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Occlusion myocardialinfarction is a clinical diagnosis Written by Willy Frick (@Willyhfrick). Recall from this post referencing this study that "reciprocal STD in aVL is highly sensitive for inferior OMI (far better than STEMI criteria) and excludes pericarditis, but is not specific for OMI." The case continues. Worrall, C.,
Background Despite the crucial role of Chest pain centers (CPCs) in acute myocardialinfarction (AMI) management, China's mortality rate for ST-segment elevation myocardialinfarction (STEMI) has remained stagnant. Conclusion CPC quality control metrics affect STEMI mortality based on Killip class.
Cath lab declined as it is not a STEMI." And now this finding is even formally endorsed as a "STEMI equivalent" in the 2022 ACC guidelines!!! Another myocardial wall is sacrificed at the altar of the STEMI/NonSTEMI mindset. Opiates are associated with worse outcomes in MyocardialInfarction. Abstract 556.
Background ST elevation myocardialinfarction (STEMI) represents a cardiac emergency. Inferior STEMI represents a dilemma for cardiologists. Methods We performed a single-centre retrospective cohort analysis of all patients admitted to our hospital from 2008 to 2020 with a diagnosis of inferior STEMI.
BackgroundIn Thailand, access to specific pharmaceuticals and medical devices for ST-elevation myocardialinfarction (STEMI) patients is restricted within certain healthcare systems, leading to inequalities in the quality of medical care among different healthcare systems.
Background It is unclear how COVID-19 pandemic affected care and outcomes among patients who are diagnosed with ST-elevation myocardialinfarction (STEMI) in the USA. Results There were 1 050 905 hospitalizations with STEMI, and there was an 8.2% reduction in admissions in 2020. reduction in admissions in 2020.
Background Despite improvements in outcomes of ST elevation myocardialinfarction (STEMI), ventricular septal rupture (VSR) remains a known complication, carrying high mortality. The contemporary incidence, mortality, and management of post-STEMI VSR remains unclear. and 10 ± 1.2%
I sent this to the Queen of Hearts So the ECG is both STEMI negative and has no subtle diagnostic signs of occlusion. Non-STEMI guidelines call for “urgent/immediate invasive strategy is indicated in patients with NSTE-ACS who have refractory angina or hemodynamic or electrical instability,” regardless of ECG findings.[1]
Their OMI Manifesto details how use of standard STEMI criteria results in an unacceptable level of inaccuracy, in which an estimated 25-30% of acute coronary occlusions are missed! The article by Aslanger, Smith et al that is featured above in today’s post has just been published.
There’s inferior ST depression which is reciprocal to subtle lateral convex ST elevation, and the precordial T waves are subtly hyperacute – all concerning for STEMI(-)OMI of proximal LAD. There’s ST elevation I/aVL/V2 that meet STEMI criteria. This is obvious STEMI(+)OMI of proximal LAD. Non-STEMI or STEMI(-)OMI?
Objectives To ascertain whether invasive assessment of coronary physiology soon after recanalisation of the culprit artery by primary percutaneous coronary intervention is associated with the development of microvascular obstruction by cardiac magnetic resonance in patients with ST-segment elevation myocardialinfarction (STEMI).
Background Despite advances in percutaneous coronary intervention (PCI) for ST segment elevation myocardialinfarction (STEMI), in-hospital mortality remains a concern, highlighting the need for the identification of additional risk factors such as serum iron levels. μmol/L) and a control group (Fe ≥7.8 μmol/L).
Data were fitted to segmented regression models with March 2020 as the breakpoint. Data on 21 001 patients were included (7057 ST-elevation myocardialinfarction (STEMI), 7649 non-ST elevation myocardialinfarction (NSTEMI) and 6295 unstable angina).
EKG from triage: Here is his previous ECG: Normal ST Elevation Resident's interpretation: Reperfusion pattern/Wellens' with biphasic T waves in V2 and V3, and in comparison to an EKG in 2020 this is new. Patient still not having chest pain however this is more concerning for OMI/STEMI. Labs ordered but not yet drawn. Aspirin given.
associated typical MyocardialInfarction therapies such as statins and ACE inhibitors with significantly decreased 1 year mortality in MINOCA patients, which suggests that they do indeed have a similar pathophysiology to MI patients with obstructive coronary disease. MINOCA I do not have the bandwidth here to write a review of MINOCA.
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.
There is an obvious inferior posterior STEMI(+) OMI. Literature cited In inferior myocardialinfarction, neither ST elevation in lead V1 nor ST depression in lead I are reliable findings for the diagnosis of right ventricular infarction Johanna E. What is the atrial activity? Is it sinus arrest with junctional escape?
Triage ECG (no prior for comparison): Computer algorithm read: "Sinus rhythm, low voltage QRS, inferior myocardialinfarction, probably old." Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI"). Academic Emergency Medicine 27(S1): S220; May 2020.
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.
Methods We adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 during the execution of this review. The models were mainly constructed using data from individuals diagnosed with ST-segment elevation myocardialinfarction (STEMI).
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%
We present the cumulative percutaneous coronary intervention (PCI) data of all comers (stable angina and acute coronary syndromes [ACS]) who presented to Hadi Clinic between January 2018 and December 2020. A total of 567 patients underwent coronary catheterisation for the three-year period between January 2018 and December 2020.
Clin Chem [Internet] 2020;Available from: [link] Smith mini-review: Troponin in Emergency Department COVID patients Cardiac Troponin (cTn) is a nonspecific marker of myocardial injury. For this reason, some argue that it should not be measured in patients unless acute myocardialinfarction is on the differential diagnosis.
