Sent by anonymous, written by Pendell Meyers
A male in his teens presented with complaints of chest discomfort and dyspnea beginning while exercising but without obvious injury. He immediately stopped exercising and symptoms started to improve. Later that evening he felt recurrent central chest discomfort, shortness of breath, and vomited. Symptoms have been constant since this second episode, and are still present on arrival, which seems to have been less than 1 to 2 hours from onset of symptoms. No similar symptoms in the past. No prior exertional complaints of chest pain, dizziness, lightheadedness, or undue shortness of breath. No family history of sudden cardiac death, cardiomyopathy, premature CAD, or other cardiac issues. He denied headache or neck pain associated with exertion.
Initial vitals: BP 116/84, RR 36, HR 85 bpm, SpO2 98% on RA
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| What do you think? |
Meyers ECG Interpretation: Easily diagnostic of LAD occlusion. Sinus rhythm, normal QRS (except for the poor R wave progression from the LAD OMI), then very obvious STE from V2-V6, Hyperacute T-waves in V2-V6, I, aVL, II, III, also TQRSD in V6 (only described as diagnostic of OMI if in V2-V3 in literature thus far). This is not "diffuse", this is simply anterior, lateral, and likely apical. 50% of LAD STEMIs do not have reciprocal findings in inferior leads, and many LAD OMIs instead have STE and/or HATWs in inferior leads instead. The ECG easily meets STEMI criteria in all leads V2-V6, as well. This was sent to me with no information and I immediately replied that it was diagnostic of LAD OMI. I calculate the 4-variable early repol vs. anterior OMI formula result at 22.34 (heavily favoring LAD OMI) using approximately 4mm STE at 60 msec after J point in V3, QTc 425, 2 mm R wave in V4, 23 mm QRS in V2.
I sent this ECG to Dr. Smith, with the only information that it is a 17 year old with chest pain. His answer was identical:
"Massive LAD OMI. Cath Lab."
"Might be an unusual myocarditis, but OMI until proven otherwise."
The ECG was interpreted as "benign early repolarization."
Initial POC Troponin I (reference range: less than 0.05 ng/mL) resulted in triage at less than 0.05 ng/mL (lower than level of detection).
CBC and BMP were within normal limits.
He was given lorazepam and olanzapine for anxiety and discomfort.
Two hours after arrival he complained on ongoing chest discomfort. He was questioned about any potential drug use, and he admitted to some marijuana after working out. He was given ketorolac and IV fluids. Urine toxicology was sent.
Three hours after arrival a repeat troponin was ordered.
This 2nd troponin returned elevated at 0.39 ng/mL.
A 3rd troponin resulted 30 minutes later at 0.88 ng/mL.
A repeat ECG was done approximately 4 hours after arrival, with ongoing pain (approximately 6 hours since pain onset as far as we can tell):
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| New RBBB, developing anterolateral pathologic Q waves, and progressing terrible LAD OMI. |
At this point a "cardiac alert" was activated, and the on call cardiologist reviewed the ECG and "did not think that he needed emergent catheterization." The patient was transferred to a tertiary care center and admitted to the PICU.
He spent several days in the PICU, undergoing workup including:
Serial troponins: rising from 5,700 ng/L (unknown if I or T) to greater than 25,000 ng/L (greater than the lab's upper limit of reporting). No further troponins were measured.
CT angiogram chest: no aortic dissection or pulmonary embolism.
Serial chest xrays: progressive bilateral pulmonary edema.
Echo: severely dilated LV, severely reduced EF at 10%, severe hypokinesis of LV from mid-apical segments with basal segments better preserved. "Pattern consistent with Takotsubo's cardiomyopathy." No apical thrombus noted using Definity contrast.
Coxsackie serologies negative.
Covid PCR negative.
UDS positive for marijuana only.
He was then transferred to quaternary care childrens hospital. There, troponins were trended up to 100,000 ng/L (still unknown if troponin I or T). Repeat CT angio chest (not CT coronary, unclear what protocol) showed possible LAD aneurysm and thrombus.
Finally, coronary angiography was performed (at least 5 days after presentation) which confirmed LAD aneurysm with large thrombus burden, TIMI 0 flow, thrombectomy performed. No further cath details available.
There was a suspicion of potentially undiagnosed Kawasaki disease as a child.
Cardiac MRI showed EF 25% with similar regional wall motion abnormalities. He was transitioned to oral heart failure medications and discharged home slightly over one week after presentation.
He was readmitted a few weeks later for a heart failure exacerbation, diuresed, and discharged again.
The last information available is that the patient was undergoing heart transplant evaluation.
Smith Major Learning Point:
The worst risk factor for a bad outcome in OMI is young age because cardiologists cannot believe that a young person can have an OMI. This gets drilled into them.
This case reminds me of this 27 year old totally healthy nurse who was previously healthy, presented with acute pulmonary edema and the below ECG that is diagnostic of proximal LAD occlusion, and was dismissed because of her age. Only after her troponin peaked at 500,000 ng/L did she get her angiogram, which showed a 100% left main occlusion due to ruptured plaque. She died before she could get a heart transplant. They just could not believe that a young woman could have an OMI.
RBBB, LAFB, and STE in I, aVL, V2 and V3.
Diagnostic of Massive OMI. Turned out to be 100% left main.
Here she is a few hours later, with new Q-waves and rising troponin. They still would not do angiography for her:
See other cases of young patients with OMI:
See this case of essentially the opposite mistake:
Learning Points:
ECG interpretation skills are critical to diagnose OMI. Use the formula (Subtle Anterior STEMI Calculator (4-Variable) - MDCalc) to help when the differential is normal variant STE ("benign early repolarization") vs. anterior OMI.
Young people can suffer acute coronary occlusion, whether by typical atherosclerotic plaque rupture, or by coronary anomalies, coronary aneurysms, dissections, spasm, etc.
In the future, an emergent CT coronary angiogram could be a reasonable option when OMI is not already diagnosed by ECG, but cardiology is reluctant to perform coronary angiography.
The wall motion abnormalities of Takotsubo cardiomyopathy and LAD OMI can be similar.
A false positive catheterization with no intervention in a young patient is nearly harmless. A missed OMI like this can be devastating.
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My Comment by KEN GRAUER, MD (1/9/2023):
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“Treat the patient — Not the age of the patient”. Today’s sad case is one for medical review. There is unfortunately no way to justify the sequence of events with resultant delay in diagnosis and treatment — and ultimate catastrophic infarction that rendered a previously healthy teenager a candidate for cardiac transplantation.
Acute MI CAN Occur in a Younger Patient
The tendency to discount new chest pain in a teenager as the 1st symptom of acute MI is understandable. Acute coronary occlusion almost always occurs in patients who are well beyond their teenage years. That said — acute MI does occur in younger patients (witness the case referred to above by Dr. Smith — as well as the links from Dr. Meyers at the end of his discussion that refer to multiple cases published on Dr. Smith’s ECG Blog of young adults with acute MI).
- There is a literature on this subject (GGF van der Schoot et al: Neth Heart J 28(6):301-308, 2020 — and — Egred et al — Postgrad Med 81(962): 741-745, 2005 — to name just 2 reports).
- Acute MI in younger patients may result from acute coronary occlusion precipitated by conventional risk factors (such as smoking begun at an early age) — in individuals with special predisposition (ie, a factor V Leiden mutation — or nephrotic syndrome — both being correlated with a hypercoagulable state) — and/or in familial entities such as genetic hypercholesterolemia.
- In addition — there is a series of nonatherosclerotic potential causes of acute infarction in younger patients. These include coronary artery spasm (as may occur from cocaine use or binge alcohol drinking) — myocardial bridging (that may be the cause of intermittent acute ischemia) — aberrant anatomy of a coronary artery (which may present with sudden rupture causing acute infarction or sudden death at any age!).
- Other types of nonatherosclerotic potential causes of acute infarction in younger patients include systematic inflammatory disease (ie, lupus, rheumatoid arthritis, Wegener granulomatosis) — thrombosis not due to coronary disease (ie, endocarditis, coagulation disorders) — pregnancy (with its hypercoagulable state).
- Causation of Endothelial damage is another potential mechanism of acute MI in a younger patient. This may occur as a result of blunt chest trauma or other acute stress that produces a sudden extreme shear force on a coronary artery (that can result in an intimal tear that leads to intraluminal thrombosis). Endothelial damage may also be seen with spontaneous dissection of a coronary artery — or result from “deceleration trauma (ie, from an auto or other vehicular accident).
- BOTTOM LINE: While the above etiologies are not common causes of acute infarction in an adolescent or young adult — they do occur! And, like most diagnostic considerations in medicine — if the differential diagnosis excludes such “other potential etiologies” simply because they are not common, or because the patient is “too young to have a heart attack” — then these other potential etiologies will be missed!
- RELEVANCE to this Case: Today’s teenage patient was “lifting weights” at the time his symptoms began. Was this coincidence? — OR — Could severe exertion and straining from lifting weights have precipitated an acute shear force — with resultant intimal tear, leading to intraluminal thrombosis (a sequence of events that might become that much more likely if this seemingly healthy young adult had some previously unrecognized predisposition, such as an anatomic coronary artery anomaly).
More Regarding Today’s CASE: Treat the Patient …
As I go back and reread the history in today’s case — I am struck by the facts in this patient’s presentation: i) The patient was a previously healthy teenager. He had not had chest pain in the past!; ii) This patient developed new chest pain and dyspnea severe enough to cause him to immediately stop his workout; and, iii) Although he temporarily felt better after stopping his workout — his symptoms recurred and were severe enough to prompt his trip to the ED that evening for persistent severe chest pain.
- BOTTOM LINE: Armed with the knowledge that acute MI can occur in younger patients — the above history places the “onus of proof” squarely on us as the medical provider, to rule out some type of acute event — rather than the other way around. We have to prove that this patient with new and severe ongoing chest pain is not having an acute event (or some other potentially treatable cause of his symptoms).
- Active search for the cause of this patient’s persistent severe chest pain is not served by waiting 4 hours before repeating the initial ECG (especially given troponin values that are beginning to rise in the face of persistent severe chest pain).
- It is also not served by cancelling the cath lab activation despite the obvious dynamic changes on the repeat ECG showing new RBBB with persistent ST elevation in the face of persistent chest pain.
- P.S.: Although the initial ECG in today’s case does not look like acute myocarditis — it's important to include this consideration whenever a younger patient presents with chest pain and acute ECG changes. Acute myocarditis is not uncommon among younger patients — and there are times when distinction between acute myocarditis vs acute OMI in a younger patient with acute-looking ECG changes and troponin elevation can only be made by cardiac catheterization.
FINAL Thoughts: Believe the ECG Despite the Patient’s Young Age
Dr. Meyers has detailed the ECG findings in the initial tracing from today’s case. This is not subtle. For clarity in Figure-1 — I've repeated this initial ECG. I'll emphasize the following:
- The height of the hyperacutely elevated ST-T wave in lead V4 of the initial ECG is nearly twice the amplitude of the QRS complex in this lead. This disproportionate increase in T wave size is not a repolarization variant.
- As noted by Dr. Meyers — Hyperacute T waves are clearly present in 5 of the 6 chest leads. In association with these hyperacute chest lead T waves — the lack of r wave progression (ie, there is no more than a 1-2 mm r wave is seen in the first 4 chest leads) — tells you this is not a repolarization variant.
- We define “hyperacute” T waves as being taller-than-they-should-be — being “fatter”-at-their-peak and wider-at-their-base than expected given QRS amplitude in the respective lead. The dramatically widened base of the T waves in lead V4 and lead V5 is not the result of a repolarization variant.
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| Figure-1: The initial ECG in today's case (from a male teenager with chest pain). |
Bottom Line in Today’s CASE:
Errors in diagnosis and management are multiple in this case.
- From what I read — this case should be reviewed. What happened to the patient in today's case should not happen again.
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