Written by Pendell Meyers
A male in his late 50s had sudden chest pain radiating to the left side and back, with nausea and diaphoresis as well as bilateral finger tingling sensation. He drove himself to the Emergency Department.
Here is his ECG on arrival at 11:33 am (unclear whether pain was persistent at this time, or if it had decreased since onset):
|What do you think?
There is a small amount of STE in II, III, and aVF, but there is not clear STD or T-wave inversion in aVL. There is STD in V2 and V3 which must be assumed to be abnormal unless proven otherwise by a baseline ECG. The T-waves in V3 and V4 are not definitively hyperacute, but could be hyperacute if a baseline ECG showed smaller baseline T-waves. If this were true, then there would be ST depression and hyperacute T-waves, which constitutes de Winter morphology and would be concerning for occlusion or near-occlusion of the LAD in this distribution. If the T-waves are not hyperacute compared to baseline, then we are left with STD maximal in V2-V3 which would be concerning for posterior OMI. But it simply doesn’t look like posterior OMI.
Apparently his pain resolved. The cath lab was not activated at that time.
Approximately 40 minutes later, he had sudden recurrence of crushing chest pain and appeared critically ill.
Here is his ECG at that time, 12:08:
|What do you see?
|Red lines show the J-points in all leads. There is sinus bradycardia with massive ST segment deviations. STE is present in V3-V6, I, aVL, II, and aVF. STD is present in lead III, aVR, and V1. This morphology in the anterolateral leads is known as “shark fin” ST elevation and is created by QRS distortion plus slurring of the J-point and ST segment which obscure the perception of STE.
The STE in V3-V6, I, and aVL implies a very large vessel which supplies anterior and lateral walls. The STD in V1 indicates posterior wall involvement. The ST segment in V2 is awkwardly isoelectric, pulled down by posterior involvement but pulled up by the massive STE of anterior OMI which is obvious from lead V3 onward. These findings alone would indicate occlusion of a very large vessel that supplies territories of both the LAD and LCX put together. And yet the STE extends even further, extending into the inferior leads as well.
Notice what is happening in lead aVR: Due to widespread massive STE in essentially all other leads, aVR registers massive reciprocal STD.
If any ECG on this blog has ever shown evidence of actual, complete left main occlusion, this is it.
Regardless of the speculation about where the lesion is, this enormous territory OMI pattern with new bradycardia portends very high risk of imminent cardiac arrest.
Another ECG was recorded 1 minute later:
|This shows diffuse “shark fin” ST Elevation.
30 seconds later, the patient suffered cardiac arrest. Apparently it was alternating between VF and “PEA” with persistent enormous ST segment deviations when the shocks were briefly successful.
ROSC could not be consistently maintained.
Cardiology was not willing to take the patient to the cath lab in this condition.
Cardiothoracic surgery was called to bedside for initiation of ECMO. However, the surgeon elected to take the patient to the OR with ongoing mechanical CPR for emergent LVAD placement (this case did not happen recently, as ECMO would be the preferred strategy in most centers today).
Amazingly, LVAD placement was successful and systemic blood flow was restored mechanically.
He went immediately from the OR to the cath lab for emergent angiography.
The angiogram revealed:
“…a saddle thrombus in the distal LMCA involving the distal LAD and LCX with significant disease in the OM and also in the RCA.”
The left main, LAD, and LCX were all 95% obstructed by the saddle thrombus at the time of cath. It is reasonable to conclude that the left main was fully occluded or almost fully occluded at the time of the second ECG above.
“Several passes were done with the thrombectomy aspiration catheter with improvement in blood flow. POBA was done to OM, LMCA/LAD, and LMCA/LCX. After discussing the case with Dr. _____ it was decided that we could not use at this time any type of stents because the patient was not a candidate for antiplatelet therapy (no aspirin or P2Y12 inhibitor). Therefore suboptimal results were obtained but TIMI flow 3 obtained in all vessels. A final revascularization approach will be decided in the future according to his status.”
Troponin I peaked at 269.05 ng/mL (extremely large MI).
Here is an ECG after these interventions:
|Extremely low voltage, which likely has to do with his LVAD being in place, as well as very small amount of remaining myocardium to conduct the action potential. ST segments resolved.
He had a meaningful baseline condition and family continued to pursue aggressive therapies. He had a very stormy course over the next month in the CTICU and ultimately passed away despite maximal therapies.
A patient with true left main occlusion will usually suffer cardiac arrest very soon thereafter. With some exceptions, only in a case like this, where the patient develops left main occlusion in front of providers, can an ECG be performed soon enough before cardiac arrest to show the ECG findings of left main occlusion.
ST elevation in lead aVR does not mean that the patient has left main occlusion. This case shows exactly the opposite: aVR in this case shows massive ST depression because it reflects the massive ST elevation in other leads. In contrast, lead aVR shows reciprocal elevation in the case of diffuse subendocardial ischemia from left main stenosis with diffuse STD and reciprocal STE in aVR.
See these other cases explaining lead aVR and left main ACS: