We learned a lot producing this Core IM 5 Pearls on Stress testing! We hope you do too!
- What are the indications for a stress test? ( 2:18)
- How to choose stress protocol in a stress test? (8:29)
- How to choose diagnostic modality in a stress test? (14:46)
- How do we interpret results from stress tests, and how should this be communicated to patients? (24:08)
- Pearl Recap (31:13)
- Is there really a big difference in risk for contrast induced nephropathy between arterial and venous contrast load? (36:02)
Pearl 1: To stress or not to stress
- There are coronary artery disease reasons and non-coronary artery disease reasons for stress testing
- Non-coronary artery disease reasons
- Exercise-induced arrhythmias
- Distinguishing aortic stenosis from pseudo- severe aortic stenosis or low-flow, low-gradient states in patient with low ejection fraction
- Coronary artery disease reasons
- Diagnosis in stable chest pain
- Risk stratification in patients with known CAD with new or worsening symptoms
- Non-coronary artery disease reasons
- Avoid in patients that are low pre-test probability
Pearl 2: Choosing the stress in the stress test
- 3 choices for stressors: exercise, inotropes and vasodilators
- Everyone who can exercise should exercise for their stress test. Patients must be able to get their heart rate to 80-85% of predicted.
- Inotropes (ex. Dobutamine) increases contractility via B1 and B2 receptors
- Con: may precipitate arrhythmias
- Vasodilators: regadenoson, adenosine, dipyridamole (RAD) causes coronary vasodilation via the adenosine receptor → cAMP production → vascular smooth muscle relaxation
- Avoid in patients with 2nd or 3rd degree heart block without a pacemaker or severe COPD/asthma
Pearl 3: Measuring response to the stressor
- 5 choices for diagnostic tools: EKG, echocardiogram, nuclear imaging, MRI and PET scans
- EKG has the lowest sensitivity and specificity for detection of coronary artery disease – 68% and 77%, respectively.
- Can’t use in patients with certain EKG abnormalities: VolksWagen Drivers Don’t Litter”: V for the V-paced rhythm, W for WPW, D for ST depressions and digoxin, and L for complete Left Bundle Branch Block
- Echocardiogram looks for new wall motion abnormalities that indicate ischemia. It is a good option to evaluate for valvular pathology, pulmonary hypertension and left ventricular outflow tract obstruction
- Diagnostic accuracy is based on skill of the sonographer and patient windows
- Nuclear imaging uses technetium-99-labeled tracer which is taken up by living myocardial cells. It relies on differences in uptake between regions of the myocardium.
- Test characteristics of of stress echos and nuclear stress are approximately equivalent.
- EKG has the lowest sensitivity and specificity for detection of coronary artery disease – 68% and 77%, respectively.
- Instead of referring to results of stress testing as “positive” or “negative” – we encourage you to describe in terms of risk.
- Read the text of the stress report for clues that about a patient’s risk. For example, The Duke Treadmill Score is a great way to translate binary results into risk for patients who undergo exercise EKG stress tests.
- If you discuss the results with patients in terms of risk it is easier to use results – even reassuring results – to discuss important lifestyle changes for our patients. Calling a test “negative” for ischemia might waste this great opportunity to encourage behavior change in our patients!
Pearl 1: What are the coronary and non-coronary reasons for stress testing?
S: I think I’m just gonna use myself as a case. I vividly remember younger Shreya (maybe this was intern year or a few months ago! will leave to your imagination) strugglingggg in clinic with ordering a stress test for a patient. So many options and things to click – I remembered feeling preemptively embarrassed at what the cardiologist might think of concoction of things I clicked just to get the order to go through
M: I’m with you, Shreya. Exercise stress, pharm stress, EKG stress, stress echo, nuclear stress . . . at one point you might have convinced me that stress colonoscopies were a thing and I would have believed you… What about stress PFTs- that sounds more real. So how do you choose the right one?
GREG KATZ: Actually, the big picture question of when to get any type of stress tests is just important, if not more important than deciding how you want to stress a patient
S: Okay, okay I got excited to dive right in but – we should back to a 30,000 foot view of when stress testing is actually indicated. And there’s two big bucket’s: the coronary artery disease reasons and the bucket that I was less familiar with, the NON-coronary artery disease reasons.
