Friday, July 29, 2022

Two patients with chest pain and LVH: Neither STEMI criteria, nor Armstrong criteria, can identify occlusion or reperfusion

Written by Jesse McLaren


Two patients presented with chest pain and LVH on ECG.

 

Patient 1: 65 year old with an hour of left sided chest pain

Patient 2: 70 year old with 30 minutes of chest pain with nausea and diaphoresis

What do you think? How do you tell which had an Occlusion MI (OMI)?







Do STEMI criteria help?

 

Both have anterior STE in two contiguous leads that exceed STEMI criteria, but both also have LVH. LVH produces tall R waves in the left sided leads with secondary ST depression and T wave inversion, and deep S waves in the right sided leads with secondary ST elevation and tall T waves. In the first patient the left sided leads don't have very tall R waves, but they do have deep right sided S waves.


Because STEMI criteria only looks at amplitude of ST elevation, it can’t differentiate between secondary and primary or superimposed causes of ST elevation, and ignores other signs of acute coronary occlusion. Instead the paradigm simply defines STEMI as ST elevation in the absence of LVH. So by definition STEMI criteria cannot be applied to these ECGs, and cannot identify which has acute coronary occlusion. Armstrong suggested using a cutoff of STE/S > 25%, but this would call both of these negative: in the second case V3 has an S wave of 28mm, which would require 7mm of STE and there’s only 4. (see this post for further discussion)

 

Do old ECGs help?

 

Here are the two cases with the old followed by the new ECG:

 

Patient 1:

 

 

If you only looked at ST segments and T waves you might be concerned about increase ST elevation and taller T waves in V1-2, but these are proportional to larger voltages in those leads. LVH can change over time, and can also be affected by lead placement: the older ECG has higher leads, with almost entirely negative P wave in V1 and biphasic P in V2. On the other hand, the prior ECG does show that the inferolateral T wave inversions are old, and they remain asymmetric and proportional to the QRS complex. So the new ECG shows LVH with secondary repolarization changes, without ECG evidence of OMI.


Patient 2:


The new ECG has greater STE in V1-3 with the same voltages, but also multiple other signs of OMI:  1) while the Q waves V1-3 are old there is loss of R wave in V4, 2) there are hyperacute T waves V3-4, and 3) there’s inferolateral ST depression especially in V5-6, which is reciprocal to anterior ST elevation. (Compare the typical LVH strain pattern from patient 1 with asymmetric T wave inversion, with ischemic reciprocal change in patient 2 with ST depression with upright T wave).

 

 

How were they managed? STEMI criteria fails to identify occlusion and reperfusion

 

Patient 1 had serial ECGs that were unchanged and serial troponin which were normal (4 and 5 ng/L, with normal < 16 in females and <26 in males). They were discharged and well on follow up.


Patient 2 had three sprays of nitro with improvement of symptoms. Here is the first ECG and repeat:


This was interpreted as resolution of ST changes, and with an initial troponin of 13ng/L the patient was observed with a plan for non-urgent angiogram based on "transient STEMI". But notice there’s been a total loss of R wave in V4, there is still a hyperacute T wave, and there is ongoing inferolateral ST depression. Despite improvement of symptoms there’s been no reperfusion.

 

Four hours later a repeat troponin was 3500ng/L and another ECG was done, with the patient reporting more pain:

 


 

There are still hyperacute T waves V3-4 and still inferolateral ST depression, and now more ST elevation V3-4. Cath lab was activated, after hours of preventable infarction, and found what the first ECG revealed: proximal LAD occlusion. While the first troponin was in the normal range, the peak was 33,000ng/L. Discharge ECG showed precordial T wave inversion, indicating reperfusion:


Take away

1.     LVH produces secondary ST and T wave changes that can vary over time

2.     STEMI criteria is defined in absence of LVH so can’t help identify OMI in the presence of LVH

3.     Other signs of OMI include loss of R waves, disproportionate ST elevation, hyperacute T waves, and reciprocal ST depression 

4.     Resolution of symptoms is not the same as reperfusion, and resolution of ST segments is not the same as reperfusion T wave inversion

5.   Initial troponins can be normal, symptoms can resolve and patients can have "transient STEMI" all in the presence of ongoing OMI and relying on these features can lead to delayed reperfusion







===================================

MY Comment, by KEN GRAUER, MD (7/29/2022):

===================================

Superb post by Dr. McLaren regarding the difficulty diagnosing acute OMI in a patient with marked LVH on ECG. As per Dr. McLaren — the "usual" STEMI criteria simply can not be used because of the changes that LVH produces in QRST size and morphology.
  • In the hope of providing additional perspective to the 2 insightful case studies described above — I focus my comments on some non-numeric "qualitative" features that have been helpful to me.
  • To illustrate these features — I've reproduced and labeled in Figure-1 the initial ECG from Dr. McLaren's Patient 2 ( = the 2nd ECG shown above).

