A man in his 30s with chest pain and a normal bedside echo, without wall motion abnormality

Submitted and written by Dominic Nicacio MD, peer reviewed by Meyers, McLaren, Grauer, Smith


A man in his early thirties with history of congenital aortic stenosis status post mechanical valve placement presented to the ED with acute onset chest discomfort starting at approximately 1800 while walking. His chest discomfort radiated to the jaw and was associated with shortness of breath and dizziness. The pain is constant and unrelieved by rest. No recent fevers, cough, congestion, nausea, sweats, or abdominal pain. He admits that he has not been taking warfarin as directed for his mechanical valve.

Triage vitals: BP 152/57 temp 97.6 F HR 62 RR 18 O2 100%

Triage ECG (1.5 hours after pain onset):

Three old ECGs on file (unfortunately the clinical history surrounding these ECGs was unavailable):

Prior ECG#1 (4 years ago):

Prior ECG#2 (12 years ago):

Prior ECG#3 (also 12 years ago):

Meyers comments on the ECG:

The triage ECG (at the top of the post) shows sinus rhythm, LVH, and STE in II, III, aVF, V3-V5. There is reciprocal STD in I and aVL. The concern until proven otherwise is for OMI involving at least the inferior leads. Comparison to Prior ECG#1 confirms the concern for the inferior leads, but interestingly Prior ECG#3 appears to have some similar but less dramatic characteristics. Nonetheless, these findings must be considered OMI until proven otherwise.

Exam: appears comfortable, unremarkable except mechanical systolic murmur

Bedside US:
No pericardial fluid, no dissection flap in descending aorta
Grossly normal LV/RV systolic function
No signs of RV strain
No WMA seen in limited parasternal long and high quality parasternal short views (no view of the apex obtained)
Collapsible IVC

Chest x-ray:
Mild central vascular congestion
Median sternotomy wires
Mildly increased size of cardiac silhouette
No pneumothorax
Mediastinum appears to be within normal limits



Based on history and the ECGs above, the cath lab was activated within about 15 minutes of arrival.

Cardiac Catheterization:
100% stenosed distal/apical LAD lesion with TIMI 0 flow, likely coronary thromboembolism from mechanical aortic valve with INR = 1.0. Type 2 MI due to coronary thromboembolism. Successful revascularization with balloon angioplasty with restoration of TIMI-3 flow. No disease seen in other coronaries. Distal LAD revascularized with balloon angioplasty with restoration of TIMI-3 flow.

Initial troponin = 10 ng/L (99% URL = 20 for men for this assay)

 
The patient was continued on heparin with transition back to therapeutic warfarin.


Repeat ECG after cath:

OMI findings resolving.

Repeat ECG next day:

OMI findings further resolving, and reperfusion T wave inversion beginning in lead III.

No further ECGs were recorded.

Repeat troponins:

2160 ng/L

8095 ng/L

7572 ng/L

Echo:

The left ventricular cavity size is moderately to severely dilated. Wall thickness is normal. Systolic function is normal. The ejection fraction is 67%. No segmental wall motion abnormalities.

Hospital course:
He was continued on heparin drip and transitioned to warfarin. Transthoracic echo showed moderately to severely dilated LV cavity, EF 67%. Aortic valve with severe paravalvular leak with normally functioning mechanical heart valve. Transesophageal echo showed 2 mobile echodensities concerning for thrombus or vegetation seen in the left ventricular outflow track and ascending aorta. Blood cultures showed no growth after 4 days. He was discharged home in good condition.

Learning Points:

Depending on the operator and interpreter, the ECG may or may not be more sensitive than echo for OMI.  In order to be fully sensitive, the echo must be done on all segments!  

Beware: echo, and especially bedside echo, can have false negatives!!

Even formal bubble contrast echo can have false negatives for ACS that needs emergent therapy!!

See this: What do you think the echocardiogram shows in this case?

And this: Wait until after the ECG to give Nitroglycerine

This case

Notice that this OMI had initial troponin within normal limits at approximately 1.5 hours after chest pain onset.

Type 1 AMI involves plaque rupture and thrombus formation as the cause of coronary ischemia. Type 2 AMI excludes plaque rupture, and includes essentially any other mechanism of supply-demand mismatch causing AMI. This case of coronary embolism is considered type 2 AMI.

The myocytes cannot "distinguish" between different etiologies of acute coronary occlusion. Any condition causing acute coronary occlusion and immediate cessation of blood flow can cause the OMI ECG progression. This case would be classified as "type 2" OMI. 

Lead aVL almost always shows reciprocal STD and or TWI when there are OMI findings in the inferior leads.

The inferior leads show findings from more myocardial territory than simply the inferior wall of the left ventricle. We believe the LV apex, inferior septum, and parts of the right ventricle also produce ECG changes in the inferior leads, in general. In this case, I believe that the infarcting LV apex was the source of the STE in this case. We specifically looked at the inferior wall of the LV on parasternal short axis in real time using bedside ultrasound, and found it to be contracting normally without WMA. We did not obtain a good view of the apex. Interestingly, the formal echo also did not show any WMA.

LVH can mimic OMI and conversely make OMI more difficult to identify. STEMI criteria are defined in the absence of LVH, meaning STEMI has no definition or criteria in cases of LVH. In significant LVH with repolarization abnormalities, the appropriately discordant STD in lateral leads and STE in right sided anterior leads frequently causes alarm for ischemia and false positive cath lab activations. 

Comparing current ECGs with prior ECGs has important limitations! Do not assume that "prior" ECGs are "baseline" ECGs. You must also know the events during the prior ECG to be able to compare it to the current ECG. The three "prior" ECGs available in this case are each quite different - highlighting the need to understand their context in better detail that we have available for this case.

Regardless of the ECG, this patient had classic ACS symptoms, ongoing ischemic pain, and rising troponin. Even if we didn't have the ECGs in this case, we must remember that the diagnosis of OMI can be made and supported by many other clinical features.

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Comment by KEN GRAUER, MD (6/17/2022):

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Superb case by Drs. Nicacio and Meyers — which emphasizes a number of important clinical points that are worthy of repetition:

• I've reproduced the initial ECG in Figure-1. Although I was not immediately convinced by this ECG that an acute OMI was ongoing — strong indication for prompt cath was nevertheless present, because the patient's history was typical for ACS — and his ischemic-sounding chest pain was unrelieved.
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• As helpful as availability of prior tracings can be for determining if ECG findings are "new" or "old" — I found the 3 prior ECGs on record for this patient to be confusing. Each showed a slightly different ECG picture, including: i) Change in frontal plane axis; ii) Differing QRS amplitudes; and, iii) Variation in ST-T wave morphology showing previous ST elevation on the more remote tracings — but fairly deep inferior lead T wave inversion on the more recent ECG from 4 years earlier. As per Drs. Nicacio and Meyers — not knowing the clinical circumstances present at the time these prior tracings showing different ECG findings were obtained — made it difficult to know what (if anything) the difference between the initial ECG in today's case, compared to this patient's prior ECGs meant.
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• PEARL: Over the years, I found it helpful in patients with multiple ECGs in their charts — to quickly skim through a representative sampling of their prior tracings. This can be done surprisingly quickly once you familiarize yourself with "the pattern" for that particular patient. For example, on occasion I'd see a patient with known heart disease show diffuse T wave inversion — which normalized on their next tracing — only to alternate over time between a pattern that looks ischemic, and one that does not. Awareness that such variation over time in ST-T wave morphology may occur in a given patient (similar to that seen in comparing the 3 prior tracings in today's case) — adds perspective for how to interpret your comparison with the newest ECG.

The Initial ECG in Today's Case:

I found the initial ECG in Figure-1 both intriguing and puzzling. As per Drs. Nicacio and Meyers — the presence of LVH can make the diagnosis of OMI much more challenging. Predominant posterior forces (from an enlarged left ventricle) will often reduce anterior r wave amplitude (if not result in frank anterior QS complexes). In addition — marked LVH that manifests with deep anterior S waves will often present with anterior ST elevation (ie, the "mirror-image" of LV "strain", that in lateral chest leads manifests as ST-T wave depression — as per My Comment in the June 20, 2020 post in Dr. Smith's ECG Blog).

• Although today's patient was a young adult in his 30s — he had a long history of heart disease (ie, with congenital aortic stenosis requiring valve replacement). So it was no surprise that ECG criteria for LVH were easily satisfied with the finding of exceedingly deep chest lead S waves (ie, 33, 26 and 31 mm in leads V2, V3, V4) — with delay in transition until lead V6 because of such marked precordial lead S wave predominance.
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• The finding of most concern in ECG #1 was ST elevation in each of the inferior leads — with reciprocal changes in high lateral leads I and aVL. That said, in view of how marked the increase in QRS amplitudes from LVH was — I thought the amount of inferior lead ST elevation was relatively modest (and a bit less, but otherwise not overly different from the ST-T wave appearance in the limb leads on prior ECG #3).

The "shape" of the ST-T wave in each of the 6 chest leads of ECG #1 is different — such that I wasn't sure how to interpret these findings. 

• The T wave inversion in lead V1 is not necessarily abnormal. But I thought the horizontal "ledge" for the ST segment in lead V2 (before finishing in an independently peaked T wave) looked strange — and not at all typical for the anterior lead appearance of LV "strain".
• I thought the ST-T wave appearance in leads V3 and V4 to be consistent with LV "strain" — although why with similar S wave depth, the T wave peaking in lead V4 should be so much more marked than in lead V3 was uncertain to me.
• The ST segment "takeoff" in lead V5 then straightened — but given the modest J-point ST elevation in this lead with a 19 mm S wave, I was again uncertain about distinction between LV "strain" vs the ST elevation from OMI. 
• The ST segment then flattened in lead V6 — but I wondered if transition from predominant precordial S waves to the relatively small R wave in lead V6 might account for this.

Figure-1: The initial ECG in the ED.

I saw 2 additional ECG findings of interest in Figure-1:

• There is definite RAD (Right Axis Deviation) — as determined from the small, but entirely negative QRS complex in lead I. The fact that the P wave in lead I is positive — with global negativity (of P wave, QRS and T wave) in lead aVR — means that this is not LA-RA lead reversal. Instead, from a "pure" ECG interpretation perspective — the presence of RAD in association with marked LVH voltage should immediately suggest the possibility of RVH. Suspicion of RVH provided yet one more reason for my uncertainty in assessing the acuity of this initial ECG. (To note that subsequent Echo revealed no sign of RV strain.).
• P wave morphology is highly unusual. All limb lead P waves are of extremely low amplitude — with a tiny bizarrely notched P wave in lead II. Yet the P wave in lead V1 is huge — with a tall, pointed initial positive component. Is this a sinus rhythm? An ectopic atrial rhythm? Or — despite the lack of prolonged P wave duration — Does the subtle P wave notching in multiple leads reflect some type of intra-atrial conduction defect?

In conclusion — our THANKS to Drs. Nicacio and Meyers for presenting today's case. As interesting as I found the initial ECG to be — the KEY point in today's case is that identification of suspicious (albeit indefinite) ECG findings in this patient with typical unrelieved chest pain merited timely cath (which was done within 15 minutes of ED presentation) — and this confirmed the need for prompt revascularization.