Myocardial infarction diagnosis
- Myocardial infarction produces clinical symptoms, EKG changes, and elevated troponins.
- Troponin elevation in acute MI has two important characteristics:
- They are detected 2-3 hours after myocardial ischemia, in other words, 2-3 hours after the onset of MI symptoms.
- Troponin elevation in acute MI (In most cases) follows a pattern of a rise to a peak and then a fall, they don’t remain stagnant! This is a stark difference between troponin elevation in acute MI and most non-MI causes.
- Assessing elevated troponin starts by taking a careful history asking for any MI symptoms, and then reviewing the EKG.
The absence of MI clinical symptoms and acute ischemic EKG changes effectively rule out MI even if troponins are elevated.
- The presence of MI symptoms in the absence of EKG changes should raise the question of whether another diagnosis is more likely. If not, proceed with MI treatment until proven otherwise.
Example (1):
A 54-year-old lady presented with acute low back pain, troponin level was ordered and came back elevated at 190 ng/L (UNL in my facility is 50 ng/L and this will apply to all examples), and EKG was negative for ischemic changes. Is this an MI or not?
Explanation:
MI symptoms are absent (LBP has a low pretest probability for AMI) along with negative EKG effectively ruling out MI in this patient! Not sure why a troponin level was ordered! Of course, we had to trend troponin levels and they came back as 200, 165 ng/L, the patient underwent an echocardiogram which was unremarkable, and the patient was discharged home.
Lessons:
- Avoid ordering troponin levels inappropriately when the pretest probability for MI is low!
- Notice the stagnant nature of troponin levels, there was no significant rise or fall!
Example (2):
A 73-year-old lady with a history of CAD and an RCA stent placed 5 years earlier presented with chest pressure 5/10 radiating to her jew and similar to the pain she had 5 years ago, she got concerned and came to the ED to be checked out! the patient’s EKG showed a subtle isolated ST elevation in AVL and a reciprocal ST depression in lead 3, the first troponin was 1000 ng/L (UNL was 50). Is this an MI or not?
Explanation:
The pretest probability of ACS is very high in this case even before reviewing the EKG or the troponin result! The patient has a full constellation of AMI with clinical symptoms, EKG changes, and elevated troponin levels, she was treated per ACS protocol, the patient underwent a coronary angiogram which revealed patent stent and clean coronaries otherwise, she was diagnosed later on with acute myocarditis following a recent URI, the third troponin was 4000 ng/L.
Lessons:
- If the pretest probability for AMI is high, any elevated troponin level is due to AMI until proven otherwise.
- If an AMI is suspected based on symptoms and EKG changes, the treatment must be started even before the troponin level is back.
- Myocarditis is a great mimic for MI that’s difficult to distinguish without a coronary angiogram. Similar to myocarditis, coronary vasospasm, spontaneous coronary artery dissection, and Takotsubo cardiomyopathy are MI mimics as well.
- Notice the rising and falling pattern of troponins.
Example (3):
A 45-year-old gentleman with no significant PMH presented with a sudden onset severe sharp/knife-like chest pain, causing the patient to seek medical attention immediately, EKG showed sinus tachycardia at a rate of 130, no ST segment or T wave ischemic changes, initial troponin was 90 ng/L (UNL is 50), is this MI or not?
Explanation:
The sharp stabbing or knife-like pain should immediately raise an alternative diagnosis to AMI! Aortic dissection is high on the differential diagnosis! It must be ruled in or out before thinking of ACS! Chest CTA confirmed a type A aortic dissection, the patient was taken for emergent surgery. the second troponin set was 200 ng/L, and no third one was obtained.
Lesson:
- History remains the single most important part of making the correct diagnosis.
- Sinus tachycardia is uncommon in AMI except in cardiogenic shock.
- You would expect some major ischemic EKG changes had this pain caused by an acute MI given the severity of chest pain.
- Notice the mild increase in troponins.
Example (4):
A 69-year-old gentleman with a history of anterior wall MI a year ago s/p stenting to LAD, presented with worsening exertional shortness of breath and lower extremity edema over the last 3 weeks, the patient’s O2 sat was 86% on RA and improved to 96% on 2 L/min O2 via NC, EKG showed Q waves in V3 and V4, and nonspecific T wave inversion in lead 3 and V1, CXR showed finding suggestive of pulmonary edema, first troponin was 200 ng/L, BNP was 950. Is this an acute MI or not?
Explanation:
It’s obvious that we are dealing with a CHF (Congestive heart failure) exacerbation probably due to ischemic cardiomyopathy, given the previous MI, the presence of Q waves, and the absence of acute ischemic changes, the patient was started on IV diuresis, EF was found to be 25%, the next two troponin sets were 250, 195.
Lessons:
- Many cardiac and noncardiac conditions may cause MI-like symptoms, history, and physical exam are essential to distinguish between them.
- The presence of pathological Q waves without ST segment and T wave changes are the sequela of an old ischemic event.
- Notice the small rise and fall in troponin.
- CHF patients may have a chronically elevated troponin level in the absence of myocardial ischemia, these patients carry worse prognosis compared to CHF patients without elevated troponins.
Example (5):
A 39-year-old diabetic noncompliant lady with ESRD on hemodialysis, she missed her last 3 HD sessions, and presented with shortness of breath and confusion, in the ED, she was hypertensive with BP 190/110, HR 110, O2 sat was 85% on RA, quickly corrected with 3 L of O2 via NC to 94%, BS199, CXR showed finding suggestive of pulmonary edema, EKG showed new a LBBB (not seen on EKG from two months ago), initial troponin was 300, is this an acute MI?
Explanation:
This patient’s shortness of breath is due to pulmonary edema from noncompliance with HD, but how about the new LBBB? There is one critical piece of info missing in the question! Can you guess what? Yes, the Potassium level was 8.5 meq/dl which explains the new LBBB, this patient underwent emergent HD, the next troponin sets were 350 and 290, potassium went down to 65.5 post-HD, and the LBBB resolved.
Lessons:
- Hyperkalemia may mimic acute MI EKG changes.
- Similar to CHF, renal patients may have a chronically elevated troponin level in the absence of myocardial ischemia, these patients carry worse prognosis compared to renal failure patients without elevated troponins.
- Notice the pattern of troponin rise and fall.
Example (6):
A 75-year-old patient was brought to ED after he woke up with an inability to speak and right-sided weakness, he was seen okay the night before, CT brain was negative, EKG showed T wave inversion in leads V3 through V6, troponin level was 190 ng/L, is this an acute MI?
Explanation:
The pretest probability of acute ischemic stroke is very high, there is no reason to suspect AMI! But what about the EKG changes and the elevated troponin level? Stroke and acute neurological conditions are known to cause ischemic-like EKG changes and elevated troponin levels in the absence of myocardial ischemia, the patient’s MRI confirmed an ischemic stroke in the right MCA territory, and the next two troponin sets were 182 and 165 ng/L, the echocardiogram was unremarkable.
Lessons:
- Stroke and acute neurological conditions may cause ischemic-like EKG changes and elevated troponin levels.
- Notice the stable level of troponin levels on serial testing.
Example (7):
A 51-year-old alcoholic patient presented with severe epigastric pain that started 2 hours before the presentation, CT abdomen showed edematous pancreas and surrounding inflammatory changes, lipase level was elevated at 1300, EKG showed sinus tachycardia at 140 with ST depression in anterior leads, initial troponin was elevated at 310 ng/L. Is this an MI?
Explanation:
The patient has acute pancreatitis, the ST segment depression on the EKG is likely due to sinus tachycardia, and the troponin elevation was likely related to tachycardia and demand ischemia (type 2 MI), this patient was diagnosed with severe alcohol-induced pancreatitis and received aggressive IVF resuscitation, serial troponins were 400, 320 ng/L and the echo showed no wall motion abnormalities.
Lessons:
- Similar to stroke, acute pancreatitis may cause ischemic-like EKG changes.
- Tachycardia, when severe, often leads to ST depression.
- Demand ischemia or type 2 MI happens when there is a mismatch between myocardial oxygen supply and demand, the treatment should address the underlying cause.
- Demand ischemia happens with:
- Decreased supply as in hypoxia and hypoperfusion, regardless of the underlying cause.
- Increased demands as in Tachycarrhythmias, LVH, RVH, and HCOM.
Example (8):
An 81-year-old gentleman presented to ED with severe shortness of breath, initial vital signs were 70/40, HR 170, O2 sat on RA was 55%, RR 39, EKG AF with RVR and diffuse ST depression, the patient was placed on 100% non-rebreather mask, and underwent immediate cardioversion with 200 joules, IVF resuscitation started simultaneously, patient converted to NSR at a rate of 92 and ST depressions have resolved, BP improved to 100/60, O2 sat was 99% on 100% non-rebreather mask, patient shortness of breath improved significantly, CXR was unremarkable, initial troponin post-cardioversion was 400 ng/L. Is this an MI?
Explanation:
The patient has AF with RVR and hemodynamic instability. Immediate synchronized cardioversion is the best next step. Post-cardioversion EKG showed no ischemic changes, the initial elevated troponin level was possibly due to a combination of demand ischemia and cardioversion, The ED physician was concerned because he believed the elevated troponin levels were higher than typically expected for demand ischemia and post-cardioversion. The patient was admitted to ICU, given a full dose of aspirin, and started on a heparin drip ( he needed that as he underwent cardioversion from Af rhythm)serial troponin levels were 500 and 420 ng/L, and echocardiogram showed EF of 35%, the patient was evaluated by cardiology and discharged a day later on oral amiodarone, apixaban, metoprolol, and lisinopril with cardiology outpatient followup in on week.
Lessons:
- Cardioversion, defibrillator shocks, ablation, pacing, cardiac contusion, and surgery may cause some troponin elevation.
- When in doubt and can’t decide if it’s an MI or an alternative diagnosis, treat it as MI until proven otherwise!
- Most non-MI causes of elevated troponin levels cause modest stable elevated troponin levels, significantly high elevated troponin levels with significant rise and fall strongly suggest MI but it isn’t diagnostic!
- Tachycardia-induced cardiomyopathy improves with medical management and adequate rate control.
- Tachycardia and hypotension are common causes of demand ischemia.
Example (9):
A 62-year-old lady was brought to the ED after a syncopal episode at a local shopping center, I only saw her the next morning and was signed out to me as a syncope case with mildly elevated troponin levels, the admission EKG was reported to be negative, 3 sets of troponin levels obtained 3 hours apart were 60, 102, then 178 ng/L, is this MI or not?
Explanation:
When I interviewed the patient I noticed she was on 4 L of O2 – She doesn’t use O2 at home -, and her CXR was unremarkable, upon further questioning, she’s been having exertional dyspnea for a week. Syncope, shortness of breath, hypoxia, and a negative CXR all raise suspicion of PE, chest CTA showed a large burden of right-sided PEs, and the patient was started on anticoagulation, at this point, it was obvious that the elevated troponin levels were due to PE and RV strain.
Lessons:
- Hypoxia regardless of the underlying cause may lead to elevated troponin levels that are usually modest.
- RV strain may cause troponin leak.
- I always teach my residents that hypoxia not explained by a CXR should raise the suspicion of PE!
- Cardiology consultation isn’t mandatory in every case of elevated troponin levels, particularly in obvious cases.
Causes of elevated troponin levels.
Non-MI Cardiac causes:
- Tachy- or bradyarrhythmias, or heart block (It isn’t just tachycardia that causes that).
- Congestive heart failure (acute and chronic).
- Cardiac contusion or other trauma including surgery, ablation, pacing, implantable cardioverter-defibrillator shocks, cardioversion, endomyocardial biopsy, cardiac surgery, and following interventional closure of atrial septal defects.
- Hypertrophic cardiomyopathy.
- Aortic valve disease.
Pulmonary causes:
- Pulmonary embolism.
- Severe pulmonary hypertension.
Neurological causes:
- Acute neurological disease, including stroke or subarachnoid hemorrhage. Stroke may, also, cause ischemic EKG changes!
Critical illness:
- Critically ill patients, especially with diabetes, respiratory failure, or sepsis.
Renal causes:
- Renal failure.
Musculoskeletal:
- Rhabdomyolysis with cardiac injury.
- Exertion.
Drugs:
- Drug toxicity or toxins (ie, adriamycin, 5-fluorouracil, Herceptin, and snake venom).
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