In My Comment at the bottom of the July 18, 2022 post of Dr. Smith's ECG Blog — I emphasized what I consider to be the 3 most important factors to consider when assessing ST-T wave changes for the likelihood of OMI ( = acute coronary occlusion). These 3 factors are: i) Shape; ii) Proportion; and, iii) Location.
  • Since reliable numeric criteria do not exist for identifying acute OMI in patients with marked LVH — we need to focus our attention on other clues. The "essence" of applying the factors of Shape — Proportion — Location — is that we are looking for QRST morphology changes "that should not be there".

  • Textbook criteria for this do not exist. Instead — we intuitively use our "memory banks" of all the hundreds (thousands, or more) tracings we've interpreted over our years of practice — to arrive at a conclusion of relative probability that an ECG in a patient with baseline LVH and new symptoms is (or is not) likely to be evolving an acute cardiac event.

  • I favor starting by search for those 1 or 2 leads on the 12-lead tracing for which I can be fairly certain that QRST appearance in a patient with new symptoms is not "normal". 
  • I then look at "neighboring leads" — to see if less obvious changes are likely to reflect a "continuation" of suspected acute changes.
  • In general — the more leads with suspected acute changes on a 12-lead ECG — the greater the likelihood that an acute process is evolving.

  • In Dr. McLaren's above discussion — he illustrates how additional information (ie, comparison with prior and/or serial tracings; troponin values; correlation with the patient's clinical response to treatment) — may assist for identifying which LVH tracings show an acute process. But initially, before this additional information becomes available — we are often faced with assessing the situation from only the initial ECG.

Figure-1: I've reproduced the 2nd ECG shown in Dr. McLaren's above discussion — which was the initial tracing obtained in the ED from his Patient 2.



MY Thoughts on ECG #2:
The ECG shown in Figure-1 was the initial ECG obtained in the ED — from a 70-year old who presented with 30 minutes of chest pain with nausea and diaphoresis.
  • There is marked baseline artifact in the limb leads. Despite this — the tracing is interpretable. 
  • The rhythm is sinus at ~75/minute. All intervals and the mean QRS axis in the frontal plane are normal.
  • There is marked LVH (very deep S wave in V3>25 mm; very tall R waves in V5,V6 greater than 30 and 20 mm, respectively).
  • There are QS complexes in leads V1,V2,V3.
  • Transition is slightly delayed — with the R wave becoming taller than the S wave is deep between leads V4-to-V5.
  • The most remarkable ECG findings are the ST-T findings (See below).

The Effect of LVH on the ECG:
Patients with marked LVH often manifest ST-T wave changes of LV "strain" in one or more leads.
  • Not all patients with Echo-proven LVH manifest LV "strain" on ECG. The Framingham Studies taught us that longterm prognosis is adversely affected when both voltage and repolarization changes of "strain" are present on ECG.
  • ST-T wave changes of LV "strain" are most commonly seen in one or more of the lateral leads (ie, in leads I, aVL; and/or V4, V5, V6). Typically — there is slow descent of the ST segment, with a more rapid rise at the end of the ST segment.
  • Some patients with LVH (especially if the frontal plane axis is vertical) — also manifest ST-T changes of LV "strain" in the inferior leads.
  • Some patients with especially deep anterior S waves — manifest the "mirror-image" picture of LV "strain" in the form of an upright ST-T wave, often with some ST elevation in these anterior leads.

  • The other major effect produced by LVH on ECG is that the increase in leftward and posterior forces forces may overshadow baseline anterior forces — with a "net result" that R wave progression is delayed (sometimes to the point of producing QS complexes in one or more anterior leads).

  • NOTE: I've reviewed my approach for ECG assessment of LVH and LV "strain" on many occasions in Dr. Smith's ECG Blog (For more — SEE My Comment in the June 20, 2020 post and the April 27, 2019 post — to name just 2 of these posts).

What Do I See of Concern in ECG #2?
To clarify the limits of the QRS complex in leads V3 and V5 — I've outlined these complexes in RED in Figure-1. I've also outlined the ST-T waves of concern in BLUE in this figure.
  • Although there is a QS complex in anterior leads V1,V2,V3 — I was not certain from this single tracing if this was the result of anteroseptal infarction at some point in time — or — simply a reflection of predominant leftward and posterior forces from marked LVH that resulted in elimination of all anterior R wave. The fact that the small QRS complex in lead V4 was isoelectric (outlined in BLUE in Figure-1) — and then followed by a dramatically tall R wave in lead V5 suggested to me that the QS complexes in anterior leads were probably the result of LVH.

  • Following my suggested approach to LOOK FIRST for those 1 or 2 leads in which I could be fairly certain that the ST-T waves were "not normal" — I focused on the T wave in lead V4. Although this V4 lead clearly represents a "transition lead" between the markedly negative QRS in lead V3 — and the markedly positive QRS in V5 — in this 70-year old with new chest pain, I thought there was NO way the T wave in lead V4 could be normal. This T wave is pointed, more than twice as tall as the R wave in this lead — and manifests a wide base. In a patient with new symptoms — I interpreted this T wave in lead V4 as hyperacute until proven otherwise!
  • Moving on to "neighboring leads" — while the initial part of the depressed ST segments in leads V5 and V6 (outlined in RED) could be consistent with LV "strain" — there was NO way the tall, pointed terminal T wave positivity in lead V5 could be normal. As a result — I thought the small, but still unusually pointed terminal T wave positivity in lead V6 was probably further extension of the same ongoing process.
  • The other "neighboring lead" to the hyperacute T wave in lead V4 — was lead V3. And while common with markedly increased anterior S waves from LVH to see fairly tall, upright ST-T waves in those anterior leads with increased voltage — the 15 mm tall, pointed T wave in lead V3 (outlined in BLUE) closely resembles the appearance of the hyperacute T wave in lead V4.

NOTE: This already makes for 4 consecutive probable hyperacute T waves (in leads V3,V4,V5,V6) in this 70-year old patient with new chest pain. Knowing this lowered my "threshold" for assessing ST-T wave appearance in the remaining leads:
  • The T wave in lead V2 (outlined in BLUE) looks hypervoluminous with respect to the relatively small QRS in this lead.
  • The ST segment in lead V1 is elevated and abnormally coved (almost a "reciprocal" mirror-image picture of the scooped ST segment depression in lateral chest leads V5,V6).
  • Subtle ST-T wave flattening is seen in limb leads III and aVF. Although this is a nonspecific change — I thought the shape of the ST-T wave in lead II (outlined in BLUE) in association with unexpected J-point depression in this lead (RED arrow) — was clearly abnormal.

BOTTOM LINE: As per Dr. McLaren — Recognition of acute OMI in a patient with marked LVH is often extremely challenging. That said — before I "read the answers" — I thought the above non-numeric qualitative features in ECG #2 strongly suggested acute OMI until proven otherwise!
  • Virtually all leads on this tracing showed abnormalities beyond that expected for simple LVH — and, given the history of new chest pain — I was suspicious of hyperacute ST-T waves in all 6 chest leads.

  • I thought chest lead T waves (especially in leads V3-thru-V5) had a deWinter-like appearance — so despite marked LVH — I thought, "acute proximal LAD occlusion" until proven otherwise.



at No comments:

Monday, July 25, 2022

A man in his 50s with hypoxemic respiratory failure from COVID pneumonia develops chest pain

Submitted by anonymous, written by Parker Hambright, MD, peer reviewed by Meyers, Smith, McLaren


A man in his 50s with a past medical history of hypertension and tobacco use disorder, who tested COVID positive 11 days prior, presented to the emergency department with worsening shortness of breath over several days. He was tachypneic and hypoxemic down to as low as 44% with reportedly good SpO2 waveform before EMS applied noninvasive ventilation with improvement to 85-89%. Although history was limited by extremis, the report is that there was no chest pain at initial presentation, only shortness of breath.


Here is his ECG on arrival, Day 1 around 0530:

What do you think?


I see some small ST depression in V3-V6, II, III, aVF, and very small reciprocal STE in aVR. In the context of known covid with severe hypoxemia and respiratory distress, I would likely feel that this ECG most likely represents subendocardial ischemia, which is well explained by hypoxemia and respiratory distress.



Evaluation was remarkable for acute hypoxemic respiratory failure secondary to COVID-pneumonia and the patient was initiated on BiPAP and admitted to the ICU. It seems that no troponin was ordered so far. While boarding in the emergency department awaiting an ICU bed, the patient developed acute onset substernal and left sided chest pain, without any worsening of his shortness of breath or any escalation in his oxygenation/ventilation parameters or work of breathing.  A repeat ECG was obtained:


ECG 2 - Day 1 around 1700:

What do you think now?











