I did a deep dive into cardiac imaging, focusing on the use of CTA for the diagnosis of coronary artery disease. I think the anatomic imaging test is leading us astray.
On the one hand, I agree with the contention that the issue is not with the test per se, but with the end users of the results of that test (and the warped financial incentives that serve at cross purposes to proper outcome-driven patient care).
OTOH, it’s a failure of regulators and gate-keepers to authorize /permit/ give credence to a test that has not shown downstream endpoint benefits to begin with. It’s yet another example of regulators failing to properly discharge their fiduciary duties.
“Coronary artery disease is part of the diverse disease of atherosclerosis. CAD treatment therefore should focus on treating atherosclerosis: diet, exercise, good control of blood pressure and cholesterol for instance.
Placing stents in stable partial blockages does not reduce the chance of future MI or death. It’s a hard concept but it’s been borne out by every clinical trial ever done. “
I agree with all the above.
I would just add that it isn’t only the question of anatomically defining a blockage. It is beholden on us as physicians to assess the physiological cardiorespiratory and prognostic significance of that anatomical blockage in the anatomical context of its location. To give but one example, a high grade distal left main blockage might cause a balanced false negative nuclear perfusion scan, and there is not a shadow of a doubt that if it was a significant stenosis, and the patient was stressed using physiologic demand testing ( exercise dobutamine etc..), RATHER THAN flow related reactive vasodilator testing, that these would be profoundly positive. The reason we have wandered down this robotic road to cardiac catheterization is that we have used the wrong tests, and the third party payors funding these tests have been slavishly endorsing it. I refer to the all prevalent issue of vasodilator nuclear flow testing, using adenosine and similar vasodilator products as stressors. The compelling impetus for adopting this stress modality, is of course that these are revenue generating, well or at least adequately reimbursed, fast accomplished convenient office tests, which are money spinners for those who do them in the outpatient office, but generate a huge number of false positive tests, or even if they are true positive, often not really indicative of any real impetus to pursue cardiac catheterization, let alone an ‘on table’ need for immediate evascularization. Adding to this are vague definitions of what are ischemic symptoms. On any given Monday (at least where I practice), you will find 80% of the patients showing up in outpatient clinics for cardiac vasodilator stress tests do not have classical angina by the Levine criteria. They have some other variant frequently atypical variants of chest pain, and or dyspnea and risk factors which are then presented as the reasons for doing this test. However, we as clinicians have to ask. Are we doing the test to determine whether the pain is cardiac so that we can manage it that way, or are we doing the test to find an ischemic area and respond to it mechanically? You’re right to point out the ISCHEMIA trial and the great prognosis of patients, who can exercise to a good degree with or without developing ischemia. This is why we should be pushing wherever and whenever possible for physiologic testing, such as exercise or even dobutamine provocative ischemia testing. (I understand the limitations of dobutamine induced rate related double product, ischemia provocation). However, we blissfully ignore to a great degree the value and importance of the treadmill test, despite years of validated confirmed prognostic information for the Duke treadmill criteria. Third party payors should be encouraging (if not financially mandating) this for all patients who can exercise, and that too with an ischemia detection modality that doesn’t overemphasize the detection of small amounts of ischemia at the expense of triggering the increasingly unnecessary use of cardiac catheterizations, and subsequent ‘on table’ do or die interventions. Incidentally, an ‘on table’ intracoronary ultrasound or provocative FFR test may very well document some validated criteria for significant flow limitation of the stenosis. I don’t doubt this. The question really is even if it is flow limiting, IS the risk benefit ratio long-term for intervening on this stenosis at that time and location, worthwhile. There isn’t a whole host of information in this regard that goes out 10 to 20 years to guide us….
Ironically perhaps, one interesting use consideration of cardiac CT coronary angiography as a testing modality, is the intriguing idea that it could be used as a ‘next’ follow up test for a positive nuclear scan (unless the region of ischemia was suggestive of multivessel or left main disease). In this way, trivial or small to moderate amounts of ischemia (ISCHEMIA trial types) could be defined anatomically and managed medically. We could then avoid the use of on-table oculo-stenotic reflexes that
compel even the bravest of interventional cardiologists from walking away from a juicy high-grade lesion from fear or guilt of professional abdication. I speak unapologetically as a former interventional cardiologist. Just food for enormous thought 💭
THANK YOU John for your always excellent analyses of the cardiac literature. Your critical "eye" for pros, cons & relevance of clinical studies is tremendously appreciated.
