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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.
Furthermore, the term "STEMI equivalent" has no reliable or definable meaning except between two practitioners who both agree on the list of entities that they believe are STEMI equivalents and can agree on how to identify it. Obvious inferoposterior STEMI. J ACC 61(4):e78-140; page e83.
Despite the absence of significant coronary stenosis on her post-arrest cath — the ECG in Figure-1 is clearly diagnostic of an extensive anterolateral STEMI ( presumably from acute LAD [ L eft A nterior D escending ] coronary artery occlusion). The rhythm in ECG #1 is regular and supraventricular at a rate of ~75/minute.
Notice on the right side of the image how the algorithm correctly measures STE sufficient in V1 and V2 to meet STEMI criteria in a man older than age 40. As most would agree, this ECG shows highly specific findings of anterolateral OMI, even with STEMI criteria in this case. Thus, this is obvious STEMI(+) OMI until proven otherwise.
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. Circulation. 2017;135(16):1490–3.
His ECG was repeated at this point: This shows a well developed anterior STEMI. To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI. It is not a missed STEMI, but it is a missed coronary occlusion. The peak troponin I was over 100.
This " imbalance of precordial T waves" is not seen very often — and in the “right” clinical setting, has been associated with recent OMI from a LCx culprit artery ( See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM ).
The precordial ST-depression pattern on this ECG (and in this clinical setting) should immediately raise suspicion of Posterior STEMI! Posterior STEMI occurs in approximately 15-20% of acute MI, but the vast majority of the time it is seen in conjunction with inferior (Infero-Posterior) or lateral (Postero-Lateral) STEMI (1).
One of our fine interns, Daniel Lee, who is also an ECG whiz, found this paper from 2013 and brought it to my attention: The delayed activation wave in non-ST-elevation myocardial infarction. They do not study whether this wave differentiates between MI and non-MI, between STEMI and NonSTEMI, or between OMI and NOMI.
Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. Also note that they allow ST depression c/w posterior MI to be a STEMI equivalent. Kurkciyan et al.
Steffen writes this case: "A few weeks ago I was able to recognize a STEMI because of what I had seen on your blog." "I Steffen wrote: " I remembered the ECG from your blog titled: "STEMI Seen Best in PVC, Diagnosed by Medic, Ignored by Physician" from 2013. I also put them side by side: What do you think?
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?
Code STEMI was activated by the ED physician based on the diagnostic ECG for LAD OMI in ventricular paced rhythm. This was several months after the 2022 ACC Guidelines adding modified Sgarbossa criteria as a STEMI equivalent in ventricular paced rhythm). LAFB, atrial flutter, anterolateral STEMI(+) OMI. Limkakeng AT.
When total LM occlusion does present with STE in aVR, there is ALWAYS ST Elevation elsewhere which makes STEMI obvious; in other words, STE is never limited to only aVR but instead it is part of a massive and usually obvious STEMI. All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
Another overlooked OMI ( Cardiologist limited by STEMI Definition — OMI evident by Mirror Test ) — See My Comment at the bottom of the page in the September 21, 2020 post on Dr. Smith’s ECG Blog. Smith’s ECG Blog. This is a free download ).
If it is STEMI, it would have to be RBBB with STEMI. Although the J-point in each of the 3 inferior leads appears depressed below the baseline — the duration of the depressed ST segment in these leads seemed much shorter to me than what is usually seen with reciprocal ST depression in association with an anterior stemi.
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.’
Although this " Imbalance " of precordial T waves is not see n very often — in the “right” clinical setting, it has been associated with recent OMI ( O cclusion-based MI ) , most often from a LCx culprit artery ( See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM — and ECG Blog #350 ).
The last section is a detailed discussion of the research on aVR in both STEMI and NonSTEMI. The additional ST Elevation in V1 is not usually seen with diffuse subendocardial ischemia, and suggests that something else, like STEMI from LAD occlusion, could be present. Current Emergency and Hospital Medicine Reports (2013) 1:4352.
Other trials that evaluated this subject were the WOEST trial (2013), Pioneer AF-PCI trial (2016), and ISAR-TRIPLE (2015). Explanation: The EKG illustrates an inferior STEMI. Explanation: The RE-DUAL PCI trial evaluated differences between triple therapy and dual therapy using antiplatelets/anticoagulant. Incorrect Answers: A and E.
A prior ECG from 1 month ago was available: The presentation ECG was interpreted as STEMI and the patient was transferred emergently to the nearest PCI center. BOTTOM Line: It can at times be extremely challenging to distinguish between anterior ST elevation from a benign Brugada Phenocopy pattern vs an acute anteroseptal STEMI.
From My Comment in the November 15, 2023 post in Dr. Smith's ECG Blog: Clinical Points about MINOCA: Given the literature citing a 5-15% estimated incidence of MINOCA in patients initially diagosed as having a STEMI or "NSTEMI" — it is important to be aware of the more common entities associated with this entity ( See Figure-2 ).
ECG Blog #193 — Reviews the concept of why the term “OMI” ( = O cclusion-based MI ) should replace the more familiar term STEMI — and — reviews the basics on how to predict the " culprit " artery. ECG Blog #218 — Reviews HOW to define a T wave as being H yperacute ? ECG Blog #351 — reviews the diagnosis of acute posterior OMI.
Although this " Imbalance " of precordial T waves is not seen very often — in the “right” clinical setting, it has been associated with recent OMI ( O cclusion-based MI ) from a LCx culprit artery ( See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM — and ECG Blog #350 ).
The HEART and EDACS scores are helpful to risk stratify patients with chest pain, but they hinge on accurate ECG interpretation: a low score doesn’t apply if the ECG shows STEMI(+)OMI, and shouldn’t be used for STEMI(-)OMI or OMI reperfusion either 2. Int J Cardiol 2013 2. Backus BE, Six AJ, Kelder JC, et al.
2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. Cardiology was consulted and they agreed that the EKG had an atypical morphology for STEMI and did not activate the cath lab. Smith comment: 1) Brugada ECG may have ST shifts in limb leads as well as precordial leads. Bicarb 20, Lactate 4.2,
Failure to do so may result in overlooking subtle ST-T wave changes in a patient "in passage" from a frank STEMI toward reperfusion changes. POINT #2: The initial tracing in today's case does not show acute changes.
Despite the clinical context, Cardiology was consulted due to concerns for a "STEMI". Hyperkalemia mimics STEMI and OMI in many distributions, but probably the most common is the Brugada morphology in V1-V2 which mimics anterior OMI for those who cannot recognize the Brugada pattern. Limb lead reversal can be easily recognized.
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. 2 The astute paramedic recognized this possibility and announced a CODE STEMI. N Engl J Med 2003; 348:1756-1763, 5/1/2013. Look at the aortic outflow tract. What do you see?
Figure 1-1 My colleague, a faithful student of ECG interpretation, handed me the tracing and said that it warranted STEMI activation because of apparent terminal QRS distortion (TQRSD) in V2. ASA 324mg was administered while a STEMI activation was simultaneously transmitted to the nearest PCI center. Attached is the first ECG.
Using person-linked hospitalisation data, we compared International Classification of Diseases (ICD)-coded data with biomarker-classified admission rates for ST-segment elevation MI (STEMI), non-STEMI (NSTEMI) and unstable angina (UA) in Western Australia (WA). Results There were 37 272 ACS admissions in 30 683 patients (64.2%
PEARL # 3: Knowing there is an acute inferior STEMI I looked next to see if there is also acute posterior involvement ( which so often accompanies inferior MI ). But larger-than-expected Q waves in each of the inferior leads ( especially in lead III ) are probably the result of this patients ongoing acute inferior STEMI.
Smith : I recognize this as a STEMI mimic. Although this is not a common phenomenon You will see it on occasion ( See the June 30, 2023 post the November 27, 2023 post and the July 24, 2013 post in Dr. Smith's ECG Blog ). Here is his ECG: There is significant ST Elevation in inferior leads, with reciprocal ST depression in aVL.
50% of LAD STEMI have Q-waves by one hour. Smith : In limb leads, the ST vector is towards lead II (STE lead II STE lead III, which is more likely with pericarditis than with STEMI). This correlates with potentially salvageable myocardium. See Raitt et al.: These findings together are more commonly seen with pericarditis. Hammill, S.
Whereas the patient's initial ECG shows sinus rhythm and nonspecific ST-T wave abnormalities just 24 minutes later , there is now profound bradycardia with a junctional escape rhythm ( YELLOW arrows highlighting retrograde P waves ) and obvious findings of an acute inferior STEMI. SanzRuiz, R., Solis, J., & & FernndezAvils, F.
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