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Name:
A 57-Year-Old with Chest Discomfort
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A 57-Year-Old with Chest Discomfort
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Upload Date:
2022-02-28T00:00:00.0000000
Transcript:
Language: EN.
Segment:0 .
[intro music]
DR. HANDY: Hi, welcome to Harrison's Podclass where we discuss important concepts in internal medicine. I'm Cathy Handy.
DR. WIENER: And I'm Charlie Wiener, and we're coming to you from the Johns Hopkins School of Medicine.
DR. HANDY: Welcome to today's episode, a 57-year-old with chest discomfort.
DR. WIENER: Great, Cathy, well, we're going to have another guest discussion today, so looking forward to that, but here's the case. You're in the emergency department seeing a 57-year-old hockey team coach with a prior history of hypertension, hyperlipidemia, and tobacco use. He presents to the emergency department tonight after experiencing chest discomfort during a practice. He tells you that he first began having similar symptoms about three weeks ago when he was skating vigorously during practice.
DR. WIENER: The discomfort typically lasts about 10 minutes, but then it resolves every time with rest. However, over the last week, it's taken less exertion to initiate the discomfort and a longer time for it to dissipate. Tonight, it occurred while he was just sitting on the bench and his assistant coach insisted that he come to the emergency department. He describes the discomfort as a pressure radiating to his jaw, but since being in the emergency department, it has resolved also.
DR. HANDY: This is the classic description of cardiac chest pain, so I would definitely begin workup for that and starting with an EKG.
DR. WIENER: Okay, well, it turns out at triage on entry they did that, and his electrocardiogram shows T wave inversions in leads I, II, aVL, V5, and V6. T wave inversions in leads I, II, aVL, V5, and V6. There are no ST elevations.
DR. HANDY: So not an ST elevation MI or a STEMI, but he could still be having an acute event. He does have changes that you mentioned, an old EKG would be essential to compare.
DR. WIENER: So his last ECG was two years ago on a routine physical examination, and these T wave inversions are clearly new.
DR. HANDY: Anything more from physical exam or history that's noteworthy? I'd want to make sure that his vital signs are stable, his pulses are symmetric, and that he doesn't have any localizing cardiac, respiratory or any neurologic findings.
DR. WIENER: Okay, good. Well, he's awake and responsive. He's worried but in no apparent distress. He was placed on nasal oxygen at triage. His blood pressure is 140/90 in both arms, his heart rate is 100, his respiratory rate is 12, and his oxygen saturation is 100% on the nasal oxygen. His pulses are present in both legs. His jugular venous pressure is not elevated, his lungs have no crackles, and the only abnormality on cardiac examination is a diffused PMI and a loud S4.
DR. WIENER: He moves all of his extremities symmetrically, and he's alert and oriented to person, place, and time.
DR. HANDY: So those are all reassuring findings. He's clearly not in cardiogenic shock and does not seem to be having a stroke or a dissection, let's tackle the question next.
DR. WIENER: So the question asks, which of the following clinical entities is an appropriate diagnosis for this hockey coach? And the options are, A. more information is required before making a diagnosis; B. non-ST elevation myocardial infarction; C. ST elevation myocardial infarction; D. stable angina; or E. unstable angina.
DR. HANDY: So of those choices, the answer is A. more information is required before we make a diagnosis, and even before we would decide on any of the other choices that you mentioned.
DR. WIENER: Why do you say that?
DR. HANDY: Well, let's go through each of the answers and rule out some of them, so it's not C. I mentioned already, he's not having an ST elevation MI, and his ECG rules that out. He could still be having an acute coronary syndrome or ACS based on the clinical presentation alone. Typically, in an ACS, the chest discomfort is severe, and it has at least one of the following three features. It occurs with rest or with minimal exertion, lasting greater than 10 minutes, it's a relatively recent onset, so within the past couple of weeks, for example, or it occurs with a crescendo pattern where it's distinctly more severe, prolonged, or more frequent than previous episodes.
DR. WIENER: So that certainly sounds like our patient, right?
DR. HANDY: Absolutely, but the question was asking for more specificity, so the diagnosis of non-ST segment elevation myocardial infarction, or an NSTEMI is established if a patient with the clinical features that we described above of ACS also develops evidence of myocardial necrosis, and that means that you would see abnormally elevated levels of biomarkers of cardiac necrosis. In this case, we didn't hear anything about laboratory values, so we'd not be able to say this right now.
DR. WIENER: So, he clearly does not have stable angina based on the worsening symptoms, right?
DR. HANDY: Right, his clinical presentation is also consistent though with accelerating or unstable angina, but we can't distinguish between NSTEMI or unstable angina without the cardiac biomarkers. If we drew them and they were elevated, then he would be having an NSTEMI.
DR. WIENER: And I presume if he had those symptoms, but his biomarkers were negative, then we'd say he has unstable angina.
DR. HANDY: That's right.
DR. WIENER: Okay, well, once again, as I mentioned, we're thrilled to have a guest discussion, Dr. Joseph Loscalzo here with us. So let's start the discussion with Dr. Loscalzo.
DR. LOSCALZO: Well, thank you, Charlie and Cathy, it's wonderful to be back with you, I really enjoy these sessions.
DR. HANDY: So making the diagnosis of acute coronary syndrome in 2021 still depends on the history and the EKG. Biomarkers so far have really not completely replaced that. So where are we with biomarkers for coronary syndromes and how do you see the diagnosis of acute coronary syndrome evolving in the next 5-10 years?
DR. LOSCALZO: Thank you for that question, Cathy, I guess the first point that I would make is that it's fairly straightforward, not invariably but generally to distinguish a STEMI from a non-STEMI, which could either be an NSTEMI or unstable angina. Distinguishing an NSTEMI from unstable angina on the other hand is more challenging but it's important because making that decision then leads to direct management decisions that are different for the two causes of an acute coronary syndrome.
DR. LOSCALZO: Now, as you say, biomarkers have evolved, but not gotten to the point that we could consider them foolproof. The most useful biomarkers these days, of course, are troponins, troponin T or I. Now we're in our fifth generation of troponin assays, they've become more and more sensitive, and as a consequence, they've lost a bit of specificity, such that we can now detect low levels of circulating troponin in more than 50% of normal healthy individuals.
DR. LOSCALZO: So as a consequence of that improved sensitivity with a potential for loss of specificity, now the European Society of Cardiology and other groups have worked out cutoffs based on measurements in populations with definable diagnoses of acute coronary syndromes. So in the initial measurement, one can comfortably rule out acute myocardial infarction if the troponin is less than 5 ng/mL, if it's greater than 52 ng/mL with the latest generation assay, one can rule in comfortably myocardial infarction.
DR. LOSCALZO: After the first hour when a second set is sent, if the level of troponin remains less than 3 ng/mL, that's consistent with a rule-out diagnosis, but now if it is equal to or exceeds 5 ng/mL, the change in troponin, that's consistent with a rule-in diagnosis. So troponin is an invaluable biomarker, but it comes with some provisos not the least of which is the sensitivity issue, but also in context, it's often difficult to interpret troponins.
DR. LOSCALZO: So for example, in patients with chronic kidney disease, especially those in dialysis, there is increased circulating levels of troponin that persist, and one needs to know what the baseline level might be in a patient before interpreting a change in that level in a patient with such severe renal disease. But there are alternate biomarkers that are now making their way through evaluation, one of course is NT-proBNP, which has been used for a while.
DR. LOSCALZO: Of course, it is another measure of stress, BNP or NT-proBNP, its precursor is released from a stressed cardiomyocyte as might occur in patients with ischemic disease. Galectin-3 is a molecule that's secreted by activated macrophages, so with plaque activation it may be a good marker for an acute coronary event. GDF-15 which is growth or differentiation factor 15 is another stress induced cytokine that is being evaluated, and copeptin, which together with troponin can very clearly identify high-risk individuals with stress induced injury like Takotsubo, is another marker that's evolving.
DR. LOSCALZO: But I would say to answer your question more succinctly, I'm not always succinct, I apologize, is that to have a really meaningful signature of biomarkers in a sort of weighted equation is really what we should move toward and over time, I believe, we'll get there.
DR. WIENER: In light of that, Joe, just the markers you just mentioned, when do you foresee that they may be ready for prime time or common usage?
DR. LOSCALZO: Well, I think a couple of them are actually making their way to prime time pretty quickly in the next couple of years, like Galectin-3 or GDF-15 as an example.