QUESTION — What do you perceive as potential role of CTA for the patient who presents to the ED for acute CP (Chest Pain)? I completely agree that incidental finding of preexisting but nonocclusive coronary disease does NOT merit prompt cath with PCI. But is it (or is it not) reasonable in the ED to do CTA looking for clear evidence of a "culprit" artery — which if found, merits cath & PCI? And, if nothing resembling an acute "culprit" iis found — then NOT pursuing prompt cath?
P.S. I ask the above from my perspective of NO LONGER believing in the outdated "STEMI paradigm" — since literature and our recent numerous case examples on Dr. Smith's ECG Blog clearly demonstrate how at least 1/3 of all acute coronary occlusions ( = "OMIs" = Occlusion based MIs) do not satisfy millimeter-based STEMI criteria, yet ARE very often able to be diagnosed by other ECG crieria (ie, hyperacute T waves, more subtle but convincing ST-T wave abnormalities in multiple leads, maximal ST depression in V2,V3 and/or V4 indicating posterior OMI — "dynamic" ST-T abnormalities on repeat ECG, etc.). My bias is that MUCH (most) of the time — awareness and attention to OMI ECG criteria can definitively obviate need for CTA, thereby greatly expediting clear indication for prompt cath.
THANK YOU in advance for your wisdom regarding the above!
I tend not to rely too much on p-values or "statistical experts.".
The authors of the SCOT Heart Trial provide a simple explanation: the reduction in myocardial infarction could be attributed to a better lifestyle, aspirin, and statin usage. The authors emphasise that the majority of MIs happened in participants with non-obstructive lesions, which the non-CTA group might have overlooked. I find this highly plausible.
However, I concur that the ISCHEMIA and COURAGE trials strongly advise against stenting a patient with an obstructive lesion causing stable angina.
I also am not an advocate of routine CTA.
I would not subject an unstable patient to a stress test, but prefer invasive angiography and proceeding appropriately.
On the one hand, I agree with the contention that the issue is not with the test per se, but with the end users of the results of that test (and the warped financial incentives that serve at cross purposes to proper outcome-driven patient care).
OTOH, it’s a failure of regulators and gate-keepers to authorize /permit/ give credence to a test that has not shown downstream endpoint benefits to begin with. It’s yet another example of regulators failing to properly discharge their fiduciary duties.
“Coronary artery disease is part of the diverse disease of atherosclerosis. CAD treatment therefore should focus on treating atherosclerosis: diet, exercise, good control of blood pressure and cholesterol for instance.
Placing stents in stable partial blockages does not reduce the chance of future MI or death. It’s a hard concept but it’s been borne out by every clinical trial ever done. “
I agree with all the above.
I would just add that it isn’t only the question of anatomically defining a blockage. It is beholden on us as physicians to assess the physiological cardiorespiratory and prognostic significance of that anatomical blockage in the anatomical context of its location. To give but one example, a high grade distal left main blockage might cause a balanced false negative nuclear perfusion scan, and there is not a shadow of a doubt that if it was a significant stenosis, and the patient was stressed using physiologic demand testing ( exercise dobutamine etc..), RATHER THAN flow related reactive vasodilator testing, that these would be profoundly positive. The reason we have wandered down this robotic road to cardiac catheterization is that we have used the wrong tests, and the third party payors funding these tests have been slavishly endorsing it. I refer to the all prevalent issue of vasodilator nuclear flow testing, using adenosine and similar vasodilator products as stressors. The compelling impetus for adopting this stress modality, is of course that these are revenue generating, well or at least adequately reimbursed, fast accomplished convenient office tests, which are money spinners for those who do them in the outpatient office, but generate a huge number of false positive tests, or even if they are true positive, often not really indicative of any real impetus to pursue cardiac catheterization, let alone an ‘on table’ need for immediate evascularization. Adding to this are vague definitions of what are ischemic symptoms. On any given Monday (at least where I practice), you will find 80% of the patients showing up in outpatient clinics for cardiac vasodilator stress tests do not have classical angina by the Levine criteria. They have some other variant