An otherwise healthy middle aged smoker complained of sudden left trapezius pain. He then began to fell very dizzy. He also had some vague left sided chest pain. His prehospital ECG was identical to the first ED ECG:
The patient's symptoms were rather atypical, and because of this and the benign appearing inferior leads, I thought that the ST depression and T-wave inversion in aVL might not be pathologic. I signed the patient out to the next team with a plan to get serial ECGs and troponins, and manage according to the results.
The patient received NTG without change in his pain.
Another ECG was recorded shortly after the first and was identical.
The initial troponin I returned at 0.018 ng/mL (normal up to 0.030).
The second trop returned at 0.28 ng/mL (positive). The patient's pain had not entirely resolved, but was at 3/10.
Persistent pain with objective evidence of MI is reason for aggressive management.
Another ECG was recorded:
He was started on antiplatelet and antithrombotic therapy.
Suddenly, the patient developed sinus brady at a rate of 30, and had a 4 beat run of VT. He was hypotensive. The bradycardia and hypotension responded to atropine.
A bedside echo showed probable inferior wall motion abnormality.
Another ECG was recorded:
These are all signs of reperfusion, and indicate that the subtle findings of the first ECGs (minimal ST elevation, T-waves, ST depression and T-wave inversion in aVL) were all due to ischemia.
He was taken to the cath lab and found to have a severe 90% thrombotic lesion of the proximal to mid RCA.
In our study of inferior STEMI vs. non-MI causes of inferior ST elevation, any ST depression in aVL was almost perfectly diagnostic (sensitive and specific) for inferior MI.
Awareness of this finding allowed for vigilant observation and serial ECGs even in the absence of a typical history.
 |
| There is minimal ST elevation in inferior leads. What caught my eye was the T-wave inversion and minimal ST depression in aVL. This should always make you scrutinize the inferior leads for signs of inferior MI, and record serial ECGs. However, to my eye, inferior ST-T complexes did not appear to show MI. |
The patient received NTG without change in his pain.
Another ECG was recorded shortly after the first and was identical.
The initial troponin I returned at 0.018 ng/mL (normal up to 0.030).
The second trop returned at 0.28 ng/mL (positive). The patient's pain had not entirely resolved, but was at 3/10.
Persistent pain with objective evidence of MI is reason for aggressive management.
Another ECG was recorded:
 |
| There are some subtle, nondiagnostic differences in the inferior T-waves, which are now smaller. There are no unequivocal signs of coronary occlusion. The ST segments and T-waves are dynamic. |
He was started on antiplatelet and antithrombotic therapy.
Suddenly, the patient developed sinus brady at a rate of 30, and had a 4 beat run of VT. He was hypotensive. The bradycardia and hypotension responded to atropine.
A bedside echo showed probable inferior wall motion abnormality.
Another ECG was recorded:
 |
| Sinus bradycardia. Now the ST depression and T-wave inversion in aVL is resolved. The inferior ST segments are completely isoelectric. The inferior T-waves are smaller. There is new T-wave inversion in III and aVF. |
He was taken to the cath lab and found to have a severe 90% thrombotic lesion of the proximal to mid RCA.
In our study of inferior STEMI vs. non-MI causes of inferior ST elevation, any ST depression in aVL was almost perfectly diagnostic (sensitive and specific) for inferior MI.
Awareness of this finding allowed for vigilant observation and serial ECGs even in the absence of a typical history.
looking at lead III in the initial ECG, does the t wave amplitude, being greater than the QRS amplitude in that lead bear any significance?
ReplyDeleteGood observation. It probably does!
DeleteSteve Smith
Your posts are always interesting but sometimes a little frightening like this one. I see a lot of people who come to ED in France complaining of atypical chest pain, and evaluating their risk factors is sometimes difficult. 1st ECG is often normal or non-specific. I can always have a 1st Troponin, sometimes difficult to get a 2d (not enough rooms). Cardiologists doesn't seem interested in these patients and sometimes they influence us to discharge these patients (without seeing the patient or ECG) and no possibilities to have a consult soon after the ED visit.
ReplyDeleteTom,
Deleteshow them these cases. where are you in France. I occasionally come and speak in France (my favorite country) and would love to talk on subtle ECGs.
Steve Smith
i thankfull or u iam learning many things
ReplyDeleteglad to hear it. thanks for the feedback!
DeleteHi Steve,
ReplyDeleteJust yesterday I found a patient with an interesting ECG that showed what looked like early repol inferiorly, but with ST depression and TWI in aVL. He also had fairly subtle biphasic T waves in V2-3 which looked to me like Wellen's, very similar to the second ECG in your post on June 17th.
The inferior changes looked like typical early repol but with the changes in aVL, took on a bit more of a worrying look.
However angiogram showed only an LAD lesion, no disease in RCA or LCX.
I'd like to see it. T-wave inversion in aVL can be acute inferior (reciprocal to inferior STEMI), or it can be reperfusion of the lateral wall (proximal LAD Wellens).
DeleteSteve
Dear doctor.,I have observed that there is st elevation in inferior. leads with irregular rhythm and there are also u waves and st suppression in lateral leads possibly because patient is hypokelimic and some st elevation in v1v2 is due to inferior. And right ventricular mi hinting RCA occlusion.please make corrections if some is missing.I am interpreting the first ecg which is diagnostic.
