Inferior lead & early repol & Diagnosed. Is it?

A 20-something male presented from an outside facility with Chest pain.  Vital signs were normal.

History: Onset of CP 2.5 hours prior to ED arrival.  "Tight and pressure, radiates to right arm, + nausea, + SOB.  No thromboembolism risks, not pleuritic, no radiation to the back.  No cardiac risk factors, no cocaine use.


He came with this ECG from the outside facility, recorded 1 hour after pain onset:

There is at least 2 mm of inferior ST elevation, with reciprocal ST depression in aVL, ST flattening in V4-V6, and T-wave inversion in V2.

Is this inferior ST elevation due to "early repolarization"?

No.  Why not? We have found in our study comparing inferior STEMI (manuscript in preparation) to inferior early repol several distinguishing characteristics.

1. There is reciprocal ST depression in aVL.  This occurred in 0 of 66 cases of early repolarization, and 99% of patients with inferior STEMI.
2. There is too much ST elevation.  In only 1 of 66 cases of early repol was there one lead with at least 2 mm STE.
3. Absence of ST elevation in V5 and V6.  In our group with inferior early repolarization, 53 of 66 had at least 1 mm of STE in V5, and 61 of 66 had at least 0.5 mm in V5.  64 of 66 had at least 1 mm of STE in V6 and 58 of 66 had at least 0.5 mm in V6.  In other words, when there is normal variant ST elevation in inferior leads, there is usually also normal variant ST elevation in V5 and V6.
4. T-waves are too tall.  T-waves in inferior leads are hyperacute, out of proportion to those in early repol
5. T-wave inversion in V2 is inconsistent with early repol, and is typical of posterior ischemia.

95 minutes later, the patient arrived in the ED and here is the triage ECG:

There is 2-2.5 mm of ST elevation in inferior leads.  There is reciprocal ST depression in I and aVL, with T-wave inversion in aVL.  There is relative ST depression in V2 (isoelectric: in a young man it there should be at least 1 mm of ST elevation), thre is also flattening of the ST segment in V2.  There is ST depression from V3-V6.  There is a negative T-wave in V3, and biphasic T-waves in V4-V6.

There should be no doubt that this is STEMI.  All of the above 5 points apply, but now all the features have evolved and are more apparent. In addition, there is ST depression, diagnostic of ischemia, in V3-V6.

Nevertheless, the cardiologist consulted diagnosed early repolarization.  The patient did not undergo immediate cath.

22 minutes later, another ECG was recorded:

It is slightly changed.  See next image for side by side comparison

Side by side comparison of leads II and III on the first two ECGs:

ST elevation is higher on the repeat ECG than on the first, especially in proportion the the R-wave.  There appears to be a diminution of the T-wave amplitude; however, not when the R-wave amplitude is taken into account.

First troponin I returns + at 0.252 ng/ml.

191 minutes after first ECG:

There is resolution of ischemic findings, spontaneously.  There are no Q-waves.  There appears to have been spontaneous reperfusion.  The minimal remaining inferior ST elevation is now consistent with early repolarization

Heparin drip started.  CCU consulted.  Admitted to CCU.  Integrilin given.  Not take directly to cath lab.

A second troponin returned at 1.71 ng/ml 3 hours later.

The patient was not taken to cath for another 6 hours after this last ECG.  It showed a 99% stenosis in the RCA, and proximal to a posterolateral branch.  A coronary aneurysm was found.  TIMI flow not reported.

Troponin I peaked at 75 ng/ml.



Next ECG available - 2 week followup:

There are inferior Q-waves of infarction, with T-wave inversions typical of completed inferior transmural MI.

This ECG, and the very elevated troponin, strongly suggest that the artery re-occluded during the extra 6 hour delay. 



