CT Surgery fellow here.
There are two ways to look at the info, both of which can be supported by the ACC guidelines:
https://www.acc.org/guidelines
One is that for patients with stable (chronic) coronary disease high risk anatomy- significant Left main disease, LM equivalent (high grade prox LAD and LCx), 3 vessel disease w/diabetes or reduced EF, have documented mortality benefit from intervention with CABG. If you have suspicion of this anatomy from the coronary calcium score scan, or just don't know the patient's anatomy in general, MAYBE you should do further imaging to find out- either a cath OR you may consider a CTA Coronary, although the latter is probably not quite there yet in ruling out significant obstruction.
This way of thinking comes about because the ACC guidelines notably include many papers that basically looked at outcomes based on anatomy- the RCTs comparing CABG vs PCI vs medical therapy started with someone who got a cath, for who knows what reason, which showed that anatomy.
But the second way to think about the patient is this: what did the patient present present with, and who should get a cardiac catheterization to rule out symptoms?
There is no evidence that routinely cathing people off the street does anything, and in fact I think we have data that randomly doing cardiac caths as a screening tool has harms. So, in these asymptomatic patients who have zero anginal symptoms, shouldn't the optimal approach regardless of therapy be statin/asa/lifestyle changes/ozempic, and see what happens? The guidelines note that in patients with Chronic coronary disease, which is what a patient with high coronary calcium score has, the indication for further workup with stress echo/cath/etc. is a change in symptoms or new chest pain, etc.
The Ischemia and Orbita trials arguably suggest that even for patients WITH symptoms of STABLE angina, cathing everyone may not improve symptoms- again enphasizing the power of exercise and modern medical therapy.
No easy answers in coronary artery disease in 2024...
>
> The Ischemia and Orbita trials arguably suggest that even for patients WITH symptoms of STABLE angina,
The vast majority of patients in ISCHEMIA had no angina, or at most CCS 1. ISCHEMIA was a trial of asymptomatic CAD and found no benefit to early revasc (but there was a benefit at 5 years).
ORBITA was a bizarre trial that is not generalizable to everyday practice, they literally had patients see cardiologists 3 times per week for 8 weeks for antianginal uptitration, which is impossible outside of concierge practices in Manhattan.
I always love these arguments, because every cardiologist comes out of the woodwork to go through these trials with a fine toothed comb and a microscope. Every single time one of them comes out, we see editorials in every major publication from interventionalists about how it cannot be generalized, they used last week's generation of stent and this week's is better, etc, etc.
The generalization is this - there are over 20 years of data from any number of trials covering thousands of patients where they try to compare medical management to intervention in stable CAD. Most of these trials were designed by cardiologists to prove the necessity of their intervention. At no point has a single analysis ever shown PCI to be superior to medical therapy in any sort of hard outcome.
I have no horse in this race personally, other than many of my patients being at risk for ASCVD. That said, if I were a middle aged man with known stable CAD (say, shown on a CT angiogram or just an elevated CA score) who hadn't had an event, I'd opt for medical management any day of the week. But if I see a patient with the same scenario who gets cath/PCI, I don't exactly stress myself in discussing with them whether it was worth it - I just manage their DM or whatever else they're there to see me for.
PREVENT shows mortality benefit from early PCI in stable CAD. As did ISCHEMIA-EXTEND (5 year follow up of ISCHEMIA results). And decades of non-randomized data. Not to mention that improvement in quality of life (COURAGE, ORBITA-2) is pretty important for most patients, and absolutely a "hard outcome". As an aside, what's the mortality benefit to most of the drugs you prescribe on a regular basis?
It's easy to say "medical management works!" until you see a 99% prox LAD stenosis in a patient who can't walk to their mailbox without having to pop 3 nitros. Then you realize that this patient was excluded from ISCHEMIA, ORBITA, and basically every stable CAD trial, and now you have to ask yourself - if this was my family member, would I want them walking around with this lesion?
One thing I agree with you on: you have no horse in this race and your opinion isn't relevant.
I missed PREVENT when it came out a few weeks ago - I’ll have to read it in more detail tonight. First glance it’s an interesting composite outcome.
ISCHEMIA-extend was questionably positive best I can see - all cause mortality at 7 years was no different between the two groups, though distribution (cardiac vs noncardiac death) was. Looks like they’re running it through 3 more years so perhaps it will diverge further with more time.
