Many people--including prominent podcasters--believe that discovering a coronary blockage is a great idea. Let's look at the actual studies. You will be surprised.
2. I think many people are confusing 'routine PCI' in all stable CAD with true ischemia driven PCI. My argument is that ETT and poor quality MPI are NOT at all 'proof of ischemia'. On table FFR (or iFR) is superior to both ETT and MPI. ETT only has 67% sensitivity and specificity. If one is familiar with MPI interpretation, then one knows the numerous technical factors (timing of injection, image acquisition and processing, and finally physician interpretation) that lead to lower sensitivity in real world setting. 85-90% sensitivity for MPI is reported in research trials (not real world community setting). The actual sensitivity in many centers is lower. Also, PCI for low risk positive MPI (SDS<4) does not carry the same indication as PCI for high risk MPI (SDS>7). Finally, balanced ischemia (left main, multi vessel) is often missed with MPI.
***
3. "by performing routine PCI we are obligating patients to more medical therapy,": Again, I'm not arguing for "routine PCI". I'm arguing against routine medical management for stable CAD UNLESS there is true high quality assessment of ischemia (FFR / iFR) AND there is diagnostic coronary anagram (or good quality coronary CTA) to ensure no left main / prox LAD). Also, have to have radiologists / cardiologists who understand 'balanced ischemia' in MPI stress testing (elevated TID is often not reported for concerns of multi vessel disease). Medical group: ASA, statin, BB, CCB, nitrate, +/- ranolazine. Medical group will often have 4-5 medications. PCI + medical group: ASA, clopidogrel for 12 months, statin, BB (3-4 medications). So, I'm not sure how PCI group is obligated to more medications. On the contrary, numerous trials demonstrate that PCI in stable CAD does lead to fewer medications for angina control.
***
One must also take into consideration occupation and special circumstances. Stress testing guidelines do not apply to airline pilots or commercial pilots, commercial truck drivers, and pre-transplant evaluation. Likewise, medical therapy for stable CAD is a hard sell for agricultural workers and construction workers (taking 4-5 medications daily, some twice daily, and having 2-3 episodes of angina requiring S/L NTG could lead to inability to perform one's occupational duties). This is not at all to suggest 'routine PCI' for everyone. It's simply to state that 'routine medical therapy' for stable CAD should not be practiced as a strict mandate for all regardless of occupation and clinical circumstances.
*****
Finally, how does one assess in a trial the anterior STEMI patient with underlying 70-90% calcified prox LAD lesion? Had this lesion been assessed and treated in a stable setting, then mechanical atherectomy could be performed in a safe manner with higher success. Now, in a community primary PCI center the on call team is dealing with a complex calcified lesion. If they don't have mechanical atherectomy they will probably have unsuccessful PCI (or poor stent deployment) or be doing CPR. How does one assess the missed multi vessel CAD because "MPI was negative" (but radiologist didn't comment on TID) that could have been treated earlier in the disease process but now has complex multivessel CAD with drop in LVEF: too high risk for CABG and not amenable to complex PCI? These are all real world examples and not hypothetical statistics.
****
I am not at all arguing for "routine PCI" without assessment of ischemia. I'm just saying the many people are treating all stable CAD as if they are all equally low risk when in fact there are subsets that benefit from FFR driven PCI.
Nearly exactly 2 years ago, I had a heart event. I ended up in ER with chest pains, although not really severe, this was something new to me. They did a few tests and gave me aspirin. I was feeling normal after a few hours and was released after about 4 1/2 hours with no drugs and no heart damage.
About a month later I saw a cardiologist after doing a stress test. He really didn't tell me what he saw but only that I needed to be put on drugs and have a catherization and probably a stent(s). I told him I needed to do research on all this (the heart drugs and stents) and he wasn't too happy. He made it almost seem like it was a critical problem and if I didn't go this route, I could have further problems.
I did much research and decided I wasn't going to do as he suggested. I now use high potency cayenne tincture with is quite a miracle herb for the heart. I take a few other supplements also. I don't smoke or drink, manage stress, get some exercise and am able to function fairly well at age 73. I have had no further episodes expect some occasional mild pains that do not last long. My diet is the biggest challenge.
As far as I could find, there is no proof that normal "cardiology" used on heart patients makes much difference except maybe in extreme cases. So you take heart drugs and get a stent. The real question, which the medical community outright refuses to ask and investigate, is why do heart problems occur.