Overall the QRS is unchanged, but there is new large STE in V1-V4, as well as tiny STE in II, III, and aVF. In comparison to the first ECG, we also see that the T waves are hyperacute in all the same leads. The slight STD in V6 is reciprocal to the right precordial STE, and the downsloping STD and TWI in aVL is reciprocal to the inferior STE/hyperacute T waves. This is diagnostic of anterior and inferior/apical OMI until proven otherwise. Pericarditis should not have any reciprocal STD or TWI. This is NOT DIFFUSE ST ELEVATION - this is focal.  This suggests occlusion of a "wraparound" LAD do the inferior wall.


ECG 2 was interpreted by the Emergency Physician as sinus rhythm with ST elevations throughout inferior and precordial leads.


The ED physician activated a code STEMI and empirically treated for ACS - ASA, atorvastatin, and heparin gtt. Cardiology was called to the bedside. The cardiologist felt the ECG more likely represented myo-pericarditis in the setting of COVID19 rather than a Type I MI, and requested for a comprehensive echocardiogram to be obtained emergently. A limited stat bedside echocardiogram was performed and demonstrated anteroseptal and apical hypokinesis with a low-to-normal LVEF in the range of 45%.

The first troponin was ordered right after this ECG, which soon returned highly elevated at 3,555 ng/L.


Despite asking for the echocardiogram ostensibly for identifying wall motion abnormalities, the cardiologist still insisted that the patients overall clinical picture was more consistent with myo-pericarditis. He refused to take the patient to the cath lab. The patient went to the ICU with ongoing chest pain (now on high flow nasal cannula for oxygen requirement).

There is no mention of anyone considering thrombolytics, all notes simply state that cardiology did not feel that the patient was having ACS. Yet they documented that cardiology recommended heparin drip, so that was given.

Serial ECGs and troponins were trended.

ECG 3 - Day 1 1750



ECG 4 - Day 1 1825




ECG 5 - Day 2 0000



Subsequent hs-troponins were 6,892 ng/L, then 9,110 ng/L, and then peaked at 10, 126 ng/L during this morning.


ECG 6 - Day 2 0921





The comprehensive echocardiogram resulted on Day 2 at 1048 and was remarkable for a reduced LVEF of 40%, proximal and mid anteroseptal hypokinesis, and distal anteroseptal and apical akinesis.


Cardiology still felt the patient’s presentation was more likely the result of myo-pericarditis.


ECG 7 - Day 3 1210
Anterolateral reperfusion without inferior reperfusion
This sometimes happens when an LAD thrombus in a wraparound LAD embolizes to the apex, resulting in anterior reperfusion but persistent inferior occlusion.





ECG 7 demonstrated evidence of coronary reperfusion with T wave inversions in the precordial leads - consistent with the OMI reperfusion sequence. This ECG further proves that the patient’s chest pain was the result of ACS rather than myo-pericarditis.


Day 4:
Anterolateral reperfusion, but active OMI in inferior leads likely corresponding to the apex, or less likely inferior septum.



Mostly the same as prior, except that the anterior leads are not proceeding down the reperfusion progression (which would show enlarging TWI), instead they appear to be turning around and going the other direction: reocclusion? Look at V3. It is trying to transition from reperfusion to reocclusion findings.



Without reasoning documented, troponins start getting ordered again around this time.

hs Troponin I:
2,008 ng/L
3,831 ng/L


Day 5:

Full re-ooclusion (in context). Anterolateral leads here would be described as pseudo-normalization (because the context tells us they are NOT normal, they are transitioning from reperfusion TWI to acute anterolateral active OMI with T waves reinflating into hyperacute T waves, if the occlusion persists).
This does NOT happen in myocarditis!!


It sounds as if the pain suddenly ceased, and no more ECGs were ordered for days.

hs Troponin I:
5,040 ng/L
3,933 ng/L
2,517 ngL



1 week later:

Mostly all areas show reperfusion, except inferior leads.



A repeat echocardiogram was performed on hospital day 7 and was remarkable for a persistent WMA with an LVEF of 40%. A large mobile apical thrombus was also noted. Left heart catheterization was deferred. He was transitioned to warfarin for long-term anticoagulation.



The patient was initiated on guideline-directed medical therapy for his HFrEF, atorvastatin and clopidogrel for his MI, and warfarin for the LV thrombus. He was discharged on hospital day 14 following recovery from COVID pneumonia complicated by an anterior OMI.

Final diagnoses:
"STEMI vs Pericarditis in context of HFrEF
LV thrombus 2/2 myocardial hypokinesia s/p STEMI v Pericarditis" 



1 month later:

Still showing reperfusion.


Months later:





A cardiac MRI was performed outpatient 4 weeks following the hospitalization. The imaging demonstrated a mid-apical inferoseptal and apical reversible defect consistent with infarct provided below.

 



Cardiac catheterization was performed 6 weeks following hospitalization. Left heart catheterization was remarkable for 90% stenosis of the proximal LAD - where a DES was subsequently placed.