Lessons:
1. Young people do have MI
          a. Some of these MIs in young people are due to anomolies: aneurysm from a disorder known to be associated  with coronary aneurysms (left out to maintain anonymity) in this case.  Young women, when they have STEMI, often have coronary dissection.
          b. Nevertheless, even young people have atherosclerosis and plaque rupture.  We have seen many, such as this young woman.    And young women have worse outcomes than other groups with STEMI because of the tendency to say, "Nah, couldn't be!"

2. When the ECG is unequivocally diagnostic, don't let young age or other atypical features deter you.

3. Know the features of STEMI look-alikes.  In this case, early repolarization was diagnosed by the cardiologist, who clearly was unaware of important differentiating features of inferior early repol from inferior STEMI (see above)

4. Once STEMI is diagnosed, the patient should go immediately to the cath lab even if the ST elevation resolves, because the risk is so high.  In this case, however, the diagnosis was also simply missed.
See this case to demonstrate the danger of reperfused STEMI!

5.  Finally, YOU have to be the expert and YOU have to advocate for the patient.  Cardiologists don't know everything, and in particular they don't know YOUR job, which is to differentiate the patients with benign symptoms (the vast majority) from those with Serious pathology.  If the cardiologist disagrees and is incorrect, the only way the patient will get good care is if YOU are the expert, YOU know what findings are true positives and true negatives, and YOU can explain why you are right and Advocate.

Cardiologists need to know a whole lot, but they don't do our everyday job of screening hundreds of symptomatic patients to find the one with the real thing.  They cannot be experts at that; you must be the expert.  They are much more likely to demand proof of disease than emergency physicians.  We demand proof of absence of disease.  And the cardiologists' opinions are of course often, or even usually, correct, but insist on a respectful conversation in which reasoning and evidence, rather than authority, direct the outcome.  That can only happen if YOU are well informed.


Here are two examples of early repolarization in the inferior leads:

First:

1. There is inferior ST elevation without reciprocal  ST depression in aVL.  This is because the ST axis is leftward, not down or to the right.  And thus the ST elevation in lead III is always less than or equal to that in lead II.  2. There is anterior and lateral ST elevation also; isolated ST elevation in inferior leads is relatively rare in limb lead early repol.        3. There are, in this ECG, well formed J-waves in leads V4-V6.  4. The QTc is less than 390, though we did not find this to be an accurate distinguishing feature of inferior ST elevation.  5. The ST elevation is at most 1 mm in inferior leads.

Second:

Slightly different, but the generalizations above apply here, too.

Found a great site for beginners in ECG, also good for experienced readers!

It's an Irish site.  It has excellent video demonstrations of the underlying pathophysiology of ECG findings correlated with simultaneous video of ECG evolution.

http://www.ecgteacher.com/

Increasing ST Elevation. STEMI vs Dynamic Early Repolarization vs Pericarditis.

Increasing ST Elevation.  STEMI vs Dynamic Early Repolarization vs Pericarditis.. Here is a series of ECGs with increasing ST elevation (STE).  They are of a young male with pleuritic, but not positional, chest pain.

Time zero:

NSR.  No remarkable findings.  Minimal STE in V2, V3, and I.  QTc 383.  LAD occlusion, early repol formula = 18.1


Time = 4.5 hours:

New, diffuse ST elevation. QTc 384, formula 19.1.  The ST axis is about 30 degrees (towards leads I and  II, such that there is STE in aVL, I, II, and aVF, but not III) and there is no reciprocal ST depression except in lead aVR).  This is very typical for pericarditis or diffuse early repolarization.  Pericarditis does not usually have T-wave voltage this high; a high T/ST ratio is more likely to be early repolarization.  Additionally, there are very well formed J-waves, typical of early repolarization.  It is highly unlikely to be acute STEMI.


There was no pericardial friction rub and echo revealed no pericardial fluid and no wall motion abnormality, and normal EF.

Time = 5.2 hours:

More ST elevation, especially in lead V2.  QTc 389, formula 20.56


Time = 7.2 hours:

No change.  QTc 389, formula 19.96



He ruled out for MI.

