Emergent angiogram (KG- Done) nine months too late

Written by Willy Frick

This case is divided into two separate hospitalizations about 9 months apart.

Part 1

A man in his late 60s with hypertension, hyperlipidemia, type 2 diabetes mellitus, and a 50 pack-year smoking history presented at around 10 AM with acute onset chest pain which began several hours earlier while he was at home. He described it as a squeezing sensation across his chest radiating into the jaw. Before you see the ECG, you know the diagnosis.

ECG 1

What do you think?

This ECG is diagnostic for inferolateral OMI. Most blog readers will recognize this one, and the Queen certainly had no trouble.

Smith: This shows the beginnings of reperfusion, with a downturn of the T-wave in III and aVF, and upturn of the T-wave in aVL.  It is "between" active and reperfused. Although not specified, I would bet that the patient's pain is improving or completely resolved.

ECG 1, QOH Explainability

This was interpreted by the emergency physician as "sinus bradycardia, ventricular rate 55, nonspecific T wave abnormality." No explanation for the delay, but 20 minutes later the physician ordered aspirin 325 mg, sublingual nitroglycerin, and troponin. There is very scarce documentation regarding progression of symptoms.

About an hour after the first ECG, cardiac troponin I (cTnI) resulted at 27.157 ng/mL (ref. < 0.033), already a huge infarct. The facility did not have cath lab services available, and apparently this troponin prompted a call to a PCI-capable facility, although the exact timeline is not clear from the notes. Repeat ECG was obtained.

ECG 2

There is some baseline wander, but it appears now completely reperfused compared to the first ECG. Patient was reportedly asymptomatic. Confusingly, this ECG is interpreted as showing "interval development of mild ST elevation in lead III, borderline ST elevation, less than 1 mm in II and aVF. Reviewed ECG with [accepting cardiologist at PCI facility] agrees no STEMI." It seems as if the baseline artifact was misinterpreted as developing STE, but this was still not considered an emergency.

At this point, the patient was listed for "priority transfer" for diagnosis NSTEMI. He received a dose of therapeutic enoxaparin and clopidogrel 600 mg. There is almost no other documentation regarding the time the patient spent waiting for transfer, although a repeat cTnI 3 hours after the first was 39.444 ng/mL.

At around 4 PM (six hours after ECG 1) the patient was loaded into an ambulance for transfer. Documentation at the receiving facility is also a bit sparse and confusing. The ambulance ride is about 15 minutes between facilities, but the next ECG (at the receiving facility) was not obtained until 7 PM, and it is shown below.

ECG 3

This ECG had the magic words printed at the top of the page.

At some point, the patient apparently had return of symptoms. He was taken for cath where he had acute thrombotic occlusion of his mid LCx which was stented. In addition, he had severe (likely non-culprit) disease in his RCA which was stented, and moderate stable disease in the LAD, angiographically graded as 60%.

Critically, because all prior ECGs were interpreted as NSTEMI, the door to balloon (D2B) timer officially begins with ECG 3. In other words, for the purposes of quality improvement efforts, this is considered a success.

Part 2

About 9 months later, the patient was admitted with sepsis secondary to complicated urinary tract infection. He has bladder cancer and obstructive uropathy which has been treated with percutaneous nephrostomy tubes. In addition, he had developed chronic HFrEF with EF 35% and inferolateral akinesis. While being monitored on telemetry, he developed salvos non-sustained ventricular tachycardia. The first ECG did not capture the VT.

ECG 4

Sinus tachycardia (always worrisome) with old inferior infarct. The patient was reportedly resting comfortably in bed. Repeat ECG was performed during an episode of sustained ventricular tachycardia.

ECG 5

In addition to being diagnostic for monomorphic VT, we can deduce the etiology. Note that the QRS is negative in the inferior leads (i.e. superior axis). This is because the tachycardia originates in the inferior wall and spreads outward (i.e. upward). This is scar mediated VT from the patient's prior OMI. There is no evidence for acute ischemia (consistent with the patient's lack of ischemic symptoms). The patient was started on amiodarone, but had recurrent VT prompting the addition of lidocaine. Still, he had more VT. 

Brief aside

It is important to know that most monomorphic VT is scar mediated. (In comparison to polymorphic VT which is often due to acute ischemia.) In this patient with known prior inferior OMI, lack of ACS symptoms, and VT with superior axis, scar mediated VT is essentially certain. When sustained VT occurs 3 or more times in a 24 hour period, we call this "electrical storm" (ES). ES is typically propagated by high adrenergic state. And it is clear this patient has high adrenergic state given his sepsis and sinus tachycardia (when he is not in VT).

The most effective medical therapy for ES is the combination of amiodarone and propranolol. In fact, the non-selective beta blocker propranolol outperformed metoprolol for management of ES in a randomized trial. Lidocaine has little role in the management of VT which is not due to acute ischemia and is inferior to beta blockers, procainamide, and sotalol.

Similarly, heart catheterization is very unlikely to be beneficial in ES in patients with monomorphic VT. In fact, Cleveland Clinic published their case series of patients with monomorphic VT causing ES and found that ischemic evaluation revealed ZERO acute culprits. Nevertheless, it is tempting for clinicians to think of monomorphic VT as an ACS presentation.