ReplyDeleteKavya,
ReplyDeleteI think you are right that the ECG is diagnostic, but it is very subtle. I don't see the ST depression except in aVL and that is what makes the ECG diagnostic! As for the U-waves, I think they are within normal limits and the patient was not hypokalemic.
Thanks for your thoughts.
Steve
Great learning case.
ReplyDeleteCan you post a link to the study/paper you referenced (re inf STEMI vs non-MI causes of ECG STE)?
Thanks,
SS
It is only in abstract form so far.
Delete21. Bischof J. Thompson RP. Tikkanen J. Porthan K. Huikuri H. Salomaa V. Smith SW. ST-segment depression in lead aVL differentiates benign ST elevation from inferior Acute STEMI. ACEP Research Forum 2012 Abstract 21. Annals of Emergency Medicine 60(4 Suppl):S8-S9; October 2012.
21 ST Depression in AVL Differentiates Inferior ST Elevation
Myocardial Infarction From Benign Causes of Inferior ST
Elevation
Bischof JE, Worrall C, Thompson R, Tikkanen J, Porthan K, Huikuri H, Salomaa
V, Smith SW/Hennepin County Medical Center, Minneapolis, MN; University of
Oulu, Oulu, Finland; Helsinki University Central Hospital, Helsinki, Finland;
Institute for Health and Welfare, Helsinki, Finland
Background: ST segment elevation in leads II, III, and/or aVF due to inferior ST
elevation acute myocardial infarction may be misdiagnosed as pericarditis or as benign
early repolarization. Conversely, these non life-threatening etiologies of ST elevation
may be confused for inferior STEMI.
Study Objectives: We sought to determine if the presence of any (reciprocal) STsegment
depression in lead aVL would differentiate inferior STEMI from these less
serious etiologies of ST elevation.
group 1 with inferior STEMI; group 2 with pericarditis, and group 3 with inferior ST
elevation due to early repolarization. For group 1, we searched the cardiac catheterization
laboratory database at Hennepin County Medical Center for all cases coded as acute
Inferior STEMI from January 2002 through March 2008. For group 2, we searched for
all patients with a discharge diagnosis of pericarditis from 1996 to 2010 who presented to
the ED with chest pain and 1 mm of ST elevation in 1 inferior lead. For group 3,
we assessed the resting baseline ECGs of 5489 asymptomatic patients from the Finnish
Health 2000 survey (44% men, mean age 50.5 years) and selected those with at least 1
mm of ST elevation in 2 consecutive inferior leads as measured by both custom software
and visual analysis. All cases were reviewed and the presenting ECG, as well as the first
ECG that was used for diagnosis of acute STEMI, were analyzed. ST segments were
measured at the J-point relative to the PR segment.
Results: Group 1: There were 156 patients with inferior STEMI. Whether or not
they met reperfusion criteria (n 134, 86%), 155 had some amount of ST depression in
lead aVL (sensitivity 99%; 95% CI: 96%-100%). Group 2: there were 67 ED pericarditis
patients with chest pain; 23 were excluded for absence of ST elevation and 5 were
excluded because the medical record could not be found, leaving 39; all rule out for acute
myocardial infarction. All 39 had some inferior ST elevation and 19 met inferior
reperfusion criteria (1 mm of ST elevation in 2 consecutive inferior leads); none of the 39
had any ST-segment depression in lead aVL, or any other lead (specificity, 100%; 95%
CI: 89%-100%). Group 3: there were 71 patients who met inferior reperfusion criteria;
after excluding patients with a paced rhythm (2), left bundle branch block (2) and Wolff
Parkinson White Syndrome (1), none of 66 had any ST depression in lead aVL
(specificity, 100%; 95% CI: 93%-100%). Overall diagnostic performance of STD in aVL
for STEMI versus no-acute myocardial infarction were sensitivity 99% (95% CI: 96%-
100%) and specificity 100% (95% CI: 95.6%-100%). Limitations: We did not include
cases with left ventricular hypertrophy by limb lead voltage; these are known to often have
baseline reciprocal STD in lead aVL.
Conclusion: When there is inferior ST segment elevation in the presence of
normal conduction (no left bundle branch block, paced rhythm, LVH, or Wolff
Parkinson White Syndrome), the presence of any ST depression in lead aVL is highly
sensitive and specific for inferior STEMI versus early repolarization or pericarditis.
Another great case Steve - the reperfused ECG seems to have some 'posterior reperfusion T-waves' as well!
ReplyDeleteSam
Indeed, Sam!
DeleteIs there any explanation for the T waves V1-V3 getting taller over the course of time?
ReplyDeleteand thanks a lot for this great blog!!
Matthias
Yes! Posterior Reperfusion T-waves.
ReplyDeletehttp://hqmeded-ecg.blogspot.com/search?q=Posterior+reperfusion+T-waves%3A+Wellens%27+syndrome+of+the+posterior+wall
Our paper on the topic: http://emj.bmj.com/content/early/2016/08/04/emermed-2016-205852.abstract