DR. WIENER: All right, Cathy well that's going to be a challenge for future podclass, I guess. Joe, assuming this patient was on appropriate medical therapy for his hypertension and his hyperlipidemia, what other preventive measures can be taken? It seems like we're always counseling our patients on lifestyle modification and diet and exercise, but success in achieving those is really hard. Do you have any tips for us or any other ancillary things that we should be thinking about?
DR. LOSCALZO: Well, I think the key is not to give up. We shouldn't give up as the patient's physician in bringing these issues to the patient's attention and the patients shouldn't give up if they attempt and fail. As you know, it takes on average about seven times before someone actually stops smoking who has an intention to do so. It's a little easier with some of the current medications, but it still takes a number of efforts before you get to a real smoke-free lifestyle in someone who smoked for much of their adulthood.
DR. LOSCALZO: Similarly for weight management, which seems literally impossible in many cases, one needs to encourage patients, celebrate even modest improvements in their weight, continue to bring to their attention ways to adjust their eating habits and the stresses that might lead to them. Again, there are new drugs on the horizon, which really do seem to make a difference, whether they will make a persistent, durable difference or not, remains to be seen.
DR. LOSCALZO: So from my perspective, I always try to take as positive an attitude as I can in discussing these kinds of issues with my patient. I also think that cardiac rehabilitation is also an important element post infarct, or post acute coronary syndrome or intervention. It may not always seem so to the patient, especially if they feel reasonably well, but they can begin to experience through the rehabilitation program and their interactions with other folks who are going through the same program, begin to experience some of the strategies that others have used with some success at improving these lifestyle issues.
DR. LOSCALZO: And of course, one can never say too much about a regular exercise prescription, even if it's just armchair stretching.
DR. HANDY: And as a vascular biologist, do you have any thoughts on the mechanisms that we'll be hearing about soon?
DR. LOSCALZO: I have lots of thoughts in that, but I only have a minute or so-
DR. HANDY: [andy and Dr. Wiener chuckle]
DR. LOSCALZO: -so I'll give you sort of a taste of some of the things that interest me. The first is that we're moving in a direction of trying to define what people call patient-based endotypes or endophenotypes, and these are really determinants of fundamental pathological mechanisms that underlie all diseases such as inflammation, thrombosis, fibrosis, so that you can imagine a day when one can identify a patient as being very strongly pro-inflammatory based on some signature or prothrombotic in which case, based on those signatures, one might approach a therapeutic strategy, both acutely as well as preventively from a more personalized basis.
DR. LOSCALZO: For example, in the case of an enhanced inflammatory response, one might explore with the appropriate biomarker signatures pathways that govern inflammation in that patient, such as senescence associated secretory phenotypes, and their downstream mediators like interleukin-1 beta, or alpha-7 nicotinic acetylcholine receptor dependent activation, or the NLRP inflammasome, or altered NAD metabolism and its consequences for inflammation.
DR. LOSCALZO: Those are some of the areas that are blossoming as potential pathological and pathobiological foci. And I'll just make one last point to this question, Cathy, that there's growing emphasis and recognition of the links between inflammation and metabolism in the blood vessel wall and its consequences for vascular function and therapeutic intervention. For example, most people don't realize that the healthy endothelium gets most of its ATP from glycolysis, not oxidative phosphorylation, even in a normal, healthy oxygen rich environment.
DR. LOSCALZO: Endothelial dysfunction modulates this glycolytic phenotype, and that is associated with enhanced endothelial inflammation, adhesion molecule expression, for example. So that kind of pathobiology begins to offer novel therapeutic targets that we haven't thought about previously.
DR. WIENER: Wow, that's just another a great example of how precision medicine is going to become more precise as we move forward and our translational research gets in from the bench to the bedside, that's great, that's really cool.
DR. LOSCALZO: Thank you.
DR. HANDY: Joe, it's always a pleasure having you here, thank you so much, and for those listening, if you want to learn more, you can read about this in Harrison's chapter on acute coronary syndromes. [outro music] [Mr. Shanahan] This is Jim Shanahan, publisher at McGraw Hill. Harrison's Podclass is brought to you by McGraw Hill's Access Medicine, the online medical resource that delivers the latest trusted content from the best minds in medicine.