Back to the case

Indeed, the physician taking care of the patient documented "given VT storm and known unrevascularized LAD territory, decision made to activate cath lab." To translate this, the patient had known stable disease in the LAD from the prior angiogram 9 months ago and the physician is considering whether that could be to blame for the current VT. This is unlikely for the two reasons discussed above:

• First, the VT has a superior axis since it is originating from the inferior wall which is unlikely to be supplied by the LAD.

• Second, the VT is monomorphic which is likely scar mediated. The likelihood of an acute culprit in a patient with monomorphic VT and no ACS symptoms is exceptionally low.

Coronary angiogram revealed no acute culprit, and troponin was undetectable.

The time for emergent cath was 9 months ago.

Learning points:

• Quality improvement efforts consistently conceal missed OMIs, systematically biasing the literature and disguising shortcomings of the STEMI paradigm

• Monomorphic VT is usually scar mediated, not due to ACS

• First line treatment of electrical storm is amiodarone and propranolol, lidocaine is less effective

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

MY Comment, by KEN GRAUER, MD (6/6/2025):

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

Today's 2-Part case by Dr. Frick contains much wisdom in his summarizing 3 powerful Learning Points. I focus my comment on a 4th essential Learning Point = The initial ECG in Part I of this case must not be interpreted as showing, a "nonspecific T wave abnormality". Awareness of this point would have expedited the emergent cath that should have been done immediately after seeing the initial ECG in Part I of today's case.

For clarity in Figure-1 — I've reproduced and labeled this initial ECG.

• The history is important. The patient in today's case is a man in his late 60s, who presented in Part I with strong coronary risk factors and several hours of sudden and severe new CP (Chest Pain). As per Dr. Frick — regular readers of this ECG Blog knew the diagnosis even before seeing the initial ECG.
• As per Dr. Smith — there is no indication as to the presence or severity of CP at the time that ECG #1 was recorded. This historical information is critical, although it is all-too-often ignored. IF (as Dr. Smith suspects) this patient's CP had decreased or resolved at the time ECG #1 was recorded — it would essentially confirm that this initial tracing represents an acute OMI that now shows reperfusion T waves. And because the "culprit" artery is in process of reperfusing — we are unlikely to find sufficient ST elevation to qualify as a STEMI.
• As a result of the preceding bullet — the 5th essential Learning Point in today's post is that you are unlikely to see enough ST elevation to qualify as a STEMI if the patient's acute OMI is in process of reperfusing. As a result — we need to stop looking for ST elevation in such tracings, and instead focus on the other ECG findings that confirm the diagnosis.

The Important ECG Findings in ECG #1:

As per Drs. Frick and Smith — ECG #1 is diagnostic of acute infero-postero-lateral OMI, now showing reperfusion T waves.

• My "eye" was immediately drawn to leads III and aVF (within the RED rectangle in Figure-1). There is ST elevation in both of these leads. The amount of ST elevation is not a lot in absolute measurement — but shape is more important than amount (albeit considering small size of the QRS in these inferior leads — the relative amount of ST elevation is considerable). 
• The shape of the elevated ST segments in leads III and aVF is coved — and — the mirror-image opposite shape of the subtle-but-real ST depression in lead aVL confirms that this high-risk patient with several hours of new, severe CP has had an acute inferior OMI (ie, lead aVL clearly shows reciprocal ST-T depression that confirms acute inferior MI — this being the "magic" relationship between leads III and aVL with acute inferior MIs that we often refer to — as per My Comment in the June 10, 2025 — the May 10, 2025 and the July 11, 2018 posts, among many others).
• In addition — there is also T wave inversion in leads III and aVF, suggestive of at least some degree of reperfusion.
• Subtle supportive findings of the above findings are seen in lead II ( = the 3rd inferior Iead — with subtle hyperacute shape of its ST segment takeoff and a hint of beginning T wave inversion) — and — in lead I ( = the other high-lateral lead that shows a similar subtle coved ST depression as we see in lead aVL).
• Indication of acute posterior OMI — is forthcoming from the already tall R wave in lead V2, that manifests a taller-than-expected T wave following a longer-than-expected flattened ST segment — consistent with posterior reperfusion.
• There is no ST elevation in lead V5. But there is subtle ST elevation in lead V6, indicative of lateral OMI (shape being more important than the amount of this elevation).
• To Emphasize: The findings that I report in leads I, II, V2 and V6 are very subtle — and may not be appreciated by even experienced providers. But the diagnostic ECG findings of acute inferior OMI in leads III,aVF and lead aVL need to be looked for given the history in today's case that, as per Dr. Frick — all-but-tells-us the diagnosis even before we see the ECG!
• 6th essential Learning Point — When we recognize several leads (such as leads III,aVF, aVL in today's case) that we know are diagnostic of acute OMI — then IF we hone our attention looking for more subtle abnormalities — we will often find them in other leads, as we do here in leads I,II V2 and V6.

Figure-1: I've reproduced and labeled today's initial ECG.