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When is a troponin elevation an acute myocardial infarction?
Misdiagnosis can have ‘downstream repercussions’
Hospitalists encounter troponin elevations daily, but we have to use clinical judgment to determine if the troponin elevation represents either a myocardial infarction (MI), or a non-MI troponin elevation (i.e. a , nonischemic myocardial injury).
It is important to remember that an MI specifically refers to myocardial injury due to acute myocardial ischemia to the myocardium. This lack of blood supply can be due to an acute absolute or relative deficiency in coronary artery blood flow. However, there are also many mechanisms of myocardial injury unrelated to reduced coronary artery blood flow, and these should be more appropriately termed non-MI troponin elevations.
Historically, when an ischemic mechanism of myocardial injury was suspected, providers would categorize troponin elevations into ST-elevation MI (STEMI) versus non-ST-elevation MI (NSTEMI) based on the electrocardiogram (ECG). We would further classify the NSTEMI into type 1 or type 2, depending on the mechanism of injury. The term “NSTEMI” served as a “catch-all” term to describe both type 1 NSTEMIs and type 2 MIs, but that classification system is no longer valid.
As of Oct. 1, 2017, ICD-10 and the Centers for Medicare & Medicaid Services have a new ICD-10 diagnosis code for type 2 MI (I21.A1), distinct from NSTEMI (I21.4) based on updated definitions from the American College of Cardiology, American Heart Association, European Society of Cardiology, and World Heart Federation. The term “NSTEMI” should be used only when referring to a type 1 MI not when referring to a type 2 MI.1
Classification of MI types
The Fourth Universal Definition of MI published in August 2018 further updated the definitions of MI (summarized in Figure 1).2 This review focuses on type 1 and type 2 MIs, which are the most common types encountered by hospitalists. Types 3-5 MI (grouped under a common ICD-10 diagnosis code for “Other MI Types,” or I21.A9) would rarely be diagnosed by hospitalists.
Figure 1: Classification of MI
MI Type | Classification |
1 | STEMI (acute coronary artery thrombosis) |
2 | Supply/demand mismatch (heterogeneous underlying causes) |
3 | Sudden cardiac death with ECG evidence of acute myocardial ischemia before cardiac troponins could be drawn |
4 | MI due to percutaneous coronary intervention (PCI) |
5 | MI due to coronary artery bypass grafting (CABG) |
The diagnosis of a type 1 MIs (STEMI and NSTEMI) is supported by the presence of an acute coronary thrombus or plaque rupture/erosion on coronary angiography or a strong suspicion for these when angiography is unavailable or contraindicated. Type 1 MI (also referred to as spontaneous MI) is generally a primary reason (or “principal” diagnosis) for a patient’s presentation to a hospital.3 Please note that a very high or rising troponin level alone is not diagnostic for a type 1 or type 2 NSTEMI. The lab has to be taken in the context of the patient’s presentation and other supporting findings.
In contrast to a type 1 MI (STEMI and NSTEMI), at type 2 MI results from an imbalance between myocardial oxygen supply and demand unrelated to acute coronary artery thrombosis or plaque rupture. A type 2 MI is a relative (as opposed to an absolute) deficiency in coronary artery blood flow triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. In type 2 MI, myocardial injury occurs secondary to an underlying process, and therefore requires correct documentation of the underlying cause as well.
Common examples of underlying causes of type 2 MI include acute blood loss anemia (e.g. GI bleed), acute hypoxia (e.g. COPD exacerbation), shock states (cardiogenic, hypovolemic, hemorrhagic, or septic), coronary vasospasm (e.g. spontaneous), and bradyarrhythmias. Patients with type 2 MI often have a history of fixed obstructive coronary disease, which when coupled with the acute trigger facilitates the type 2 MI; however, underlying CAD is not always present.
Diagnosing a type 2 MI requires evidence of acute myocardial ischemia (Figure 2) with an elevated troponin but must also have at least one of the following:2
- Symptoms of acute myocardial ischemia such as typical chest pain.
- New ischemic ECG changes.
- Development of pathological Q waves.
- Imaging evidence of new loss of viable myocardium, significant reversible perfusion defect on nuclear imaging, or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.
Distinguishing a type 1 NSTEMI from a type 2 MI depends mainly on the clinical context and clinical judgment. A patient whose presenting symptoms include acute chest discomfort, acute ST-T wave changes, and a rise in troponin would be suspected of having a type 1 NSTEMI. However, in a patient presenting with other or vague complaints where an elevated troponin was found amongst a battery of tests, a type 2 MI may be favored, particularly if there is evidence of an underlying trigger for a supply-demand mismatch. In challenging cases, cardiology consultation can help determine the MI type and/or the next diagnostic and treatment considerations.
