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ST-elevation myocardial infarction (STEMI) is a critical cardiovascular emergency characterized by acute coronary artery occlusion and subsequent myocardial injury. The pathophysiology of MVO is systematically reviewed, followed by an evaluation of clinical studies on thrombus aspiration and intracoronary thrombolysis in STEMI management.
Background Despite restoration of epicardial blood flow in acute ST-elevation myocardial infarction (STEMI), inadequate microcirculatory perfusion is common and portends a poor prognosis. IC thrombolysis was associated with a significantly lower incidence of MACE (RR=0.65, 95% CI 0.51 to 2.67; I 2 =25%; p<0.0001).
Time window s for intervention for thrombolysis in STEMI starts from onset of chest pain, but when it comes to primary PCI, a different time window takes the center stage pushing the former to the background. How can we have uniform std of 90-120 minutes D2B in all STEMI cases ? Why is this disparity?
Introduction Differences in pathophysiology, clinical presentation, and natural course of ST-elevation myocardial infarction in female patients due to either spontaneous dissection (SCAD-STEMI) or atherothrombotic occlusion (type 1 STEMI) have been discussed. vs. 1.8 ± 5.1%, p = 0.002). vs. 1.8 ± 5.1%, p = 0.002).
Linear regression identified prepercutaneous coronary intervention Thrombolysis in Myocardial Infarction flow (=3.35,P<0.001) CONCLUSIONS:EGE-derived MSI was associated with prepercutaneous coronary intervention Thrombolysis in Myocardial Infarction flow and microvascular injuries.
Is primary PCI superior to thrombolysis in the first hour of STEMI ? Steg PG, Bonnefoy E, Chabaud S, Lapostolle F, Dubien PY, Cristofini P, Leizorovicz A, Touboul P; Comparison of Angioplasty and Prehospital Thrombolysis In acute Myocardial infarction (CAPTIM) Investigators. No, it is not. Read ref 1, 2. Reference 1.
BackgroundST-segment elevation myocardial infarction (STEMI) persists to be prevalent in the elderly with a dismal prognosis. Nevertheless, the influence of aging on the functionality of EPCs in STEMI is not fully understood.MethodThis study enrolled 20 younger STEMI patients and 21 older STEMI patients.
“ 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?
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).
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.
Methods:STEMI patients who underwent coronary revascularization therapy and cardiac magnetic resonance (CMR) at about 4 days and 6 months between 2017 and 2023 were included.
A second 12 Lead ECG was recorded: This is a testament to the dynamic nature of coronary thrombosis and thrombolysis. it has been subsequently deemed a STEMI-equivalent. The patient verbalized spontaneous improvement just before 324mg ASA administration. But the lesion is still active!
Smith : there is some minimal ST elevation in V2-V6, but does not meet STEMI criteria. Transient STEMI has been studied and many of these patients will re-occlude in the middle of the night. Is it normal STE? The computer thinks so, and the physician thinks that is quite possible. However , there is terminal QRS distortion in lead V3.
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.
Permanently deferred PCI is other wise called medical management , is practiced by some inferior cardiologists or GPs who never refer such patients to higher centers after a stand alone thrombolysis) * The FFR, iFR RFR, related stuff What if if we are completely blinded to the status of Non IRA vessel ? What do you mean ?
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."
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.
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. LV Thrombus , 1.5 0 0 1 95 544 MMRF 4 1 638 14.0 Methods: Vermeer et al.
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.
I am going to code this as an acute STEMI as he had transient ST elevation which started to evolve in the emergency department but I think this is most appropriately termed STEMI." When is it anterior STEMI? No formal echo was done, and EF was normal on ventriculogram during cath, with no obvious wall motion abnormalities.
Smith15, and PERFECT Study Author Group 1 Hennepin County Medical Center, 2 Minneapolis Medical Research Foundation, 3 Background : The Smith-modified Sgarbossa criteria (MSC) are frequently recommended for diagnosing acute coronary occlusion (ACO; STEMI-equivalent) in the setting of ventricular paced rhythm (VPR).
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.
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.
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.
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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