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The Queen of Hearts disagrees, diagnosing OMI with high confidence: Case Continued: The EKG was not immediately recognized by the emergency provider, who ordered a CT scan to rule out aortic dissection at 1419. Most STEMI have peak troponin I over 1000 ng/L and most NSTEMI below that level.
An echocardiogram confirmed aorticstenosis with a large pressure gradient. Thus, this patient had increased ST elevation (current of injury) superimposed on the ST elevation of LVH and simulating STEMI. The next day, and angiogram showed normal coronary arteries. He awoke and did well.
is very specific for STEMI , and there is some evidence, as well as rationale, that a paced rhythm behaves similarly. Here is one case of anterior STEMI in a paced rhythm. Here is a case of lateral STEMI in a paced rhythm. He has had previous angiograms showing "large vessels" and "no significant coronary disease."
Look at the aortic outflow tract. Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. The diagnostic coronary angiogram identified only minimal coronary artery disease, but there was a severely calcified, ‘immobile’ aortic valve.
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? His response: “subendocardial ischemia.
The estimated left ventricular ejection fraction is 58 % Aorticstenosis, mild, 9.0 We found that 38% of out of hospital ventricular fibrillation was due to STEMI. The patient thus did not need immediate angiography. An echocardiogram showed: Left ventricular hypertrophy concentric. mmHg mean gradient. cm^2 valve area.
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 aorticstenosis. We also looked at his aortic root by both parasternal and suprasternal views, and the aorta was normal.]
Smith : there is some minimal ST elevation in V2-V6, but does not meet STEMI criteria. They also wanted an aortic CT which was negative. Transient STEMI has been studied and many of these patients will re-occlude in the middle of the night. Is it normal STE? However , there is terminal QRS distortion in lead V3.
But limitation of this ST elevation to a single lead is not consistent with any distribution of a STEMI. The plan was to proceed as soon as possible with aortic valve replacement. This patient needed prompt aortic valve replacement. Then there is the significant ST elevation we see in lead V1.
It may be difficult to read STEMI in the setting of RBBB. There is, however, a long QT also, with abnormal T-waves, but this is not STEMI. An elderly patient with a ruptured abdominal aortic aneurysm: Formal ECG Interpretation (final read in the chart!) : "Inferior ST elevation, lead III, with reciprocal ST depression in aVL."
When total LM occlusion does present with STE in aVR, there is ALWAYS ST Elevation elsewhere which makes STEMI obvious; in other words, STE is never limited to only aVR but instead it is part of a massive and usually obvious STEMI. All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
LAD plaque with 0-25 percent stenosis. No signs for aortic dissection or pulmonary embolus. --"Results were discussed with the ordering physician. The LAD has moderate 40% ostial-proximal LAD stenosis and severe 90% mid LAD stenosis involving first diagonal branch. --The Transient STEMI is at high risk of re-occlusion.
Due to the severity of the pain and the high BP, they obtained an aortic dissection CT. Here is the repeat ECG at 52 minutes after arrival to triage: Obvious posterolateral STEMI Angiographic findings: 1. Left main: no significant stenosis. RCA: Dominant: Mid 50-60% stenosis. At this point, the cath lab was activated.
They found non-obstructive CAD, with only a 20% stenosis of OM2 and 10% RCA. The next morning the patient went for his routine echocardiogram, where the operator noticed a dilated aortic root at 5.47 cm with severe aortic insufficiency. A repeat ECG was performed and cardiology was re-consulted: Roughly unchanged. Pericarditis?
There is ventricular hypertrophy in the absence of abnormal loading conditions, such as aorticstenosis, or hypertension, for example – of which the most common variant is Asymmetric Septal Hypertrophy. This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital.
Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). Also see these posts of Type II STEMI. An EKG from a year prior was available for comparison: The ED physician noted Initial EKG here read by the computer as a STEMI, however, there is a very poor baseline and a lot of artifact. See reference and discussion below.
The cath lab was deactivated by cardiologist on arrival at ED because it was "not a STEMI". No thoracic aortic hematoma, aneurysm or dissection. First obtuse marginal also had an 80% stenosis and was stented. Pt received 324 ASA and 2 sprays of nitro with improvement. Cath lab was activated by EMS and transported emergent."
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