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Theres ST elevation in V3-4 which meets STEMI criteria, which could be present in either early repolarization, pericarditis or injury. Lets see what happens in the current STEMI paradigm. Emergency physician: STEMI neg but with elevated troponin = Non-STEMI The first ECG was signed off. What do you think?
Interpretation : diagnostic of acute anterior OMI with STE less than STEMI criteria in V1-V4, hyperacute T waves in V2-V4, and suspiciously flat isoelectric ST segments in III and aVF suspicious for reciprocal findings. Now it even meets STEMI criteria, and HATWs continue to inflate. The patient survived with unknown long term outcome.
Cath lab declined as it is not a STEMI." There is probably a trickle of flow which is why there is both subendocardial ischemia (ST depression) and early subepicardial ischemia (hyperacute T-waves). And now this finding is even formally endorsed as a "STEMI equivalent" in the 2022 ACC guidelines!!! It is a mass delusion.
The first ECG was labeled “anterior subendocardial ischemia”, but subendocardial ischemia does not localize. If there were diffuse ischemic STD, with precordial STDmaxV5-6 and reciprocal STE-aVR, this would be non-specific subendocardial ischemia from ACS or supply-demand mismatch. Do you need posterior leads?
Cardiogenic shock (CS)is the most feared event following STEMI. We tend to perceive CS as an exclusive complication of STEMI. The incidence is half of that of STEMI, i.e., 2.5-5%. might show little elevation with considerable overlap of left main STEMI vs NSTEMI ) 2.Onset ACS pathophysiology is not that simple.
There may be ischemia present, but it is not evident on the ECG. LVH and the diagnosis of STEMI - how should we apply the current guidelines? This one mimics inferior STEMI (Figure 4): Concentric LVH, NO wall motion abnormality Case 5. How about diagnosing anterior STEMI in the setting of LVH? Birnbaum Y and Mahboob A.
Methods and Results Patients with confirmed ST elevation myocardial infarction (STEMI) treated by emergency medical services were included in this retrospective cohort analysis of the AVOID study. And as we have shown before, morphine leads to slower times to treatment and worse outcomes. 414 patients were included in the analysis.
He had an immediate ED ECG: There is artifact, but the findings appear to be largely gone now The diagnosis is acute MI, but not STEMI. There is about 1 mm of STE in aVR I con sidered but rejected subendocardial ischemia. Is it subendocardial ischemia, or inferior MI? Outcome : Was it RCA or LCX with inferior MI?
See my formula for differentiating anterior LV aneurysm (that is to say, persistent ST elevation after old MI) from acute anterior STEMI. Both support acute anterior STEMI. After the hyperacute phase, the ST segments rise and only fall with either 1) reperfusion or 2) prolonged ischemia leading to irreversible infarction.
Acute Q waves are a marker of severe ischemia and a predictor for delayed reperfusion. This patient could have very easily been overlooked, both because the ECG was STEMI negative and because the Q waves were attributed to an “old infarct”. Fortunately, Dr. Cho was not looking for STEMI ECG criteria but for an acute coronary occlusion.
This was a machine read STEMI positive OMI. In this patient's case, the RV ischemia manifested as dramatic anterior hyperacute T waves. This degree of STE is a bit atypical for LAD ischemia. the investigators reviewed outcomes in 118 patients presenting with NSTEMI. His ECG is shown below.
ST depression in the setting of acute transmural ischemia (STEMI) is almost ALWAYS due to reciprocal change. Outcome: The patient went to the cath lab, but we have no further followup. The elevation is higher in Lead III than in Lead II, a reliable sign of RCA occlusion. Reciprocal depression in Leads aVL and I.
1-3] But these studies were very short duration and used cardiology interpretation of ECGs or emergent angiography rather than patient outcomes. 4,5] We have now formally studied this question: Emergency department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review.[6]
You can subscribe for news and early access (via participating in our studies) to the Queen of Hearts here: [link] queen-form This EMS ECG was transmitted to the nearby Emergency Department where it was remotely reviewed by a physician, who interpreted it as normal, or at least without any features of ischemia or STEMI.
Echo on the day after admission showed EF of 30-35% and antero-apical wall akinesis with an LV thrombus [these frequently form in complete or near complete (no early reperfusion) anterior STEMI because of akinesis/stasis] 2 more days later, this was recorded: ST elevation is still present. The LAD has reperfused early. This was recorded 2.5
Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI"). Smith : the profound persistent STE suggests either persistent occlusion or " no reflow " with persistent downstream ischemia. Long term outcome unknown but obviously bleak.
If this STD were due to LVH or to subendocardial ischemia, rather than posterior OMI, it would be maximal in V5 and V6. If I saw this without the STD V2-V4, I would not make anything of it, and even with that precordial STD, I am not convinced that it is a manifestation of ischemia. Because we are hypnotized the STEMI paradigm. "If
We have also shown several cases in which atrial flutter hides true, active ischemia. Is this inferor STEMI? Atrial Flutter with Inferior STEMI? The EM provider asked if the cardiologist thought it was a "STEMI." Long-term outcome is unknown. Christmas Eve Special Gift!! Tachycardia and ST Elevation.
This suggests further severe ischemia. STEMI MINOCA versus NSTEMI MINOCA STEMI occurs in the presence of transmural ischaemia due to transient or persistent complete occlusion of the infarct-related coronary artery. This has resulted in an under-representation of STEMI MINOCA patients in the literature. From Gue at al.
Computer read: "Non-specific ST abnormality, consider anterior subendocardial ischemia" There are very poor R-waves in V1-V4 suggesting old anterior MI. Firstly, subendocardial ischemia does not localize on 12-Lead ECG. But the real question at hand is: Are these precordial ST-depressions a result of subendocardial ischemia?
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. His response: “subendocardial ischemia. Anything more on history? POCUS will be helpful.”
Step 1 to missing posterior MI is relying on the STEMI criteria. A prospective validation of STEMI criteria based on the first ED ECG found it was only 21% sensitive for Occlusion MI, and disproportionately missed inferoposterior OMI.[1] But it is still STEMI negative. A 15 lead ECG was done (below). In a study last year, 14.4%
This is diagnostic of infero-posterior OMI, but it is falsely negative by STEMI criteria and with falsely negative posterior leads (though they do show mild ST elevation in V4R). They were less likely to have STEMI on ECG, and more likely to be initially diagnosed as non-ACS. Circulation 2007 2. Khan et al.
In any case, the ECG is diagnostic of severe ischemia and probably OMI. So this could be myocarditis but in my opinion needs an angiogram before making that diagnosis. == Dr. Nossen Comment/Interpretation: Evaluation of ischemia on an ECG can be very challenging. Concordant STE of 1 mm in just one lead or 2a.
STE limited to aVR is due to diffuse subendocardial ischemia, but what of STE in both aVR and V1? The last section is a detailed discussion of the research on aVR in both STEMI and NonSTEMI. Alternatively, it is a variant of diffuse subendocardial ischemia, with STE in V1 reciprocal to ST depression in inferior and lateral leads.
Non-randomized trials show better outcomes (neurologic survival) using this device; see this article in Resuscitation: Head and Thorax Elevation during cardiopulmonary resuscitation using circulatory adjuncts is associated with improved survival. Finally, head-up CPR (which was not used here), makes for better resuscitation.
Repeat ECG showing no STEMI, only non-specific ST-segment and T-wave abnormalities, unchanged from prior" Transferred to surgery for exploration but diagnostic studies were too indeterminate to be certain of intra-abdominal pathology. Trop T now very high, well into the range one sees with a STEMI; very unusual in type II MI.
The ECG in the chart was read as "no obvious ST changes," (even though no previous ECG was available) and the formal read by the emergency physicians was: "ST deviation and moderated T-wave abnormality, consider lateral ischemia." New ST elevation diagnostic of STEMI [equation value = 25.3 Computerized QTc = 417. Gottlieb SO, et al.
The baseline ECG is basically normal with no ischemia. You can see in the lead-specific analysis that she "sees" the STD in V5, V5, and II, with STE in aVR as signs of "Not OMI", because subendocardial ischemia pattern is not the same as OMI. In my opinion, I think it looks more like subendocardial ischemia.
None of these findings are diagnostic of ischemia, but they should give you a high index of suspicion and prompt serial ECGs at a minimum. Anterolateral STEMI. He underwent PCI and had a good outcome. Ischemia comes and goes. mm of STE at 60 ms after the J-point in lead V3, 400 ms QTc, and 6 mm of R-wave amplitude in V4.