Unfortunately, the patient has experienced multiple complications since discharge requiring recurrent hospitalizations due to UGIBs in the setting of anticoagulation and antiplatelet agents. This case highlights the importance of timely intervention with PCI for OMI in order to reduce the incidence of post-MI complications and the complications from medical management.


Learning Points:

In this case, the patient's management disagrees with both the current ACC/AHA NSTEMI guidelines which give a 1A recommendation for emergent cath for NSTEMI with ongoing ischemia, as well as the 2020 AHA statement on myocarditis, which states: 

"A nonvascular distribution of ST-segment elevations is common in fulminant myocarditis but should not delay angiographic assessment of the coronary anatomy." Also: "Although an elevated serum cardiac troponin (cTn) is almost always present in fulminant myocarditis, there should be a low threshold for evaluation with coronary angiography because acute coronary syndrome is the most common cause of a cardiac presentation with elevated biomarkers."

Myocarditis and takotsubo cardiomyopathy can closely mimic OMI. In some cases, the ECG cannot differentiate these conditions. However, myocarditis should not mimic the OMI progression including reperfusion and reocclusion, as we saw in the case above. With myopericarditis having a much lower incidence than OMI and the consequence of missing an OMI being severe, having a low threshold for early angiography is an appropriate approach to diagnostic evaluation.

Clinical context and ancillary tests other than the ECG can help differentiate these conditions. This patient had features including rapidly rising troponin and focal wall motion abnormality, both of which should of course be considered due to OMI until proven otherwise. Myocarditis as a cause of this case can only be entertained after emergent angiogram. An emergent coronary CT angio would also be a reasonable plan for a patient for whom the diagnosis of OMI is in doubt due to possible myocarditis or takotsubo. This cardiologist seems to be able to ignore almost any possible clinical feature, but imagine if the primary team had obtained CT coronary angio showing occlusion or high grade stenosis of the LAD.


A case series from the NEJM (Bangalore et al., in references below), further highlights the difficulty in discerning OMI from myopericarditis in COVID-19 patients. This series identified 18 patients with COVID19 who presented with ECG features suggesting STEMI. Following additional evaluation, 8 patients were determined to have OMI and 10 patients were determined to have non-coronary myocardial injury. The ST segment elevation was identified as diffuse in 4/10 of the non-coronary myocardial injury cases and focal in 6/10 of the non-coronary myocardial injury cases. This series emphasizes the lack of specificity of ST segment changes and distribution in distinguishing OMI from myo-pericarditis.

Many patients will unfortunately present with vague symptoms that cannot be used to confidently discern these two pathologies. Laboratory evaluation using a CRP/troponin ratio may provide some additional insight. A CRP/troponin ratio >500 was found to have an 85% specificity for myopericarditis and >1000 has a 92% specificity for myopericarditis. The consequence of missing an OMI, however, is exceptionally high and using the CRP/troponin ratio as the sole reason to defer cardiac catheterization is risky. Better to consider myocarditis as a diagnosis that is only possible to make after the angiogram and other features rule out OMI.


References:

Bangalore S, Sharma A, Slotwiner A, et al. ST-segment elevation in patients with COVID-19 – a case series. New England Journal of Medicine. June 2020; 382: 2478-2480. https://www.nejm.org/doi/full/10.1056/NEJMc2009020


Bangalore S, Sharma A, Slotwiner A, et al. ST-segment elevation in patients with COVID-19 — a case series; Supplementary appendix. New England Journal of Medicine. 2020; 382:2478-80. https://www.nejm.org/doi/suppl/10.1056/NEJMc2009020/suppl_file/nejmc2009020_appendix.pdf

Circulation 2020: ACC/AHA Statement on Management of Fulminant Myocarditis:
https://www.ahajournals.org/doi/10.1161/CIR.0000000000000745

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0248365





===================================

MY Comment, by KEN GRAUER, MD (7/25/2022):

===================================

Brilliant discussion of today's case by Dr. Parker Hambright — with contributions from Drs. Meyers, Smith and McLaren. At the risk of repetition — I'll reemphasize KEY points brought out regarding the distinction between acute OMI vs Myocarditis.
  • By itself, the initial ECG can not reliably distinguish between acute OMI vs Myocarditis. There is simply too much overlap of ECG findings between these 2 entities to provide a definitive diagnosis based on a single tracing.
  • Use of serial ECGs may faciliate distinction — as was seen in today’s case with the appearance of reperfusion T waves. Unfortunately, this ECG finding was not seen until ECG #7 (done on Day-3 at 12:10) — at a time that was well beyond that likely to provide benefit from PCI.
  • Long before the "tell-tale" ECG sign of reperfusion T waves — presumptive diagnosis of acute OMI until you prove otherwise was evident from focal evolution of ECG findings (recognized as soon as ECG #2 became available to compare with ECG #1).
  • Bedside Echo provided further support of focal injury (serving as an additional indication to assume acute OMI until you prove otherwise).
  • Cardiac MRI could distinguish between OMI vs Myocarditis — but this modality will not be available to many (most) providers in a timely-enough fashion to positively impact treatment.

