Is it important to try to determine the culprit vessel based on ECG?

Written by Willy Frick

A man in his 60s with hypertension and prior stroke presented with three days of crushing chest pain. He reported intermittent chest pain for the last few months, but never lasting this long. He described it as substernal with radiation into the right arm.

With all of this information, we can feel reasonably confident even before looking at the ECG that we are dealing with OMI.

What do you think?

Right away, we notice different populations of R waves. On the V1 rhythm strip, R4 and R5 look like natively conducted beats. (Note, they are not sinus since the P waves are upside down in aVF. It looks like a low atrial rhythm.) The other beats are wider and have a different origin -- more on this later. Unfortunately, although natively conducted beats are the best ones for evaluating ischemia, we only have a few! Or do we?

Although printed ECGs in North America typically display 2.5 seconds of each lead plus one or more 10 second rhythm strips, most machines actually gather data for 10 seconds of all 12 leads! (I recently learned from Dave Richley that modern machines collect 10 seconds of data from leads I and II plus V1-V6. They do not actually measure III, aVL, aVR, aVF but rather calculate them.)

Smith comment: this is one of the major obstacles that Powerful Medical needed to overcome in digitizing 12-lead ECG images: all digital ECG recordings are 10 seconds of each lead, but the images only display 2.5 seconds.  So 75% of the image is missing!  Most computer scientists in the 12-lead ECG world said it was impossible.  But they did it.  They were also able to produce an XML file with 10 seconds of each lead out of these JPG, PNG, or PDF files.  This is critical because AI needs an XML file for analysis.

Case Continued

I like to take advantage of this fact by opening up the ECG in the reading software and reformatting it into 12 channels of rhythm.

Before reading further, see if you can figure out the rhythm. My interpretation is described in reference to the lead II rhythm strip below with annotations for clarity.

• Beats 4 and 5 have the narrowest QRS of all. These must be natively conducted beats. Note that the P waves indicated by the blue arrows have a superior axis (i.e. they are inverted in the inferior leads). Sinus rhythm has an inferior axis, so this must be a low atrial rhythm.

• Beats 1-2 and 7-10 are wider, uniform, and regular. In context of reperfused OMI (I will come back to this), we commonly see AIVR. This QRS complex is almost exactly 120 ms, which is on the narrow end for ventricular origin. And AIVR is commonly closer to 80-110 bpm. Still, this would be very fast for a junctional or ventricular escape rhythm under normal circumstances, so I favor AIVR.

• The red arrows associated with R waves 3 and 6 indicate P waves with sinus morphology -- upright in  I, II, aVF. (They are upside down in V1 and V2, but this is probably because the electrodes are too high.) Additionally, the PR intervals are very short and the QRS complexes are intermediate in morphology between the AIVR beats. Hence they are fusion beats [fusion between ventricular (wide) and conducted (narrow)].  R3 is mostly AIVR morphology, and R6 is mostly sinus conducted morphology.

• The green arrows indicate atrial activity that appears to have been beaten out by the AIVR (i.e., did not conduct because the AIVR beat came first). I doubt retrograde conduction because the RP interval is variable between 8 and 9. If the atrial activity were due to retrograde conduction, the interval from the R wave to the retrograde P wave would likely be the same between the two beats.

Moving on to ischemia, the ECG shows reperfused inferoposterior infarct. Specifically focusing on beats 4 and 5, we see:

• TWI in II, III, aVF

• Overly upright posterior reperfusion T waves most pronounced in V2-3*

• Reciprocally upright T waves in I/aVL (we would expect them to be inverted with the LVH strain pattern)

*Some of this may be the expected T wave in a patient with LVH strain pattern. It is hard to be sure, but this nuance does not impact the overall diagnosis.

Back to the case:

Unfortunately for the patient, he presented on Friday morning to a facility that did not have cath lab coverage until the following Monday. The cardiology consultant notes that pain is "almost resolved."

Remember that in OMI, chest pain is a sign of ongoing infarction. "Almost resolved" means it is NOT resolved. There is active infarction. There either is ischemic chest pain or there is not.

The patient was loaded with aspirin and clopidogrel and started on continuous heparin infusion with plan for cath Monday. The note says that "if symptoms become refractory," the patient will need to be transferred for urgent cath over the weekend. (What does refractory mean if not days of unresolved chest pain which persists after starting medical therapy?) Initial hsTnI was 14,114 ng/L, repeat 12,651 ng/L, none further checked. Echocardiogram showed inferior wall hypokinesis. The patient was evaluated Saturday with no changes to plan.

On Sunday, the patient complained of dyspnea and angina while ambulating. Repeat ECG is shown.

Again, we see reperfusion in the inferior and posterior territories. There is just a hint of coving in leads III and aVF suggesting a component of active ischemia which fits with persistent pain.

The Queen of Hearts recognizes this as reperfused OMI:

This was interpreted by cardiology as "suggestive of anterior wall ST elevation MI." Yes, you read that right. It was hand written in two places in the note, so definitely not an accident.

Smith: yes, it is suggestive of anterior MI -- of OLD anterior MI.  But also of subacute inferior OMI.

Perhaps the cardiologist was attempting serial comparison and thought there was new STE in V3 without realizing that the prior ECG shows AIVR and fusion beats in V3. Fortunately for the patient, this mistaken interpretation at least got him urgently transferred to a cath capable facility where he underwent urgent angiography.

If interested, you can review the angiography in detail on my coronary angiography guide where you will find a lot more information about coronary angiography generally.

Here is an LAO cranial view showing TIMI 0 in the mid to distal RCA

Angiography was interpreted as showing chronic total occlusion of the RCA. (We know from the ECG that the RCA is actually the acute culprit!) The patient received DES to mid LAD and DES to diagonal, with no intervention to the culprit RCA.

Unfortunately, wrong vessel PCI is very common. In a prospective cohort of patients presenting with NSTEMI, 27% of patient receiving PCI had intervention solely to uninvolved arteries. In the same cohort, almost HALF (46%) have either the wrong infarct related artery selected, or the ultimate diagnosis is not ischemic in the first place!

Not surprisingly, the patient had persistent pain after PCI, continuing through the night. The following day, he returned to lab where a different operator performed repeat angiography. The second operator described the RCA as an acute thrombotic occlusion and placed three overlapping stents. The final shot is shown.

Learning points:

• Just because the cath report describes a lesion as "CTO" does not mean it is. It may still be an acute culprit.

• Wrong vessel PCI is very common, it happens in about 1 in 4 NSTEMIs.

• Angiography has inherent limitations. About half of NSTEMI diagnoses are incorrect.

• As always, effective OMI care requires putting the ECG in context of the patient's symptoms.

Here is another video explanation of a case in which the ECG was critical in finding the culprit:

Right Ventricular MI seen on ECG helps Angiographer to find Culprit Lesion

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MY Comment, by KEN GRAUER, MD (1/5/2025):

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Awareness that many modern ECG machines do not display all of the data they gather when writing out an ECG is a greatly underused concept. That said, uncovering much of this unused extra data by routinely displaying each beat in each of the 12 leads would not only prove cumbersome — but it would be unnecessary in the great majority of tracings that lack the great degree of morphology variation seen in today's case.

• Today's case by Dr. Frick illustrates an exception to the above generality. By reformatting the data collected into 12 channels of the rhythm — Dr. Frick facilitated interpretation not only of today's initial 12-lead ECG — but he also provides insight into the mechanism of today's fascinating initial rhythm.
• I focus my comment on exploring this mechanism.

Thanks to Dr. Frick — I was able to obtain a long lead II rhythm strip. In Figure-1 — I combine this derived lead II with the already displayed lead V1 rhythm strip to facilitate clarifying atrial activity in today's initial tracing.