frequently atypical variants of chest pain, and or dyspnea and risk factors which are then presented as the reasons for doing this test. However, we as clinicians have to ask. Are we doing the test to determine whether the pain is cardiac so that we can manage it that way, or are we doing the test to find an ischemic area and respond to it mechanically? You’re right to point out the ISCHEMIA trial and the great prognosis of patients, who can exercise to a good degree with or without developing ischemia. This is why we should be pushing wherever and whenever possible for physiologic testing, such as exercise or even dobutamine provocative ischemia testing. (I understand the limitations of dobutamine induced rate related double product, ischemia provocation). However, we blissfully ignore to a great degree the value and importance of the treadmill test, despite years of validated confirmed prognostic information for the Duke treadmill criteria. Third party payors should be encouraging (if not financially mandating) this for all patients who can exercise, and that too with an ischemia detection modality that doesn’t overemphasize the detection of small amounts of ischemia at the expense of triggering the increasingly unnecessary use of cardiac catheterizations, and subsequent ‘on table’ do or die interventions. Incidentally, an ‘on table’ intracoronary ultrasound or provocative FFR test may very well document some validated criteria for significant flow limitation of the stenosis. I don’t doubt this. The question really is even if it is flow limiting, IS the risk benefit ratio long-term for intervening on this stenosis at that time and location, worthwhile. There isn’t a whole host of information in this regard that goes out 10 to 20 years to guide us….
Ironically perhaps, one interesting use consideration of cardiac CT coronary angiography as a testing modality, is the intriguing idea that it could be used as a ‘next’ follow up test for a positive nuclear scan (unless the region of ischemia was suggestive of multivessel or left main disease). In this way, trivial or small to moderate amounts of ischemia (ISCHEMIA trial types) could be defined anatomically and managed medically. We could then avoid the use of on-table oculo-stenotic reflexes that
compel even the bravest of interventional cardiologists from walking away from a juicy high-grade lesion from fear or guilt of professional abdication. I speak unapologetically as a former interventional cardiologist. Just food for enormous thought 💭
THANK YOU John for your always excellent analyses of the cardiac literature. Your critical "eye" for pros, cons & relevance of clinical studies is tremendously appreciated.
QUESTION — What do you perceive as potential role of CTA for the patient who presents to the ED for acute CP (Chest Pain)? I completely agree that incidental finding of preexisting but nonocclusive coronary disease does NOT merit prompt cath with PCI. But is it (or is it not) reasonable in the ED to do CTA looking for clear evidence of a "culprit" artery — which if found, merits cath & PCI? And, if nothing resembling an acute "culprit" iis found — then NOT pursuing prompt cath?
P.S. I ask the above from my perspective of NO LONGER believing in the outdated "STEMI paradigm" — since literature and our recent numerous case examples on Dr. Smith's ECG Blog clearly demonstrate how at least 1/3 of all acute coronary occlusions ( = "OMIs" = Occlusion based MIs) do not satisfy millimeter-based STEMI criteria, yet ARE very often able to be diagnosed by other ECG crieria (ie, hyperacute T waves, more subtle but convincing ST-T wave abnormalities in multiple leads, maximal ST depression in V2,V3 and/or V4 indicating posterior OMI — "dynamic" ST-T abnormalities on repeat ECG, etc.). My bias is that MUCH (most) of the time — awareness and attention to OMI ECG criteria can definitively obviate need for CTA, thereby greatly expediting clear indication for prompt cath.
THANK YOU in advance for your wisdom regarding the above!
I tend not to rely too much on p-values or "statistical experts.".
The authors of the SCOT Heart Trial provide a simple explanation: the reduction in myocardial infarction could be attributed to a better lifestyle, aspirin, and statin usage. The authors emphasise that the majority of MIs happened in participants with non-obstructive lesions, which the non-CTA group might have overlooked. I find this highly plausible.
However, I concur that the ISCHEMIA and COURAGE trials strongly advise against stenting a patient with an obstructive lesion causing stable angina.
I also am not an advocate of routine CTA.
I would not subject an unstable patient to a stress test, but prefer invasive angiography and proceeding appropriately.