Just as hyperacute T-waves can be reciprocal to T-wave inversion ( last case ),T-wave inversion can be reciprocal to STEMI of opposite wall! Answer : There is very abnormal T-wave inversion in aVL which is typical of subtle transmural/subepicardial (due to occlusion) ischemia to the inferior wall. This case was sent by Arthur Lee.
Here is the prehospital ECG, with pain: Hyperacute anterolateral STEMI The medics had activated the cath lab and the patient went for angiogram and had a 95% stenotic LAD with TIMI-3 flow. For those who depend on echocardiogram to confirm the ECG findings of ischemia, this should be sobering. Type B waves are deeper and symmetric.
Jason asked me if I thought it is due to occlusion (without either of us knowing the outcome), and this was my answer: This is a posterolateral MI. Down-up T-waves in inferior leads are almost always reciprocal to ischemia in the territory underlying aVL. Therefore it is not a STEMI. Some are STEMI-equivalents.
The patient with no prior cardiac history presented in the middle of the night with acute chest pain, and had this ECG recorded during active pain: I did not see any ischemia on this electrocardiogram. This is a case I had quite a while back. There is a normal amount of ST elevation in the precordial leads.
Outcome of case 2? Another missed OMI by the False STEMI-NonSTEMI Dichotomy Don't miss them!!! In addition — there is transmural ischemia of the septum , most often resulting from occlusion proximal to the 1st septal perforator branch of the LAD. Admitted for NSTEMI. Cath days later showed complete occlusion of the LAD, stented.
There is normal R-wave progression in the precordial leads with no evidence of ischemia. Troponin T peaked at 2074 ng/L (very high, typical of OMI/STEMI). Here the image quality is enhanced using the PM Cardio app. What do you think? The presenting ECG shows SR with narrow QRS complexes. The LV EF was 57% at formal echo.
We have found in our study comparing inferior STEMI (manuscript in preparation) to inferior early repol several distinguishing characteristics. T-wave inversion in V2 is inconsistent with early repol, and is typical of posterior ischemia. In addition, there is ST depression, diagnostic of ischemia, in V3-V6.
I do not think this ECG is by itself diagnostic of OMI (full thickness, subepicardial ischemia ), b ut comparison to a previous might reveal this ECG as diagnostic of OMI. Immediate and early percutaneous coronary intervention in very high-risk and high-risk Non-STEMI patients. Lupu L, et al. mg/dL, K 3.5 Abstract 556.
Full case details and outcomes are below. The Queen of Hearts correctly says: Smith : Why is this ECG which manifests so much ST Elevation NOT a STEMI (even if it were a 60 year old with chest pain)? Physician interpretation: "No STEMI." Physician: "No STEMI." Case 1: Case 2: Case 1: What do you think?
He wrote in his note that "The EKG showed early repolarization in I, V2-V3 but no clear STEMI pattern." If the patient had been "lucky," his symptoms from the prior day might have been due to ischemia prolonged and intense enough to result in small troponin increase. Of the 418 patient with ACO, 29% did not meet “STEMI criteria.”
While this ECG is negative for “posterior STEMI”, the resolution of anterior ST depression (accompanied by the troponin elevation) confirms posterior OMI with spontaneous reperfusion. The second opportunity to make the diagnosis and expedite angiography was missed because the ECG never met STEMI criteria and continued to be labeled ‘normal.’
At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high). The patient’s angiogram should have been expedited, but the EKG change was not recognized as recurrence of transmural ischemia. At 1605, another repeat troponin resulted at 5.271 ng/mL.
These kinds of cases were excluded from the study as obvious anterior STEMI. --QTc Case 1 Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)? Appropriately, the physicians repeated the ECG 20 minutes later and it was diagnostic of anterior STEMI. QTc is the computer measurement. 100% LAD occlusion.
It is equivalent to a transient STEMI. Now you have ECG and troponin evidence of ischemia, AND ventricular dysrhythmia, which means this is NOT a stable ACS. It they are static, then they are not due to ischemia. This is better evidence for ischemia than any other data point. Again, cath lab was not activated.
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