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No ischemia. This is a conundrum, because it is clear that the patient is having an acute MI, the ECG is dynamic, but the pain is very mild and there is no ECG evidence of active transmural ischemia. We already know that the ischemia is ongoing, though mild (because of the persistent pain). The culprit was opened and stented.
He underwent coronary stenting (uncertain which artery). Such T-waves are almost always reciprocal to ischemia in the region of aVL (although aVL looks n ormal here) , and in a patient with chest pain are nearly diagnostic of ischemia. Ischemia on the ECG can be very subtle and is easily missed. Lesson : 1.
Important point: when there is diffuse subendocardial ischemia but no OMI, a wall motion abnormality will not necessarily be present. They agreed ischemia was likely in the setting of demand given DKA and infection. That this is all demand ischemia is unlikely. Lung exam showed diffuse B lines bilaterally. Aslanger's pattern.
Angiogram reportedly showed acute thrombotic occlusion of the first obtuse marginal which was stented. V5-V6) of any amplitude, is specific for Occlusion MyocardialInfarction (vs. non-occlusive ischemia) Ongoing ischemic symptoms in NSTEMI is already an indication for emergent cath, regardless of the ECG.
This EKG is diagnostic of transmural ischemia of the inferior wall. Smith: note also the terminal QRS distortion in lead III (absence of S-wave without a prominent J-wave). . __ Smith comment 1 : the appropriate management at this point is to lower the blood pressure (lower afterload, which increases myocardial oxygen demand).
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. The baseline ECG is basically normal with no ischemia. In my opinion, I think it looks more like subendocardial ischemia.
In any case, the ECG is diagnostic of severe ischemia and probably OMI. So this could be myocarditis but in my opinion needs an angiogram before making that diagnosis. == Dr. Nossen Comment/Interpretation: Evaluation of ischemia on an ECG can be very challenging. The ECG is diagnostic of occlusion myocardialinfarction (OMI).
By Magnus Nossen, edits by Grauer and Smith The patient is a 70-something female with DMII, HTN and an extensive prior history of coronary artery disease and myocardialinfarctions. ECG#1 Assessing ischemia on an ECG with wide QRS complexes (AIVR, ventricular pacing, BBB, etc) can be challenging. What do you think?
A stent was placed. For those who depend on echocardiogram to confirm the ECG findings of ischemia, this should be sobering. In this case, the duration of ischemia was so brief that there was no such evolution, and there was near-normalization. Wellens' syndrome represents a state of reperfusion of the infarct related artery 2.
Written by Jesse McLaren A 70 year old with prior MIs and stents to LAD and RCA presented to the emergency department with 2 weeks of increasing exertional chest pain radiating to the left arm, associated with nausea. But no ECG met STEMI criteria so the patient was referred to cardiology as Non-STEMI. Clin Cardiol 2022 4. McLaren and Smith.
Precordial ST depression may be subendocardial ischemia or posterior STEMI. I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia. The OM-1 was opened and stented, then the LAD was stented 3 days later. There is no ST elevation. How can we tell the difference?
Here is the EMS ECG: Obviously massive diffuse subendocardial ischemia, with profound STD and STE in aVR Of course this pattern is most often seen from etoliogies other than ACS. The ECG only tells you there is ischemia, not the etiology of it. Nevertheless, the clinical situation made other etiologies unlikely. NTG drip started.
The pain will resolve and you will think the ischemia is gone when it is only hidden ! Just before 10 AM, the patient received a stent to the culprit OM. Immediate and early percutaneous coronary intervention in very high‐risk and high‐risk non‐st segment elevation myocardialinfarction patients. & Griffin, J.
The ECG in the chart was read as "no obvious ST changes," (even though no previous ECG was available) and the formal read by the emergency physicians was: "ST deviation and moderated T-wave abnormality, consider lateral ischemia." Consequences of reocclusion after successful reperfusion therapy in acute myocardialinfarction.
An open 90% LAD was stented. Here is the ECG the next AM: There was so little infarction that there are lateral, but no anterior reperfusion T-waves (normally, there would be Wellens' type waves after LAD reperfusion). Here is some older but very interesting literature on TIMI myocardial perfusion grade and ST resolution : 1.
It was a 60yo with a history of stents to the circumflex and right coronary arteries, who presented with 9 hours of fluctuating central chest pain. 2] Here there is no posterior ST elevation, but the anterior ST depression is also less—so it is dynamic, confirming acute ischemia. But it is still STEMI negative.
A very large myocardialinfarction. The next day the ECG not unexpectedly shows a completed transmural inferior and posterior wall infarction. The patient, albeit very delayed was referred for angiography where a 99% stenosed pRCA was stented. No further episodes of atrial fibrillation occurred during monitoring.
All these factors, again, support an ECG diagnosis of LVH The patient was nonetheless taken for emergency angiography, and a 99% mid-LAD lesion was found and stented. However, the ST segments in patients with LVH may show significant variation over time in the absence of ischemia. Interestingly, few signs of LVH at this point.
I do not think this ECG is by itself diagnostic of OMI (full thickness, subepicardial ischemia ), b ut comparison to a previous might reveal this ECG as diagnostic of OMI. Association between opioid analgesia and delays to cardiac catheterization of patients with occlusion MyocardialInfarctions. Abstract 556.
This is diagnostic of myocardialinfarction. Now you have ECG and troponin evidence of ischemia, AND ventricular dysrhythmia, which means this is NOT a stable ACS. The lesion was stented. It they are static, then they are not due to ischemia. This is better evidence for ischemia than any other data point.
There is broad subendocardial ischemia as demonstrated by STE aVR with concomitant STD that almost appears appropriately maximal in Leads II and V5. There is LBBB-like morphology with persistent patterns of subendocardial ischemia. A mid-LAD culprit lesion was identified and stented. Pacing Clin Electrophysiol. 40; 1234-1241.
Although not striking, this is clearly a diagnostic ECG for infero"posterior" myocardialinfarction due to coronary occlusion (OMI), most likely due to left circumflex (LCx) artery occlusion. mm STE even in the fourth universal definition of myocardialinfarction. Considerations on the naming of myocardialinfarctions.
He did, found the true culprit, and went back in to stent it. His astute observation is worthy of brief discussion: Rituparna et al document a case study report, in which J waves appeared to be induced by ischemia ( Pacing Clin Electrophysiol 30(6):817-819, 2007 ). You can listen to my explanation by playing the video.
He was rushed to the Cath Lab where an LAD culprit lesion was stented. Here is the LAD after stent placement. Electrocardiographic differentiation of early repolarization from subtle anterior ST-segment elevation myocardialinfarction. It’s important to stress the presence of a normal QRS (i.e., References 1] Smith, S.
In the STEMI/NSTEMI dichotomy, NSTEMI is supposed to mean non-occlusive myocardialinfarction, but this patient had transient Occlusion MI that was at risk for re-occlusion (like ‘transient STEMI’). Notice also that there is new T-wave inversion in III with upright T-wave in aVL, confirming inferior infarction.
Angiogram: Culprit for the patient's inferior ECG changes and non-ST elevation myocardialinfarction is a 100% acute thrombotic occlusion of the proximal RCA. It was opened and stented. Traditionally , Occlusion MI (OMI) myocardialinfarctions that are not STEMI are called NonSTEMI.
He reported a history of ischemic cardiomyopathy with coronary stent placement approximately 10 years prior, but could not recall the specific artery involved. A 99% LAD occlusion was stented. Terminal QRS distortion is present in anterior myocardialinfarction but absent in early repolarization. 3] Smith, S.
The patient was then taken to the cath lab an found to have a proximal RCA 100% thrombotic occlusion which was successfully stented. Progression of V2 showing posterior involvement. J Electrocardiology January–February, 2018; Volume 51, Issue 1, Pages e5–e6.
Chest pain with New LBBB: It helps to actually measure the ST/S ratio A Fascinating Demonstration of ST/S Ratio in LBBB and Resolving LAD Ischemia The cath lab was activated. It was opened and stented. Shortly thereafter, the first troponin I returned at 0.689 ng/mL (URL = 0.034), all but diagnostic of acute MI.
Electrocardiographic Differentiation of Early Repolarization FromSubtle Anterior ST-Segment Elevation MyocardialInfarction. After many hours, the decided that it was appropriate to do an angiogram and they found a distal LAD occlusion which was opened and stented. It was stented. There was no wall motion abnormality.
Stone, MD Mount Sinai Health System tim.hodson Wed, 04/02/2025 - 15:26 March 31, 2025 Using intravascular imaging (IVI) to guide stent implantation during complex stenting procedures is safer and more effective for patients with severely calcified coronary artery disease than conventional angiography, the more commonly used technique.
The 2 coprimary outcomes were target lesion revascularization and myocardialinfarction. The secondary outcomes included ischemia-driven target lesion revascularization, target vessel myocardialinfarction, death, cardiac death, target vessel revascularization, stent thrombosis, and major adverse cardiac events.
In some cases the ischemia can be seen "through" the flutter waves, whereas in other cases the arrhythmia must be terminated before the ischemia can be clearly distinguished. First , there can simply be diffuse ST depressions (which obligates reciprocal STE in aVR) associated with tachycardia which are not indicative of ischemia.
indicates inducible ischemia while an FFR above 0.80 excludes ischemia in 90% of cases. If the FFR normalizes after stenting, the restenosis rates at six months is less than 5%. If the FFR normalizes after stenting, the restenosis rates at six months is less than 5%. myocardialinfarction rate and 3.2%
The impact of this narrowing can ultimately result in angina (chest pain), which has been shown to double the risk of major cardiovascular events,1 as well as myocardialinfarction ( heart attack ) or even death.
Background Untreated multivessel disease (MVD) in acute myocardialinfarction (AMI) has been linked to a higher risk of recurrent ischemia and death within one year. The immediate non-IRA PCI is associated with a significantly lower occurrence of unplanned ischemia-driven PCI (OR 0.60; confidence interval [CI] 0.44–0.83)
This was stented. If there is polymorphic VT with a long QT on the baseline ECG, then generally we call that Torsades, but Non-Torsades Polymorphic VT can result from ischemia alone. I have read articles that say that patients without ischemia are at low risk of complications from hypokalemia, But it is not entirely without risk.
His father and brother both died of myocardialinfarction at ages 61 and 45, respectively. There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1]
Diagnosis of Acute MyocardialInfarction in the Presence of Left Bundle Branch Block using the ST Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Electrocardiographic Diagnosis of Acute Coronary Occlusion MyocardialInfarction in Ventricular Paced Rhythm Using the Modified Sgarbossa Criteria.
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" That said, complete LM occlusion would be expected to have subepicardial ischemia (STE) in these myocardial territories: STE vector 1.
Background:Patients with atrial fibrillation were excluded from clinical trials evaluating carotid artery stent(CAS) or carotid endarterectomy (CEA).We Background:Patients with atrial fibrillation were excluded from clinical trials evaluating carotid artery stent(CAS) or carotid endarterectomy (CEA).We versus 18.8%
Objective:To compare the 1-month stroke, myocardialinfarction (MI), and/or death rates among symptomatic patients undergoing either CAS or CEA according to the timing of the procedure in Carotid Revascularization Endarterectomy versus Stenting Trial (CREST).Methods:We
Appearance of abnormal Q waves early in the course of acute myocardialinfarction: implications for efficacy of thrombolytic therapy. It was treated with and dual "kissing balloons" and drug eluting stents. Midlateral wall rupture secondary to infero-postero-lateral infarction from circumflex occlusion was most common (34%).
LAD 80% mid LCx occluded mid (acute infarct lesion) RCA 80% mid. distal stent patent. PCI mid LCx So this is an OMI (Occlusion MyocardialInfarction), but not a STEMI Echo: Decreased left ventricular systolic performance, mild/moderate. Repeat ECG shows modest ST elevation in I and aVL and depression in inferior leads."
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