This is why I will continue to avoid the modern medical establishment. There is NO reason anyone should ever need drugs (other than if a few rare cases). If you do, then it is most likely because you have abused your body. It has become a broken down pit of toxicity. No drugs, tests or procedures are going to fix negligence and stupidity.
While still in practice, I was disappointed how many of my patients continued to undergo PCI for stable or asymptomatic CAD years after these studies were published suggesting a course correction. Old habits, beliefs, mixed incentives, I don't know. One patient story stands out. Gentleman in his mid 60s with stable CAD (no angina or angina equivalent symptoms), previous MI, previous CABG receiving optimal medical therapy, scheduled for elective surgery, I believe hip replacement, referred by the surgeon to his cardiologist for preop cardiac clearance. Cardiologist performed a stress test which was abnormal though as I recall, consistent with his known disease. He then performed a Cath and in the process of attempting a PCI and stent, caused a dissection in the vessel, an acute MI, a near fatal disaster requiring additional instrumentation to salvage the patient. He recovered and eventually had his hip replaced.
There still are “prominent podcasters” who promote open artery hypothesis and plumbing solutions for systemic vascular problems?!? In 2023?!?
Courage had some limitations. But I was practicing “courage” protocol even before courage, and nothing before or since has made me need to substantially reconsider.
No doubt you will be reviewing Orbita and Ischemia is this series, which addresses some of the limitations of courage and further cement the primacy of medical therapy for most people with stable CAD.
I'm an Interventional Cardiologist and I've been at this since 1983, the early days of simple balloon angioplasty. And as Payam states, my ego/status/tenure/funding is involved in the care of heart disease. I will state that I see the vast majority of my colleagues transition to these new guidelines. Cardiologists are unique in that heart disease is so common, that our procedures have been tested in randomized studies in tens of thousands of patients in all ethnic, age, and economic groups. We tend to listen and adjust. I only place a coronary stent today in the setting of an Acute Coronary Syndrome, i.e. acute MI, unstable angina, or markedly abnormal stress test. Was the procedure done unnecessarily in the past to many patients? Yes. I guess the upside of overutilization of the procedure is that the technology evolved to an incredible high level and now we can effectively treat acute MI's with great success and improvement in outcomes. So there lies the ethical dilema . Yes, it was overutilized, but yes, we are very very good at treating and saving those suffering from a STEMI (ST Elevation Myocardial Infarction).
Thanks for writing this. The Courage trial compared optimal medical therapy alone vs optimal medical therapy plus a stent. That trial was conducted over a decade ago. Still our system is focused on finding blockages and opening them We do that but we don't provide optimal medical therapy and the consequences are terrible. If you are on optimal medical therapy after the discovery of heart artery disease, you are ten times as likely to be alive in 5 years compared with usual care-the care that most people receive.
A common cause of myocardial infarction and stroke is the rupture of atherosclerotic plaques. The exact location of plaque ruptures has previously been unknown, but now researchers at Lund University have mapped this. The research team has also identified an enzyme, a marker, that they hope will help predict who is at risk of having a myocardial infarction or a stroke due to a ruptured atherosclerotic plaque.
In atherosclerosis , fat is accumulated in the artery walls creating atherosclerotic plaques. Plaques that rupture can cause a stroke or myocardial infarction, and a deeper understanding of the mechanisms underlying plaque rupture is needed to prevent serious complications. Research at Lund University, Sweden,now shows that atherosclerotic plaques in the carotid arteries often rupture at the beginning of the plaque, at a location closest to the heart. The study has been published in the Journal of the American College of Cardiology (JACC).
“In our study, we were able to pinpoint exactly where plaques rupture. This is an important step, allowing for a better understanding of why they rupture. Previous studies have focused more on how plaques are formed while we have studied the precise area where they rupture, which no previous human study has done”, says Isabel Goncalves, who led the study.
1. COURAGE did not adequately assess ischemia (70% had MPI stress testing and there is no comment on degree of ischemia. The remainder presumably had treadmill stress test which does not have high sensitivity or specificity for ischemia). Subsequent trials using invasive assessment of ischemia (FFR / iFR) did prove benefit of PCI in stable CAD. Also, MPI with high ischemia burden (high risk ischemia, SDS>10) does have proven benefit. Also, it is unclear if the MPI stress testing was adjudicated in a core lab to ensure consistency of interpretation. So, yes: COURAGE did not adequately assess ischemia.
2. All patients did have diagnostic coronary angiography in COURAGE to definite the coronary anatomy (to ensure no left main). So, the takeaway should not be that stable CAD has no proven benefit of diagnostic coronary angiography (or coronary CTA).
3. Also, COURAGE evaluated MI and death: it did not assess time off from work, declining physical function, arrhythmias, poloypharmacy, etc.
ALL of the Doctors are already on the TAKE...personal fees....
How does that NOT color the results at all?
Dr. Bangalore reports grants from National Heart, Lung, and Blood Institute , during the conduct of the study; grants and personal fees from Abbott Vascular, personal fees from Biotronik, personal fees from Pfizer, personal fees from Amgen, personal fees from Reata, outside the submitted work; .
Dr. Ali reports grants from National Heart, Lung, and Blood Institute, during the conduct of the study; grants and personal fees from Abbott Vascular, grants and personal fees from Cardiovascular Systems Inc, personal fees from Amgen , personal fees from Astra Zeneca, personal fees from Abiomed, personal fees from Boston Scientific, personal fees from Cardinal Health , personal fees from Opsens Medical, personal fees from Acist Medical , other from Shockwave Medical, outside the
COURAGE was an an important (landmark) trial to curtail the occulostenotic impulse to perform PCI in all visual CAD. However, it had severe limitations. 57% of the patients in each arm had ETT as 'proof of ischemia'. ETT has 67% sensitivity and specificity and is hardly robust 'proof of ischemia'. Only ~70% in each arm had MPI stress testing. Has anyone seen MPI stress test interpretation (in the absence of a centralized core lab or 2 independent physicians to corroborate findings)? I have numerous examples of radiologist reading the MPI stress test as 'normal' but missing actual reversible perfusion defect. If read properly: MPI has great sensitivity but not so great specificity. So, COURAGE didn't actually have robust protocol to prove then absence of presence of ischemia.
So, COURAGE is a bit of a straw man argument: if one does PCI in stable CAD *without* adequate ischemia testing THEN there is no proven benefit in reducing MI and death. Ischemia driven PCI (FFR / iFR) in 'stable CAD' has proven benefit in hard outcomes.
We should also underscore that 'stable' Left Main and proximal LAD are different subsets benefiting from revascularization.
And one doesn't know if LM, proximal LAD or FFR/iFR are applicable to a particular patient without at least a diagnostic coronary angiogram (or in modern times coronary CTA).
So, none of the 'conservative' management trials (medical management alone) should lead one to conclude that for everyone diagnostics coronary angiogram is not needed. Unselected PCI (without robust ischemia testing) is indeed questionable at best (no proven benefit).
Finally, let's remember that these are real life human beings and not mere statistics. Trials like COURAGE do not take into account: quality of life (yes, they hint at decreased angina and decreased number of anti-anginal medications). However, this should not be an afterthought. For most people who perform physical labor: reduced angina and reduced number of anti-anginal medications directly correlates with professional productivity. Decreased number of medications also means increased compliance and decreased drug-drug interactions from polypharmacy (especially in older people). People with chronic 'stable' angina on 2-3 medications to control the angina are sometimes unable to perform their daily professional duties (if they perform physical labor).
Hard endpoints (MI and mortally) are easier to measure in trials and need smaller sample size. But quality of life (psychological and physical), professional productivity (time off from work due to cardiac testing, doctor and ER visits, etc), and improved exercise performance: these have never been adequately assessed in any major trial.
Also, untreated CAD *can* increase the risk of developing AFib (or other arrhythmias) or exacerbate pre-existing arrhythmias. This could further lead to time off from work and polypharmacy.
For AFib: we went 180 degrees (from emphasis on rate control to now once again emphasis on rhythm control).
I have no doubt that true ischemia-driven PCI in 'stable CAD' will be better assessed with more comprehensive contextualized decision making. PCI for every visual (angiographic) coronary stenosis is most certainly a waste of resources and has no proven benefit. But this should not be confused with ischemia (FFR, iFR) driven PCI nor should it categorically preclude diagnostic coronary angiography to ensure no left main or proximal LAD stenosis.
Thanks for your comment.
1. Please see link below for mortality benefit in FFR driven PCI (https://onlinelibrary.wiley.com/doi/full/10.1002/ccd.30310). I don't have access to full article so am unable to critique it in detail.
***
2. I think many people are confusing 'routine PCI' in all stable CAD with true ischemia driven PCI. My argument is that ETT and poor quality MPI are NOT at all 'proof of ischemia'. On table FFR (or iFR) is superior to both ETT and MPI. ETT only has 67% sensitivity and specificity. If one is familiar with MPI interpretation, then one knows the numerous technical factors (timing of injection, image acquisition and processing, and finally physician interpretation) that lead to lower sensitivity in real world setting. 85-90% sensitivity for MPI is reported in research trials (not real world community setting). The actual sensitivity in many centers is lower. Also, PCI for low risk positive MPI (SDS<4) does not carry the same indication as PCI for high risk MPI (SDS>7). Finally, balanced ischemia (left main, multi vessel) is often missed with MPI.
***
3. "by performing routine PCI we are obligating patients to more medical therapy,": Again, I'm not arguing for "routine PCI". I'm arguing against routine medical management for stable CAD UNLESS there is true high quality assessment of ischemia (FFR / iFR) AND there is diagnostic coronary anagram (or good quality coronary CTA) to ensure no left main / prox LAD). Also, have to have radiologists / cardiologists who understand 'balanced ischemia' in MPI stress testing (elevated TID is often not reported for concerns of multi vessel disease). Medical group: ASA, statin, BB, CCB, nitrate, +/- ranolazine. Medical group will often have 4-5 medications. PCI + medical group: ASA, clopidogrel for 12 months, statin, BB (3-4 medications). So, I'm not sure how PCI group is obligated to more medications. On the contrary, numerous trials demonstrate that PCI in stable CAD does lead to fewer medications for angina control.
***
One must also take into consideration occupation and special circumstances. Stress testing guidelines do not apply to airline pilots or commercial pilots, commercial truck drivers, and pre-transplant evaluation. Likewise, medical therapy for stable CAD is a hard sell for agricultural workers and construction workers (taking 4-5 medications daily, some twice daily, and having 2-3 episodes of angina requiring S/L NTG could lead to inability to perform one's occupational duties). This is not at all to suggest 'routine PCI' for everyone. It's simply to state that 'routine medical therapy' for stable CAD should not be practiced as a strict mandate for all regardless of occupation and clinical circumstances.
*****
Finally, how does one assess in a trial the anterior STEMI patient with underlying 70-90% calcified prox LAD lesion? Had this lesion been assessed and treated in a stable setting, then mechanical atherectomy could be performed in a safe manner with higher success. Now, in a community primary PCI center the on call team is dealing with a complex calcified lesion. If they don't have mechanical atherectomy they will probably have unsuccessful PCI (or poor stent deployment) or be doing CPR. How does one assess the missed multi vessel CAD because "MPI was negative" (but radiologist didn't comment on TID) that could have been treated earlier in the disease process but now has complex multivessel CAD with drop in LVEF: too high risk for CABG and not amenable to complex PCI? These are all real world examples and not hypothetical statistics.
****
I am not at all arguing for "routine PCI" without assessment of ischemia. I'm just saying the many people are treating all stable CAD as if they are all equally low risk when in fact there are subsets that benefit from FFR driven PCI.
Nearly exactly 2 years ago, I had a heart event. I ended up in ER with chest pains, although not really severe, this was something new to me. They did a few tests and gave me aspirin. I was feeling normal after a few hours and was released after about 4 1/2 hours with no drugs and no heart damage.
About a month later I saw a cardiologist after doing a stress test. He really didn't tell me what he saw but only that I needed to be put on drugs and have a catherization and probably a stent(s). I told him I needed to do research on all this (the heart drugs and stents) and he wasn't too happy. He made it almost seem like it was a critical problem and if I didn't go this route, I could have further problems.
I did much research and decided I wasn't going to do as he suggested. I now use high potency cayenne tincture with is quite a miracle herb for the heart. I take a few other supplements also. I don't smoke or drink, manage stress, get some exercise and am able to function fairly well at age 73. I have had no further episodes expect some occasional mild pains that do not last long. My diet is the biggest challenge.
As far as I could find, there is no proof that normal "cardiology" used on heart patients makes much difference except maybe in extreme cases. So you take heart drugs and get a stent. The real question, which the medical community outright refuses to ask and investigate, is why do heart problems occur.
This is why I will continue to avoid the modern medical establishment. There is NO reason anyone should ever need drugs (other than if a few rare cases). If you do, then it is most likely because you have abused your body. It has become a broken down pit of toxicity. No drugs, tests or procedures are going to fix negligence and stupidity.
While still in practice, I was disappointed how many of my patients continued to undergo PCI for stable or asymptomatic CAD years after these studies were published suggesting a course correction. Old habits, beliefs, mixed incentives, I don't know. One patient story stands out. Gentleman in his mid 60s with stable CAD (no angina or angina equivalent symptoms), previous MI, previous CABG receiving optimal medical therapy, scheduled for elective surgery, I believe hip replacement, referred by the surgeon to his cardiologist for preop cardiac clearance. Cardiologist performed a stress test which was abnormal though as I recall, consistent with his known disease. He then performed a Cath and in the process of attempting a PCI and stent, caused a dissection in the vessel, an acute MI, a near fatal disaster requiring additional instrumentation to salvage the patient. He recovered and eventually had his hip replaced.
I’m really looking forward to the rest of this series!
There still are “prominent podcasters” who promote open artery hypothesis and plumbing solutions for systemic vascular problems?!? In 2023?!?
Courage had some limitations. But I was practicing “courage” protocol even before courage, and nothing before or since has made me need to substantially reconsider.
No doubt you will be reviewing Orbita and Ischemia is this series, which addresses some of the limitations of courage and further cement the primacy of medical therapy for most people with stable CAD.
Well glad Cardiologists aren't like Oncologists (that sell the same drugs they get to RX).
Kinda reminds me of when GI was initially turned on it’s ear when H. Pylori became “a common cause” of peptic ulcers!
I'm an Interventional Cardiologist and I've been at this since 1983, the early days of simple balloon angioplasty. And as Payam states, my ego/status/tenure/funding is involved in the care of heart disease. I will state that I see the vast majority of my colleagues transition to these new guidelines. Cardiologists are unique in that heart disease is so common, that our procedures have been tested in randomized studies in tens of thousands of patients in all ethnic, age, and economic groups. We tend to listen and adjust. I only place a coronary stent today in the setting of an Acute Coronary Syndrome, i.e. acute MI, unstable angina, or markedly abnormal stress test. Was the procedure done unnecessarily in the past to many patients? Yes. I guess the upside of overutilization of the procedure is that the technology evolved to an incredible high level and now we can effectively treat acute MI's with great success and improvement in outcomes. So there lies the ethical dilema . Yes, it was overutilized, but yes, we are very very good at treating and saving those suffering from a STEMI (ST Elevation Myocardial Infarction).
Thanks for writing this. The Courage trial compared optimal medical therapy alone vs optimal medical therapy plus a stent. That trial was conducted over a decade ago. Still our system is focused on finding blockages and opening them We do that but we don't provide optimal medical therapy and the consequences are terrible. If you are on optimal medical therapy after the discovery of heart artery disease, you are ten times as likely to be alive in 5 years compared with usual care-the care that most people receive.
https://pubmed.ncbi.nlm.nih.gov/20973686/
It’s hard to get someone to believe something when their income (or ego, status, tenure, funding, etc) depends on not believing it.
Really good, as always!
A common cause of myocardial infarction and stroke is the rupture of atherosclerotic plaques. The exact location of plaque ruptures has previously been unknown, but now researchers at Lund University have mapped this. The research team has also identified an enzyme, a marker, that they hope will help predict who is at risk of having a myocardial infarction or a stroke due to a ruptured atherosclerotic plaque.
In atherosclerosis , fat is accumulated in the artery walls creating atherosclerotic plaques. Plaques that rupture can cause a stroke or myocardial infarction, and a deeper understanding of the mechanisms underlying plaque rupture is needed to prevent serious complications. Research at Lund University, Sweden,now shows that atherosclerotic plaques in the carotid arteries often rupture at the beginning of the plaque, at a location closest to the heart. The study has been published in the Journal of the American College of Cardiology (JACC).
“In our study, we were able to pinpoint exactly where plaques rupture. This is an important step, allowing for a better understanding of why they rupture. Previous studies have focused more on how plaques are formed while we have studied the precise area where they rupture, which no previous human study has done”, says Isabel Goncalves, who led the study.
https://www.eurekalert.org/news-releases/991111
HT https://www.fightaging.org/
Thanks for the response.
In short:
1. COURAGE did not adequately assess ischemia (70% had MPI stress testing and there is no comment on degree of ischemia. The remainder presumably had treadmill stress test which does not have high sensitivity or specificity for ischemia). Subsequent trials using invasive assessment of ischemia (FFR / iFR) did prove benefit of PCI in stable CAD. Also, MPI with high ischemia burden (high risk ischemia, SDS>10) does have proven benefit. Also, it is unclear if the MPI stress testing was adjudicated in a core lab to ensure consistency of interpretation. So, yes: COURAGE did not adequately assess ischemia.
2. All patients did have diagnostic coronary angiography in COURAGE to definite the coronary anatomy (to ensure no left main). So, the takeaway should not be that stable CAD has no proven benefit of diagnostic coronary angiography (or coronary CTA).
3. Also, COURAGE evaluated MI and death: it did not assess time off from work, declining physical function, arrhythmias, poloypharmacy, etc.
ALL of the Doctors are already on the TAKE...personal fees....
How does that NOT color the results at all?
Dr. Bangalore reports grants from National Heart, Lung, and Blood Institute , during the conduct of the study; grants and personal fees from Abbott Vascular, personal fees from Biotronik, personal fees from Pfizer, personal fees from Amgen, personal fees from Reata, outside the submitted work; .
Dr. Ali reports grants from National Heart, Lung, and Blood Institute, during the conduct of the study; grants and personal fees from Abbott Vascular, grants and personal fees from Cardiovascular Systems Inc, personal fees from Amgen , personal fees from Astra Zeneca, personal fees from Abiomed, personal fees from Boston Scientific, personal fees from Cardinal Health , personal fees from Opsens Medical, personal fees from Acist Medical , other from Shockwave Medical, outside the
submitted work; .
COURAGE was an an important (landmark) trial to curtail the occulostenotic impulse to perform PCI in all visual CAD. However, it had severe limitations. 57% of the patients in each arm had ETT as 'proof of ischemia'. ETT has 67% sensitivity and specificity and is hardly robust 'proof of ischemia'. Only ~70% in each arm had MPI stress testing. Has anyone seen MPI stress test interpretation (in the absence of a centralized core lab or 2 independent physicians to corroborate findings)? I have numerous examples of radiologist reading the MPI stress test as 'normal' but missing actual reversible perfusion defect. If read properly: MPI has great sensitivity but not so great specificity. So, COURAGE didn't actually have robust protocol to prove then absence of presence of ischemia.
FFR guided PCI (https://www.nejm.org/doi/full/10.1056/NEJMoa1408758) has proven benefit in stable CAD.
So, COURAGE is a bit of a straw man argument: if one does PCI in stable CAD *without* adequate ischemia testing THEN there is no proven benefit in reducing MI and death. Ischemia driven PCI (FFR / iFR) in 'stable CAD' has proven benefit in hard outcomes.
We should also underscore that 'stable' Left Main and proximal LAD are different subsets benefiting from revascularization.
And one doesn't know if LM, proximal LAD or FFR/iFR are applicable to a particular patient without at least a diagnostic coronary angiogram (or in modern times coronary CTA).
So, none of the 'conservative' management trials (medical management alone) should lead one to conclude that for everyone diagnostics coronary angiogram is not needed. Unselected PCI (without robust ischemia testing) is indeed questionable at best (no proven benefit).
Finally, let's remember that these are real life human beings and not mere statistics. Trials like COURAGE do not take into account: quality of life (yes, they hint at decreased angina and decreased number of anti-anginal medications). However, this should not be an afterthought. For most people who perform physical labor: reduced angina and reduced number of anti-anginal medications directly correlates with professional productivity. Decreased number of medications also means increased compliance and decreased drug-drug interactions from polypharmacy (especially in older people). People with chronic 'stable' angina on 2-3 medications to control the angina are sometimes unable to perform their daily professional duties (if they perform physical labor).
Hard endpoints (MI and mortally) are easier to measure in trials and need smaller sample size. But quality of life (psychological and physical), professional productivity (time off from work due to cardiac testing, doctor and ER visits, etc), and improved exercise performance: these have never been adequately assessed in any major trial.
Also, untreated CAD *can* increase the risk of developing AFib (or other arrhythmias) or exacerbate pre-existing arrhythmias. This could further lead to time off from work and polypharmacy.
For AFib: we went 180 degrees (from emphasis on rate control to now once again emphasis on rhythm control).
I have no doubt that true ischemia-driven PCI in 'stable CAD' will be better assessed with more comprehensive contextualized decision making. PCI for every visual (angiographic) coronary stenosis is most certainly a waste of resources and has no proven benefit. But this should not be confused with ischemia (FFR, iFR) driven PCI nor should it categorically preclude diagnostic coronary angiography to ensure no left main or proximal LAD stenosis.
Peace,
Sanjay Verma, MD FACC
Interventional Cardiologist.
https://ratical.org/radiation/CNR/RMP/
It looks like something is going on in the long run.