E: Yeah, so those non-coronary disease reasons to get a stress test would be something like exercise induced arrhythmias, or, in the case of WPW, to assess the risk of a patient’s accessory pathway. A fun fact to know on rounds for WPW is that a rapidly disappearing delta wave suggests a lower risk variant. One last non-coronary reason for stress-testing that Greg will expound on is distinguishing aortic stenosis from pseudo severe aortic stenosis or low-flow, low-gradient states in pts with low EF.
GREG KATZ: If somebody has a low ejection fraction, you can have falsely low ejection fraction through the LVOT and that can make it look like non severe aortic stenosis is severe when you use the continuity equation to calculate the aortic valve area. And so if you’re trying to distinguish between pseudo severe AS and severe AS, the dobutamine stress echo can be helpful because by increasing someone’s contractility and improving flow through their LVOT, you might be able to show that a previously calculated aortic valve area of 0.8 is actually 1.2cm so its not severe.
M: How-freakin-cool-is-that! I am so forcing a discussion about aortic stenosis next time I’m on rounds just so I can drop a “pseudosevere aortic stenosis” bomb on the residents.
S: Oh goodness easy, easy Marty. Before you get too carried away we are gonna focus the majority of the podcast on the coronary reasons for stress testing.
M: Can’t wait for some more stress bombs.
E: Oh they’re coming Marty, just you wait. In the meantime, Greg provides a pretty nice description of that relatively common situation in clinic when a patient’s chest pain partly sounds like angina, and partly sounds like something else altogether:
GREG KATZ: Any time you’re seeing a patient who has either symptoms or risk factors, one of the things that’s going through your head is, ‘How likely do I think that it is that this patient has coronary artery disease? and also how severe is this patient’s coronary artery disease? Very often the story that you’re left with is this very unsatisfying situation where there are some features of the chest pain that are very concerning and some features that are a lot more reassuring. So stress testing can be helpful when you’re trying to figure out if symptoms or lack of perfection that you’re able to clarify about someone’s history is due to obstructive coronary disease.
E: So stress testing is probably most beneficial in patients with stable angina or in cases as Greg puts it, “unsatisfying stories,” where you are not sure if their symptoms could be an anginal equivalent or not.
M: And what we’re really talking about are those patients who fall in the intermediate-risk population. Remember, when we’re talking about risk, we’re talking about factoring in the patient’s age, sex, and chest pain character to help you estimate the pre-test probability of coronary disease. We could spend an entire podcast discussing Bayesian probability and clinical epi, but the important take-away is that stress testing probably won’t help you much in very low-risk or very high-risk patients.
S: #ThingsWedoForNoReason stress testing in low risk chest pain – shout out to Tony Breu on Twitter. We will get more into why when thinking of the false positives later but the final point to build this framework out for stress tests: stress tests don’t only serve a diagnostic purpose if these symptoms are possible from obstructive coronary disease, they serve a prognostic purpose as well.
GREG KATZ: The other big group is you have a patient who you know has coronary disease and you want to figure out how high risk they are: Do you need to get anatomical imaging ? Do they need to go for cath before they go for surgery? Are they somebody you should think more closely about revascularizing because there are number of other risk factors in their presentation. Stress testing if you look at population based data, you see that people who have more ischemia on stress tests, have a much higher incidence of major adverse cardiovascular events (MACE) moving forward and so even semi-quantifying how much ischemia that somebody has on a stress test can be helpful as you are talking to that patient in clinic and trying to figure out how intensely do you need to convince them to take their statin or how aggressive do you need to be their diet and lifestyle modifications.
M: More on that to come but to recap this pearl, which was really a framework: there are non-coronary reasons for stress testing and cornary reasons for stress testing. A few examples from the former group are arrhythmia and valvular evaluations. Thinking about coronary disease there are also two purposes- diagnosis and prognosis. We want to stress those intermediate probability folks with the iffy stories to see if ischemia is causing their symptoms. And we also might stress people with known coronary disease in whom we may be interested in better defining the clinical significance of their disease like ischemia
Pearl 2: How do you choose the stressor in the stress test?