DR. HANDY: Go to accessmedicine.com to learn more.
Segment:0 .
[intro music]
DR. HANDY: Hi, welcome to Harrison's Podclass where we discuss important concepts in internal medicine. I'm Cathy Handy.
DR. WIENER: And I'm Charlie Wiener, and we're coming to you from the Johns Hopkins School of Medicine.
DR. HANDY: Welcome to today's episode, a 57-year-old with chest discomfort.
DR. WIENER: Great, Cathy, well, we're going to have another guest discussion today, so looking forward to that, but here's the case. You're in the emergency department seeing a 57-year-old hockey team coach with a prior history of hypertension, hyperlipidemia, and tobacco use. He presents to the emergency department tonight after experiencing chest discomfort during a practice. He tells you that he first began having similar symptoms about three weeks ago when he was skating vigorously during practice.
DR. WIENER: The discomfort typically lasts about 10 minutes, but then it resolves every time with rest. However, over the last week, it's taken less exertion to initiate the discomfort and a longer time for it to dissipate. Tonight, it occurred while he was just sitting on the bench and his assistant coach insisted that he come to the emergency department. He describes the discomfort as a pressure radiating to his jaw, but since being in the emergency department, it has resolved also.
DR. HANDY: This is the classic description of cardiac chest pain, so I would definitely begin workup for that and starting with an EKG.
DR. WIENER: Okay, well, it turns out at triage on entry they did that, and his electrocardiogram shows T wave inversions in leads I, II, aVL, V5, and V6. T wave inversions in leads I, II, aVL, V5, and V6. There are no ST elevations.
DR. HANDY: So not an ST elevation MI or a STEMI, but he could still be having an acute event. He does have changes that you mentioned, an old EKG would be essential to compare.
DR. WIENER: So his last ECG was two years ago on a routine physical examination, and these T wave inversions are clearly new.
DR. HANDY: Anything more from physical exam or history that's noteworthy? I'd want to make sure that his vital signs are stable, his pulses are symmetric, and that he doesn't have any localizing cardiac, respiratory or any neurologic findings.
DR. WIENER: Okay, good. Well, he's awake and responsive. He's worried but in no apparent distress. He was placed on nasal oxygen at triage. His blood pressure is 140/90 in both arms, his heart rate is 100, his respiratory rate is 12, and his oxygen saturation is 100% on the nasal oxygen. His pulses are present in both legs. His jugular venous pressure is not elevated, his lungs have no crackles, and the only abnormality on cardiac examination is a diffused PMI and a loud S4.
DR. WIENER: He moves all of his extremities symmetrically, and he's alert and oriented to person, place, and time.
DR. HANDY: So those are all reassuring findings. He's clearly not in cardiogenic shock and does not seem to be having a stroke or a dissection, let's tackle the question next.
DR. WIENER: So the question asks, which of the following clinical entities is an appropriate diagnosis for this hockey coach? And the options are, A. more information is required before making a diagnosis; B. non-ST elevation myocardial infarction; C. ST elevation myocardial infarction; D. stable angina; or E. unstable angina.
DR. HANDY: So of those choices, the answer is A. more information is required before we make a diagnosis, and even before we would decide on any of the other choices that you mentioned.
DR. WIENER: Why do you say that?
DR. HANDY: Well, let's go through each of the answers and rule out some of them, so it's not C. I mentioned already, he's not having an ST elevation MI, and his ECG rules that out. He could still be having an acute coronary syndrome or ACS based on the clinical presentation alone. Typically, in an ACS, the chest discomfort is severe, and it has at least one of the following three features. It occurs with rest or with minimal exertion, lasting greater than 10 minutes, it's a relatively recent onset, so within the past couple of weeks, for example, or it occurs with a crescendo pattern where it's distinctly more severe, prolonged, or more frequent than previous episodes.
DR. WIENER: So that certainly sounds like our patient, right?
DR. HANDY: Absolutely, but the question was asking for more specificity, so the diagnosis of non-ST segment elevation myocardial infarction, or an NSTEMI is established if a patient with the clinical features that we described above of ACS also develops evidence of myocardial necrosis, and that means that you would see abnormally elevated levels of biomarkers of cardiac necrosis. In this case, we didn't hear anything about laboratory values, so we'd not be able to say this right now.
