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Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Bedside cardiac ultrasound with no obvious wall motion abnormalities. Conversely, pathological evaluation, as shown in Fig 2, will correctly identify the percentage of cross-sectional area occupied by plaque.
MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli , and coronary dissection; myocardial disorders, including myocarditis, takotsubo cardiomyopathy, and other cardiomyopathies. Thus, intracoronary imaging modalities are crucial in this setting. From Gue at al.
We did a bedside cardiac ultrasound. This is as clear a STEMI as you can get. So this is classic inferoposterior STEMI on the ECG but is NOT acute coronary syndrome! The ECG and ultrasound could not have been differentiated from acute plaque rupture with occlusion of the RCA. 3 points gets you an MI by Sgarbossa.
The scan also showed “scattered coronary artery plaques”. __ Smith comment 1 : the appropriate management at this point is to lower the blood pressure (lower afterload, which increases myocardial oxygen demand). Smith comment : Is the ACS (rupture plaque) with occlusion that is now reperfusing?
Bedside ultrasound with no apparent wall motion abnormalities, no pericardial effusion, no right heart strain. Patient still not having chest pain however this is more concerning for OMI/STEMI. Wellens' syndrome is a syndrome of Transient OMI (old terminology would be transient STEMI). Labs ordered but not yet drawn.
The commonest causes of MINOCA include: atherosclerotic causes such as plaque rupture or erosion with spontaneous thrombolysis, and non-atherosclerotic causes such as coronary vasospasm (sometimes called variant angina or Prinzmetal's angina), coronary embolism or thrombosis, possibly microvascular dysfunction. It is not rare.
Although it is statistically unlikely, multiple plaque ruptures are possible. On intravascular ultrasound (IVUS), the mid RCA plaque was described as "cratered, inflamed, and bulky," and the OM plaque was described as "bulky with evidence of inflammation and probably ulceration." Heitner et al.
This case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!!
This is a troponin I level that is almost exclusively seen in STEMI. So this is either a case of MINOCA, or a case of Type II STEMI. If the arrest was caused by acute MI due to plaque rupture, then the diagnosis is MINOCA. I believe the latter (type II STEMI) is most likely. Troponin I rose to 44.1 What is Type 2 MI?
Prehospital Conventional algorithm interpretation: ANTERIOR INFARCT, STEMI Transformed ECG by PM Cardio: PM Cardio AI Bot interpretation: OMI with High Confidence What do you think? On arrival, lung ultrasound confirmed pulmonary edema (B lines). Mild Plaque no angiographically significant obstructive coronary artery disease.
This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. aVR ST segment elevation: acute STEMI or not? aVR ST Segment Elevation: Acute STEMI or Not?
Could this be Septal STEMI (STE in V1 and aVR, with reciprocal ST depression in V4-V6?), In Septal STEMI , transmural ischemia of the septum is recorded by the overlying lead V1 as ST Elevation. Lead III is also on the right and might manifest ST Elevation in Septal STEMI. with ADDED STE in III?
EMS recorded these ECGs: Time 0: In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 Here are a couple shots with strain, or "speckle tracking" on ED Echo: To, me these look like anterior wall motion abnormality, but I showed them to one of our ultrasound fellows who is very interested in this. She called 911.
Here’s the angiogram of the RCA : No thrombus or plaque rupture in the RCA (or any coronary artery) was found. This MI wasn’t caused by a ruptured plaque of CAD - it was a coronary artery dissection of the RCA. A recent study found that SCAD causes almost 20% of STEMI in young women. A study by Hassan et al. Lobo et al.
EMS recorded these prehospital ECGs: Time 0: In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 To, me these look like anterior wall motion abnormality, but I showed them to one of our ultrasound fellows who is very interested in this. She was having a transient STEMI, briefly. She called 911.
This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. This was diagnosed by IVUS (intravascular ultrasound) as a ruptured plaque. As there was ruptured plaque, this is NOT Prinzmetal's angina. Here is his triage ECG: There is massive STE in V3-V6, and also STE in II, III, aVF.
There is an obvious inferior STEMI, but what else? Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1. This STE is diagnostic of Right Ventricular STEMI (RV MI). In fact, the STE is widespread, mimicking an anterior STEMI. EKG is pictured below: What do you think?
As in all ischemia interpretations with OMI findings, the findings can be due to type 1 AMI (example: acute coronary plaque rupture and thrombosis) or type 2 AMI (with or without fixed CAD, with severe regional supply/demand mismatch essentially equaling zero blood flow). Now another, with ultrasound. What is the Diagnosis?
50% of LAD STEMIs do not have reciprocal findings in inferior leads, and many LAD OMIs instead have STE and/or HATWs in inferior leads instead. The ECG easily meets STEMI criteria in all leads V2-V6, as well. 24 yo woman with chest pain: Is this STEMI? Beware a negative Bedside ultrasound. Diagnostic of Massive OMI.
She had this ECG recorded: Obvious massive anterior STEMI She was quickly brought to the critical care area and the cath lab was activated. Here is the ECG at 25 minutes: Terrible LAD STEMI (+) OMI So a CT scan was done which of course showed a normal aorta. This was ruptured plaque with thrombus. She was a walk-in at triage.
They recorded this ECG: Obvious inferior STEMI/OMI What else? Provocative testing is very helpful for this Coronary Thrombus with lysis (one must do optical coherence tomography or at least intravascular ultrasound to find thes non-obstructive plaques that ruptured. He called 911. Medics recorded a BP of 79/52 with pulse of 47.
Nevertheless, the operator performed intravascular ultrasound and saw erupted calcium nodule consistent with plaque erosion. Limitations of registry data: This patient presented with STEMI (-) OMI and developed STEMI the following day. Does anyone think that this is a "false positive" STEMI because the vessel was open?
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