When there is only elevated troponin levels (or even a rise and fall in troponin) without new symptoms or ECG/imaging evidence of myocardial ischemia, it is most appropriate to document a non-MI troponin elevation due to a nonischemic mechanism of myocardial injury.
Non-MI troponin elevation (nonischemic myocardial injury)
The number of conditions known to cause myocardial injury through mechanisms other than myocardial ischemia (see Figure 2) is growing, especially in the current era of high-sensitivity troponin assays.4
Common examples of underlying causes of non-MI troponin elevation include:
- Acute (on chronic) systolic or diastolic heart failure: Usually due to acute ventricular wall stretch/strain. Troponin elevations tend to be mild, with more indolent (or even flat) troponin trajectories.
- Pericarditis and myocarditis: Due to direct injury from myocardial inflammation.
- Cardiopulmonary resuscitation (CPR): Due to physical injury to the heart from mechanical chest compressions and from electrical shocks of external defibrillation.
- Stress-induced (takotsubo) cardiomyopathy: Stress-induced release of neurohormonal factors and catecholamines that cause direct myocyte injury and transient dilatation of the ventricle.
- Acute pulmonary embolism: Result of acute right ventricular wall stretch/strain, not from myocardial ischemia.
- Sepsis without shock: Direct toxicity of circulating cytokines to cardiac myocytes. In the absence of evidence of shock and symptoms/signs of myocardial ischemia, do not document type 2 MI.
- Renal failure (acute kidney injury or chronic kidney disease): Multiple etiologies, but at least partially related to reduced renal clearance of troponin. In general, renal failure in the absence of symptoms/signs of ischemia is best classified as a non-MI troponin elevation. ESRD patients who present with volume overload due to missed dialysis also typically have a non-MI troponin elevation.
- Stroke/intracranial hemorrhage: Mechanisms of myocardial injury and troponin elevation are incompletely understood, but may include catecholamine surges that injure the heart.
Some underlying conditions can cause a type 2 MI or a non-MI troponin elevation depending on the clinical context. For example, hypertensive emergency, severe aortic valve stenosis, hypertrophic cardiomyopathy, and tachyarrhythmias (including atrial fibrillation with rapid ventricular response) may cause increased myocardial oxygen demand, and in patients with underlying CAD, could precipitate a type 2 MI.
However, these same conditions could cause a non-MI troponin elevation in patients without CAD and could also cause myocardial injury and troponin release by causing acute left ventricular stretch/strain. Distinguishing the diagnose of type 2 MI vs. non-MI troponin elevation depends on documenting whether there are ancillary ischemic symptoms, ECG findings, imaging, and/or cath findings of acute myocardial ischemia.
Case examples
1. A 60-year-old male presents with fever, cough, shortness of breath, and an infiltrate on CXR and is diagnosed with sepsis secondary to pneumonia. His initial troponin of 0.07 (normal < 0.05) rises to 0.11, peaks at 0.23, then subsequently trends down.
While some may be tempted to diagnose a type 2 MI, remember that sepsis can cause direct myocardial cell injury via direct cell toxicity. Unless this patient had at least one additional criteria (anginal chest pain, new ischemic ECG changes, or imaging evidence of new loss of viable myocardium, which does not recover with treatment of sepsis), this was most likely myocardial injury via direct cell toxicity, and should be documented as a non-MI troponin elevation due to sepsis without shock.
If there were ischemic ECG changes and the patient had chest pain, one would have to use clinical suspicion to differentiate between a type 1 NSTEMI and a type 2 MI. If there is a high clinical suspicion for an acute plaque rupture/thrombus, one would call it an NSTEMI and would have to document treatment as such (e.g. start heparin drip). Again, cardiology consultation can be helpful in cases where it may be hard to decide how to manage. Many times, the true mechanism is not determined until the patient is taken to the cath lab and if no acute plaque rupture is seen, then it was likely a type 2 MI.
2. A 70-year-old male with chronic systolic heart failure, noncompliant with medications, presents with 3 days of dyspnea on exertion and lower extremity edema. He had no chest discomfort. Exam shows bibasilar crackles and hepatojugular reflux. ECG shows no ischemic changes. Serial troponin values over 48 hours were: 0.48, 0.58, 0.51. A transthoracic echocardiogram reveals an LVEF of 40% with poor movement in the apex, similar to his prior echo.
This patient had no overt evidence of ischemia (no chest pain, ischemic ECG, or imaging changes) so the troponin elevation was most likely a non-MI troponin elevation secondary to acute on chronic systolic heart failure (in which the mechanism of troponin elevation is left ventricular chamber stretch from volume overload, and not demand ischemia). Generally, it is uncommon for a heart failure exacerbation to cause a type 2 MI.
Why is it so important to get this diagnosis right?
Misdiagnosing an MI when the patient does not have one can have multiple downstream repercussions. Because it stays on their medical record, it impacts their ability to get insurance and their premium costs. We expose patients to additional medications (e.g. dual antiplatelet therapy, statins), which can have adverse effects. As a result, it is very important to classify the etiology of the troponin elevation and treat accordingly.
Finally, when we incorrectly label a patient as having an MI, this can impact billing and reimbursement, DRG denials, insurance premiums, and quality metrics for both the hospital and the physicians. Hospitals’ 30-day readmission rates for AMI will suffer and quality metrics can be significantly impacted. We must be diligent and as precise as possible with our diagnoses and documentation to ensure the maximum benefit for our patients and our health care system.
Dr. Nave is assistant professor of medicine in the division of hospital medicine at Emory University, Atlanta. Dr. Goyal is associate professor of medicine (cardiology), at Emory University, and chief quality officer, Emory Heart and Vascular Center, Emory Healthcare. He is also codirector of nuclear cardiology at Emory University Hospital.
Key points
- A diagnosis of a type 1 MI is supported by evidence or strong suspicion of acute coronary artery thrombus or plaque rupture/erosion.
- A very high troponin level alone is not diagnostic for a type 1 or type 2 MI. It has to be contextualized with the patient’s presentation and other supporting findings.
- Type 2 MI is a mismatch between myocardial oxygen supply and demand unrelated to acute coronary thrombosis or plaque rupture triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. Type 2 MI should be documented along with its underlying cause.
- To diagnose an MI (either type 1 or type 2 MI), in addition to the troponin elevation, the patient must have symptoms of acute ischemia, ischemic ECG findings, and/or imaging suggestive of new ischemia.
- An elevated troponin level without new symptoms or ECG/imaging evidence of myocardial ischemia should be documented as a non-MI troponin elevation secondary to an underlying cause.
References
1. Goyal A, Gluckman TJ, Tcheng JE. What’s in a name? The new ICD-10 (10th revision of the international statistical classification of diseases and related health problems) codes and type 2 myocardial infarction. Circulation. 2017;136:1180-2.
2. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018;Aug 25:[Epub ahead of print].
3. Goyal, et al. Translating the Fourth Universal Definition of Myocardial Infarction into Clinical Documentation: Ten Pearls For Frontline Clinicians. Cardiology Magazine. Nov 2018.
4. Roongsritong C, Warraich I, Bradley C. Common causes of troponin elevations in the absence of acute myocardial infarction: incidence and clinical significance. Chest. 2004;125:1877-84.
Misdiagnosis can have ‘downstream repercussions’
Misdiagnosis can have ‘downstream repercussions’
Hospitalists encounter troponin elevations daily, but we have to use clinical judgment to determine if the troponin elevation represents either a myocardial infarction (MI), or a non-MI troponin elevation (i.e. a , nonischemic myocardial injury).
It is important to remember that an MI specifically refers to myocardial injury due to acute myocardial ischemia to the myocardium. This lack of blood supply can be due to an acute absolute or relative deficiency in coronary artery blood flow. However, there are also many mechanisms of myocardial injury unrelated to reduced coronary artery blood flow, and these should be more appropriately termed non-MI troponin elevations.
Historically, when an ischemic mechanism of myocardial injury was suspected, providers would categorize troponin elevations into ST-elevation MI (STEMI) versus non-ST-elevation MI (NSTEMI) based on the electrocardiogram (ECG). We would further classify the NSTEMI into type 1 or type 2, depending on the mechanism of injury. The term “NSTEMI” served as a “catch-all” term to describe both type 1 NSTEMIs and type 2 MIs, but that classification system is no longer valid.
As of Oct. 1, 2017, ICD-10 and the Centers for Medicare & Medicaid Services have a new ICD-10 diagnosis code for type 2 MI (I21.A1), distinct from NSTEMI (I21.4) based on updated definitions from the American College of Cardiology, American Heart Association, European Society of Cardiology, and World Heart Federation. The term “NSTEMI” should be used only when referring to a type 1 MI not when referring to a type 2 MI.1
Classification of MI types
The Fourth Universal Definition of MI published in August 2018 further updated the definitions of MI (summarized in Figure 1).2 This review focuses on type 1 and type 2 MIs, which are the most common types encountered by hospitalists. Types 3-5 MI (grouped under a common ICD-10 diagnosis code for “Other MI Types,” or I21.A9) would rarely be diagnosed by hospitalists.
Figure 1: Classification of MI
MI Type | Classification |
1 | STEMI (acute coronary artery thrombosis) |
2 | Supply/demand mismatch (heterogeneous underlying causes) |
3 | Sudden cardiac death with ECG evidence of acute myocardial ischemia before cardiac troponins could be drawn |
4 | MI due to percutaneous coronary intervention (PCI) |
5 | MI due to coronary artery bypass grafting (CABG) |
The diagnosis of a type 1 MIs (STEMI and NSTEMI) is supported by the presence of an acute coronary thrombus or plaque rupture/erosion on coronary angiography or a strong suspicion for these when angiography is unavailable or contraindicated. Type 1 MI (also referred to as spontaneous MI) is generally a primary reason (or “principal” diagnosis) for a patient’s presentation to a hospital.3 Please note that a very high or rising troponin level alone is not diagnostic for a type 1 or type 2 NSTEMI. The lab has to be taken in the context of the patient’s presentation and other supporting findings.
In contrast to a type 1 MI (STEMI and NSTEMI), at type 2 MI results from an imbalance between myocardial oxygen supply and demand unrelated to acute coronary artery thrombosis or plaque rupture. A type 2 MI is a relative (as opposed to an absolute) deficiency in coronary artery blood flow triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. In type 2 MI, myocardial injury occurs secondary to an underlying process, and therefore requires correct documentation of the underlying cause as well.
Common examples of underlying causes of type 2 MI include acute blood loss anemia (e.g. GI bleed), acute hypoxia (e.g. COPD exacerbation), shock states (cardiogenic, hypovolemic, hemorrhagic, or septic), coronary vasospasm (e.g. spontaneous), and bradyarrhythmias. Patients with type 2 MI often have a history of fixed obstructive coronary disease, which when coupled with the acute trigger facilitates the type 2 MI; however, underlying CAD is not always present.
Diagnosing a type 2 MI requires evidence of acute myocardial ischemia (Figure 2) with an elevated troponin but must also have at least one of the following:2
- Symptoms of acute myocardial ischemia such as typical chest pain.
- New ischemic ECG changes.
- Development of pathological Q waves.
- Imaging evidence of new loss of viable myocardium, significant reversible perfusion defect on nuclear imaging, or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.
Distinguishing a type 1 NSTEMI from a type 2 MI depends mainly on the clinical context and clinical judgment. A patient whose presenting symptoms include acute chest discomfort, acute ST-T wave changes, and a rise in troponin would be suspected of having a type 1 NSTEMI. However, in a patient presenting with other or vague complaints where an elevated troponin was found amongst a battery of tests, a type 2 MI may be favored, particularly if there is evidence of an underlying trigger for a supply-demand mismatch. In challenging cases, cardiology consultation can help determine the MI type and/or the next diagnostic and treatment considerations.
When there is only elevated troponin levels (or even a rise and fall in troponin) without new symptoms or ECG/imaging evidence of myocardial ischemia, it is most appropriate to document a non-MI troponin elevation due to a nonischemic mechanism of myocardial injury.
Non-MI troponin elevation (nonischemic myocardial injury)
The number of conditions known to cause myocardial injury through mechanisms other than myocardial ischemia (see Figure 2) is growing, especially in the current era of high-sensitivity troponin assays.4
Common examples of underlying causes of non-MI troponin elevation include:
- Acute (on chronic) systolic or diastolic heart failure: Usually due to acute ventricular wall stretch/strain. Troponin elevations tend to be mild, with more indolent (or even flat) troponin trajectories.
- Pericarditis and myocarditis: Due to direct injury from myocardial inflammation.
- Cardiopulmonary resuscitation (CPR): Due to physical injury to the heart from mechanical chest compressions and from electrical shocks of external defibrillation.
- Stress-induced (takotsubo) cardiomyopathy: Stress-induced release of neurohormonal factors and catecholamines that cause direct myocyte injury and transient dilatation of the ventricle.
- Acute pulmonary embolism: Result of acute right ventricular wall stretch/strain, not from myocardial ischemia.
- Sepsis without shock: Direct toxicity of circulating cytokines to cardiac myocytes. In the absence of evidence of shock and symptoms/signs of myocardial ischemia, do not document type 2 MI.
- Renal failure (acute kidney injury or chronic kidney disease): Multiple etiologies, but at least partially related to reduced renal clearance of troponin. In general, renal failure in the absence of symptoms/signs of ischemia is best classified as a non-MI troponin elevation. ESRD patients who present with volume overload due to missed dialysis also typically have a non-MI troponin elevation.
- Stroke/intracranial hemorrhage: Mechanisms of myocardial injury and troponin elevation are incompletely understood, but may include catecholamine surges that injure the heart.
Some underlying conditions can cause a type 2 MI or a non-MI troponin elevation depending on the clinical context. For example, hypertensive emergency, severe aortic valve stenosis, hypertrophic cardiomyopathy, and tachyarrhythmias (including atrial fibrillation with rapid ventricular response) may cause increased myocardial oxygen demand, and in patients with underlying CAD, could precipitate a type 2 MI.
However, these same conditions could cause a non-MI troponin elevation in patients without CAD and could also cause myocardial injury and troponin release by causing acute left ventricular stretch/strain. Distinguishing the diagnose of type 2 MI vs. non-MI troponin elevation depends on documenting whether there are ancillary ischemic symptoms, ECG findings, imaging, and/or cath findings of acute myocardial ischemia.
Case examples
1. A 60-year-old male presents with fever, cough, shortness of breath, and an infiltrate on CXR and is diagnosed with sepsis secondary to pneumonia. His initial troponin of 0.07 (normal < 0.05) rises to 0.11, peaks at 0.23, then subsequently trends down.
While some may be tempted to diagnose a type 2 MI, remember that sepsis can cause direct myocardial cell injury via direct cell toxicity. Unless this patient had at least one additional criteria (anginal chest pain, new ischemic ECG changes, or imaging evidence of new loss of viable myocardium, which does not recover with treatment of sepsis), this was most likely myocardial injury via direct cell toxicity, and should be documented as a non-MI troponin elevation due to sepsis without shock.
If there were ischemic ECG changes and the patient had chest pain, one would have to use clinical suspicion to differentiate between a type 1 NSTEMI and a type 2 MI. If there is a high clinical suspicion for an acute plaque rupture/thrombus, one would call it an NSTEMI and would have to document treatment as such (e.g. start heparin drip). Again, cardiology consultation can be helpful in cases where it may be hard to decide how to manage. Many times, the true mechanism is not determined until the patient is taken to the cath lab and if no acute plaque rupture is seen, then it was likely a type 2 MI.
2. A 70-year-old male with chronic systolic heart failure, noncompliant with medications, presents with 3 days of dyspnea on exertion and lower extremity edema. He had no chest discomfort. Exam shows bibasilar crackles and hepatojugular reflux. ECG shows no ischemic changes. Serial troponin values over 48 hours were: 0.48, 0.58, 0.51. A transthoracic echocardiogram reveals an LVEF of 40% with poor movement in the apex, similar to his prior echo.
This patient had no overt evidence of ischemia (no chest pain, ischemic ECG, or imaging changes) so the troponin elevation was most likely a non-MI troponin elevation secondary to acute on chronic systolic heart failure (in which the mechanism of troponin elevation is left ventricular chamber stretch from volume overload, and not demand ischemia). Generally, it is uncommon for a heart failure exacerbation to cause a type 2 MI.
Why is it so important to get this diagnosis right?
Misdiagnosing an MI when the patient does not have one can have multiple downstream repercussions. Because it stays on their medical record, it impacts their ability to get insurance and their premium costs. We expose patients to additional medications (e.g. dual antiplatelet therapy, statins), which can have adverse effects. As a result, it is very important to classify the etiology of the troponin elevation and treat accordingly.
Finally, when we incorrectly label a patient as having an MI, this can impact billing and reimbursement, DRG denials, insurance premiums, and quality metrics for both the hospital and the physicians. Hospitals’ 30-day readmission rates for AMI will suffer and quality metrics can be significantly impacted. We must be diligent and as precise as possible with our diagnoses and documentation to ensure the maximum benefit for our patients and our health care system.
Dr. Nave is assistant professor of medicine in the division of hospital medicine at Emory University, Atlanta. Dr. Goyal is associate professor of medicine (cardiology), at Emory University, and chief quality officer, Emory Heart and Vascular Center, Emory Healthcare. He is also codirector of nuclear cardiology at Emory University Hospital.
Key points
- A diagnosis of a type 1 MI is supported by evidence or strong suspicion of acute coronary artery thrombus or plaque rupture/erosion.
- A very high troponin level alone is not diagnostic for a type 1 or type 2 MI. It has to be contextualized with the patient’s presentation and other supporting findings.
- Type 2 MI is a mismatch between myocardial oxygen supply and demand unrelated to acute coronary thrombosis or plaque rupture triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. Type 2 MI should be documented along with its underlying cause.
- To diagnose an MI (either type 1 or type 2 MI), in addition to the troponin elevation, the patient must have symptoms of acute ischemia, ischemic ECG findings, and/or imaging suggestive of new ischemia.
- An elevated troponin level without new symptoms or ECG/imaging evidence of myocardial ischemia should be documented as a non-MI troponin elevation secondary to an underlying cause.
References
1. Goyal A, Gluckman TJ, Tcheng JE. What’s in a name? The new ICD-10 (10th revision of the international statistical classification of diseases and related health problems) codes and type 2 myocardial infarction. Circulation. 2017;136:1180-2.
2. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018;Aug 25:[Epub ahead of print].
3. Goyal, et al. Translating the Fourth Universal Definition of Myocardial Infarction into Clinical Documentation: Ten Pearls For Frontline Clinicians. Cardiology Magazine. Nov 2018.
4. Roongsritong C, Warraich I, Bradley C. Common causes of troponin elevations in the absence of acute myocardial infarction: incidence and clinical significance. Chest. 2004;125:1877-84.
Hospitalists encounter troponin elevations daily, but we have to use clinical judgment to determine if the troponin elevation represents either a myocardial infarction (MI), or a non-MI troponin elevation (i.e. a , nonischemic myocardial injury).
It is important to remember that an MI specifically refers to myocardial injury due to acute myocardial ischemia to the myocardium. This lack of blood supply can be due to an acute absolute or relative deficiency in coronary artery blood flow. However, there are also many mechanisms of myocardial injury unrelated to reduced coronary artery blood flow, and these should be more appropriately termed non-MI troponin elevations.
Historically, when an ischemic mechanism of myocardial injury was suspected, providers would categorize troponin elevations into ST-elevation MI (STEMI) versus non-ST-elevation MI (NSTEMI) based on the electrocardiogram (ECG). We would further classify the NSTEMI into type 1 or type 2, depending on the mechanism of injury. The term “NSTEMI” served as a “catch-all” term to describe both type 1 NSTEMIs and type 2 MIs, but that classification system is no longer valid.
As of Oct. 1, 2017, ICD-10 and the Centers for Medicare & Medicaid Services have a new ICD-10 diagnosis code for type 2 MI (I21.A1), distinct from NSTEMI (I21.4) based on updated definitions from the American College of Cardiology, American Heart Association, European Society of Cardiology, and World Heart Federation. The term “NSTEMI” should be used only when referring to a type 1 MI not when referring to a type 2 MI.1
Classification of MI types
The Fourth Universal Definition of MI published in August 2018 further updated the definitions of MI (summarized in Figure 1).2 This review focuses on type 1 and type 2 MIs, which are the most common types encountered by hospitalists. Types 3-5 MI (grouped under a common ICD-10 diagnosis code for “Other MI Types,” or I21.A9) would rarely be diagnosed by hospitalists.
Figure 1: Classification of MI
MI Type | Classification |
1 | STEMI (acute coronary artery thrombosis) |
2 | Supply/demand mismatch (heterogeneous underlying causes) |
3 | Sudden cardiac death with ECG evidence of acute myocardial ischemia before cardiac troponins could be drawn |
4 | MI due to percutaneous coronary intervention (PCI) |
5 | MI due to coronary artery bypass grafting (CABG) |
The diagnosis of a type 1 MIs (STEMI and NSTEMI) is supported by the presence of an acute coronary thrombus or plaque rupture/erosion on coronary angiography or a strong suspicion for these when angiography is unavailable or contraindicated. Type 1 MI (also referred to as spontaneous MI) is generally a primary reason (or “principal” diagnosis) for a patient’s presentation to a hospital.3 Please note that a very high or rising troponin level alone is not diagnostic for a type 1 or type 2 NSTEMI. The lab has to be taken in the context of the patient’s presentation and other supporting findings.
In contrast to a type 1 MI (STEMI and NSTEMI), at type 2 MI results from an imbalance between myocardial oxygen supply and demand unrelated to acute coronary artery thrombosis or plaque rupture. A type 2 MI is a relative (as opposed to an absolute) deficiency in coronary artery blood flow triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. In type 2 MI, myocardial injury occurs secondary to an underlying process, and therefore requires correct documentation of the underlying cause as well.
Common examples of underlying causes of type 2 MI include acute blood loss anemia (e.g. GI bleed), acute hypoxia (e.g. COPD exacerbation), shock states (cardiogenic, hypovolemic, hemorrhagic, or septic), coronary vasospasm (e.g. spontaneous), and bradyarrhythmias. Patients with type 2 MI often have a history of fixed obstructive coronary disease, which when coupled with the acute trigger facilitates the type 2 MI; however, underlying CAD is not always present.
Diagnosing a type 2 MI requires evidence of acute myocardial ischemia (Figure 2) with an elevated troponin but must also have at least one of the following:2
- Symptoms of acute myocardial ischemia such as typical chest pain.
- New ischemic ECG changes.
- Development of pathological Q waves.
- Imaging evidence of new loss of viable myocardium, significant reversible perfusion defect on nuclear imaging, or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.
Distinguishing a type 1 NSTEMI from a type 2 MI depends mainly on the clinical context and clinical judgment. A patient whose presenting symptoms include acute chest discomfort, acute ST-T wave changes, and a rise in troponin would be suspected of having a type 1 NSTEMI. However, in a patient presenting with other or vague complaints where an elevated troponin was found amongst a battery of tests, a type 2 MI may be favored, particularly if there is evidence of an underlying trigger for a supply-demand mismatch. In challenging cases, cardiology consultation can help determine the MI type and/or the next diagnostic and treatment considerations.
When there is only elevated troponin levels (or even a rise and fall in troponin) without new symptoms or ECG/imaging evidence of myocardial ischemia, it is most appropriate to document a non-MI troponin elevation due to a nonischemic mechanism of myocardial injury.
Non-MI troponin elevation (nonischemic myocardial injury)
The number of conditions known to cause myocardial injury through mechanisms other than myocardial ischemia (see Figure 2) is growing, especially in the current era of high-sensitivity troponin assays.4
Common examples of underlying causes of non-MI troponin elevation include:
- Acute (on chronic) systolic or diastolic heart failure: Usually due to acute ventricular wall stretch/strain. Troponin elevations tend to be mild, with more indolent (or even flat) troponin trajectories.
- Pericarditis and myocarditis: Due to direct injury from myocardial inflammation.
- Cardiopulmonary resuscitation (CPR): Due to physical injury to the heart from mechanical chest compressions and from electrical shocks of external defibrillation.
- Stress-induced (takotsubo) cardiomyopathy: Stress-induced release of neurohormonal factors and catecholamines that cause direct myocyte injury and transient dilatation of the ventricle.
- Acute pulmonary embolism: Result of acute right ventricular wall stretch/strain, not from myocardial ischemia.
- Sepsis without shock: Direct toxicity of circulating cytokines to cardiac myocytes. In the absence of evidence of shock and symptoms/signs of myocardial ischemia, do not document type 2 MI.
- Renal failure (acute kidney injury or chronic kidney disease): Multiple etiologies, but at least partially related to reduced renal clearance of troponin. In general, renal failure in the absence of symptoms/signs of ischemia is best classified as a non-MI troponin elevation. ESRD patients who present with volume overload due to missed dialysis also typically have a non-MI troponin elevation.
- Stroke/intracranial hemorrhage: Mechanisms of myocardial injury and troponin elevation are incompletely understood, but may include catecholamine surges that injure the heart.
Some underlying conditions can cause a type 2 MI or a non-MI troponin elevation depending on the clinical context. For example, hypertensive emergency, severe aortic valve stenosis, hypertrophic cardiomyopathy, and tachyarrhythmias (including atrial fibrillation with rapid ventricular response) may cause increased myocardial oxygen demand, and in patients with underlying CAD, could precipitate a type 2 MI.
However, these same conditions could cause a non-MI troponin elevation in patients without CAD and could also cause myocardial injury and troponin release by causing acute left ventricular stretch/strain. Distinguishing the diagnose of type 2 MI vs. non-MI troponin elevation depends on documenting whether there are ancillary ischemic symptoms, ECG findings, imaging, and/or cath findings of acute myocardial ischemia.
Case examples
1. A 60-year-old male presents with fever, cough, shortness of breath, and an infiltrate on CXR and is diagnosed with sepsis secondary to pneumonia. His initial troponin of 0.07 (normal < 0.05) rises to 0.11, peaks at 0.23, then subsequently trends down.
While some may be tempted to diagnose a type 2 MI, remember that sepsis can cause direct myocardial cell injury via direct cell toxicity. Unless this patient had at least one additional criteria (anginal chest pain, new ischemic ECG changes, or imaging evidence of new loss of viable myocardium, which does not recover with treatment of sepsis), this was most likely myocardial injury via direct cell toxicity, and should be documented as a non-MI troponin elevation due to sepsis without shock.
If there were ischemic ECG changes and the patient had chest pain, one would have to use clinical suspicion to differentiate between a type 1 NSTEMI and a type 2 MI. If there is a high clinical suspicion for an acute plaque rupture/thrombus, one would call it an NSTEMI and would have to document treatment as such (e.g. start heparin drip). Again, cardiology consultation can be helpful in cases where it may be hard to decide how to manage. Many times, the true mechanism is not determined until the patient is taken to the cath lab and if no acute plaque rupture is seen, then it was likely a type 2 MI.
2. A 70-year-old male with chronic systolic heart failure, noncompliant with medications, presents with 3 days of dyspnea on exertion and lower extremity edema. He had no chest discomfort. Exam shows bibasilar crackles and hepatojugular reflux. ECG shows no ischemic changes. Serial troponin values over 48 hours were: 0.48, 0.58, 0.51. A transthoracic echocardiogram reveals an LVEF of 40% with poor movement in the apex, similar to his prior echo.
This patient had no overt evidence of ischemia (no chest pain, ischemic ECG, or imaging changes) so the troponin elevation was most likely a non-MI troponin elevation secondary to acute on chronic systolic heart failure (in which the mechanism of troponin elevation is left ventricular chamber stretch from volume overload, and not demand ischemia). Generally, it is uncommon for a heart failure exacerbation to cause a type 2 MI.
Why is it so important to get this diagnosis right?
Misdiagnosing an MI when the patient does not have one can have multiple downstream repercussions. Because it stays on their medical record, it impacts their ability to get insurance and their premium costs. We expose patients to additional medications (e.g. dual antiplatelet therapy, statins), which can have adverse effects. As a result, it is very important to classify the etiology of the troponin elevation and treat accordingly.
Finally, when we incorrectly label a patient as having an MI, this can impact billing and reimbursement, DRG denials, insurance premiums, and quality metrics for both the hospital and the physicians. Hospitals’ 30-day readmission rates for AMI will suffer and quality metrics can be significantly impacted. We must be diligent and as precise as possible with our diagnoses and documentation to ensure the maximum benefit for our patients and our health care system.
Dr. Nave is assistant professor of medicine in the division of hospital medicine at Emory University, Atlanta. Dr. Goyal is associate professor of medicine (cardiology), at Emory University, and chief quality officer, Emory Heart and Vascular Center, Emory Healthcare. He is also codirector of nuclear cardiology at Emory University Hospital.
Key points
- A diagnosis of a type 1 MI is supported by evidence or strong suspicion of acute coronary artery thrombus or plaque rupture/erosion.
- A very high troponin level alone is not diagnostic for a type 1 or type 2 MI. It has to be contextualized with the patient’s presentation and other supporting findings.
- Type 2 MI is a mismatch between myocardial oxygen supply and demand unrelated to acute coronary thrombosis or plaque rupture triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. Type 2 MI should be documented along with its underlying cause.
- To diagnose an MI (either type 1 or type 2 MI), in addition to the troponin elevation, the patient must have symptoms of acute ischemia, ischemic ECG findings, and/or imaging suggestive of new ischemia.
- An elevated troponin level without new symptoms or ECG/imaging evidence of myocardial ischemia should be documented as a non-MI troponin elevation secondary to an underlying cause.
References
1. Goyal A, Gluckman TJ, Tcheng JE. What’s in a name? The new ICD-10 (10th revision of the international statistical classification of diseases and related health problems) codes and type 2 myocardial infarction. Circulation. 2017;136:1180-2.
2. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018;Aug 25:[Epub ahead of print].
3. Goyal, et al. Translating the Fourth Universal Definition of Myocardial Infarction into Clinical Documentation: Ten Pearls For Frontline Clinicians. Cardiology Magazine. Nov 2018.
4. Roongsritong C, Warraich I, Bradley C. Common causes of troponin elevations in the absence of acute myocardial infarction: incidence and clinical significance. Chest. 2004;125:1877-84.