Diagnosis: probable dynamic early repolarization.  Could it be pericarditis?  Yes, but if there is no pericardial effusion and there is good cardiac function with negative troponins (not myocarditis with myocardial dysfunction), then pericarditis would be treated with Nonsteroidal antiinflammatory medications only.

In other words, the really important differential is this: is this STEMI, or is it a more benign etiology?  And to make this determination, it is important to know that early repolarization may be dynamic (1, 2).  And it may even change from hour to hour, or with heart rate or exercise.   We have seen this many times, though it is not common.

The use of the LAD-BER formula may be of great help and lead one to obtain an echocardiogram rather than activating the cath lab.

1. Kambara H, Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976;38(2):157-61. 

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation.  Elevations in inferior leads were less than 0.5mm in 18 of 20 cases.  Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.


2. Mehta MC. Jain AC.  Early Repolarization on the Scalar Electrocardiogram.  The American Journal of the Medical Sciences 309(6):305-11; June 1995. 

Sixty thousand electrocardiograms were analyzed for 5 years. Six hundred (1%) revealed early repolarization (ER). Features of ER were compared with race-, age-, and sex-matched controls (93.5% were Caucasians, 77% were males, 78.3% were younger than 50 years, and only 3.5% were older than 70). Those with ER had elevated, concave, ST segments in all electrocardiograms (1-5 mv), which were located most commonly in precordial leads (73%), with reciprocal ST depression (50%) in aVR, and notch and slur on R wave (56%). Other results included sinus bradycardia in 22%, shorter and depressed PR interval in 38%, slightly asymmetrical T waves in 96.7%, and U waves in 50%. Sixty patients exercised normalized ST segment and shortened QT interval (83%). In another 60 patients, serial studies for 10 years showed disappearance of ER in 18%, and was seen intermittently in the rest of the patients. The authors conclude that in these patients with ER: 1) male preponderance was found; 2) incidence in Caucasians was as common as in blacks; 3) patients often were younger than 50 years; 4) sinus bradycardia was the most common arrhythmia; 5) the PR interval was short and depressed; 6) the T wave was slightly asymmetrical; 7) exercise normalized ST segment; 8) incidence and degree of ST elevation reduced as age advanced; 9) possible mechanisms of ER are vagotonia, sympathetic stimulation, early repolarization of sub-epicardium, and difference in monophasic action potential observed on the endocardium and epicardium.

What You Need to Know About Angina Pectoris

What You Need to Know About Angina Pectoris. Angina pectoris is the result of myocardial ischemia caused by an imbalance between myocardial blood supply and oxygen demand.

An episode of angina is not a heart attack. Having angina means you have an increased risk of having a heart attack.
A heart attack is when the blood supply to part of the heart is cut off and that part of the muscle dies (infarction).Angina can be a helpful warning sign if it makes the patient seek timely medical help and avoid a heart attack.Prolonged or unchecked angina can lead to a heart attack or increase the risk of having a heart rhythm abnormality. Either of those could lead to sudden death.

People who are at risk of angina are:
Men above 55 years old,Women above 65 years old,Obese or overweight,Cigarette smokers,Having high blood pressure,Having high cholesterol levels,Physically inactive,Having kidney disease,Having diabetes mellitus, andHaving family history of premature cardiovascular disease (men who suffer from heart disease below the age of 55 or women who suffer from the same disease below 65 year old).

Generally, angina pectoris is recognized in two types:
Stable angina is found more often in people. The symptoms of this type occur regularly and are predictable. Usually, people with this type suffer from the chest discomfort during exercise and stress, or after consuming heavy meals. Generally, the symptoms last not more than five minutes and improve when the patient rests or takes medications such as nitroglycerin, amlodipine besylate, or ranolazine.Unstable angina is found less often but more serious than the first type. Unlike the stable one, the occurrence of unstable angina cannot be predicted. The symptoms of this type also tend to be more severe. Unstable angina usually creates more pain and occurs longer and more frequent. Usual medication or resting cannot improve the symptoms. While unstable angina differs from heart attack, it is often noted as the precursor to heart attack.