S: Okay so back to wide-eyed younger Shreya in clinic, pulling my hair out trying to sort out which stress test to order. Mr. Cory Nary is 60 something year old man with a whiff of glucose intolerance, LDL in the mid 150s, family history of heart disease who presented with new quote-unquote indigestion when walking up the stairs. I remember thinking that reflux just with stairs was a little odd and with all his his risk factors, felt pretty confident he needed a stress test, so let’s Monday-morning quarterback this and go through how I should have chosen the next test….
M: Yeahh I’m still kind of pushing for the stress PFTs here… But seriously, the way to select a stress test is to separate the two components of the test.
GREG KATZ: Making sure we’re sharing the same mental model. Anytime you are sending somebody for a stress test, you’re making two decisions, how do I stress them and how do I image them?
M: Ok love me a good framework! First, pick a method of stressing the patient – typically exercise, vasodilator or inotropes. Second, we choose the diagnostic method – typically EKG or one of many imaging modalities that we’ll talk about in the next pearl.
S: Yep, let’s focus on the stressor – okay if my options are exercise, vasodilators and inotropes – how do I choose?
GREG KATZ: So everyone who can exercise should exercise, and when you’re deciding about the type of stress test you want to do, you want to stress somebody, and you want to replicate the experiences that they do in their life as best as you can. So if you have someone who is really active, you want to encourage them to push themselves . . . so that you can replicate and bring out whatever symptoms they may be having in their regular life. If you have a patient who is very sedentary, you still want to exercise them because you get a lot of prognostic information based on how far someone is able to go on a stress test. So everyone who can exercise should exercise.
S: Okay so Mr Nary says his exercise tolerance limited by bad knee pain. So I don’t think he will get his HR up to 80-85% of maximum heart rate so how much I choosing between the pharmacological stressors – the vasodilators and inotropes? Greg makes me feel a little better that there isn’t necessarily a right or wrong answer here.
GREG KATZ: Majority of how people are deciding this is based on their arbitrary n of 1 experience across the population. And I mean there are data to look at it but the data don’t really show that there’s one that is unequivocally superior to another
M: Exactly but we can highlight some nuances. Starting with the inotropes- we often see in the US as dobutamine – its a direct B1 and B2 agonist so its going increase that cardiac squeeze to stress it. So you tell the patient “heads up they’re gonna inject a medicine. Its gonna make your heart beat faster and take pictures of how your heart responds.”
S: Oh nice it being B1 B2 agonist makes sense why dobutamine is contraindicated in pts with ventricular arrhythmias history- dobutamine is quite safe but can see how it can precipitate arrhythmias. Let’s move on to vasodilators? What do you got for me here?
E: The flavors of vasodilators are adenosine, dipyridamole, and regadenoson. (M: If I was Andy from the Office I’d say Reggggggadenson) Each of the vasodilators activate the adenosine receptor, which increases cyclic AMP production, vascular smooth muscle relaxation, and, at last, coronary vasodilation.
GREG KATZ: What it does is it dilates the resistance vessels dilate to the arterioles. And so that lets you see, because there’s no more resistance in the coronary bed, if there’s an epicardial obstruction that is significant enough to cause an asymmetric distribution of blood flow
M: So the idea here is that we’re opening the flood gates to coronary flow – if there is nothing preventing blood flow then the whole heart gets a little extra juice and everything lights up normally. If there is an impediemnt to flow – like a coronary blockage – then that area gets less juice than the rest of the heart. Any if I’ve learned anything from being a father to a 3-year-old is that less juice is always a bad thing..
S: Anyway, what are some contraindications I should keep in mind with those vasodilators?
E: First, that increase cyclic AMP’s effect on the SA node may reduce chronotropy resulting in bradycardia and hypotension, which is why we should avoid vasodilators in patients with second or third degree HB w/o a pacemaker to protect them. Second one to keep in mind is, adenosine receptor activation also induces histamine and acetylcholine release, which may lead to bronchoconstriction in patients with severe COPD or asthma.
M: And while that list of contraindications may sound scary, they are pretty rare and we do have a reversal agent – which is aminophylline
S: Right, and you also wanna tell patients 2 things before their stress test 1) in general no B-blocker the morning of the stress and 2) no caffeine before a vasodilator stress test because fun fact, it can competitively block the adenosine receptor, making the vasodilator stressor less effective
M: To sum this up – remember that if they can exercise, they should exercise.
E: In this group think about anyone with a comorbidity that would make it unlikely they could achieve the target HR of 85% predicted for age. And if they can’t or shouldn’t (S: or straight up won’t!) then pharmacologically stress ‘em
M: And if you’re dropping a pharma stress-bomb, dobutamine and vasodilators are your main weapons. Dobutamine is your squeeze-machine and the vasodilators open the floodgates to expose hidden impidents to your juice-flow. Remember that both classes of drugs have their own sets of contraindications that you should think about when stressing your patients.
Pearl 3: How do you choose the diagnostic modality of the stress test?
M: Okay after choosing the stressor then the next step is to choosing how we want to measure the response to that stressor. Super basic question – what are my options here?
E: Yeah, thankfully you have a few. With all of them, the idea is that you get baseline diagnostic test and then repeat it after the stressor, looking for a change. Straight up EKG works for low-intermediate risk patients, and there’s also 4 others: echocardiogram, nuclear imaging and even MRI and PET scans if you want to get real saucy.
M: Yes! Hashtag #saucystress – coming soon to a tweetorial near you!
S: Alright guys – let’s rein this in a bit. Starting with the ECG, which patients might we target for these?
E: The 1st thing to ask yourself — is the baseline EKG interpretable or not? In other words, is there anything that might prevent ischemic changes from showing up after the stressor.
S: Right to help me keep straight the 5 things that are no bueno in baseline ECGs is tied up nicely in an acronym “VolksWagen Drivers Don’t Litter”: V for the V-paced rhythm, W for WPW, D for depressions and digoxin, and L for complete LBBB. As an aside, we have no idea if driving a Volkswagen has anything to do with littering but maybe the mnemonic will stick
E: If you can get away with it – don’t have V-paced rhythm, any baseline depressions, LBBB on the EKG, stress EKG tests are nice because they are cheap and radiation-free.
M: An important pearl to remember is that ST elevations during the stress test localize to coronary distribution but the ST depressions do not.
E: Righteous point Fried. But stress EKGs are the least sensitive and specific of all diagnostic modalities, coming in at about pooled sensitivity of 68% and specificity of 77% for detection of CAD. That sensitivity drops even more with its comes to women and in the elderly. So we usually reserve these for patients in whom our pretest probability is relatively low to begin with.
S: If my stats are correct that means you have to be okay a decent amount of false positives and false negatives. So that’s probably why stress ECGs rarely used in isolation today.
GREG KATZ: Everybody who gets a stress test gets EKG imaging- that’s done automatically. The people who need imaging beyond EKG imaging are people who you have anything other than a really low index of suspicion. And so if you are thinking, ‘I’m pretty sure this person does not have coronary disease,’ then an exercise EKG stress test is usually a good choice as the test that you’re doing.
S: So sounds like for Mr Cory Nary is intermediate risk with his risk factors and story, so I definitely want add some imaging to the ECG. And for further imaging I often find myself deciding btw stress echos and stress nuclear scans – what are the pros and cons between the two?
E: Good news is echo and nuclear scans have similar sensitivity and specificity – roughly around 80%, which is better than exercise ECG alone.
S: Yeah that’s helpful to understand and we’ll have the more detailed #s of sensitivities and specificities in our infographic for the episode if you really want to delve into it.
M: Right on, so w/ echos, we’re essentially looking with echos are wall motion abnormalities. If a resting wall motion abnormality is present, then we interpret that as scar which is “old ischemia.” If there is a new wall motion abnormality with stress, then that is indicative of “new ischemia.” Other pluses with echo is it gives you info on valvular pathology, pulmonary HTN and Left ventricular outflow track obstruction.
E: The drawback with stress echos is that the diagnostic performance of the test is heavily reliant on the skill level of the sonographer. They have to obtain clear windows at rest, and then again at maximum stress, which can be insanely difficult.