• Without Dr. Frick's reformatting the 10 beats in today's initial tracing into 12 channels of rhythm — I would never have realized that there are 2 atrial foci in the initial rhythm. (Although P wave morphology of sinus P waves may vary some from one beat to the next — I would not expect as much variation as we abruptly see for just 2 beats in today's initial rhythm).
• As per Dr. Frick — the P waves that precede beats #4 and #5 are predominantly negative in lead II, therefore presumably of low atrial origin (BLUE arrow P waves in Figure-1).
• RED arrows in Figure-1 highlight sinus P waves that are upright in lead II. Of these, P waves c and f are the only P waves clearly seen. Dr. Frick pointed out P waves h and i that appear shortly after beats #8 and 9 in lead II (albeit they are not seen in lead V1).
• Given sinus P waves f, h and i — it seems logical that another on-time sinus P wave will almost certainly be hiding within the QRS complex of beat #7 (WHITE arrow).
• Motivated to look even closer for "hidden" P waves — the slight angulation just before the QRS of beat #2 is not present in other beats (strongly suggesting that b represents another on-time sinus P wave).
• Finally — the subtle notch that simulates an r' deflection at the end of the QRS of beat #1 falls in a perfect place to be hiding a final on-time sinus P wave. (This rhythm simply makes more sense if we postulate more regular atrial activity — and the highlighted atrial deflections support this premise).

Whereas atrial activity is best displayed in the long lead II rhythm strip of today's initial ECG — I thought the variation in QRST morphology to be best displayed in the long lead V1.

• As per Dr. Frick — the pathology underlying today's case is an acute inferior OMI — now with reperfusion T waves (best seen in the inferior leads of this initial tracing) and with AIVR (Accelerated IdioVentricular Rhythm) that is so commonly seen as a reperfusion arrhythmia.
• Focusing on QRST morphology in lead V1 of Figure-1 — beats #1,2; and 7,8,9,10 are all wide and not preceded by any P wave. These are all ventricular beats at a regular and slightly accelerated rate of ~60/minute (which is perfectly consistent with AIVR).
• The 2 low atrial P waves ( = d and e) are conducted normally to the ventricles (ie, beats #4 and 5 are narrow QRS complexes).
• Beats #3 and #6 are Fusion beats (F). We know this — because both of these beats: i) Manifest a QRS and T wave morphology that is intermediate to the beat before and the beat after it (ie, QRST morphology of beat #3 is intermediate to that of beats #2 and #4 — and QRST morphology of beat #6 is intermediate to that of beats #5 and #7); — and, ii) Both beats #3 and 6 are preceded by P waves that have a chance to partially conduct (and as would be expected with fusion beats — beat #6 with a slightly longer PR interval provides slightly more time for the sinus P wave preceding it to conduct in the ventricles, which is why fusion beat #6 looks more like normally conducted beats #4 and 5 than does beat #3 which is preceded by a shorter PR interval).

Why was AIVR able to appear in this initial tracing?

• Whereas the R-R interval of ventricular beats in Figure-1 remains quite constant — the atrial rate of sinus P waves varies somewhat. As a result — slowing of the sinus P wave rate facilitates intermittent appearance of either a low atrial escape rhythm or of AIVR.
• P.S.: As often occurs — there may be slight lag in the intermittent appearance of AIVR. But the "theme" of this initial rhythm, is that OMI reperfusion results in a slightly accelerated AIVR that in general makes its presence around the time that the sinus rate slows. A longer period of monitoring would be needed to know for certain — but the back-and-forth between wide and narrow QRS complexes is almost like that seen with isorhythmic AV dissociation, albeit complicated by low atrial escape.

Figure-1: Combined lead II and lead V1 rhythm strip.

My Proposed Laddergram:

• Sinus P waves a,b and g are not conducted to the ventricles — because ventricular beats #1,2 and 7 have rendered the AV nodal area refractory to supraventricular impulses.
• Sinus P waves h and i are not conducted to the ventricles — because these P waves occur after the QRS of beats #8 and 9 during the ARP (Absolute Refractory Period).
• Escape low atrial impulses d and e occur at just the right time to be able to conduct normally to the ventricles to produce beats #4 and 5.
• Sinus P wave c occurs just before the QRS of beat #3. As a result — this P wave is only able to conduct a short distance in the ventricles before being stopped by the AIVR impulse. This fusion beat therefore looks very much like other AIVR impulses.
• Sinus P wave f manifests a slightly longer PR interval than did c. As a result — this P wave penetrates further in the ventricles — which leads to a fusion beat that looks much more like normally conducted beats #4 and #5.

Figure-2: Proposed laddergram for today's initial rhythm.