Your doctor or nurse will examine you and measure your blood pressure. Tests that may be done include:
Coronary angiographyCoronary risk profile (special blood tests)ECGExercise tolerance test (stress test or treadmill test)Nuclear medicine (thallium) stress testStress echocardiogram
Your doctor may give you one or more medicines to help prevent you from having angina.
ACE inhibitors to lower blood pressure and protect your heartBeta-blockers to lower heart rate, blood pressure, and oxygen use by the heartCalcium channel blockers to relax arteries, lower blood pressure, and reduce strain on the heartNitrates to help prevent anginaRanolazine (Ranexa) to treat chronic angina

A Tough ECG, But Learn From It!

A Tough ECG, But Learn From It!. I have to tell this story from my point of view because I don't want anyone to think that the recognition of LAD occlusion was made in retrospect.  I want all to know that, with the right mind preparation, and the use of the early repol/LAD occlusion formula, extremely subtle coronary occlusion can be detected prospectively, with no other information than the ECG.

The Case:

I was reading dozens of leftover ECGs from over a weekend and saw this one:

There are symmetric T-waves and poor R-wave progression.  There is 1 mm of ST elevation at the J-point in leads V2 and V3.  This formerly met "criteria" for thrombolytics in the ACC/AHA guidelines of 2004, though of course this amount of ST elevation is very nonspecific.  It is nonspecific because normal variant ST elevation can be even much greater.  However, normal variant ST elevation always has better R-wave progression and asymmetric T-waves which have a slow upstroke and a rapid downstroke.  See image below:

Slow upstroke, fast downstroke.  Asymmetric.

This was my thought: if this patient presented to the ED with chest pain, then this is an LAD occlusion.  So I went to look at the chart and here is the history:

This patient with no h/o CAD had a couple of episodes of chest pain during the day, then presented with one hour of substernal chest pain that had some reproducibility but also improved from 10/10 to 5/10 with nitroglycerine.

This is such a subtle ECG that I was worried that it had gone unnoticed, and, in fact, it did go unnoticed:  

His pain continued and his ECG was read as normal.  His first troponin was normal.  He was admitted to the hospital for a "rule out."  His second troponin I returned at t = 5 hours and was + at 3.8 ng/ml.  His ECG was repeated at this point:

This shows a well developed anterior STEMI.

The cath lab was activated and an LAD occlusion was opened.  The peak troponin I was over 100.  On echocardiogram, there was a 40% ejection fraction with anterior wall motion abnormality.

I applied the LAD occlusion/early repol formula and, with a QTc of 402ms, STE60V3 of 1.5, and R-wave amplitude in V4 of 3 mm, the result was = 24.5, which is in the range of LAD occlusion (even if you read the STE as 1.0, the result is 23.9, greater than 23.4).  The formula results in such a high number because of the very low R-wave amplitude, which (in comparing subtle LAD occlusion to early repol) is the single best predictor of LAD occlusion, better than ST elevation.

To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI.  

It is not a missed STEMI, but it is a missed coronary occlusion.  As you can see, the subtle findings are apparent and, with a prepared mind, can be detected.  Studies show that 30% of NonSTEMI have an occluded infarct artery at the time of angiography done 24 hours after presentation.  This is because of subtle ECG findings.  These patients have worse outcomes: higher mortality, more CHF, higher biomarkers, and worse ejection fractions than the NonSTEMI patients with open arteries.


This patient had continued and ongoing pain.  If there had been serial ECGs, then the evolution of ST elevation would have been detected much earlier and there would be less myocardial injury.  

Fesmire et al. showed that, with continuous ST segment monitoring, the sensitivity of the ECG for STEMI rises from 48% to 62% of all MI as diagnosed by CK-MB.  In other words, NonSTEMIs are frequently diagnosed as STEMIs if you give them time to evolve.