GREG KATZ: And the downside of a stress echo is if you don’t have good windows, the validity of the test is really low. It’s technically a little bit more difficult to image because you are getting somebody from a position on a treadmill and then immediately putting them, onto a table and then taking images. And so you might miss peak exercise in that patient because it takes so long to get the images and to get them in the right position
S: Right gotta keep in mind some ppl might just have bad windows – sometimes our COPD pts or pts with high BMIs (hope my POCUS colleagues are proud I remember who gets bad windows usually)
E: Now that we have the pros and cons of stress echo down, let’s move to stress nuclear scans, or the so-called Stress MIBI or nuclear SPECT aka “single positron emission” CT for ppl who didnt know what SPECT was (Guilty!) A Tc-99 labeled tracer, usually sestamibi, is injected. Healthy myocardial cells take up tracer, and dead or ischemic cells do not. Rest images are captured using SPECT. The patient then undergoes the chosen stressor, tracer is injected again, and stress images are captured. Again we’re looking at the difference in the before and after pictures and also differences in the tracer distribution within the heart itself.
S: Right so that tracer will light up the living cells and nonviable cells will be dark; this is particularly helpful for pts who have undergone revascularization and you’re trying to figure out if there’s healthy tissue for further intervention.
M: But the downside with nuclear scans is that there is radiation involved. And let’s not forget that similar to echo’s there are some user-dependent subjectivity as well.
GREG KATZ: When you put up nuclear images, it looks like you’re looking at a doughnut across the room and trying to gauge the symmetric distribution of sprinkles. There’s this huge arbitrary component how you’re interpreting it. I may be overstating it a little bit in terms of the arbitrariness because it’s standardized to some extent, but there’s a large degree of subjectivity in interpreting. Similarly, there’s a degree of subjectivity and interpreting echo
S: Yep no perfect tests. Another small but pearl-worthy possible downside to keep in mind with nuclear scans is something called balanced ischemia.
M: To understand “Balanced ischemia” we have to understand that ischemia on the nuclear SPECT relies on the reduced uptake of tracer in a particular segment relative to the other segments of the LV. BUTTT, if a person has severe proximal or three vessel disease, the myocardium is globally ischemic, and there is no major difference in tracer distribution within the heart so there is a higher chance the scan will appear normal when in reality severe ischemia is present.
E: But fear not, Greg has a really interesting contingency plan for cases of balanced ischemia:
GREG KATZ: To get around the concept of balanced ischemia, a nuclear stress test will also report something called TID or transient ischemic dilation. And the idea is that if you have TID that is present on nuclear imaging, the ventricle is enlarging and it probably has globally reduced function . . . if you see transient ischemic dilation on the nuclear imaging report that is a very high-risk feature that alludes to the decent probability of there being either left main or triple-vessel disease.
M: How about THAT for a stress bomb! A TID higher than 1.3, higher is worrisome global ischemia. I’m about ready to call this section and move on…
E: Almost Marty, but not quite. The stress ECG, stress echo and stress nuclear scan are probably the most high-yield for many internists – but for completeness sake we should probably touch on pharmacologic PET and MRI scans. These are your Cadillacs of functional testing, in both quality and cost. For example, it has been estimated that for a particular facility to even offer pharmacologic PET may cost as much as $450,000 per year.
S: Eesh that is pricey. Cardiac MRI can assess essentially anything you want to know about the heart. It’s able to quantify both myocardial perfusion and flow reserve, myocardial fibrosis and providing assessment of RV function. A negative stress cardiac MRI is associated with a 99.2% 3-year event free survival.
M: Nice. Can I recap now?
S: Hold on, one more thing Marty- we should talk about costs of each. We already talked about the cadallics of stress testing but the three most common stress tests: Stress ECGs obviously the cheapest, rings around ~$175 stress echos are bit more expensive at about $500. Nuclear scans are twice as much about $950
M: So start saving now for your Christmas SPECT scans… Ok I’m recapping now. Stress EKGs is probably best reserved for your patients in whom you have a low suspicion of CAD, who are able to exercise, and whose baseline ECG is interpretable. For most patients the choice probably comes down to echo or nuclear imaging. In the hands of a skilled echo tech the test characteristics are pretty close. Echo has the benefit of better valvular evaluation while nuclear scans are the test of choice for patients with a history of revascularization.
Pearl 4: How should we interpret stress tests and discuss with patients?
S: Okay so back to our case. Younger Shreya ended up getting a dobutamine stress echo because she thought she heard a murmur and wanted to if there was influence of any valvular pathologies. Younger Shreya thought the pain was over, but then the results came back and I remember being confused again – how do I interpret the results… and how do I explain that to a patient in a way that makes sense.
E: I totally agree, Shreya. It turns out that describing a stress test is “positive” or “negative” might be the easy thing to do, but it’s probably not the most accurate.
S: Yeah how many times have seen in the chart negative stress test in 2017 and no one bats an eye any further?
GREG KATZ: When you’re an internist who is sending somebody for a stress test, there are, there’s a lot of information that you can get from the body of results of the text that doesn’t get communicated if you just think of a stress test as positive or negative
M: Oh boy, I’m going to have to addended a progress note from Friday…
GREG KATZ: if you look at exercise stress testing, you get prognostic information from how far does somebody go and what degree of ST depressions do they have during the test and not to sort of over quantify things. But you can look at something like the Duke treadmill score, which is the number of minutes that you walk on the stress test essentially minus a factor of how many millimeters of ST Depression do you have. And that gives you great prognostication for major adverse cardiovascular events for a patient moving forward over the course of a period of years. Similarly, if you get nuclear imaging on somebody, the amount of ischemia that somebody has gives prognostic information about their MACE (Major Adverse Cardiovascular Event) risk over the future next couple of years
S: Check out bottom of the infographic using scores like the Duke Treadmill score to estimate risk.
M: Right someone who gets symptomatic or has EKG changes at 3 mins is very different from someone who’s EKG changes occur at minute 9.
S: so that’s what stress tests can tell us but just as important as that is what it doesnt tell you! These stress tests will tell you about the physiologic consequences of blockages, but not always about the presence of blockages.
Greg KATZ: Stress tests don’t tell you anything about coronary disease that is not causing an epicardial coronary obstructions. You can have intermediate amounts of plaque or large quantities of plaque but if they are not blocking 70% or so of the artery, you are not going to pick them up on a stress test.
E: So stress tests are not binary – they do not say obstruction or no obstruction – stress tests tell us if there is an amount of coronary obstruction that cause ischemia during the stress.
GREG KATZ: Instead of describing a stress test as positive or negative, I describe a stress test as low risk or higher risk. I’m looking at how severe is this? Is it mild, moderate, or is it very severe? And I’m also looking at how many segments of the wall or how much of the myocardium is involved. And immediately if somebody walks on the Bruce Protocol for 12 minutes and they have nuclear images that are completely perfect, they still have a possibility of having an MI in the next 12 months. It’s really low.
S: Marty’s opening up EPIC right now and changing “negative stress” test to low risk
M: That did just happen. But seriously, what I found compelling from speaking with all these cardiologists was that we often get tricked by the positive stress test in a person found to have clean coronaries or, even worse, the tragic stories of major cardiac events shortly after quote negative tests.
GREG KATZ: None of these tests are perfect and you’re always in the back of your mind wondering how reliable is this test and to what extent do I believe the results?
E: And this gets into that Baysesian pre-test probability for significant coronary disease – something that is nearly impossible to capture in a clinical guideline. Greg thinks about this in terms of populations:
GREG KATZ: You will be fooled by abnormal nuclear imaging in patients who have totally patent epicardial vessels and whether that reflects microvascular disease, endothelial dysfunction or some other issue that isn’t cardiac at all. It’s impossible to tell. But you will be fooled in both directions. Across populations, and even though stress testing is really good at prognosticating across the population, if that person has an event, their probability of the event is 100% and all of a sudden you’re getting somebody who on a population level wasn’t supposed to have something happen but they do have something happen. So stress testing is not perfect. And I keep harping on that because it’s super important and like the whole goal of ordering these tests is to figure out how are you treating somebody and how are you empowering them and giving them the tools to change their lifestyle that will reduce their risk of cardiovascular events and cardiovascular morbidity and mortality.
M: Wow – let’s talk about that! I’ve never thought of using stress tests to empower patients to change their lifestyle in meaningful ways… In fact I wonder if there are actually harms done when we slap a “negative” label – for example, if we give them a false sense of confidence by describing the test as ‘negative’ when they can still benefit from lifestyle changes that provide the greatest benefit. This, my friends, might be the hashtag stress bomb to top all others…
GREG KATZ: It doesn’t help your decision about whether that treat their hypertension or treat their diabetes or give them a statins because I don’t think it gives you enough certainty about the presence or absence of the diagnosis to modify the way that you’re treating those risk factors.
