Typical Chest Pain: Would you activate the cath lab? Would you advocate if the interventionalist was not interested?

A 50-something woman complained of acute chest pain radiating to the left arm, onset while driving.  It would briefly improve with NTG.

Here is the first ED ECG:

What do you think?

When I saw this, I immediately said: "This is Aslanger's Pattern." 

1. Inferior OMI, with STE in lead III only, and reciprocal STD in aVL.

2. Diffuse subendocardial ischemia (ST depression, STD, in I, II, V3-V6) with reciprocal STE in aVR.

Aslanger's pattern is a combination of inferior OMI and diffuse subendocardial ischemia.  The subendocardial ischemia produces an ST depression vector toward leads II and V5 (with reciprocal STE in aVR) and the simultaneous inferior OMI results in STE in lead III only, but not in the other inferior leads.  

If there is inferior OMI, why is there no STE in II and aVF?  Because the ST depression (STD) vector towards lead II cancels part of the STE vector that would otherwise manifest in II and aVF.  That STD vector cannot, however, cancel the STE in III, which is too far to the right.  In fact, the STE vector must be directly rightward (180 degrees, or minus 180 degrees) in order not to register in lead aVF.  But of course, that rightward STE vector also registers as STE in aVR.  

When there is subendocardial ischemia alone, the STE vector is towards aVR, or actually a bit higher than aVR; thus, there is no STE in III or any other inferior lead.

So: lead III registers STE of subepicardial ischemia due to inferior MI and lead aVR registers reciprocal STE, reciprocal to the STD vector towards II. 

Since the ECG shows BOTH inferior OMI AND subendocardial ischemia, this pattern is associated with BOTH:

1. RCA/Circumflex occlusion (depending on dominance) AND 

2. At least one other ischemic vessel, and often 3 vessel disease, simultaneously.

See below a description of the article by Aslanger.  

Clinical Progression

The team activated the cath lab, but the interventionalist was skeptical.

An initial troponin I returned slightly elevated (0.379 ng/mL), and the patient's pain worsened.

Another ECG was recorded:

The findings are slightly worse.

Does this patient need immediate cath?  

There is ECG evidence of OMI.  There is refractory chest pain and clear ACS.  If the patient could be made pain free, then cath could be delayed.  But that was not the case here.

The patient was taken to the cath lab and was found to have 3 vessel disease:

LAD: 70% stenosis

Circ: 90% proximal, 90% first obtuse marginal.  It seems that these were not recognized as possible culprits for inferior OMI.

RCA: Prox: 50%, Mid: 50%, Distal: 90%

He underwent CABG to the posterior descending artery (PDA) of the RCA and internal mammary to LAD.  

The circumflex lesions were not intervened upon, either by PCI or CABG.

Here was the immediate post CABG EKG:

NEW Inferior and anterior STEMI (+) OMI

This looks like a wraparound LAD, but could also be 2 STEMIs at once.

The patient was immediately taken back to the cath lab, where they found:

--100% occlusion of the internal mammary graft to the LAD, AND 

--3 TIMI-2 occlusions in the circumflex:  

90% ostial circumflex culprit with TIMI-2 flow

90% 1st obtuse marginal with TIMI-2 flow

90% ostial circumflex culprit with TIMI-2 flow

These 4 occlusions of the 2 arteries resulted in inferior and anterior OMI:

The mid LAD was successfully stented (not the graft) and all 3 circ lesions were successfully stented.

Aslanger's Pattern:

I helped him a little bit and so I am a co-author. 

A new electrocardiographic pattern indicating inferior myocardial infarction

Highlights

•

We define a new ECG pattern that is not uncommon among patients classified as non-STEMI (6.3%).

•

This new pattern has only 1 lead with any ST elevation.  Guidelines require 2 consecutive leads to make the diagnosis of STEMI.  Thus, those with only 1 lead, especially if less than 1 mm, are labelled Non-STEMI.

13.3% of inferior STEMIs presents with this pattern and may be deprived of primary PCI because of the incorrect label of non-STEMI.

•

It indicates an acute atherothrombotic event that is frequently due to inferior MI despite ECG not showing contiguous STE.

•

The patients with this pattern have higher short- and long-term risk for mortality.

•

Since there is more than one critical lesion, it may cause confusion about which lesion should be emergently opened.

2 Groups below:

Group IA is NonSTEMI with Aslanger's pattern 

Group IB is NonSTEMI without Aslanger's pattern

Group IA was compared with Group IB in terms of clinical outcomes, the patients in Group IA had a higher troponin rise in the first 24- hours, higher infarct size as evidenced by 24-hour troponin levels, higher frequency of angiographic culprit lesion and higher frequency of composite ACO endpoint (Table 2). They also had a higher frequency of circumflex artery involvement as the infarct-related artery, higher frequency of multivessel disease, higher frequency of the presence of concurrent chronic total occlusion, and a higher in-hospital and one year mortality compared to Group IB.

Although the patients with this pattern are classified as non-STEMI, they have an acute atherothrombotic event frequently resulting in inferior OMI (more often occlusion or near occlusion of the circumflex artery than the right coronary artery) with at least one accompanying stable but critical stenosis in one of the non-infarct-related arteries. They tend to have multiple vessel disease, multiple comorbidities and higher baseline risk, and show an increased short- and long-term mortality.