So we activated the Cath Lab Angiogram: Impression and Recommendations: Culprit for the patient's anterior ST segment myocardialinfarction and out of hospital V-fib cardiac arrest is a thrombotic occlusion of the mid LAD The first troponin returned barely elevated at 36 ng/L (URL = 35) In our study of initial troponin in STEMI, 26.8%
They recorded a third ECG before intervention: No significant difference Angiogram : Impression and Recommendations: Culprit for the patient's non-ST elevation myocardialinfarction is a thrombotic occlusion of the mid circumflex Formal Echo Normal left ventricular cavity size, normal wall thickness and normal LV systolic function.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. Troponin T peaked at 38,398 ng/L ( = a very large myocardialinfarction, but not massive-- thanks to the pre-PCI spontaneous reperfusion, and rapid internvention!! ). The below ECG was recorded. Inotropic medication was continued.
The ECG is diagnostic of occlusion myocardialinfarction (OMI). It definitely does not fulfill STEMI criteria, and I would argue that it would not lead to cath lab activation in most centers. The overall read is OMI with HIGH confidence. == Below is the ECG of Patient #2 — as interpreted by the QOH.
This is a troponin I level that is almost exclusively seen in STEMI. In this case, profound shock for 1 hour would result in the same degree of infarction. A followup ECG was recorded 2 days later: No definite evidence of infarction. So this is either a case of MINOCA, or a case of Type II STEMI. Troponin I rose to 44.1
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.’
If it is STEMI, it would have to be RBBB with STEMI. Only 5-18% of ED patients with chest pain have a myocardialinfarction of any kind. The patient presented with chest pain. Here is the ECG: What do you think? I frankly did not know what to think. Is it Brugada pattern? But in a very unusual pattern. Only 1-5% have OMI.
Angiogram: Culprit for the patient's inferior ECG changes and non-ST elevation myocardialinfarction is a 100% acute thrombotic occlusion of the proximal RCA. The patient was diagnosed with a"Non-STEMI." Here is the main learning point: The infarct was due to an occluded artery (Occlusion MI, OMI).
Here is the ED ECG on arrival: Less STE/STD Provider's Clinical Impression: "findings concerning for myocardialinfarction, likely proximal LAD or Left main." The artery is open, but flow is insufficient to perfuse the entire myocardial thickness (subendocardial AND subepicardial). NTG drip started. Pain better still.
Such cases are classified as MINOCA (MyocardialInfarction with Non-Obstructed Coronary Arteries). 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. It can only be seen by IVUS.
I knew that, if the patient had presented with chest discomfort, that this ECG is diagnostic of inferior posterior OMI, even though it is not a STEMI. Unusual and puzzling, as there was a large focal acute MI) Final Diagnosis: Acute MI, Non ST Elevation MyocardialInfarction.
The ECG was read as "No STEMI" and the patient was treated like an average chest pain patient (despite the fact that a chest pain patient with active pain and active subendocardial ischemia is very high risk). A New ST-segment elevation myocardialinfarction equivalent pattern? Academic Emergency Medicine 27(S1): S220; May 2020.
There is clearly sufficient STE for STEMI criteria in leads V2 and aVL, but lead I has less than 1.0 mm of STE - thus, technically this ECG does not meet STEMI criteria, although it is a quite obvious OMI. This ECG was immediatel y discussed with the on-call cardiologist who said the ECG was "concerning but not a STEMI."
His father and brother both died of myocardialinfarction at ages 61 and 45, respectively. STEMI was activated and the patient went to Cath on arrival. New insights into the use of the 12 Lead Electrocardiogram for diagnosing Acute MyocardialInfarction in the emergency department. 2] Aslanger, E., 3] deWinter, R.
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. Am J Emerg Med 2020 3. Shin YS, Ahn S, Kim YJ. Bracey A, Meyers HP, Smith SW.
Practice putting the probe on the chest of someone with an obvious STEMI(+) OMI in order to look for regional wall motion abnormalities. In this study, Smith and others show that the initial high sensitivity troponin is often below the 99th percentile in true STEMI (+) OMI (and sometime even below a very low threshold). [1] Gray, A.,
V5-V6) of any amplitude, is specific for Occlusion MyocardialInfarction (vs. OMI that are not STEMI can be very subtle and difficult to diagnose even though the findings are very specific. Posterior infarctions often ( though not always ) result in an increase in R wave amplitude in anterior leads.
Alternatively , it is someone who has an old myocardialinfarction and is now very sick with something else. Dyspnea, Right Bundle Branch block, and ST elevation Here are two more cases where the differential diagnosis is acute OMI vs. LV aneurysm: Is this acute STEMI? Below is my response. There is sinus tach. LV Aneurysm?
Here is the repeat ECG at 52 minutes after arrival to triage: Obvious posterolateral STEMI Angiographic findings: 1. page 1932 • “The application of STEMI ECG criteria on a standard 12-lead ECG alone will miss a significant minority of patients who have acute coronary occlusion. (21) Left main: no significant stenosis.
See our publication: ST depression in lead aVL differentiates inferior ST-elevation myocardialinfarction from pericarditis There is STE in inferior leads, high lateral leads, and V4-V6. Smith and Meyers to diagnose both obvious (STEMI) and subtle OMI. And there is ST depression in V2 and V3, all but diagnostic of posterior OMI.
== MY Comment by K EN G RAUER, MD ( 9/17/2020 ): == Todays patient is a previously healthy, 60-something year-old woman who presented with chest pain that began at a reception. However, the cath lab activation was cancelled by the on-call interventionalist who felt the diagnosis of acute STEMI could not be made because of the LBBB.
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