S: Right in terms of mgmt, lets bust the myth that everyone with an abnormal stress goes to cath lab. It’s a case-by-case decision between the patient, primary clinician and cardiologist
M: Something to think about as we wrap up the episode.
S: So much food for thought indeed, to recap what are hearing – if we avoid labeling studies “positive” and “negative” in favor of more nuanced terms like “high” and “low” risk that leaves much more room for discussions around risk modification. These tests give us a ton of information that we can use to estimate risk – for example the Duke Treadmill Score. And if we use the results of the tests to gain buy-in from our patients we will probably make a bigger difference than if we ignored all quote-unquote negative stress tests and sent all positive stress tests to cath.
E: And with that we would like to introduce our peer reviewer Dr. Eugene Yuriditsky, a cardiologist at NYU to recap our Stress test take home points before we move on the throwback pearl
Pearl 5 – Throwback – Revisiting sticking points of contrast-induced nephropathy
M: Ok, let’s pump the brakes on the squeeze machine and revisit pearls from a prior episode on the unsung heroes of human physiology – the beans.
S: Several episodes ago we discussed – wait, Marty did you just call the heart the squeeze machine?
E: Did you just call the kidneys the “beans”.
M: yes, yes I did.
S: Not a hundred percent sure how I feel about that, but I’ll allow it for now. Anyway – we covered contrast-induced nephropathy back in the day and felt that all this talk about coronary health is a good place to revisit one of the biggest perceived threats to the kidneys – intravascular contrast. (dun-dadun)
M: Yes, fine, true. But Shreya, let’s be honest what’s the real reason why we’re doing this now?
S: One of our biggest takeaways from the podcast episode was that the risk of contrast induced nephropathy has been described more in the arterial contrast literature and not as much of a risk with venous contrast – and in fact the risk is very low in intravenous contrast studies like CT abdomen with contrast. Our great friend and colleague Dr. Swapnil Hiremath (M: @hswapnil on the tweet machine) pushed us to even question the data behind contrast-induced nephropathy in the arterial contrast literature.
E: So the problem with the contrast induced nephropathy literature that deals with intra-arterial contrast is that they have so many confounders – we might see an increased risk of AKI after coronary catheterizations, but patients undergoing intra arterial angiography after a STEMI, for example, simply put have more reasons that they could suffer from AKI than those undergoing a more routine CT chest with contrast.
S: The confounders include things like poor renal perfusion at baseline, to propagation of atheroemboli, to higher effective concentrations of contrast seen by the kidneys. Bottom line is that intra-arterial studies likely carry higher risk of post contrast AKI, and are very difficult to compare to studies of AKI post intra-venous contrast.
M: The other big issue here is that the optimal strategy for prevention of contrast -induced nephropathy hasn’t been determined yet.
E: Several methods of prevention have been studied, some more robustly than others. These include hydration with isotonic saline, sodium bicarbonate, and n-acetylcysteine.
M: While prophylaxis with isotonic saline before during and after arterial contrast studies has been the tried and true means of reducing risk of post-contrast AKI, we want to make sure to introduce a bit more skepticism thanks to some recent high quality data
E: A recent prospective study showed that saline prophylaxis was no better at preventing contrast induced AKI compared to no prophylaxis in patients with CKD undergoing elective contrast studies. This was the AMACING study.
M: That’s AMACING with a C and not a Z.
S: We are still far from case closed – while these studies certainly do throw some shade on the routine usefulness of isotonic saline to prevent post contrast AKI, it’s worth noting that the procedures in AMACING study was are elective – read no STEMIs, likely no hypoperfusion to the kidneys and likely ok volume status – and so might represent a group of less vulnerable kidneys not as sensitive to contrast.
M: We clearly still have quite a bit to learn with this topic, but we greatly appreciate Swapnil’s comments and everyone else who drops us a line to help refine our points and make a better podcast for our audience.
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Tags: cardiac risk stratification, Chest pain