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ST-elevation myocardial infarction (STEMI) is a critical cardiovascular emergency characterized by acute coronary artery occlusion and subsequent myocardial injury. However, despite successful revascularization, microvascular obstruction (MVO) remains a major challenge, contributing to adverse clinical outcomes.
Background Despite restoration of epicardial blood flow in acute ST-elevation myocardial infarction (STEMI), inadequate microcirculatory perfusion is common and portends a poor prognosis. Intracoronary (IC) thrombolytic therapy can reduce microvascular thrombotic burden; however, contemporary studies have produced conflicting outcomes.
“ Since Intravenous lysis looks too simplistic, that do not need expertise, and lacks a commercial trail, it is wrongly depicted as inferior management strategy in STEMI “ Every one of us is equally responsible for this sorry state of affairs. In this context, we need a movement to revive the pre-hospital thrombolysis.
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). A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty.
Will evolve into STEMI by prothrombotic trigger of lytic agent ECG will get normalised with clinical stability in some Nothing happens. Majority of Wellens end up as NSTEMI, statistics tells us about 20% of them can be STEMI in incognito mode demanding lysis or emergency PCI. ECG will remain same. How to manage Wellen syndrome?
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.
Background:Slow flow phenomenon is impaired coronary flow during percutaneous coronary intervention (PCI) in absence of mechanical obstruction, and it is associated with deteriorated outcome.
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).
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? J Electrocardiol 2013;46:240-8 2.
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. Type B waves are deeper and symmetric. When the patient had chest pain, prior to nitroglycerine, what do you think the ECG showed ? A stent was placed.
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."
cm diameter in the apex The presence of thrombus led the clinicians to state that this was a "late presentation STEMI." It does take some time for thrombus to form, but the EKG and the troponin profile show that this was NOT a late presentation STEMI. Findings: Greater reciprocal ST depression correlated strongly with poor outcome.
See these posts for Wellens' mimics: Pseudo-Wellens' Syndrome due to Left Ventricular Hypertrophy (LVH) Anterior STEMI? It even meets STEMI criteria: 2.5 A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty. Am Heart J.
Details cannot be shared here, but suffice it to say that inability to recognize acute occlusive myocardial infarction in the presence of ventricular paced rhythm contributed to a poor outcome. Blinded physicians adjudicated angiogram reports for coronary lesions and thrombolysis in myocardial infarction (TIMI) flow score.
He has a history of coronary artery disease and a STEMI two years prior that was treated with primary PCI. At the time of this initial ED ECG, his symptoms were improving ECG #1 on admission to the ED The patient was not seen quickly in the ED as it was a busy shift and the ECG did not meet STEMI criteria. The below ECG was recorded.
It is a long read, meant only for those who want to know the hidden intricacies in the concept of “Time window” in STEMI and its important Implication in patient care. [08/11, 08/11, 12:07] Dr S Venkatesan: Is the therapeutic time window for primary PCI and thrombolysis same ? [08/11, How can they be different? [08/11,
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