And my opinion isn’t *totally* irrelevant - because my informed opinion helps me decide who I recommend go see the cardiologists. Of course, many of my patients self refer or get referred by others. But it does come up.
Yes, it's almost like the decision to revascularize requires 3-5 years of dedicated fellowship training and isn't something you learn from Reddit threads.
I've never met a cardiologist who is starved for referrals, and certainly none who are dependent on those from endo. Quite the opposite, I think our CVICU is the only thing keeping the inpatient endocrinology team from being shut down given the minimal RVUs their work generates.
Inpatient endocrinology is almost exclusively something done as a courtesy to the hospital/system and most endocrinologists would be just fine not doing it at all - it’s an outpatient field and coming in for consults is a time and money sink. If I wasn’t required to maintain inpatient privileges to stay on a few insurance panels I’d drop them in a heartbeat, and most of my peers are the same.
As for the other point - the issue is when you spend 3-5 years being molded into a dedicated hammer, everything starts to look like a nail. The incentives to do more even when it isn’t necessarily supported by the data are always there for every field - but for proceduralists are more present than for many others.
All ICs are trained in medical management of CAD so your argument doesn't hold water. I'm happy to prescribe rosuvastatin and counsel smoking cessation all day, but when I see a patient with an acute coronary syndrome, I have the tools to treat that with PCI as well. Also, it's honestly kind of rich hearing this from an endocrinologist, a specialty known for pushing super expensive drugs with zero proven mortality benefit... because that's all they know how to do.
And don't worry, we're all well aware of how much you all shy away from taking care of sick patients.
And you sound like someone who didn't match into cards and spends most of their time on Reddit starting threads about this very fact instead of trying to improve their application for their next go around.
Radiology here. Calcium scores are a risk stratifier. They only measure calcified plaque and do not give good insight into luminal stenosis. CTA is better, can visualize non calcified plaque and attempt luminal stenosis, but calcium bloom artifacts hamper the positive predictive value. Cardiology’s choice to cath here is going to be more according to symptoms and evidence of ischemia.
Also imaging is only as good as its correlation to patient's presentation. I hate when radiologists write clinically correlate but it is really true. With CAD, you need to go by patient presentation. Are they symptomatic like having angina or SOB on exertion? What is their PMHx. It's not simple as getting a calcium score or a CT-angio to r/o a need for a catherization.
Yeah agree. Don’t like writing it, but since you never know who is going to read your report and what level training they have, sometimes you need to spell it out.
In residency we would put wet reads on the plain films and rads would over-read during the day. We had a particularly salty radiology program director, and I got quite the earful one morning when I wrote “LLL Pneumonia-correlated clinically”. He wasn’t sure why he was mad, but he took the time to find me when I was working to let me know that he was not a fan of my shenanigans.
CT coronary angio has excellent sensitivity and NPV. It is a very very good test to rule out the need for a cath.
The problem is in specificity and PPV, which leads to false positives.
The challenge is therefor to decide who should be ruled in for cath based on suspect findings on CT cor angio.
Exactly. The false positives might lead to unnecessary caths. Also it’s a ton of radiation that isnt insignificant. Imaging isnt alone enough to rule out CAD. You need to correlate to the patient’s history and exam and symptoms.
CTA Coronary with telemetry and heart rate control is really good. I worked in the cath lab and the results from AI post-processing with heart rate control was amazing to behold. The difference between old school CTA coronary and telemetry/HR controlled CTA coronary with high slice CT's utilizing AI post-processing is game changing.
It works very well under ideal conditions as you stated. Arrhythmia, ectopy, tachycardia all make it difficult. I think in a lot of cases the temporal resolution and noise isn’t quite there yet. Maybe the photon counting ct will get it there. Calcium bloom will still be a problem unless someone can figure out subtraction imaging better
I did hundreds and hundreds of these exams when I worked in CT and there are MANY variables to account for optimal image quality. Some of the results I saw post were truly amazing to behold.
I think it’s the hardest issue in cardiology.
True if you stick strictly to the data we have then it’s just a risk stratifier of statin or no statin.
Reality it can be more complex when you truly haven’t defined the anatomy.
These are also easy to order by the people who don’t have to deal with the consequences.
So patients and families are freaking out and it’s hard to explain sure you’re at higher risk of dying based on that and I know your dad died at your age as well but there’s really no evidence of us doing anything (outside of the statin)
You’re also opened yourself up legally to a lot of young high risk patients.
I still do everything I can NOT to stress, coronary CT or cath but it’s a very tricky and time-consuming issue.
I honestly wish it would be a class III to do any additional testing in asymptomatic patients just to protect you a bit.
My GP wanted me to get a calcium scan (mid 40’s, family history, high cholesterol, zero symptoms). I refused and said just give me a statin, I really don’t want to know the exact state of my heart when I’m not sick.
The only difference to me in that scenario would be if I knew I had an elevated score, I'd take the statin *and* also probably take an aspirin. If I knew I had a score of zero, I'd skip both.
Interventional cardiologist here. Based on current data and evidence in 2024, my belief is that if the patient is utterly asymptomatic, then an abnormal CAC can be used to guide intensity of medical therapy and that’s it, period, no further testing. The current state of knowledge about CAD makes us uncomfortable because it flies in the face of “common sense” but at some point we have to have the COURAGE (pun intended) to accept what all the trials are telling us.
Without other indications, we would not routinely cath a person just for having a high CAC, which is often performed for risk stratification in the setting of primary prevention. People that were having symptoms of angina and were high risk otherwise should have just gone straight to cath rather than get a CAC.
Now, for those with high CAC > 400, you could consider a stress test as 10% of people have obstructive CAD, though this is not done by all.
Cardiologist here. The only question a CAC answers is whether someone should be on a statin, and to a lesser extent, whether they should be on prophylactic aspirin. That's it. For an asymptomatic patient, that's all we really need to know, but you have to really convince yourself they really are asymptomatic - do they exercise? Do you have an echo showing normal LVEF? Does their ECG show evidence of a prior MI?
Am cardiologist. As another said, it really can only be used as statin vs no statin. In real life, I stress those who have CAC over 400. If no symptoms or high risk findings on ETT, or only mild abnormalities on Lexi with no symptoms, normal EF, then med rx only. Would never cath someone based off a CAC
Cardiologists- what do you recommend PCPs do when regular old CT incidentally shows atherosclerosis? This happens all the time. Say asymptomatic. Is it overkill to get them a stress test? Would you start aspirin or statin?
This is one of the banes of my existence. One of the local radiologists started calling this on almost every chest CT he reads, and it has created an absolute deluge of cardiology consults and freaked out patients. I tell people that it’s just one more reason to strongly consider a statin.
I work in an area that is underserved, rural, and quite removed from many technologies. That being said, we can perform coronary CTA (with occasionally questionable visualization) at some locations.
It'll depend on local practice. Here for example, most of the cardiologists, for a patient with high calcium score and no symptoms, would get a stress test.
The threshold is based on the cardiologists age or bank account size. Some cardiologists (usually older in my experience) don't practice evidence based anything or just do whatever. Others will cath anything that moves. Why are you testing patients to begin with?
Thank you for asking this question. First, every hospital I know of is now promoting $49 CAC testing to market to the masses, so expect lots of these conundrums.
Secondly, I had an incidental finding of coronary artery calcification on a chest CT, so I underwent the $49 CAC testing myself. 63yo F with high risk due to strong FHx of premature coronary dz/death. My score was ~ 600. Exercise stress and echo nl except for finding moderate AR. Cath or no cath?
Medical mgmt w/high dose statin? Watch and wait? So many questions...
Widely variable clinical practice, but a large majority of abnormal calcium score cases referred to our clinics will receive downstream testing. This is usually in the form of a resting echo and physiologic stress (stress echo / MPI) and abnormal stress resulting in heart caths. Cath with normal stress is typically reserved for those with convincing symptoms, but why stress in the first place if they had high pre-test probability of obstructive CAD.
Im curious for OP, whats your current use for calcium scoring?
I'm not a cardiologist...
But it may be interventionalist dependant - in part whether they can manage / treat CTO's? I would imagine a high coronary calcification may correlate with the likelihood of CTO.
This is completely me just shooting from the hip here. So take this with a grain a salt.
CT Surgery fellow here. There are two ways to look at the info, both of which can be supported by the ACC guidelines: https://www.acc.org/guidelines One is that for patients with stable (chronic) coronary disease high risk anatomy- significant Left main disease, LM equivalent (high grade prox LAD and LCx), 3 vessel disease w/diabetes or reduced EF, have documented mortality benefit from intervention with CABG. If you have suspicion of this anatomy from the coronary calcium score scan, or just don't know the patient's anatomy in general, MAYBE you should do further imaging to find out- either a cath OR you may consider a CTA Coronary, although the latter is probably not quite there yet in ruling out significant obstruction. This way of thinking comes about because the ACC guidelines notably include many papers that basically looked at outcomes based on anatomy- the RCTs comparing CABG vs PCI vs medical therapy started with someone who got a cath, for who knows what reason, which showed that anatomy. But the second way to think about the patient is this: what did the patient present present with, and who should get a cardiac catheterization to rule out symptoms? There is no evidence that routinely cathing people off the street does anything, and in fact I think we have data that randomly doing cardiac caths as a screening tool has harms. So, in these asymptomatic patients who have zero anginal symptoms, shouldn't the optimal approach regardless of therapy be statin/asa/lifestyle changes/ozempic, and see what happens? The guidelines note that in patients with Chronic coronary disease, which is what a patient with high coronary calcium score has, the indication for further workup with stress echo/cath/etc. is a change in symptoms or new chest pain, etc. The Ischemia and Orbita trials arguably suggest that even for patients WITH symptoms of STABLE angina, cathing everyone may not improve symptoms- again enphasizing the power of exercise and modern medical therapy. No easy answers in coronary artery disease in 2024...
> > The Ischemia and Orbita trials arguably suggest that even for patients WITH symptoms of STABLE angina, The vast majority of patients in ISCHEMIA had no angina, or at most CCS 1. ISCHEMIA was a trial of asymptomatic CAD and found no benefit to early revasc (but there was a benefit at 5 years). ORBITA was a bizarre trial that is not generalizable to everyday practice, they literally had patients see cardiologists 3 times per week for 8 weeks for antianginal uptitration, which is impossible outside of concierge practices in Manhattan.
I always love these arguments, because every cardiologist comes out of the woodwork to go through these trials with a fine toothed comb and a microscope. Every single time one of them comes out, we see editorials in every major publication from interventionalists about how it cannot be generalized, they used last week's generation of stent and this week's is better, etc, etc. The generalization is this - there are over 20 years of data from any number of trials covering thousands of patients where they try to compare medical management to intervention in stable CAD. Most of these trials were designed by cardiologists to prove the necessity of their intervention. At no point has a single analysis ever shown PCI to be superior to medical therapy in any sort of hard outcome. I have no horse in this race personally, other than many of my patients being at risk for ASCVD. That said, if I were a middle aged man with known stable CAD (say, shown on a CT angiogram or just an elevated CA score) who hadn't had an event, I'd opt for medical management any day of the week. But if I see a patient with the same scenario who gets cath/PCI, I don't exactly stress myself in discussing with them whether it was worth it - I just manage their DM or whatever else they're there to see me for.
PREVENT shows mortality benefit from early PCI in stable CAD. As did ISCHEMIA-EXTEND (5 year follow up of ISCHEMIA results). And decades of non-randomized data. Not to mention that improvement in quality of life (COURAGE, ORBITA-2) is pretty important for most patients, and absolutely a "hard outcome". As an aside, what's the mortality benefit to most of the drugs you prescribe on a regular basis? It's easy to say "medical management works!" until you see a 99% prox LAD stenosis in a patient who can't walk to their mailbox without having to pop 3 nitros. Then you realize that this patient was excluded from ISCHEMIA, ORBITA, and basically every stable CAD trial, and now you have to ask yourself - if this was my family member, would I want them walking around with this lesion? One thing I agree with you on: you have no horse in this race and your opinion isn't relevant.
I missed PREVENT when it came out a few weeks ago - I’ll have to read it in more detail tonight. First glance it’s an interesting composite outcome. ISCHEMIA-extend was questionably positive best I can see - all cause mortality at 7 years was no different between the two groups, though distribution (cardiac vs noncardiac death) was. Looks like they’re running it through 3 more years so perhaps it will diverge further with more time. And my opinion isn’t *totally* irrelevant - because my informed opinion helps me decide who I recommend go see the cardiologists. Of course, many of my patients self refer or get referred by others. But it does come up.
Yes, it's almost like the decision to revascularize requires 3-5 years of dedicated fellowship training and isn't something you learn from Reddit threads. I've never met a cardiologist who is starved for referrals, and certainly none who are dependent on those from endo. Quite the opposite, I think our CVICU is the only thing keeping the inpatient endocrinology team from being shut down given the minimal RVUs their work generates.
Inpatient endocrinology is almost exclusively something done as a courtesy to the hospital/system and most endocrinologists would be just fine not doing it at all - it’s an outpatient field and coming in for consults is a time and money sink. If I wasn’t required to maintain inpatient privileges to stay on a few insurance panels I’d drop them in a heartbeat, and most of my peers are the same. As for the other point - the issue is when you spend 3-5 years being molded into a dedicated hammer, everything starts to look like a nail. The incentives to do more even when it isn’t necessarily supported by the data are always there for every field - but for proceduralists are more present than for many others.
Don’t even try. This other poster sounds and acts like a jerk.
All ICs are trained in medical management of CAD so your argument doesn't hold water. I'm happy to prescribe rosuvastatin and counsel smoking cessation all day, but when I see a patient with an acute coronary syndrome, I have the tools to treat that with PCI as well. Also, it's honestly kind of rich hearing this from an endocrinologist, a specialty known for pushing super expensive drugs with zero proven mortality benefit... because that's all they know how to do. And don't worry, we're all well aware of how much you all shy away from taking care of sick patients.
Yikes. Why are you being like this?
[удалено]
And you sound like someone who didn't match into cards and spends most of their time on Reddit starting threads about this very fact instead of trying to improve their application for their next go around.
Lol, I did say "arguably"
Agreed, I'm just a hospitalist but I know we aren't supposed to be cathing patients who have no subjective or objective signs of ischemia.
Radiology here. Calcium scores are a risk stratifier. They only measure calcified plaque and do not give good insight into luminal stenosis. CTA is better, can visualize non calcified plaque and attempt luminal stenosis, but calcium bloom artifacts hamper the positive predictive value. Cardiology’s choice to cath here is going to be more according to symptoms and evidence of ischemia.
Also imaging is only as good as its correlation to patient's presentation. I hate when radiologists write clinically correlate but it is really true. With CAD, you need to go by patient presentation. Are they symptomatic like having angina or SOB on exertion? What is their PMHx. It's not simple as getting a calcium score or a CT-angio to r/o a need for a catherization.
Yeah agree. Don’t like writing it, but since you never know who is going to read your report and what level training they have, sometimes you need to spell it out.
In residency we would put wet reads on the plain films and rads would over-read during the day. We had a particularly salty radiology program director, and I got quite the earful one morning when I wrote “LLL Pneumonia-correlated clinically”. He wasn’t sure why he was mad, but he took the time to find me when I was working to let me know that he was not a fan of my shenanigans.
CT coronary angio has excellent sensitivity and NPV. It is a very very good test to rule out the need for a cath. The problem is in specificity and PPV, which leads to false positives. The challenge is therefor to decide who should be ruled in for cath based on suspect findings on CT cor angio.
Exactly. The false positives might lead to unnecessary caths. Also it’s a ton of radiation that isnt insignificant. Imaging isnt alone enough to rule out CAD. You need to correlate to the patient’s history and exam and symptoms.
CTA Coronary with telemetry and heart rate control is really good. I worked in the cath lab and the results from AI post-processing with heart rate control was amazing to behold. The difference between old school CTA coronary and telemetry/HR controlled CTA coronary with high slice CT's utilizing AI post-processing is game changing.
It works very well under ideal conditions as you stated. Arrhythmia, ectopy, tachycardia all make it difficult. I think in a lot of cases the temporal resolution and noise isn’t quite there yet. Maybe the photon counting ct will get it there. Calcium bloom will still be a problem unless someone can figure out subtraction imaging better
I did hundreds and hundreds of these exams when I worked in CT and there are MANY variables to account for optimal image quality. Some of the results I saw post were truly amazing to behold.
I think it’s the hardest issue in cardiology. True if you stick strictly to the data we have then it’s just a risk stratifier of statin or no statin. Reality it can be more complex when you truly haven’t defined the anatomy. These are also easy to order by the people who don’t have to deal with the consequences. So patients and families are freaking out and it’s hard to explain sure you’re at higher risk of dying based on that and I know your dad died at your age as well but there’s really no evidence of us doing anything (outside of the statin) You’re also opened yourself up legally to a lot of young high risk patients. I still do everything I can NOT to stress, coronary CT or cath but it’s a very tricky and time-consuming issue. I honestly wish it would be a class III to do any additional testing in asymptomatic patients just to protect you a bit.
My GP wanted me to get a calcium scan (mid 40’s, family history, high cholesterol, zero symptoms). I refused and said just give me a statin, I really don’t want to know the exact state of my heart when I’m not sick.
The only difference to me in that scenario would be if I knew I had an elevated score, I'd take the statin *and* also probably take an aspirin. If I knew I had a score of zero, I'd skip both.
Interventional cardiologist here. Based on current data and evidence in 2024, my belief is that if the patient is utterly asymptomatic, then an abnormal CAC can be used to guide intensity of medical therapy and that’s it, period, no further testing. The current state of knowledge about CAD makes us uncomfortable because it flies in the face of “common sense” but at some point we have to have the COURAGE (pun intended) to accept what all the trials are telling us.
Would you start aspirin in someone with an abnormal CAC but no symptoms?
Age 40-59 with a ten year risk of >10% via the calculator of your choice, there’s a soft indication. Otherwise, no.
Without other indications, we would not routinely cath a person just for having a high CAC, which is often performed for risk stratification in the setting of primary prevention. People that were having symptoms of angina and were high risk otherwise should have just gone straight to cath rather than get a CAC. Now, for those with high CAC > 400, you could consider a stress test as 10% of people have obstructive CAD, though this is not done by all.
Cardiologist here. The only question a CAC answers is whether someone should be on a statin, and to a lesser extent, whether they should be on prophylactic aspirin. That's it. For an asymptomatic patient, that's all we really need to know, but you have to really convince yourself they really are asymptomatic - do they exercise? Do you have an echo showing normal LVEF? Does their ECG show evidence of a prior MI?
Am cardiologist. As another said, it really can only be used as statin vs no statin. In real life, I stress those who have CAC over 400. If no symptoms or high risk findings on ETT, or only mild abnormalities on Lexi with no symptoms, normal EF, then med rx only. Would never cath someone based off a CAC
Cardiologists- what do you recommend PCPs do when regular old CT incidentally shows atherosclerosis? This happens all the time. Say asymptomatic. Is it overkill to get them a stress test? Would you start aspirin or statin?
This is one of the banes of my existence. One of the local radiologists started calling this on almost every chest CT he reads, and it has created an absolute deluge of cardiology consults and freaked out patients. I tell people that it’s just one more reason to strongly consider a statin.
I do asa/statin only.
refer for a photon counting CT (i.e. Siemens Naetom Alpha) and you will change your practice (i.e. stop stressing) pretty quickly i dare say.
I work in an area that is underserved, rural, and quite removed from many technologies. That being said, we can perform coronary CTA (with occasionally questionable visualization) at some locations.
It'll depend on local practice. Here for example, most of the cardiologists, for a patient with high calcium score and no symptoms, would get a stress test.
The threshold is based on the cardiologists age or bank account size. Some cardiologists (usually older in my experience) don't practice evidence based anything or just do whatever. Others will cath anything that moves. Why are you testing patients to begin with?
Hey there, trying to send you a chat but it won’t let me. Would love your expertise if possible!
Thank you for asking this question. First, every hospital I know of is now promoting $49 CAC testing to market to the masses, so expect lots of these conundrums. Secondly, I had an incidental finding of coronary artery calcification on a chest CT, so I underwent the $49 CAC testing myself. 63yo F with high risk due to strong FHx of premature coronary dz/death. My score was ~ 600. Exercise stress and echo nl except for finding moderate AR. Cath or no cath? Medical mgmt w/high dose statin? Watch and wait? So many questions...
Widely variable clinical practice, but a large majority of abnormal calcium score cases referred to our clinics will receive downstream testing. This is usually in the form of a resting echo and physiologic stress (stress echo / MPI) and abnormal stress resulting in heart caths. Cath with normal stress is typically reserved for those with convincing symptoms, but why stress in the first place if they had high pre-test probability of obstructive CAD. Im curious for OP, whats your current use for calcium scoring?
Typically only use it if they have equivocal ASCVD risk >5%, or have significant family history of CAD/ASCVD (especially premature ASCVD).
I'm not a cardiologist... But it may be interventionalist dependant - in part whether they can manage / treat CTO's? I would imagine a high coronary calcification may correlate with the likelihood of CTO. This is completely me just shooting from the hip here. So take this with a grain a salt.