Profound ST depression in II, III, aVF

This 29 year old African American patient was found down, unconscious, not breathing and was given 2 mg of intranasal naloxone by a bystander.  He then received bag-valve-mask ventilations for several minutes until he became responsive.

He had a prehospital ECG that was worrisome to the medics, so they called me to see him at the door.

On arrival to the ED, the patient was diaphoretic, tachycardic. and had dilated pupils. He was alert and oriented.  He remained somewhat altered, and history was not reliable.

His prehospital ECG showed "inferior" ST depression and high voltage, with tachycardia. I did not think it was due to ACS, but we ordered an ED ECG immediately:

What do you think?

There is profound "inferior" ST Depression. Usually, this is reciprocal to high lateral ST elevation which may be very subtle.  But in this case the clinical scenario is not right for acute ACS with OMI, and there is very high voltage, and the patient is very young, (though beware of young patients, even 29 year olds!!, both here and here).  

The precordial findings are typical for a young AA male  See 20 similar cases here.

I suspected no OMI, that this could be due to LVH plus tachycardia.  I was not worried for a coronary etiology.

But I wasn't certain, and so we planned on a Bedside echo (which was normal), and serial troponins.

Looking through the records, we found an ECG from 2 years prior:

There is some similarity in the inferior leads, so I suspected that today's ECG was an exaggeration of this STD

ECG 2 years prior at slower heart rate

At a slower heart rate, there is less STD

I sent today's ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict:

First hs-troponin I returns at 250 ng/L.

4.5 hours ECG:

Not much change

hs troponin I peaks at 500 ng/L

8 hours

Next morning

Urine drug screen: 

Amphetamine, Methamphetamine, Fentanyl, Fentanyl metabolite

Formal Bubble Contrast Echocardiogram:

Indications for Study: Silent Ischemia.

 

SUMMARY

 

Normal left ventricular cavity size.

Normal estimated left ventricular ejection fraction .

No wall motion abnormality .

The estimated left ventricular ejection fraction is 67 %.

The estimated pulmonary artery systolic pressure is 29 mmHg + RA pressure.

Conclusion:

Type II MI probable due to hypoxia and tachycardia from resp arrest and amphetamine use.  Whether the ST Depression on the ECG represents ischemia or not is uncertain, but it does not represent acute coronary syndrome.

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MY Comment, by KEN GRAUER, MD (7/27/2023):

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The most interesting aspects of today’s case are: i) The tale told by the 6 ECGs; and, ii) The surprise finding of positive troponins! 

The Sum is More than Each of its Parts:

If we look back at the initial ECG in today’s case — it’s easy to let one’s attention be “captured” by the inferior lead ST depression (especially the “eye-catching” sharp and deep descent of the ST segment in lead III) + the mirror-image opposite shape of the ST elevation (with overly straight ST segment take-off) in lead aVL. Under most circumstances — this combination of ECG findings would point to an acute event. But — the sum of this initial ECG is more than each of its parts. Regarding specifics of this initial ECG:

• QRS amplitude in multiple leads is huge! Even though I did not know the patient’s age at the time I saw this initial tracing — it was obvious that voltage for LVH would be easily satisfied. The lateral chest lead ST depression (with terminal T wave inversion in leads V4,V5) supports my impression of marked LVH by the typical ST-T wave appearance of LV “strain”.
• 
  
• PEARL #1: The frontal plane axis in this initial ECG is vertical (small amplitude, nearly isoelectric QRS in lead I — in the face of huge inferior lead R waves). Increased voltage and ST-T wave changes of LV “strain” are commonly seen not only in lateral leads, but also in inferior leads in the presence of marked LVH when there is an inferior frontal plane axis. Given my initial “sum” impression of this tracing (ie, marked LVH with LV “strain”) — I did not think the inferior lead ST depression was disproportionate in view of the relatively fast heart rate (of ~90/minute) and the huge inferior lead R waves of >25mm!
• 
  
• Additional notable findings on this 1st ECG included: i) Very deep infero-lateral Q waves (ie, >8mm in lead III!); — ii) A surprisingly tall R wave (>10 mm) as early as lead V2; — iii) ST elevation with an alarmingly straight ST segment takeoff in lead V2; — and, iv) An unusual biphasic T wave appearance in lead V3.
• 
  
• My Impression of this 1st ECG: Taking all of the above findings into account, I thought — The sum is more than each of its parts! Even without yet knowing the full history — I interpreted this 1st ECG as showing marked LVH with LV “strain” — perhaps in an African-American young adult male with a component of a repolarization variant — but not suggestive of acute OMI. I was not expecting troponins to be positive.

The Sum Total of All 6 ECGs:

Rather than describe all findings on each of these 6 tracings — I thought the “overall picture” conveyed by these tracings provided the more important message. Markedly increased QRS amplitude was seen in each tracing.

• Prominent J-point notching with ST elevation typical of a repolarization variant was seen in prior tracings (both of which were recorded at slower heart rates). The relative amount of inferior lead ST depression was clearly less in these earlier tracings.
• On the 4 serial ECGs recorded on this current admission — heart rate was extremely variable — slowing to ~80/minute @ 4.5 hours after admission — but increasing to a surprisingly fast 135/minute on the ECG done the next morning. The “theme” of ST-T wave appearance over the course of these 4 serial tracings — was a lessening of the ST depression, with nonspecific ST-T wave flattening in the most tachycardic tracing recorded the following morning.
• 
  
• BOTTOM Line: While possibly indicative of some ischemia — my “sum total” assessment of the 4 serial tracings from the current admission, in the context of the 2 prior tracings — was marked LVH with a repolarization variant + rate-related ST-T wave changes reflecting this patient’s evolution of his underlying medical condition — but nothing to suggest an acute cardiac event.
• 
  
• PEARL #2: Although I always advocate systematic interpretation with lead-to-lead comparison of serial ECG changes — Sometimes you just have to “stand back” from the tracings and take in the “overall theme” of what these multiple ECGs are showing. While impossible to explain the nuances of all changes on the above 6 ECGs — the “theme” is no acute OMI.

Positive Amphetamines:

While we don’t know details of this patient’s medical admission that might account for the fastest heart rate being seen on his last ECG (done the next morning) — the most plausible explanation is longterm drug abuse with acute use of amphetamines.

• Peak plasma concentration of amphetamines is rapid (within minutes) following inhalation or injection. The duration of amphetamine effect is highly variable (depending on multiple factors) — but may last hours, which may account for this patient’s labile vital signs even on the day after his admission!
• Potential cardiovascular effects of acute amphetamine use are multiple. While hypertension and sinus tachycardia are the most common manifestations — a variety of other tachyarrhythmias (including VT leading to cardiac arrest) and acute MI may be seen.
• 
  
• PEARL #3: The pathophysiologic mechanism for producing amphetamine-induced acute MI is unclear (Bazmi et al — SQUMJ 17(10); e31-37, 2017 — and — Sinha et al — Case Rep Cardiol, 2016). Possible explanations include: i) Coronary vasospasm, with a brief period of coronary occlusion; ii) Supply-demand mismatch (Type II MI) — precipitated by amphetamine-induced catecholamine surge; and/or, iii) Catecholamine-mediated platelet aggregation with subsequent thrombus formation. While OMI from acute thrombus formation is the least common of these mechanisms — acute thrombotic coronary occlusion can occur (Vichairuangthum — Arch Med Sci Atheroscler Dis 5:e45-48, 2020).

BOTTOM Line in Today’s CASE:

I was surprised by the elevated troponins in today’s case. That said — adverse effects of acute amphetamine use are well documented — and it is important to remember that acute MI from one of several potential mechanisms must be considered.

• An OMI is always a possibility with acute amphetamine use. That said — the nature of the serial ECGs in today’s case + bedside Echo that failed to show any localized wall motion abnormality excluded the need for cath lab activation in today’s case.
• In Retrospect — the marked inferior lead ST-T wave depression on the initial ECG most probably was a reflection of this patient’s Type II MI — as these inferior lead changes lessened with subsequent tracings. That said — providers were aware of the increased troponins, and clinical management throughout the case was completely appropriate.