Can you localize the culprit lesion on angiogram without taking ECG findings into account?

Written by Willy Frick

A woman in her 60s with very severe hyperlipidemia (LDL >200 mg/dL) presented with acute onset chest pain. Her symptoms began while getting off the bus. She described the pain as moderate in severity, and said it had come and gone several times over the next few hours before ultimately resolving. On day of presentation, the pain returned and was very severe with associated dyspnea and vomiting. Given this, the pre-test probability of OMI is very high. High enough that a bland ECG is not immediately reassuring.

ECG 1

What do you think?

To me, this ECG is not diagnostic. The inferior T waves are a bit generous, but they could be baseline. There is low voltage in the precordium which always makes reading ischemia harder. There is sort of an eerie flatness to the ST segments in V2-3. But if you call every ECG that looks like this OMI, you are going to have a lot of false positives. In the ER, the patient received nitroglycerin paste. Pain was unresolved, so she received a nitroglycerin tablet and IV morphine with resolution of her pain.

Smith: it is highly suspicious for inferior OMI, but not 100% diagnostic. It has some morphologic features of LVH, but not the voltage. The Queen of Hearts does not diagnose OMI.  

In ACS, chest pain is the warning sign of ongoing ischemia. I have said before, treating angina with morphine and continuing non-emergent management is like taking the batteries out of an actively alarming smoke detector during a house fire and going back to sleep.

Smith: As Willy says, and as we've said many times before, morphine will resolve pain without resolving ischemia.  So ongoing symptoms must be assumed if opiates have been given.  ONLY give opiates if the pain is intolerable or you will activate the cath lab at the first objective evidence of coronary ischemia.

No further ECGs were obtained for the rest of the day. The first high sensitivity troponin I (hsTnI) was 745 ng/L.  

Smith: At this point, it is acute MI with presumed persistent refractory symptoms and the cath lab should be activated.

Case continued

Alas, this simple rule was ignored.

Subsequent troponins climbed: 588 ng/L, and 4189 ng/L (reference: < 14 ng/L). The following tracing is taken from telemetry around midnight:

From chart review, it looks as if VF persisted for 20 minutes before successful termination. Documentation indicates that the patient was shocked 4 times (with no comment on energy level) and received amiodarone 300 mg IV and magnesium 2 g IV. Getting patients out of VT/VF is the number one priority. A shock can fail for two reasons, and this can be addressed with two different approaches:

1. The shock terminates VT/VF, but then it comes back immediately
2. The shock never terminates VT/VF, even for a second

In the first case, the shock did its job but there are other factors promoting VT/VF such as unrevascularized ischemia. In this case, you can give anti-arrhythmics and address the underlying cause (OMI). In the second case, the patient never converted meaning the shock did not do its job at all. In this case, you should get a second defibrillator and perform double sequential external defibrillation (DSED). Simply attach a second defibrillator as shown in the diagram below and deliver max shocks from both devices simultaneously.

Smith: often, providers think that the above rhythm is torsade (or polymorphic VT due to long QT).  But torsades and ventricular fibrillation cannot be distinguished by the monitor.  They can only be distinguished by:

1) if there are pulses, then it is not VF

2) if it spontaneously resolves, then it is not VF, with rare exceptions

DOSE VF, New England Journal 2022

Remember that in the trial DOSE VF, pre-hospital use of DSED increased the likelihood of survival to hospital discharge by 17.1% in absolute terms! That's a number needed to treat of just under 6 and it costs almost nothing.

Back to the case:

Repeat ECG after return of spontaneous circulation is shown.

ECG 2

We now have clear inferior, posterior, and lateral OMI. The patient was taken to lab for coronary angiography. All the angiograms (and much more) are available on the angiography guide if you wish you read in more detail.  For this post, I have included the most important angiogram followed by my narrated explanation. The rest of the angiograms are here.

And here is my narrated explanation:

The patient had intervention to his proximal LAD. No intervention was performed on the LCx. The report says that there was "occlusion of a smaller lateral branch." Repeat ECG twelve hours later is shown below.

ECG 3

This ECG shows persistent posterolateral occlusion. The inferior infarct appears nearly complete (prominent Q-waves with T-wave inversion).  Thus, it appears as if the top ECG was truly an inferior OMI. There is no evidence of reperfusion, only progression of untreated infarct. Serial hsTnI beginning at the time of the arrest were 9652 ng/L, 12,747 ng/L, and 21,112 ng/L. None further checked. Echocardiogram was technically difficult but showed preserved ejection fraction and mid to distal inferolateral hypokinesis.

The patient remained intubated for several days following this. Even after extubation, she was amnestic for the events leading up to hospitalization, so it is unknown whether she was experiencing persistent chest pain while intubated after stent to the LAD. She was awake and following commands, but no more specific details about her neurologic exam are available.

Discussion:

This case very likely represents another case of wrong vessel PCI. Many similar cases have been featured on the blog. I shared this case with several people, and no one was completely certain which vessel was the culprit.

I think it is likely the OM for the reasons I mentioned in the narrated video, however it is worth wondering whether a vessel that small could produce ECG changes that extensive. And it is definitely possible that a more proximal LCx lesion ruptured and produced distal embolism. Some others worried about the RCA as a possible culprit.

Uncertainty about culprit vessel is very common. In fact, in this elegant study by Heitner et al., investigators found that among patients receiving revascularization, 27% received revascularization solely to non-culprit coronary arteries!

A 2017 trial named CULPRIT SHOCK found that in patients with cardiogenic shock, a strategy of culprit vessel PCI only was associated with better outcomes than immediate multivessel PCI. After CULPRIT SHOCK, many shied away from multivessel PCI in the acute setting. However, we must bear in mind two things when translating this evidence to clinical practice. First, these were patients in shock. And second, this presupposes clear identification of culprit (an inclusion criterion for that trial). Many patients may not have a clear culprit.

Other trials have found a benefit to revascularizing non-culprit lesions when a patient presents with ACS, the largest of which was COMPLETE, and more recently MULTISTARS AMI. Although I believe the results of these trials, I always had trouble squaring these findings with the results of COURAGE, BARI 2D, ISCHEMIA, REVIVED-BCIS2 which showed that stenting stable lesions does not result in improvements in major adverse cardiovascular events (MACE). And in a study like COMPLETE or MULTISTARS AMI, you are stenting an acute plaque rupture (the culprit) and non-ruptured, non-culprit and hence essentially stable plaques.

So to summarize, we have evidence that:

1. Wrong vessel PCI is very common, perhaps nearly a third of patients (Heitner et al.)
2. Stenting stable lesions in most patients does not reduce MACE (COURAGE, BARI 2D, ISCHEMIA, REVIVED-BCIS2)
3. Stenting all lesions (stable and unstable) in patient with ACS does reduce MACE (COMPLETE, MULTISTARS AMI)

It begs the question of whether the benefit seen in COMPLETE and MULTISTARS AMI could be mediated in part by reducing or eliminating the possibility of missing the culprit?

All the more reason to use intravascular imaging (IVUS or OCT) to identify plaque rupture and confirm the culprit, especially since the use of intravascular imaging was shown to reduce all-cause mortality by 25%.

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MY Comment, by KEN GRAUER, MD (3/25/2025):

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I'd suggest as one of the "themes" for Dr. Frick's thought-provoking case from today being — Back to Basics — with not following this fundamental concept leading to the unfortunate occurrences in today's case.

• In a higher-risk patient (as today’s patient was) — If the initial ECG is laden with artifact that prevents accurate interpretation — then immediately repeat the ECG. Instead — no ECG was repeated for the rest of the day.
• Even if no artifact at all would have been present — in a higher-risk patient with ongoing symptoms, ECGs should be repeated every 15-30 minutes until a definitive diagnosis can be made.
• As described above by Dr. Frick: Morphine was given — Troponins were elevated and climbing — yet cardiac cath was delayed (being performed only after a prolonged resuscitation that perhaps could have been avoided had the basics been followed).
• And, perhaps because multi-vessel disease was found on cath with no clear "culprit" being evident — PCI was applied to the wrong artery. As per Dr. Frick — use of intravascular imaging (IVUS or OCT) could have helped to find plaque rupture and identify the "true" culprit. 
• Following through with frequent serial ECGs on this patient might also have helped to identify "tell-tale" ST-T wave changes that would have identified the vascular area(s) contributing to the acute event.

The Initial ECG:

Given how much depends on assessment of the initial ECG — this initial ECG should be immediately repeated if it is not adequately interpretable.

• To illustrate this point in Figure-1 — I've reproduced today's initial tracing in the TOP panel. Baseline artifact is clearly distorting ST-T wave morphology in each of the 6 limb leads. 
• QUESTION: Which of the 3 or 4 QRST complexes in leads II,III,aVF — and in lead aVL — manifest the "true appearance" of ST-T wave morphology in these leads?

In the BOTTOM panel of Figure-1 — I picked the middle QRST complex.

• In today's 60+ year old woman with new-onset severe CP (Chest Pain) — IF the ST-T waves that I show in the BOTTOM panel are the "true" representation of ST-T wave morphology in these 4 leads — Isn't this worrisome? 
• At least in leads II and aVF — I thought the T waves looked disproportionately larger-than-expected (possibly hyperacute) — with what appears to be reciprocal ST depression in lead aVL.
• In this context of new-onset severe CP and potential inferior OMI — I thought the clearly abnormal ST segment flattening in lead V2 and the more subtle (but nevertheless abnormal) ST segment straightening in lead V3 was in support of my concern about an infero-postero OMI.

How do we know IF I picked the "true" ST-T wave morphology?

• Answer: We don't know — because "garbage in = garbage out" — and there is simply too much artifact to tell. Perhaps if this initial ECG had been immediately repeated — and followed up by a 2nd ECG within 15-20 minutes — we might have seen enough "dynamic" ST-T wave change to qualify as an acute event in need of prompt cath (and the VFib episode might never have occurred).

Figure-1: I've labeled the initial ECG in today's case.