jama paper recently put, in the supplemental material, the cases of death in conservative arm, sudden death was present before symptoms …… ? What are your thought about it?
Conflict of interest
Study done by those that profit
Cherry picking results
You could have stopped right there!?!
Let us physicians strive to make people feel better rather than hope to improve outcomes with spurious treatments.
Profit is replacing evidence-based medicine, with medical journals becoming exceedingly complicit.
I could not agree more. This is simply about profit for both the manufacturers, the physicians and hospitals involved. Of course no one really has the patients best interests at heart.
Secondly who defines what is symptomatic.
And thirdly and I constantly berate the point the numbers(n) in both trials were just too small( irrespective of whatever statistical methods were employed.)