Written by Pendell Meyers, with edits by Steve Smith
I received a text message with no clinical information other than the following ECG, with the question "Is this Wellens? No prior ECG available."
What do you think?
I responded that this ECG represented benign T-wave inversion (BTWI), not Wellens. I asked for more history.
It turns out this was a 25 year old male with no past medical history presenting after he was found "passed out" or laying down on the floor of the nursing home facility where he works. He was reported to be intermittently answering questions and seeming "not himself." Family reported that he had 2 similar episodes in the past 3 months, which the patient describes as similar to "bad trips," including increased fatigue, confusion, and vague hallucinations. He had been evaluated last month at an outside hospital by a psychiatrist. He denied any substance use on the day of presentation. There was no history of exertional syncope or sudden death in the family.
Apparently a single troponin was ordered on the basis of the perceived ECG findings, which was negative. Three serial ECGs were performed which were all identical (though BTWI is not necessarily always perfectly constant).
He was discharged.
Two days later he presented again with a similar story. Here is his ECG on arrival from the second visit:
 |
| This ECG shows sinus rhythm around 65 bpm. The QRS complex has moderately high voltage but otherwise normal morphology. There is STE in V1-V3 of 1.0, 1.5, and 1.5 millimeters, which is completely normal. There are prominent J-waves in leads V4-V6, as well as leads II, III, and aVF. Lead V3 shows the first and third complexes with terminal T-wave inversions, but the second complex does not appear to have this terminal T-wave inversion - whether this is due to a brief episode of baseline wandering / lead manipulation, or beat to beat variation is unknown, but I believe it is more likely brief baseline movement. The terminal T-wave inversion is no longer present in V4 as it was in the first presentation. Overall the second ECG is better characterized as "benign early repolarization" or simply "benign ST elevation" than by BTWI. |
Another single troponin was normal. He was discharged with outpatient psychiatry and primary care.
How do I recognize this as BTWI?
Most importantly because it matches the examples of BTWI I have seen on this blog, and does not match Wellens syndrome. The T-wave inversion in lead V3 of the initial ECG just does not look like reperfusion. Lead V4 of the initial ECG has the complete morphologic package of BTWI, including high voltage (large R wave), smaller S-wave, prominent J-wave followed by minimal STE and then characteristic terminal T-wave inversion. The history obviously helps as well, as this was a young African-American patient with symptoms of near-zero pretest probability of ACS. Some cases will not be so easy clinically.
Also important, "Wellens' syndrome" requires clinical factors in addition to ECG findings, including chest pain which resolved prior to recording of the ECG. Wellens' syndrome is not diagnosed during ongoing pain, as this would not be consistent with reperfusion (which should produce resolution of pain). On the ECG Wellens' syndrome also requires that there are preserved R-waves in the precordial leads.
Below I have reproduced a list of findings of BTWI from a series of other blog posts on this topic on this site, and we will go through each one with respect to the first presentation ECG:
1. There is a relatively short QT interval (QTc less than 425)
YES. Computerized QTc in this case was 424 msec.
2. The leads with T-wave inversion often have very distinct J-waves
YES. J-waves are present in V4-6, as well as II, III, aVF.
3. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which they are V2-V4)
Here the TWI is in leads V3-4 only. So this doesn't really distinguish. Also, Wellens' syndrome is simply one particular example of reperfusion (in this case, of the anterior wall). Reperfusion can obviously happen in any coronary distribution, and the same pattern of findings will happen in any affected wall.
