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He denied any known history of CAD, but did report ASCVD risk factors to include HTN, HLD, and DM. I interpreted the ECG as VT with two primary etiological possibilities: 1. Abrupt plaque ulceration of Type 1 ACS leading to VT. Readers of the Smith ECG Blog will probably recognize this a very subtle inferior OMI.
This was sent by an undergraduate (not yet in medical school, but applying now) who works as an ED technician (records all EKGs, helps with procedures, takes vital signs) and who reads this blog regularly. Smith comment : Is the ACS (rupture plaque) with occlusion that is now reperfusing? The ST depressions in I and aVL have resolved.
By Magnus Nossen This ECG is from a young man with no risk factors for CAD, he presented with chest pain. ACS then becomes less likely. Before the lab values returned this patient had a n emergent coronary CT angiogram done that ruled out CAD. How would you assess this ECG? How confident are you in your assessment?
The patient presented to an outside hospital An 80yo female per triage “patient presents with chest pain, also hurts to breathe” PMH: CAD, s/p stent placement, CHF, atrial fibrillation, pacemaker (placed 1 month earlier), LBBB. This case was sent by Amandeep (Deep) Singh at Highland Hospital, part of Alameda Health System.
Similarly, if a patient with known CAD presents with refractory ischemic chest pain, the ECG barely matters: the pre-test likelihood of acute coronary occlusion is so high that they need an emergent angiogram. 1] European guidelines add "regardless of biomarkers".
He had a history of CAD with CABG. Does this patient have ACS? He did not have ACS. The remainder were due to other etiologies, (including NonSTEMI ACS). But approximately 50% were due to non-ACS etiologies. A middle-aged male had a V Fib arrest. There is profound ST depression especially in I, II, V2-V6.
However, a smooth tapering of the mid-RCA was seen, highlighted in red below: How do we explain the MI if no sign of CAD was found? This MI wasn’t caused by a ruptured plaque of CAD - it was a coronary artery dissection of the RCA. SCAD isn’t rare, especially in women Historically SCAD had been identified in 22% of ACS cases in women.
Sent by Anonymous, written by Pendell Meyers A man in his 60s with history of CAD and 2 prior stents presented to the ED complaining of acute heavy substernal chest pain that began while eating breakfast about an hour ago, and had been persistent since then, despite EMS administering aspirin and nitroglycerin. Pre-intervention.
A man in his 70s with past medical history of hypertension, dyslipidemia, CAD s/p left circumflex stent 2 years prior presented to the ED with worsening intermittent exertional chest pain relieved by rest. In our opinion it should not be given in ACS unless you are committed to the cath lab.
Submitted and written by Alex Bracey with edits by Pendell Meyers and Steve Smith Case A 50ish year old man with a history of CAD w/ prior LAD MI s/p LAD stenting presented to the ED with chest pain similar to his prior MI, but worse. link] He was admitted to the cardiology unit for serial troponin measurements and concern for possible ACS.
If this is ACS with Aslanger's pattern , the ST depression vector of subendocardial ischemia (due to simultaneous 3 vessel or left main ACS) is directed toward lead II (inferior and lateral). Thus, this apparently is Aslanger's Pattern (inferior OMI with single lead STE in lead III, with simultaneous subendocardial ischemia).
So, I'm a follower of your blog, and I think I have a interesting case that I attended yesterday." Remember: these findings above are included as STEMI equivalent findings in the 2022 ACC Expert Consensus Decision Pathway on ACS Patients in the ED. Since then, I started looking for OMI EKG findings and not just STEMI.
But it does prove that the patient has coronary disease and makes the probability that his chest pain is due to ACS very very high. It is proven better than angiography alone in stable angina , and also has been shown to improve decisions on stenting non-culprit lesions in ACS. It could be acute, though probably is not.
The fire department, who operate at an EMT level in this municipality, arrived before us and administered 324 mg of baby aspirin to the patient due to concern for ACS. Just because you don't see hemodynamically significant CAD on angiogram does not mean it is not OMI. I could have told you this (and did tell you this) without an MRI.
A middle aged male with no h/o CAD presented with one week of crescendo exertional angina, and had chest pain at the time of the first ECG: Here is the patient's previous ECG: Here is the patient's presenting ED ECG: There is isolated ST depression in precordial leads, deeper in V2 - V4 than in V5 or V6. There is no ST elevation.
The axiom of "type 1 (ACS, plaque rupture) STEMIs are not tachycardic unless they are in cardiogenic shock" is not applicable outside of sinus rhythm. This case represents the same physiologic event as OMI in terms of the result on the myocardium, therefore with identical ECG features, however there may not be ACS!
But if they do present: The very common presentation of diffuse STD with reciprocal STE in aVR is NOT left main occlusion , though it might be due to sub total LM ACS, but is much more often due to non-ACS conditions, especially demand ischemia. Beware crescendo angina in patient with known CAD ST Elevation in aVR Case 7.
These findings are very subtle but suspicious for LAD occlusion, as we have seen in many similar (but less difficult) cases on this blog: A man in his sixties with chest pain at midnight with undetectable troponin How long would you like to wait for your Occlusion MI to show a STEMI? He also had non-acute CAD of the RCA (50%) and LCX (50%).
Written by Pendell Meyers A man in his late 40s with several ACS risk factors presented with a chief complaint of chest pain. The cardiologists felt that the ECG did not represent ACS, and thought it was more likely pericarditis, so they did not take him to the cath lab. His first troponin T then resulted elevated at 0.19
She had zero CAD risk factors. Now you have ECG and troponin evidence of ischemia, AND ventricular dysrhythmia, which means this is NOT a stable ACS. hours of substernal chest pressure. It was non-radiating and without other associated symptoms except for nausea. Here was her ECG at time zero: What do you think?
Although this is considered a "STEMI equivalent" and the ACC/AHA guidelines even approve of thrombolytics for ACS with this ECG, the usual criteria used to alert the cath lab team of an inbound Code STEMI are not met by this ECG. For instance: sepsis, bleeding, dehydration, hypoxia, and mild ACS.
CAD-RADS category 1. --No CT Coronary angiogram is usually used to make ACS much less likely in the context of a patient who is ruled out for acute MI by troponins. Now, with elevated troponins, Wellens' syndrome is likely. A CT Coronary angiogram was ordered. Here are the results: --Minimally obstructive coronary artery disease. --LAD
A middle-aged male with h/o CAD and stents presented with typical chest pressure. It is highly associated with proximal LAD occlusion or severe left main ACS and with bad outcomes. Here is his ECG: The resident was alarmed at the "ST elevation in III with reciprocal ST depression in aVL" Are you alarmed? This is a very common misread.
She did not receive any opioids (which would mask her pain without affecting any underlying ACS). She also had non-acute CAD of the left main (50%) and LCX (75%). By the time the patient arrived at our facility, she had received aspirin and nitroglycerin, and her pain had apparently completely resolved. They opened it.
The patient was transferred immediately for angiogram which revealed no significant CAD, and no intervention was performed. Learning Points: The myocardium doesn't know the etiology of OMI (ACS, spasm, dissection, embolus, etc.), That said, ACS is by far the most common and treatable cause.
He did have a family history notable for early CAD. A final ECG was perfomed on hospital day 2: Persistent ST elevation in the inferior leads with slight reciprocal ST depression in aVL Teaching points - It is essential to consider ACS in all age groups. He denied drug or alcohol use. ng/mL (ULN 16,000 ng/L, mildly elevated CRP of 8.4
But thankfully, when the clinical context is clearly and highly concerning for ongoing ischemia from ACS, this distinction doesn't matter much. The procedure was described as very complex due to severe multivessel CAD, but ultimately PCI was successfully performed to the ostial LCX. Pre-intervention.
Negative trops and negative angiogram does not rule out coronary ischemia or ACS. It is a judgment call retrospectively, but to assume there is no ACS at presentation is very risky, especially in a patient with previously diagnosed severe CAD and poor LV function. It must be diagnosed with IVUS or Optical Coherence Tomography.
Case A 68 year old man with a medical history of hypertension, hyperlipidemia, and CAD with stent deployment in the RCA presented to the emergency department with chest pain. html ) Despite an undetectable troponin and three normal EKGs, the nature of the patients symptoms and his positive cardiac history warranted concern for ACS.
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