  • BOTTOM Line: As emphasized above by Drs. Hambright, Meyers, Smith & McLaren — there are times when cardiac catheterization may be the only way to definitively distinguish between OMI vs Myocarditis. The clinical lesson is to expedite identification of which patients need prompt cath — because we recognize that without prompt cath, we simply may not be able to distinguish between acute OMI vs Myocarditis in problematic cases.



What Happened in Today's Case:
Unfortunately — the diagnosis of acute OMI was significantly delayed in today's case because of oversights pointed out above in Dr. Hambright's discussion. To facilitate appreciation of these oversights — I thought it worthwhile to take another LOOK at the first 2 tracings in today's case (Figure-1):


Figure-1: Comparison between the first 2 tracings in today’s case (See text).


Comparing the 2 ECGs in Figure-1:
The point I would emphasize about ECG #1 — is that this is not a "normal" tracing. I completely agree with Dr. Hambright that the subtle-but-real ST depression in at least 6 leads (with hint of ST elevation in lead aVR) — is consistent with diffuse subendocardial ischemia (which is not unexpected given the clinical context of Covide-related acute respiratory failure).
  • I'd add that while not depressed — the ST segment in lead V2 of ECG #1 is abnormally straightened — with angulation at the point that it joins the T wave. Considering modest size of the QRS complex in this lead — I thought the T wave in lead V2 was taller-than-expected, and in the context of the straightened ST segment — possibly hyperacute.
  • Given the association of severe Covid illness with acute cardiac disorders (such as myocarditis and OMI) — these ECG findings in this initial tracing (even in the absence of chest pain at this time) would seem to merit: i) Ordering troponin (which was not done in today's case until after ECG #2); and, ii) Repeating the ECG much sooner than was done (ECG #2 was not done until 11 1/2 hours later — and then only because the patient had chest pain). 
  • I can't help but wonder if that overly tall T wave in lead V2 of ECG #1 might had heralded the beginning of this patient's LAD occlusion.

I chose to put ECGs #1 and #2 together in the same Figure-1 — because the changes that occurred between these 2 tracings are so striking. Almost every lead shows evolution!
  • Whereas the "amount" of ST elevation in the inferior leads of ECG #2 is not great — this most definitely is a dynamic ST-T wave change when you consider how flat the ST segments were in ECG #1.
  • Although the QRS in lead aVL of ECG #2 is tiny — the change from an upright T wave in this lead in ECG #1 — to a negative ST-T wave in ECG #2 is a real indication of reciprocal change.
  • The amount that the ST segments in leads V3 and V4 of ECG #2 have elevated — is even more than what one might think when you factor in the starting point of ST depression in these leads that was present in ECG #1.
  • Even the flat ST segments in leads V5,V6 of ECG #2 represent some elevation of ST segments considering the ST depression that was present in ECG #1.

The conclusion from comparing ECG #2 with the initial tracing in today's case is compelling:
  • The patient has severe Covid-related illness. He is therefore predisposed to acute cardiac disorders such as myocarditis and OMI. The onus of distinguishing between acute myocarditis vs OMI is on us.
  • While a single ECG by itself might not be able to reliably distinguish between these 2 entities — the patient has new chest pain and has clearly evolved focal ST elevation with dynamic ST-T wave changes in multiple leads.

  • BOTTOM Line: It was OK not to be 100% certain at this point in the case as to whether the patient had acute myocarditis or acute OMI (neither Echo nor troponins were yet done). Regardless — it should have already been evident that prompt cardiac cath was needed for definitive diagnosis (since you otherwise will not be able to rule out acute OMI).


at No comments:

Thursday, July 21, 2022

A woman in her 40s with intractable nausea and vomiting, dyspnea, and lightheadedness

 Submitted and written by Oriane Longerstaey MD, peer reviewed by Meyers, Smith, and McLaren


A woman in her 40s with diabetes and HLD presented with nausea and vomiting x3 days. She was seen on day 1 of symptoms at an outside ED, no ECG performed, and sent home with return precautions and zofran, which she had been taking around the clock for persistent nausea and vomiting. She presented on day 3 of symptoms because of new onset dyspnea, tachycardia, lightheadedness, and heart palpitations. She had a "burning" sensation in her chest but no "pain".



A 12 lead EKG was obtained at triage:





 - Sinus rhythm at 96 bpm
 - Narrow, normal QRS
 - ST depressions in V3-V6, II, III, and aVF, with reciprocal STE in aVR, V1, (and potentially reciprocal in aVL)
 - Extremely long QT interval due to both prolonged ST segment and prolonged T wave, concerning for acquired long QT, drug induced long QT, hypokalemia, hypomagnesemia, or Takotsubo cardiomyopathy. Long QT can be subdivided by ECG into cases with long long QT due to long ST segment (hypocalcemia), long QT due to T wave (meds, takotsubo, etc.) and long QU (usually due to hypokalemia).



The computer QT/QTc was 486/540 msec (heart rate 96 bpm).


My quick QT interval measurement is at least 520 msec, with Bazett QTc 658 msec.






Given the long QT, she was given 2g magnesium.

Her initial high sensitivity troponin I was markedly elevated at 1950 ng/L.



Repeat ECG was performed about an hour after the first:

Mostly similar.




Several repeat troponins (ng/L) were:
1688
1659
880


Cardiology was consulted and felt that the overall clinical picture was not ACS, and advised against heparin for ischemia. She was admitted to medicine.


Inpatient Course:

QTC prolongation attributed to Zofran. QT prolonging agents held.

Echocardiogram and coronary CT ordered.


Repeat EKG the next morning with worsening QT prolongation and TWI in V1, V2.

 





Formal echocardiogram:

LV: cavity size is normal, moderate to severe concentric hypertrophy, EF 61%, severe hypokinesis of the basal anterior myocardium.

RV: systolic function is mildly reduced

No significant valve stenosis or regurgitation

Pericardium: small pericardial effusion anterior to the heart and at the apex, maximal 1cm.




Coronary CT results: mild to moderate nonobstructive coronary atherosclerosis.


CALCIUM SCORE: Not performed.
CORONARY ORIGINS AND COURSE: Normal
DOMINANCE: Right dominant coronary anatomy.

LEFT MAIN: Plaque - None. Stenosis - None.

LEFT ANTERIOR DESCENDING:
Proximal- Plaque - Noncalcific. Stenosis <25%.
Mid- Plaque - Noncalcific. Stenosis <25%.
Distal- Plaque - None. Stenosis - None.
1st Diagonal- Plaque - Noncalcific. Stenosis <25%.
2nd Diagonal- Plaque - None. Stenosis - None.

CIRCUMFLEX:
Proximal- Plaque - None. Stenosis - None.
Distal- Plaque - Noncalcific. Stenosis <25%.
1st Obtuse Marginal- Plaque - None. Stenosis - None.
2nd Obtuse Marginal- Plaque - None. Stenosis - None.

RIGHT CORONARY ARTERY:
Proximal- Plaque - Noncalcific. Stenosis 25-49%.
Mid- Plaque - None. Stenosis - None.
Distal- Plaque - Noncalcific. Stenosis 25-49%.
Right Posterior Descending- Plaque - None. Stenosis - None.
Right Posterolateral- Plaque - None. Stenosis - None.

IMPRESSION:
Mild to moderate nonobstructive coronary atherosclerosis. Recommend aggressive risk factor management and medical therapy.




She next underwent EGD due to her intractable nausea and vomiting, which revealed some scattered musocal erosions but no other findings. CT abdomen was unremarkable.



After about 24 hours, her ECG began to normalize:




What happened to this patient? What is the diagnosis?

I think some unusual form of takotsubo cardiomyopathy fits best, though the echo is not at all typical of takotsubo (or of reverse takotsubo, for that matter). The CT coronary angiogram findings confirm the presence of CAD, and do not rule out ACS as the cause, but with all clinical information together it just does not seem like ACS to me. The bizzare T waves and extremely long QT remind me of many cases of takotsubo that I've seen and published on this blog. 

But there is still uncertainty in this case.



Learning points:

Current computer algorithms are suboptimal for measuring the QT interval. In this case the computer identified prolonged QT, though it still underestimated the QT interval.

We believe that bizarre long QT interval is sometimes a feature of takotsubo cardiomyopathy that may help to differentiate it from other etiologies of ECG abnormalities. It is unusual in my experience for OMI to have an extremely long QT interval.

Troponin should not be elevated in cases of simple drug-induced prolonged QT.


See these other relevant cases:











Spiked Helmet Sign







===================================

MY Comment, by KEN GRAUER, MD (7/21/2022):

===================================

Fascinating case presented today by Drs. Longerstaey and Meyers. Unfortunately — we do not have a definitive answer. That said — lack of a definitive diagnosis allows me the opportunity to offer another way of looking at this case.
  • I agree with Drs. Longerstaey and Meyers that this case most likely reflects "some unusual form of Takotusbo Cardiomyopathy".