4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', which always evolves)
There is certainly no evolution consistent with continued reperfusion from OMI (occlusion MI), as there would be in the case of Wellens' syndrome. The changes from presentation 1 to 2 are clear, but these are potentially explainable by lead placement or simply the normal variation of ECG findings in normal healthy patients from day to day or hour to hour (we don't really know the answer to this, except to say that we have a large amount of personal experience showing many cases of benign ECG patterns which show changes with repeat ECGs). We have shown many times on this blog that essentially no normal ECG is 100% guaranteed to be completely stable over time. See this case. And this case. And this case. And this very recent case with supporting references:
Huge Precordial ST Elevation in an ED Patient
The opposite, however, is fairly reliable: if the patient has OMI or reperfusion from OMI, the ECG abnormalities will evolve along the expected progression (depending upon continued occlusion and infarction or reperfusion). Therefore, lack of serial ECG changes in the appropriate time frame can be interpreted as evidence against ischemia, but presence of changes is not necessarily indicative of ischemia (it might be, but it might not because there is a significant amount of variation based on lead placement, day to day, etc). Those who have studied cases of OMI versus benign ECG patterns from this blog can usually tell the difference.
5. The leads with T-wave inversion (left precordial) usually have some ST elevation
In the first presentation ECG there is minimal STE. In the second presentation there is slightly more.
6. Right precordial leads often have ST elevation typical of classic early repolarization
In the first presentation, no. In the second presentation, yes.
7. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves
YES, seen in V4 of the first presentation ECG.
8. The T-wave inversion in leads V4-V6 is preceded by high R-wave amplitude
YES, again seen in V4 of the first presentation ECG.
9. II, III, and aVF also frequently have T-wave inversion
YES, the first presentation ECG does have flat/minimally inverted T-waves in the inferior leads.
Learning Points:
Benign T-wave Inversion is recognizable and (with experience) reliably differentiated from anterior reperfusion (Wellens).
Almost all the patterns of normal variant ECGs may show some changes upon serial ECGs. This may be due to lead placement and/or actual primary morphologic change of unknown etiology and significance. These changes can be distinguished from ischemic progression changes.
If you record serial ECGs and there is no evolution over an appropriate time frame, then the lack of evolution is a fairly strong piece of evidence against ischemic ECG changes. The presence of dynamic changes on repeat ECGs, however, may be either progression of ischemia or meaningless, normal variation in a patient's baseline - with the experience provided by this blog these are usually not difficult to differentiate.
References
1. Kambara et al. Early repol is not stable over time. https://www.sciencedirect.com/science/article/pii/0002914976901429
2. Mahaveer C. Mehta, MD. Abnash C. Jain, MD. Early Repolarization on Scalar Electrocardiogram. The American Journal of the Medical Sciences. June 1995; 309(6):305–311.
ABSTRACT
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.
3. Here is a good review of early repolarization by Mehta:
Thanks for the post!
ReplyDeleteCan the J-waves actually be Epsilon waves in a young man with syncope due to ARVD? Would be another explanation for the negative T-waves as well..
Cheers, Rick T.
Epsilon waves look different. ARVD has T-wave inversions in V1-V3. No reliably sensitive ECG findings though. see this reference: https://www.jstage.jst.go.jp/article/circj/79/5/79_CJ-15-0288/_html/-char/ja/
Delete3 Repolarization abnormalities
Major
Inverted T waves in right precordial leads (V1, V2, and V3) or beyond in individuals >14 years of age (in the absence of complete RBBB
QRS ≥120 ms)
Minor
Inverted T waves in V1 and V2 in individuals >14 years of age (in the absence of complete RBBB) or in V4, V5, and V6
Inverted T waves in leads V1, V2, V3, and V4 in individuals >14 years of age in the presence of a complete RBBB
4 Depolarization/conduction abnormalities
Major
Epsilon wave (reproducible low-amplitude signals between end of QRS complex to onset of T wave) in the right precordial leads (V1–3)
Minor
Late potentials by SAECG in ≥1 of 3 parameters in the absence of a QRSd ≥110 ms on standard ECG
Filtered QRS duration (fQRS) ≥114 ms
Duration of terminal QRS <40 microV ≥38 ms
Root-mean-square voltage of terminal 40 ms ≤ micro V
Terminal activation duration ≥55 ms measured from the nadir of the end of the QRS, including R’, in V1, V2, or V3 in absence of complete
RBBB
Great case! I always find the subtleties of T-wave inversions to be quite fascinating to discuss, since they can be pivotal in several critical diagnosis'.
ReplyDeleteI was wondering if you could speak to the possibility of Arrhythmogenic Right Ventricular Cardiomyopathy for this patient, and how you'd go about ruling it out in this case? Am I right to assume that you considered this, and that's why you brought up this patient's lack of exertional syncope, or the lack of SCD in his family history?
However, would it be fair to consider those to be 'Epsilon waves' at the terminal portion of the QRS in the inferior and low-lateral leads?
I'm still somewhat novice in this realm, so I'm very eager to see your response. I always learn so much from this blog. Thank you in advance for your time!
Please see Dr. Smith's much better response above. I have seen a very small number of true epsion waves, and I do not feel as though I am experienced enough to teach about it. I consider the ECG inadequately sensitive to find ARVD if I were worried about it. So I look for epsilon waves, ask the history you discussed and make the best clinical decision available. See this case: https://hqmeded-ecg.blogspot.com/search/label/Arrhythmogenic%20Right%20ventricular%20dysplasia
DeleteThanks for the question, sorry I do not have a great answer!
Thank you for your response! I've never knowingly come across ARVD in my practice as of yet. So i value your input! Thanks
DeleteI am curious if this was from a black individual. My understanding of the "International criteria for electrocardiographic interpretation in athletes" is this is considered a normal pattern in black individuals, but not necessarily in white (or other races). Additionally if the TWI extends beyond V4 in black individuals this may warrant eval for cardiomyopathy, etc. I work in military medicine and see this pattern frequently in young black male athletes, but rarely in others.
ReplyDeleteIndeed, the individual was a 25 year old African American male. It has also been my understanding that this population has a much higher incidence of BTWI.
DeleteSo my question is this, if this was a white individual would you pursue a work up for genetic cardiomyopathy? This is what my understanding of the current guidelines suggest. Or would you instead still diagnose this as BTWI based on appearance despite these guidelines?
DeleteI am not familiar with these guidelines, please send the details/reference and feel free to respond to educate us and our readers about the guidelines you're describing. In a patient with no clinical history suggestive of cardiomyopathy (such as this patient) with an ECG pattern which is also not concerning to me because in my experience it matches that of a benign pattern, my very inexperienced trainee opinion would be that I am not concerned for genetic cardiomyopathy. Unless you or the guidelines you mention have data explaining otherwise, that would be my take.
DeletePlease tell us your approach for this concern and explain the guidelines and data behind them, thanks for the insightful comments!
Pendell,
DeleteTo be clear I also do not consider myself an expert, but rather an improving novice. I will give my input and perhaps some more experience will give input.
Sudden cardiac death in athletes is a rare but devastating problem. SCD in athletes is most often found to be cardiac in origin from a variety of abnormalities including hypertrophic cardiomyopathy, ARVC, Brugada and other channelopathies, etc. The ECG has been used as a screening to determine who needs further cardiac work up prior to sports activities. Unfortunately, the ECG is very poorly specific, so several groups have tried to define what is normal and abnormal in a young athlete’s ECG to better define who needs further work up. The European Society of Cardiology published guidelines in 2010 (updated from the 2005 and 2007 guidelines)1. These guidelines were reported as fairly sensitive (89-90%) but specificity very poor, especially in the subgroup of African Americans who had very high rates of false positives based on these guidelines. Since that time there have been several attempts to improve on these. Stanford criteria where published in 20112, Seattle criteria in 20123, in 2014 the refined Seattle criteria4 were published (the most commonly used I believe) and in 2017 the International criteria of ECG interpretation in athletes was published5.
These are all studies looking at asymptomatic individuals being screened for participation in sporting events. Clearly, this is not the situation with most patients we see in the ED. However, as a military physician this is a population we see not infrequently. We have huge numbers of young males passing through basic training regularly, and despite best attempts still have occasional deaths from an undiagnosed cardiac abnormality. We often have young males sent to the ED from a troop medical clinic (often staffed by NPs, etc. who have very little experience) for abnormal ECGs and because the computerized reading at the top is scary. Most the time these are benign changes as per the case presented here, however, part of my job is to decide if this asymptomatic individual need a cardiac work up (echo, possible cardiac MRI) before returning to training. Certainly if they had symptoms of an undiagnosed cardiomyopathy I would be very concerned (IE exertional syncope, early sudden death in family member).
Back to your case, the ECG presented would be categorized as normal in a black athlete in the most recent guidelines (table 1 lays this out clearly), but would not necessarily be considered normal in a white athlete. Again, this may not fit the clinical scenario you are in, this person may not be participating in any physically strenuous activity, etc. But I think you still have to consider whether to do anything with it if it meets these criteria. If he goes out and runs with the cross country team tomorrow and dies of SCD I imagine you could be held responsible. I think since this is not what the person is there for I would tell them to follow up with their primary doctor prior to any strenuous physical activity for an abnormal ECG and let the PCP decide if they will do further work up. This is different from the population I see given that the all will be forced to participate in strenuous activity on a daily basis- and I would treat this very differently. Again, given that the pt in you case was black, this is a normal ECG by these criteria and I would do nothing further.
Delete1. Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J. 2010;31(2):243-259. doi:10.1093/eurheartj/ehp473
2. Uberoi A, Stein R, Perez M V., et al. Interpretation of the electrocardiogram of young athletes. Circulation. 2011;124(6):746-757. doi:10.1161/CIRCULATIONAHA.110.013078
3. Drezner JA, Ackerman MJ, Anderson J, et al. Electrocardiographic interpretation in athletes: the “Seattle criteria”. Br J Sports Med. 2013;47(3):122-124. doi:10.1136/bjsports-2012-092067
4. Sheikh N, Papadakis M, Ghani S, et al. Comparison of electrocardiographic criteria for the detection of cardiac abnormalities in elite black and white athletes. Circulation. 2014;129(16):1637-1649. doi:10.1161/CIRCULATIONAHA.113.006179
5. Drezner JA, Sharma S, Baggish A, et al. International criteria for electrocardiographic interpretation in athletes: Consensus statement. Br J Sports Med. 2017;51(9):704-731. doi:10.1136/bjsports-2016-097331
Pendell,
DeleteTo be clear I also do not consider myself an expert, but I will give my input and perhaps some others will have input.
Sudden cardiac death in athletes is a rare but devastating problem. SCD in athletes is most often found to be cardiac in origin from a variety of abnormalities including hypertrophic cardiomyopathy, ARVC, Brugada and other channelopathies, etc. The ECG has been used as a screening to determine who needs further cardiac work up prior to sports activities. Unfortunately, the ECG is very poorly specific, so several groups have tried to define what is normal and abnormal in a young athlete’s ECG to better define who needs further work up. The European Society of Cardiology published guidelines in 2010 (updated from the 2005 and 2007 guidelines)1. These guidelines were reported as fairly sensitive (89-90%) but specificity very poor, especially in the subgroup of African Americans who had very high rates of false positives based on these guidelines. Since that time there have been several attempts to improve on these. Stanford criteria where published in 20112, Seattle criteria in 20123, in 2014 the refined Seattle criteria4 were published (the most commonly used I believe) and in 2017 the International criteria of ECG interpretation in athletes was published5.
These are all studies looking at asymptomatic individuals being screened for participation in sporting events. Clearly, this is not the situation with most patients we see in the ED. However, as a military physician this is a population we see not infrequently. We have huge numbers of young males passing through basic training regularly, and despite best attempts still have occasional deaths from an undiagnosed cardiac abnormality. We often have young males sent to the ED from a troop medical clinic (often staffed by NPs, etc. who have very little experience) for abnormal ECGs and because the computerized reading at the top is scary. Most the time these are benign changes as per the case presented here, however, part of my job is to decide if this asymptomatic individual need a cardiac work up (echo, possible cardiac MRI) before returning to training. Certainly if they had symptoms of an undiagnosed cardiomyopathy I would be very concerned (IE exertional syncope, early sudden death in family member).
Back to your case, the ECG presented would be categorized as normal in a black athlete in the most recent guidelines (table 1 lays this out clearly), but would not necessarily be considered normal in a white athlete. Again, this may not fit the clinical scenario you are in, this person may not be participating in any physically strenuous activity, etc. But I think you still have to consider whether to do anything with it if it meets these criteria. If he goes out and runs with the cross country team tomorrow and dies of SCD I imagine you could be held responsible. I think since this is not what the person is there for I would tell them to follow up with their primary doctor prior to any strenuous physical activity for an abnormal ECG and let the PCP decide if they will do further work up. This is different from the population I see given that the all will be forced to participate in strenuous activity on a daily basis- and I would treat this very differently. Again, given that the pt in you case was black, this is a normal ECG by these criteria and I would do nothing further.
1. Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J. 2010;31(2):243-259. doi:10.1093/eurheartj/ehp473
Delete2. Uberoi A, Stein R, Perez M V., et al. Interpretation of the electrocardiogram of young athletes. Circulation. 2011;124(6):746-757. doi:10.1161/CIRCULATIONAHA.110.013078
3. Drezner JA, Ackerman MJ, Anderson J, et al. Electrocardiographic interpretation in athletes: the “Seattle criteria”. Br J Sports Med. 2013;47(3):122-124. doi:10.1136/bjsports-2012-092067
4. Sheikh N, Papadakis M, Ghani S, et al. Comparison of electrocardiographic criteria for the detection of cardiac abnormalities in elite black and white athletes. Circulation. 2014;129(16):1637-1649. doi:10.1161/CIRCULATIONAHA.113.006179
5. Drezner JA, Sharma S, Baggish A, et al. International criteria for electrocardiographic interpretation in athletes: Consensus statement. Br J Sports Med. 2017;51(9):704-731. doi:10.1136/bjsports-2016-097331
Thanks so much for this valuable contribution!
DeleteOverall, my initial impression of this consensus statement (reference #5) is that it's a great resource. However, I am deeply confused to see their list of T-wave inversion criteria, because I think this list would turn out to be unbelievably nonspecific, with downstream overtesting and other unforeseeable harms. I worry that this document could be used retrospectively to prosecute EM physicians and other specialties for cardiograms that were within normal limits, or unable to be differentiated from cardiograms that are within normal limits. The interrater reliability of these findings would be off the charts in the bad direction.
I cannot imagine the number of cardiology consults and genetic CM workups that would ensue if EM physicians obeyed these T-wave inversion guidelines in young patients presenting with syncope.
Dr. Smith what do you think about these guidelines and the T-wave criteria specifically?
This comment has been removed by the author.
DeleteYes, makes sense, thanks.
DeleteThis particular patient did not actually have syncope. He was African American. No concerning history.
But this discussion is all helpful for the many patients we will see who do have syncope and/or concerning history.
I think that an echocardiogram is indicated if the patient had syncope (although in this case it does not sound like syncope). But the point of the post is that this is not an ECG indicative of ischemia, which so many emergency physicians would be concerned about. In that sense, it is a false positive. However, if this ECG were recorded in an aysmptomatic white person, further evaluation as outpatient would be indicated. Or in this patient, who did have syncope (and who is African American, correct?), further outpatient workup (echo) is indicated because of the ECG in the context of syncope, which sounds quite worrisome).
DeleteDoes that make sense?