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A male in his 40's who had been discharged 6 hours prior after stenting of an inferoposterior STEMI had sudden severe SOB at home 2 hours prior to calling 911. Is this acute STEMI? Is this an acute STEMI? -- Unlikely! The hypertension alone is the likely etiology of the pulmonary edema. He had no chest pain.
We discover that for STEMI/OMI vs subendocardial ischemia, we should look for STEMI(-)OMI, subacute OMI, and OMI in the presence of LBBB and RBBB, and consider the differential for diffuse ST depression with reciprocal ST elevation in aVR.
A 63 year old man with a history of hypertension, hyperlipidemia, prediabetes, and a family history of CAD developed chest pain, shortness of breath, and diaphoresis after consuming a large meal at noon. He called EMS, who arrived on scene about two hours after the onset of pain to find him hypertensive at 220 systolic.
Written by Pendell Meyers, few edits by Smith A man in his 60s with history of stroke and hypertension but no known heart disease presented with chest pain that started on the morning of presentation at around 8am. So it is very unclear to me whether or not "posterior STEMI" is actually a recognized entity under our current guidelines.
He had some cardiac risk factors including hypertension, on meds, but no previous coronary disease. He had an immediate ED ECG: There is artifact, but the findings appear to be largely gone now The diagnosis is acute MI, but not STEMI. His pain was intermittent and he was vague about when it was present and when it was resolved.
So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. The patient was admitted as ‘NSTEMI’ which is supposed to represent a non-occlusive MI, but the underlying pathophysiology is analogous to a transient STEMI. See these posts: Chest Pain, ST Elevation, and an Elevated Troponin: Should we Activate the Cath Lab?
Her vitals signs were remarkable for marked hypertension. would require the ST/S ratio to be 25% for diagnosis of STEMI in LVH. The physician was concerned about STEMI, but also worried that she was overreacting, with the potential that LVH was producing a "STEMI-mimic." The criteria of Armstrong et al. References 1.
He learned more about the patient: A 77 year old female with a past medical history of hypertension and hyperlipidemia presented to the ED at around 0520 after waking up at 0400 with 10/10 chest heaviness radiating to both arms. The patient had continued to have chest pain.
The Minneapolis Heart Institute Foundation (MHIF) is presenting leading research focused on trends in ST-elevation myocardial infarction (STEMI), the most severe form of a heart attack, at the American College of Cardiology’s Annual Scientific Session (ACC.24), 24), being held April 6-8 in Atltanta, GA.
The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. The paramedic notes called STEMI into question: “EMS disagree with monitor for STEMI callout. Past medical history included diabetes and hypertension.
Purpose Construction of a prediction model to predict the risk of major adverse cardiovascular events (MACE) in the long term after percutaneous coronary intervention (PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI).
Written by Willy Frick with edits by Ken Grauer A woman in her 70s with a history of hypertension presented with acute onset shortness of breath. The conventional machine algorithm interpreted this ECG as STEMI. See this post of RV MI with both McConnell sign and "D" sign: Inferior and Posterior STEMI.
A 50-something male with hypertension and 20- to 40-year smoking history presented with 1 week of stuttering chest pain that is worse with exertion, which takes many minutes to resolve after resting and never occurs at rest. Patient still not having chest pain however this is more concerning for OMI/STEMI. Aspirin given. Am J Cardiol.
Sent by anonymous, edited by Pendell Meyers A man in his 50s with history only of hypertension presented with acute chest pain that started 45 minutes prior to presentation while doing yard work. Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI").
Written by Willy Frick A man in his 50s with history of hypertension, hyperlipidemia, and a 30 pack-year smoking history presented to the ER with 1 hour of acute onset, severe chest pain and diaphoresis. For national registry purposes, this will be incorrectly classified as a STEMI.) Most STEMI have peak cTnI greater than 10.0.
It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI. A mong patients with STEMI, ventricular septal rupture is the most common and free wall rupture is the least common.
Written by Willy Frick A 67 year old man with a history of hypertension presented with three days of chest pain radiating to his back. The cardiologist agreed that the ECG was suggestive of STEMI, but the facility's cath lab was apparently not available and he therefore recommended emergent transfer to a cath capable facility.
He stated that it is "an acute change from previous" in an elderly smoker with hypertension, syncope, and abdominal pain. However, there are morphologies of Takotsubo that cannot be distinguished from STEMI. Takotsubo This looks like and infero-posterior STEMI, but the QT is bizarrely long. Here are some examples: 1.
She is somewhat hypertensive, but her vital signs are otherwise normal. These elevations meet STEMI criteria ( ≥ 1mm in 2 contiguous leads). While this may be change that is reciprocal to an Acute/Subacute Inferior STEMI, the problem is that LV aneurysm may also manifest with this reciprocal change. This case is tough.
The computer calls it a STEMI. Never chest pain but had to treat as hypertensive emergency. In fact, severe hypertension by itself can lead to greatly increased oxygen demand and type 2 acute MI, sometimes with ST Elevation. See this case of Type 2 STEMI due to severe hypertension. Here are more Type II STEMI.
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?
Case submitted and written by Mazen El-Baba MD, with edits from Jesse McLaren and edits/comments by Smith and Grauer A 90-year old with a past medical history of atrial fibrillation, type-2 diabetes, hypertension, dyslipidemia, presented with acute onset chest/epigastric pain, nausea, and vomiting. BP was 110 and oxygen saturation was normal.
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 He had no further risk factors for atherosclerosis besides hypertension. Steffen wrote: " I remembered the ECG from your blog titled: "STEMI Seen Best in PVC, Diagnosed by Medic, Ignored by Physician" from 2013.
The "criteria" for posterior STEMI are 0.5 Is it STEMI or NonSTEMI? The patient had no hypertension, no tachycardia, a normal hemoglobin, no drug use, no hypotension/shock, no murmur of aortic stenosis. The troponin I returned at 4.1 ng/mL (ULN = 0.030 ng/mL) , diagnostic of myocardial injury. mm STE in one lead.
A middle-aged woman with a history of hypertension presented with typical chest pain. Her BP was 160/80. Here was her presenting ECG, with chest pain: Inferior leads show hyperacute T-waves and reciprocal STD in aVL, with a reciprocally hyperacute T-wave in aVL. This is all but diagnostic of inferior OMI. There is also subtle STE in V1-V3.
Case An 82 year old man with a history of hypertension presented to the ED with chest pain at 1211. His EKG with worse pain now shows enough ST elevation to meet STEMI criteria. The EKG was read by the conventional computer algorithm as diagnostic of “ACUTE MI/STEMI”. There is pericardial tamponade.
A 50-something man with history only of alcohol abuse and hypertension (not on meds) presented with sudden left chest pain, sharp, radiating down left arm, cramping, that waxes and wanes but never goes completely away. Because we are hypnotized the STEMI paradigm. "If It was not a STEMI) 1. Symptoms were classic for MI 3.
Vital signs were noted to be unremarkable with respect to any hypo-hypertensive crisis, hypoxia, etc. He denied any known medical history, specifically: coronary artery disease, hypertension, dyslipidemia, diabetes, heart failure, myocardial infarction, or any prior PCI/stent. Fire/EMS crews found him clammy and uncomfortable.
As always, LAD OMI need not meet STEMI criteria and usually does NOT! Septal STEMI with ST elevation in V1 and V4R, and reciprocal ST depression in V5, V6 Case 8. Missed LAD Occlusion with Swirl, peak trop 80 ng/mL (equivalent to 80,000 ng/L), diagnosed as "Non-STEMI" Case 9. A 49 year old man with chest pain.
Any cause of pulmonary hypertension. Troponin T peaked at 2074 ng/L (very high, typical of OMI/STEMI). large ASD, partial anomalous pulmonary venous return, significant tricuspid regurgitation, carcinoid valvular disease, etc,) 2) Conditions causing pressure overload of the RV. The LV EF was 57% at formal echo.
This was a male in his 50's with a history of hypertension and possible diabetes mellitus who presented to the emergency department with a history of squeezing chest pain, lasting 5 minutes at a time, with several episodes over the past couple of months. New ST elevation diagnostic of STEMI [equation value = 25.3
This meets "STEMI criteria" However, there is very high voltage, with a very deep S-wave in V2 and tall R-wave in V4. The morphology is not right for STEMI. My interpretation: LVH with secondary ST-T abnormalities, exaggerated by stress, not a STEMI. This is very good evidence that the ST elevation is not due to STEMI.
The patient was in his 50s with history of hypertension, diabetes, seizure disorder, and smoking, but no known coronary artery disease. He wrote in his note that "The EKG showed early repolarization in I, V2-V3 but no clear STEMI pattern." See far below for data on 24 troponin T in STEMI and NSTEMI, and correlation with infarct size.
The Queen of Hearts correctly says: Smith : Why is this ECG which manifests so much ST Elevation NOT a STEMI (even if it were a 60 year old with chest pain)? He was mildly tachycardic (105-110 bpm) and hypertensive (157/92 mm Hg) on arrival. Physician interpretation: "No STEMI." Physician: "No STEMI."
He had a history of hypertension, but no history of heart problems. Computer interpretation: SINUS RHYTHM NON-DIAGNOSTIC ANTEROLATERAL ST ELEVATION BORDERLINE ECG The overreading cardiologist confirmed the computer interpretation (did not diagnose OMI or STEMI). Since the threshold for "STEMI" is 2.0 LAD occlusion.
We hypothesize that cardiopulmonary exercise testing (CPET) may be helpful in clinical assessment of patients reporting SOB on ticagrelor.Case presentation:66-yo female with history of arterial hypertension, DM type 2 and prior MI presented with STEMI and successfully underwent urgent PCI of RCA and LAD. plus low-dose aspirin.
Some patients will not progress (or not as quickly) to obvious STEMI, as in this case. Sometimes serial ECGs minimizes the delay. What will you do for this patient transferred to you who is now asymptomatic? Nevertheless, they also will get enormous benefit from emergent cath due to preemption of progression to full thickness MI.
This patient, who is a mid 60s female with a history of hypertension, hyperlipidemia and GERD, called 911 because of chest pain. A mid 60s woman with history of hypertension, hyperlipidemia, and GERD called 911 for chest pain. This has resulted in an under-representation of STEMI MINOCA patients in the literature. Circulation.
Sent by Drew Williams, written by Pendell Meyers A man in his 50s with history of hypertension was standing at the bus stop when he developed sudden onset severe pressure-like chest pain radiating to his neck and right arm, associated with dyspnea, diaphoresis, and presyncope. When is it anterior STEMI? Is this Acute Ischemia?
His medical history includes hypertension, a decade-long battle with diabetes, ischemic heart disease, a coronary bypass graft surgery ten years ago, a diagnosis of congestive heart failure for the last five years, and a prior ICD implantation five years ago. That was also my initial concern. No "baseline" ECG is available for comparison.
A woman in her 40's who was healthy, except for hypertension, was at work when she suddenly complained of neck and shoulder pain and then collapsed. The last section is a detailed discussion of the research on aVR in both STEMI and NonSTEMI. It was witnessed, and CPR was performed by trained individuals. see below).
Here is a repeat ECG 45 minutes later with persistent chest pain: Obviously progressing into a clear STEMI. Meets formal STEMI criteria in V2-V3. The ECG was interpreted as non-ischemic. The patient was closely monitored. Also notice clearly hyperacute T waves in V2-V4, as well as worsening STD in V5-6 and II, III, aVF.
A 56 year old male with a history of diabetes, dyslipidemia, hypertension, and coronary artery disease presented to the emergency department with sudden onset weakness, fatigue, lethargy, and confusion. At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high).
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