DR. WIENER: So, he clearly does not have stable angina based on the worsening symptoms, right?
DR. HANDY: Right, his clinical presentation is also consistent though with accelerating or unstable angina, but we can't distinguish between NSTEMI or unstable angina without the cardiac biomarkers. If we drew them and they were elevated, then he would be having an NSTEMI.
DR. WIENER: And I presume if he had those symptoms, but his biomarkers were negative, then we'd say he has unstable angina.
DR. HANDY: That's right.
DR. WIENER: Okay, well, once again, as I mentioned, we're thrilled to have a guest discussion, Dr. Joseph Loscalzo here with us. So let's start the discussion with Dr. Loscalzo.
DR. LOSCALZO: Well, thank you, Charlie and Cathy, it's wonderful to be back with you, I really enjoy these sessions.
DR. HANDY: So making the diagnosis of acute coronary syndrome in 2021 still depends on the history and the EKG. Biomarkers so far have really not completely replaced that. So where are we with biomarkers for coronary syndromes and how do you see the diagnosis of acute coronary syndrome evolving in the next 5-10 years?
DR. LOSCALZO: Thank you for that question, Cathy, I guess the first point that I would make is that it's fairly straightforward, not invariably but generally to distinguish a STEMI from a non-STEMI, which could either be an NSTEMI or unstable angina. Distinguishing an NSTEMI from unstable angina on the other hand is more challenging but it's important because making that decision then leads to direct management decisions that are different for the two causes of an acute coronary syndrome.
DR. LOSCALZO: Now, as you say, biomarkers have evolved, but not gotten to the point that we could consider them foolproof. The most useful biomarkers these days, of course, are troponins, troponin T or I. Now we're in our fifth generation of troponin assays, they've become more and more sensitive, and as a consequence, they've lost a bit of specificity, such that we can now detect low levels of circulating troponin in more than 50% of normal healthy individuals.
DR. LOSCALZO: So as a consequence of that improved sensitivity with a potential for loss of specificity, now the European Society of Cardiology and other groups have worked out cutoffs based on measurements in populations with definable diagnoses of acute coronary syndromes. So in the initial measurement, one can comfortably rule out acute myocardial infarction if the troponin is less than 5 ng/mL, if it's greater than 52 ng/mL with the latest generation assay, one can rule in comfortably myocardial infarction.
DR. LOSCALZO: After the first hour when a second set is sent, if the level of troponin remains less than 3 ng/mL, that's consistent with a rule-out diagnosis, but now if it is equal to or exceeds 5 ng/mL, the change in troponin, that's consistent with a rule-in diagnosis. So troponin is an invaluable biomarker, but it comes with some provisos not the least of which is the sensitivity issue, but also in context, it's often difficult to interpret troponins.
DR. LOSCALZO: So for example, in patients with chronic kidney disease, especially those in dialysis, there is increased circulating levels of troponin that persist, and one needs to know what the baseline level might be in a patient before interpreting a change in that level in a patient with such severe renal disease. But there are alternate biomarkers that are now making their way through evaluation, one of course is NT-proBNP, which has been used for a while.
DR. LOSCALZO: Of course, it is another measure of stress, BNP or NT-proBNP, its precursor is released from a stressed cardiomyocyte as might occur in patients with ischemic disease. Galectin-3 is a molecule that's secreted by activated macrophages, so with plaque activation it may be a good marker for an acute coronary event. GDF-15 which is growth or differentiation factor 15 is another stress induced cytokine that is being evaluated, and copeptin, which together with troponin can very clearly identify high-risk individuals with stress induced injury like Takotsubo, is another marker that's evolving.
DR. LOSCALZO: But I would say to answer your question more succinctly, I'm not always succinct, I apologize, is that to have a really meaningful signature of biomarkers in a sort of weighted equation is really what we should move toward and over time, I believe, we'll get there.
DR. WIENER: In light of that, Joe, just the markers you just mentioned, when do you foresee that they may be ready for prime time or common usage?
DR. LOSCALZO: Well, I think a couple of them are actually making their way to prime time pretty quickly in the next couple of years, like Galectin-3 or GDF-15 as an example.
DR. WIENER: All right, Cathy well that's going to be a challenge for future podclass, I guess. Joe, assuming this patient was on appropriate medical therapy for his hypertension and his hyperlipidemia, what other preventive measures can be taken? It seems like we're always counseling our patients on lifestyle modification and diet and exercise, but success in achieving those is really hard. Do you have any tips for us or any other ancillary things that we should be thinking about?
DR. LOSCALZO: Well, I think the key is not to give up. We shouldn't give up as the patient's physician in bringing these issues to the patient's attention and the patients shouldn't give up if they attempt and fail. As you know, it takes on average about seven times before someone actually stops smoking who has an intention to do so. It's a little easier with some of the current medications, but it still takes a number of efforts before you get to a real smoke-free lifestyle in someone who smoked for much of their adulthood.
DR. LOSCALZO: Similarly for weight management, which seems literally impossible in many cases, one needs to encourage patients, celebrate even modest improvements in their weight, continue to bring to their attention ways to adjust their eating habits and the stresses that might lead to them. Again, there are new drugs on the horizon, which really do seem to make a difference, whether they will make a persistent, durable difference or not, remains to be seen.
DR. LOSCALZO: So from my perspective, I always try to take as positive an attitude as I can in discussing these kinds of issues with my patient. I also think that cardiac rehabilitation is also an important element post infarct, or post acute coronary syndrome or intervention. It may not always seem so to the patient, especially if they feel reasonably well, but they can begin to experience through the rehabilitation program and their interactions with other folks who are going through the same program, begin to experience some of the strategies that others have used with some success at improving these lifestyle issues.
DR. LOSCALZO: And of course, one can never say too much about a regular exercise prescription, even if it's just armchair stretching.
DR. HANDY: And as a vascular biologist, do you have any thoughts on the mechanisms that we'll be hearing about soon?
DR. LOSCALZO: I have lots of thoughts in that, but I only have a minute or so-
DR. HANDY: [andy and Dr. Wiener chuckle]
DR. LOSCALZO: -so I'll give you sort of a taste of some of the things that interest me. The first is that we're moving in a direction of trying to define what people call patient-based endotypes or endophenotypes, and these are really determinants of fundamental pathological mechanisms that underlie all diseases such as inflammation, thrombosis, fibrosis, so that you can imagine a day when one can identify a patient as being very strongly pro-inflammatory based on some signature or prothrombotic in which case, based on those signatures, one might approach a therapeutic strategy, both acutely as well as preventively from a more personalized basis.
DR. LOSCALZO: For example, in the case of an enhanced inflammatory response, one might explore with the appropriate biomarker signatures pathways that govern inflammation in that patient, such as senescence associated secretory phenotypes, and their downstream mediators like interleukin-1 beta, or alpha-7 nicotinic acetylcholine receptor dependent activation, or the NLRP inflammasome, or altered NAD metabolism and its consequences for inflammation.
DR. LOSCALZO: Those are some of the areas that are blossoming as potential pathological and pathobiological foci. And I'll just make one last point to this question, Cathy, that there's growing emphasis and recognition of the links between inflammation and metabolism in the blood vessel wall and its consequences for vascular function and therapeutic intervention. For example, most people don't realize that the healthy endothelium gets most of its ATP from glycolysis, not oxidative phosphorylation, even in a normal, healthy oxygen rich environment.
DR. LOSCALZO: Endothelial dysfunction modulates this glycolytic phenotype, and that is associated with enhanced endothelial inflammation, adhesion molecule expression, for example. So that kind of pathobiology begins to offer novel therapeutic targets that we haven't thought about previously.
DR. WIENER: Wow, that's just another a great example of how precision medicine is going to become more precise as we move forward and our translational research gets in from the bench to the bedside, that's great, that's really cool.
DR. LOSCALZO: Thank you.
DR. HANDY: Joe, it's always a pleasure having you here, thank you so much, and for those listening, if you want to learn more, you can read about this in Harrison's chapter on acute coronary syndromes. [outro music] [Mr. Shanahan] This is Jim Shanahan, publisher at McGraw Hill. Harrison's Podclass is brought to you by McGraw Hill's Access Medicine, the online medical resource that delivers the latest trusted content from the best minds in medicine.
DR. HANDY: Go to accessmedicine.com to learn more.
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