Written by Pendell Meyers
84 yo M with history of a “valve problem” presented for sudden onset chest pain and trouble breathing while eating lunch.
He was sitting bolt upright, diaphoretic, tachypneic, with bilateral crackles. Although his BP was 126/84, he was in acute cardiogenic shock.
Here is his initial ECG:
|Sinus tach with occasional PACs. Relatively normal QRS complex with diffuse significant ST depression including leads V2-V6, I, aVL, II, III, and aVF, with ST elevation in aVR. The vector of ST depression is maximal in leads V5 and II, consistent with diffuse subendocardial ischemia. There is no evidence of any single vessel OMI (Occlusion MI). This is not consistent with posterior OMI, which would have ST depression maximal in V2-V4 usually without diffuse ST depression.
The differential for acute chest pain and cardiogenic shock without evidence of OMI on ECG includes:
(still) OMI – the ECG is not perfectly sensitive for OMI
3 Vessel disease with superimposed non-occlusive ACS
Non-occlusive ACS of any major vessel, including left main
Acute aortic stenosis or other acute severe valvular abnormality
Any other cause of acute severe supply-demand mismatch
Any combination of the above
The ECG does not differentiate the above etiologies, it simply signifies that there is severe diffuse global supply-demand mismatch, whatever the etiology.
Bedside ultrasound revealed significant LVH and an extremely bright, dense, nearly non-moving aortic valve (video not available).
He went to the cath lab semi-emergently. He was found to have severe aortic stenosis (area 0.87cm2, mean gradient 22mm Hg) as well as significant CAD:
Left main: 60% stenosis, with 90% ostial LAD and LCX stenosis, and 70% ramus intermedius stenosis
mid RCA: 50% stenosis
It seems as though the angiographers were unsure whether any of these lesions represented acute ACS or whether they were pre-existing without acute ACS.
Here are the images:
|The left main ends with a trifurcation (LAD, Ramus, LCX) that shows a severe stenosis at ostia of all three vessels.
|This is the “spider view” of the same lesion.
|Diseased but grossly patent RCA.
The max troponin T was 2.40 ng/mL.
The patient required urgent bioprosthetic aortic valve replacement and CABG including LIMA to LAD, SVG to ramus, and SVG to OM1.
Here is his ECG after interventions:
Diffuse ST depression maximal in V4-V6 and lead II, with ST elevation in aVR, signifies diffuse subendocardial ischemia. Some etiologies of diffuse subendocardial ischemia, including unstable 3-vessel or left main ACS likely benefit from emergent revascularization, whereas other etiologies of global demand such as sepsis, hypotension, GI bleeding do not.
Make sure you can recognize the difference between diffuse ST depression and localized ST depression maximal in V2-V4 which signifies posterior Occlusion MI. See these examples for comparison: