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BACKGROUND:Lower-limb amputation rates in patients with chronic limb-threatening ischemia vary across the United States, with marked disparities in amputation rates by gender, race, and income status. Circulation: Cardiovascular Interventions, Ahead of Print. Mean age, 76.6
The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). What do you think?
As a result, the ST elevation ( with especially tall, peaked T wave in lead V2) — is not indication of acute ischemia. As suggested by Figure-4 below in the ADDENDUM — assessment of the ST-T waves in leads V2,V3 and V5,V6 — is consistent with ischemia and / or LV "strain".
My written interpretation on a tracing such as this one would read, "Marked LVH and 'strain' and/or ischemia — with need for clinical correlation." BOTTOM LINE: ECG changes of LV "strain" and/or ischemia that we see on today's initial ECG — were not present 9 years earlier. Please see ECG Blog #73 for additional details ).
When I was shown this ECG, I said it looks like such widespread ischemia that is might be a left main occlusion, or LM ischemia plus circumflex occlusion (high lateral and posterior OMI). In Figure-1 — I reproduce major points that I've summarized from Dr. Smith's August 9, 2019 post on the subject. There is STE in aVR.
In this patient's case, the RV ischemia manifested as dramatic anterior hyperacute T waves. This degree of STE is a bit atypical for LAD ischemia. We've highlighted a considerable number of acute RV MI cases in Dr. Smith's ECG Blog ( See the October 7, 2019 and May 10, 2024 posts , to name just two ).
A prior ECG was available for comparison: Normal One might be tempted to interpret the ST depression as ischemia, but as Smith says, "when the QT is impossibly long, think of hypokalemia and a U-wave rather than T-wave." QUESTION #2: If it were not for the markedly prolonged QTc — Wouldn't ECG #1 look like diffuse 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. Concordant STE of 1 mm in just one lead or 2a.
ECG#1 Assessing ischemia on an ECG with wide QRS complexes (AIVR, ventricular pacing, BBB, etc) can be challenging. Many health care providers will simply not attempt to assess ischemia in the presence of a wide QRS. In the ECG above there are several features indicative of ongoing transmural ischemia. What do you think?
There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( Some residual ischemia in the infarct border might still be present. Both episodes are initiated by an "R-on-T" phenomenon.
The company is also pursuing an indication for non-invasive measurement of fractional flow reserve (FFR CT ), uniquely derived from its plaque algorithm, to measure coronary blockages and the extent of ischemia. 6 (3) (2019). 2017 23, April 2020; Available from: [link]. Cardiovasc.
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.
Subendocardial Ischemia from another Cause ( ie, sustained tachyarrhythmia; cardiac arrest; shock or profound hypotension; GI bleeding; anemia; "sick patient" , etc. ). To EMPHASIZE: This pattern of diffuse Subendocardial Ischemia does not suggest acute coronary occlusion ( ie, it is not the pattern of an acute MI ).
It should be kept in mind that on occasions, beta-one agonist can result in increased ventricular ectopy e.g., in severe myocardial ischemia (by increasing myocardial demand), or sometimes with congenital long-QT syndrome. Smith, this can be accomplished by either using beta-one agonists or temporary transvenous pacing. J Am Coll Cardiol.
You can subscribe for news and early access (via participating in our studies) to the Queen of Hearts here: [link] queen-form This EMS ECG was transmitted to the nearby Emergency Department where it was remotely reviewed by a physician, who interpreted it as normal, or at least without any features of ischemia or STEMI.
Contrary to what Ken stated, the ST vector remains mostly posterior __ What about subendocardial ischemia? Subendocardial ischemia results in ST depression, but unfortunately, and rather mysteriously, it does not localize to the ischemic wall. Similarly, STD in aVL is usually reciprocal to inferior ST elevation, not "lateral ischemia."
We sought to evaluate PFO closure rates and indications relative to the timing of regulatory approval and publication of key randomized trials.Methods:We performed a retrospective cohort study using the OptumLabs Data Warehouse of US commercial insurance enrollees from 2006 to 2019. per 100 000 person-years in 2019. female, 29.2%≥60
His response: “subendocardial ischemia. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. With the history of Afib, CTA abdomen was ordered to r/o mesenteric ischemia vs ischemic colitis vs small bowel obstruction. Am J Med 2019, 132(5):622-630.
The same reciprocal relationship is seen in severe subendocardial ischemia, just with opposite vector direction where V1 can show ST elevation) Below you can find the 3D model of the heart and coronary vessels. Each main coronary artery (LAD, RCA and LCx) are shown in separate images.
IntroductionTransient Ischemic Attack (TIA) is a common neurologic condition characterized by temporary, focal cerebral ischemia that results in reversible neurological deficits without tissue infarction. from 2016‐2019 and secondary diagnosis of T2DM. Diabetics were more likely to be younger (70.43
This study aimed to evaluate the safety and technical feasibility of left TRA-CAS in comparison to right TRA-CAS.Methods:We conducted a retrospective review of consecutive patients who underwent TRA-CAS using a 6-French Simmons guiding sheath between 2019 and 2024. Patients who underwent proximal balloon-protected CAS were excluded.
or basilar ischemia. Rather than loss of both a J wave and S wave — there is a "slur" ( J-point equivalent ) in lead V2 of ECG #2 ( See My Comment in the November 14, 2019 post for illustration of T-QRS-D ). EKG on arrival to the ED is shown below: What do you think? However, T waves do not appear to be hyperacute or hyperkalemic.
Our chief of cardiology, Gautam Shroff, interprets it differently and thinks this is indeed ischemia. She was taken to the cath lab and her coronaries were clean!! There was no MRI, but the presumptive diagnosis is myocarditis. I have seen this pattern in severe acute AI also."
This is secondary to delayed postoperative cerebral ischemia and infarction caused by vasospasm.7 7 Clinical indicators like delirium can play a role in evaluating for delayed cerebral ischemia and infarction leading to timely management of vasospasms.5,8,9
2] Here there is no posterior ST elevation, but the anterior ST depression is also less—so it is dynamic, confirming acute ischemia. The absence of STE in V7-V9 is often due to resolution of ischemia, as seen by resolution of ST depression in V7-V9. Int J Cardiol 2019 2. -- Meyers HP, Bracey, Smith et al.
The terminology favored to describe these ECG findings is diffuse subendocardial ischemia ( See ECG Blog #271 — for more on diffuse subendocardial ischemia ). Figure-3: Reasons for the varied ECG presentation of acute LMain occlusion — with this summary synthesized from Dr. Smith’s 8/9/2019 post in his ECG Blog.
That said — I did not interpret these differences as the result of acute ischemia. An additional criterion that has sometimes been cited as helpful for making the diagnosis of acute Pericarditis — is the ST/T Wave Ratio in Lead V6 ( Please see My Comment at the BOTTOM of the page in the December 13, 2019 post of Dr. Smith's ECG Blog ).
mg reduced the risk of cardiovascular death, MI or heart attack, ischemic stroke, or ischemia-driven coronary revascularization by 31% compared with placebo.34 2019 Sep 10;140(11):e649-e650] [published correction appears in Circulation. Published 2019 Feb 28. 12 Colchicine, 0.5 34 Colchicine, 0.5 References: 1. Circulation.
Stroke: Vascular and Interventional Neurology, Ahead of Print. Descriptive statistics including medians (interquartile range) and proportions were used as appropriate.
Background:Myocardial infarction with nonobstructive coronary artery disease (MINOCA) is a special syndrome with clear evidence of myocardial ischemia, but no clear stenosis of coronary artery imaging sign. Circulation, Volume 150, Issue Suppl_1 , Page A4143007-A4143007, November 12, 2024. month follow-up.
A majority (62.5%) of those presenting with ‘normal’ ECGs had the cath lab activated without any ECG being labeled ‘STEMI’ by automated interpretation – based on signs of Occlusion MI including ECG changes, regional wall motion abnormality on bedside ultrasound, or refractory ischemia. 2019 ; 54 : 79 - 81. Acad Emerg Med.
Final diagnosis of cerebral ischemia was made in 662/1043 patients (63.5%) and stroke mimic was diagnosed in 381/1043 patients (36.5%). Detailed chart review was conducted to extract both the variables needed to apply the mimic scales the final diagnosis confirmed by final imaging and discharge diagnosis (cerebral ischemic vs stroke mimic).
BACKGROUND:Abnormal orthostatic blood pressure (BP) regulation may result in cerebral hypoperfusion and brain ischemia and contribute to dementia. The primary outcome was adjudicated dementia ascertained through 2019.RESULTS:Among Hypertension, Ahead of Print. RESULTS:Among 11 644 participants (mean [SD] age, 54.5 [5.7]
In the days before I learned to look for OMI, back when I was counting ST elevation boxes, I used to save ischemia for last.) I interpret tracings systematically in "real time" ( including my assessment for acute ischemia ). My approach (which is not unique) is rate, rhythm, axis, hypertrophy, intervals. (In
Though this association may be related to impaired cerebral oxygen delivery, it is unclear whether these changes relate to cerebral ischemia. Patients who had a brain MRI and serial hemoglobin measurements were included.
Part of the ST depression with deep T wave inversion in the lateral chest leads clearly reflects LV "strain" from the marked LVH — but despite the very large QRS amplitudes, this ST-T wave appearance looks disproportionate, suggesting at least a component of ischemia.
The company is also pursuing an indication for non-invasive measurement of fractional flow reserve (FFR CT ), uniquely derived from its PlaqueIQ technology, to measure coronary blockages and the extent of ischemia. 6 (3) (2019). Hafiane, Vulnerable plaque, characteristics, detection, and potential therapies , J. Cardiovasc.
She requires maximal medical management per all current guidelines (including heparin and P2Y12 inhibitor per cardiology), as well as consideration for emergent cath in the case of persistent ischemia. I believe this is by far the most common outcome for this patient around the world in 2019. So what will you do for this patient?
JAMA Intern Med 2019 9. We are told that the Stress Echo that was performed showed objective evidence of inducible ischemia ( confirmed apparently by both wall motion abnormalities and ECG changes ). Was this objective evidence of inducible ischemia accompanied by chest pain? Gulati M, Levy P, Mukherjee D, et al.
Accurate identification is absolutely necessary as this pattern can be easily misinterpreted for something less nefarious: for example, generic “subendocardial ischemia.” Accurate identification is absolutely necessary as this pattern can be easily misinterpreted for something less nefarious: for example, generic “subendocardial ischemia.”
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. This is the initial ECG: The QRS is widened with a regular cadence, and there are no discernable P waves.
Followup ECG: No Change Absence of evolution is the best evidence against ischemia as the etiology. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chest pain for the ischemia and potential syncope for brugada. Ischemia/infarction. Acute febrile illness. Hypothermia.
This can be simply a equivalent of HT, with no true supply side ischemia with LVF with global ST depression ) Management *More or less similar to STEMI with aggressive opening of culprit lesions with few differences. SCAI 2019 Catheter Cardiovasc Interv.2019;94:29–37 PMID: 35743628; PMCID: PMC9224589. Circ Cardiovasc Qual Outcomes.
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