  • Formal cardiac cath apparently was not done. Coronary CT scan revealed, "mild-to-moderate non obstructive coronary atherosclerosis". But as per Drs. Longerstaey and Meyers — synthesis of all clinical information (and especially assessment of serial ECGs) just does not appear consistent with an acute MI.

  • Assessment of LV function in today's case is limited to formal Echo results — which revealed an EF = 61%, but with severe hypokinesis of the basal anterior myocardium. Although this localized hypokinesis on Echo would seem more consistent with acute MI — as noted above, the rest of the clinical presentation in today's case is not suggestive of ACS.
  • These Echo results are clearly not consistent with typical Takotsubo — which generally presents with akinesia of the apical and mid-ventricular segments (often with apical "ballooning") — while the basal segments are hypercontractile. 

Regarding "Typical" Takotsubo:
We've reported numerous cases of Takotsubo Cardiomyopathy on Dr. Smith's ECG Blog. To name just 3 of many: 
  • In My Comment at the bottom of the page in the March 25, 2020 post in Dr. Smith's Blog — I reviewed KEY features for the ECG diagnosis of typical Takotsubo Cardiomyopathy. As a reminder — I've reproduced below in Figure-2 (from this March 25, 2020 post) — a summary for ECG diagnosis of this entity.
  • The January 22, 2018 post in Dr. Smith's ECG Blog showed the typical evolution of Takotsubo Cardiomyopathy.
  • The March 27, 2014 post reviewed tips on distinguishing between Takotsubo vs acute MI.

What About "Reverse" Takotsubo?
Areas other than the apex may be affected with disorders related to "typical" Takotsubo. Included among these is the variant known as Inverted (or "Reverse") Takotsubo Cardiomyopathy.
  • With "Reverse" Takotsubo — Echo shows sparing of the apex — with instead akinesis of the mid-ventricular and all basal LV (left ventricular) segments. That said — there can be variations and an evolution of the specific LV segments involved (Manzanal et al: Tex Heart Inst J 40(1):56-59, 2013) — Elikowski et al: Pol Merkur Lekarski 41(243):136-140, 2016).

  • The ECG pattern of "Reverse" Takotsubo is also variable — but in addition to QTc prolongation — "Reverse" Takotsubo tends to manifest diffuse ST depression rather than ST elevation or deep T wave inversion (Awad et al: Ann Translational Medicine 6(23), 2018 — Elikowski et al — with similar suggestion of this ECG pattern in the June 24, 2014 and September 4, 2018 posts in Dr. Smith's ECG Blog).

  • So, the Echo in today's case is not what we'd expect for "Reverse" Takotsubo (because hypokinesis was limited to the anterior basal segment). That said — perhaps the "moderate-to-severe concentric hypertrophy" that was found on Echo might have had an effect on contractility that altered results — and/or — perhaps the Echo pattern was in process of evolving ...

Use of the "Mirror" Test:
Since the anatomic abnormalities encountered with "Reverse" Takotsubo are in a sense, a mirror-image of what we expect to see with typical Takotsubo Cardiomyopathy (ie, basal rather than apical akinesis with compensatory hyperkinesis of other areas) — I thought it might be interesting to produce a mirror-image ECG (in which I invert the inferior and lateral chest leads, which are those leads that view the LV apex).
  • I reproduce the initial ECG on today's case in the TOP tracing shown below in Figure-1. Doesn't this initial tracing present a striking picture of diffuse ST depression with large terminal T wave positivity and a markedly prolonged QT interval?

  • After inverting the infero-lateral leads (BOTTOM tracing in Figure-1) — Doesn't the ECG picture this produces now look much more like the ECG picture of typical Takotsubo?

BOTTOM LINE — I completely agree with Drs. Longerstaey and Meyers that acute MI is an unlikely explanation for today's presentation. Serial ECGs in today's case are also not as expected for typical Takotsubo. For this reason — the most logical explanation for the overall clinical picture in today's case seems most consistent with some unusual form of Takotsubo Cardiomyopathy.
  • Although not perfect — I thought clinical features in today's case come closest to being consistent with the "Reverse" form of Takotsubo Cardiomyopathy.

  • I wish we had a definitive answer ...

Figure-1: Comparison of the initial ECG (TOP) — with superimposed mirror-image pictures of the inferior and lateral chest leads (BELOW).


Figure-2: ECG Findings in the "typical" form of Takotsubo Cardiomyopathy — adapted from Namgung in Clin Med Insights Cardiol (See text).



at No comments: