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Wellens Syndrome

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161. Early Repolarization: Not as Innocent as Once Thought!

, the practitioner should rule out all more commonly studied ischemic and non-ischemic causes, including, but not limited to, the long-QT syndrome, the short-QT syndrome, the Brugada syndrome, and arrhythmogenic right ventricular dysplasia (i). Once these conditions have been excluded, it can be implied that the inferolateral J point elevation which represents early repolarization in an area with increased current density is what predisposed to the event. As such, these studies presented above suggest (...) the prevalence of early repolarization and evaluate its potential relationship with any observed arrhythmias, as monitored by implantable defibrillators. In the study, early repolarization prevalence was compared between case subjects who had previously experienced an episode of IVF prior to the study and control subjects with no known heart disease. Early repolarization occurred statistically more frequently in the case subjects with IVF than the control subjects (31% vs. 5%, P<0.001). Furthermore

2011 Clinical Correlations

162. Right Precordial T-wave Inversion

must not be measured in V2 or V3. The QT as measured in other leads is about 420 ms, with a preceding RR of 1500ms, resulting in a Bazett corrected QT interval of 345 ms . This short QT at least makes ischemia all but impossible. ERP is, of course, associated with an increased long term risk of sudden death, but only marginally and only if in inferior or lateral locations : In addition, many readers of this Facebook post were worried about ischemia , including Wellen's syndrome ("What (...) that some have tried to restrict its use to the syndrome of J-waves and QRS slurring/notching which predicts a higher long term risk of sudden death. For the purposes of STEMI mimics, which is an entirly different context "early repolarization" remains in widespread usage. And indeed, patients with normal variant ST elevation in leads V2-V4 do have short QT intervals due to rapid repolarization! As for the QT interval, there are many correction formulas, none work very good, and the only way to actually

2016 Dr Smith's ECG Blog

163. Syncope Several Times, Complete Heart Block, And a Surprise ECG in the ED!

. Transient STEMI is usually due to brief thrombotic occlusion that then lyses. This occlusion happened several times. The first time it did not result in chest pain but did result in complete heart block. In Acute Coronary Syndrome, a thrombotic event, a culprit is not always found. And the coronary disease may be mild in such cases: the thrombosis just happens at a minimally stenotic, but vulnerable lesion. It is even possible to have thrombosis with a completely normal angiogram, though in less than 1 (...) to make that less likely." He thought it might be vasospasm of two different coronary arteries. ECG 7. At 0428 the burning persisted and this was recorded: Now they are inferior again!! 7 minutes later the burning was gone and this ECG was recorded at 0435: All STE has resolved again. The Cath Lab was activated. Here is the last ECG before he left for the cath lab at 0449: There are now inferior reperfusion T-waves (inferior Wellens' waves!) This supports some degree of infarction. The troponin

2016 Dr Smith's ECG Blog

164. I saw this on the computer. Most physicians, at first glance, get this wrong. What is it?

(and no obvious reperfusion T waves / "Wellens"), and hs-TnT that went from 59 to 358 ng/L (<15) where coronary angiography the following day showed three vessel disease (with Cx as the probable culprit) Peter, sure, any ischemia can cause it! Steve Good! The first thought that struck me after I looked at the upgoing QRS in avR was, are leads properly attached. fantastic teaching case. thank you. Thanks for the feedback! fantastic teaching case. thank you Really great case. Learnt some incredibly interesting (...) the underlying sinus rate so that it inhibits the AIVR. 4. Antidysrhythmics are not indicated and will not help: this is not a re-entrant rhythm; rather it is an automatic rhythm. 5. If it is not a situation of reperfusion, consider other causes: digoxin toxicity and other structure heart diseases. Posted by Steve Smith at Reactions: 15 comments: Would you say that AIVR can be seen in NonSTEMI also? I happen to have a case of AIVR where there was no ST elevation while the patient were in sinus rhythm

2016 Dr Smith's ECG Blog

165. How do you explain these inferior hyperacute T-waves?

, in retrospect, to have been MI and a misread ECG. Remember that unstable angina still exists. At presentation, this EKG was recorded: Alberto's interpretation: "Inverted biphasic T waves in V1-V4, inverted T waves in D1-aVL ." Smith comment: I agree, consistent with Wellens' syndrome of the anterolateral wall, due to proximal LAD ACS. Bedside echo was normal. First troponin was 16 ng/L (0.016 ng/mL), second 22 ng/L, third 28 ng/L ( so, just barely positive : cut-off at our institution is 13 ng/L (...) ). In the telemetry ward, 18 hours later, the patient had chest pain and another EKG was taken as shown in image 2 Alberto's interpretation: "There are deeply inverted T waves with minimal ST depression in V2-V3 and D1-aVL, hyperacute T waves in the inferior leads, especially III and aVF , long QT. Looks like Wellens' Syndrome." The crux of Alberto's inquiry: "Why are there "hyperacute T-waves" in inferior leads??" Smith answer: The Wellens' syndrome has evolved as it normally does, with increasingly inverted T

2016 Dr Smith's ECG Blog

166. Just as hyperacute T-waves can be reciprocal to T-wave inversion (last case),.....

in the setting of posterior MI (or posterolateral, inferoposterior), in which case the patient still has symptoms (e.g. chest pain) or 2. indicative of reperfusion of the myocardial wall beneath that lead (V2-V4 in anterior ischemia), in which case the pain is resolved (e.g., Wellens' syndrome); I call these "reperfusion T-waves". Can you specify point one as how to distinguish between ischemic vs reciprocal TWI during ongoing symptoms? If the patient is now pain free, then the T-wave inversion is likely (...) . Posted by Steve Smith at Reactions: 7 comments: Medical student here, this might be a very silly question but how would you differentiate this from antero-lateral wall ischemia? I.e. how to differentiate ischemic T-wave inversion on lateral leads from reciprocal changes of infero-posterior MI? First, it looks subtle different. Look up Wellens' cases on this blog. More to the point, however, T-wave inversion is either 1. reciprocal to active ischemia/occlusion (aVL in the setting of inferior MI, V2

2016 Dr Smith's ECG Blog

167. One reason we get ECGs in stroke patients

strokes and some atherosclerotic cerebrovascular disease, which could have been the source of the stroke. However, because of the ECG findings, an echocardiogram was done which confirmed LV aneurysm and showed: 1. Decreased left ventricular systolic performance moderate to moderately severe 2. Estimated left ventricular ejection fraction of 35%. 3. Regional wall motion abnormality distal anterior wall and apex diastolic distortion with dyskinesis (aneurysm). 4. A 1.2 x 1.3 cm mural thrombus (...) . It would look much more acute. These all look like chronic findings. Steve Smith Anonymous Wow, so much information packed into one ECG. This is why I love ECGs, they are often diagnostic if one knows what to look for. Would you say that the inverted Wellens'-like T-waves in V3-V5 are indicative of CNS pathology? Thanks for the great case. Dan Dan, these are NOT acute findings. Stroke is the result, not the cause of the ECG findings. ST-T changes are much less striking than QRS (Q-wave) findings. Steve

2016 Dr Smith's ECG Blog

168. A Patient with Ischemic symptoms and a Biventricular Pacemaker

manifest in reperfusion of VPR cases. Here is the next day ECG: Deeper T-wave inversion, evolving just like in Wellens' syndrome (which is a condition of reperfusion of the LAD after brief occlusion). Learning Point: STEMI may be diagnosed in VPR!! We are starting a large study of this, at multiple sites. We'll see how well the Modified Sgarbossa Criteria work for VPR. has some great comments on this post here: If EVER you wanted to learn more about how you may sometimes see definitive evidence (...) not so wise) that states that no further interpretation is possible in VPR. In this case, the VPR beats show the STEMI. The Non-VPR beats do NOT show it. Furthermore, the VPR showed reperfusion changes after PCI: There is electrical alternans of unknown etiology. There is r esolution of most ST elevation (indicating reperfusion) and T-wave inversion ("Wellens' waves, reperfusion T-waves) in V2 and V3, and also in half of the V5 and V6 waves, depending on the QRS. Thus, even T-wave inversion may

2016 Dr Smith's ECG Blog

169. A 37 year old woman with Chest Pain

that i can persuade them to use lytics in such cases? Is there any literature convincing enough(for them not me..i am just the resident)? Thank you very much Can you get an immediate high quality echo? Prove to them with wall motion abnormality. Also, Wellens' is NOT a STEMI equivalent! Wellens' is a syndrome when the patient has had pain, is not pain free, and the artery is open. The T-wave inversions are due to reperfusion of an artery that was occluded at the time of the pain, but spontaneously (...) and other clinical factors do not tell the whole story, but when they do, the troponin often leads us astray! Steve The converse is true also in that a mildly positive troponin doesn't necessarily mean acute coronary syndrome either. Recently Professor Jean Marco from France visited our department and highlighted this point very well in showing a case with positive troponins which was sent to the cardiology team who took the patient to the cath lab.. they found some disease but nothing critical

2016 Dr Smith's ECG Blog

170. My Very Smart Colleagues are Getting Very Good at Diagnosing Subtle Occlusion

My Very Smart Colleagues are Getting Very Good at Diagnosing Subtle Occlusion Dr. Smith's ECG Blog: My Very Smart Colleagues are Getting Very Good at Diagnosing Subtle Occlusion Friday, May 20, 2016 My very smart colleagues are getting very good at this! A male in his 40's with a significant history of coronary disease and stents called 911 for sudden onset "terrible" left sided chest pain radiating to the jaw, with diaphoresis and vomiting. He appeared very uncomfortable. Here is his (...) for patients with ongoing, refractory chest pain and high suspicion of coronary syndrome, even in the absence of ECG or biomarker evidence of ischemia . In this case, there is even very good ECG evidence. As with 50% of STEMI, the initial troponin was negative (Initial cTnI = 0.028 ng/mL, 99% upper reference level = 0.030 ng/mL). My very astute colleagues simply activated the cath lab after giving aspirin, heparin and ticagrelor. The interventionalist was skeptical but gladly took the patient to the cath

2016 Dr Smith's ECG Blog

171. Articles of the month (May 2017)

are good, but have a plan to manage this awareness. Wellen’s syndrome Morris N, Howard L. BET 1: In patients with suspected acute coronary syndrome, does Wellens’ sign on the electrocardiograph identify critical left anterior descending artery stenosis? Emergency medicine journal 34(4):264-266. 2017. PMID: This review looks at 6 papers trying to answer the question: in adult patients with suspected acute coronary syndrome, does Wellen’s sign on the ECG identify critical stenosis of the left anterior (...) surrogate. The heterogeneity here doesn’t allow for a single estimate, but if you identify Wellen’s syndrome, there is a high likelihood (somewhere between 50-90% in these studies) that the patient has a >70% LAD lesion. The thing to remember is that Wellen’s is not an ECG finding alone, but rather an ECG finding in combination with history. Part of the definitions of Wellen’s syndrome is a recent history of angina. Bottom line: We should know what Wellen’s syndrome is and watch for it ACEP policy

2017 First10EM

172. ECG of the Week - 25th September 2017 - Interpretation

the patient was taken for angiography. There was no evidence of vessel disease but appearance was typical for Takotsubo cardiomyopathy likely secondary to exertional stress from triathlon. What are the potential complications of endurance sports ? Injury Rhabdomyolysis Dehydration Acute renal failure Myocardial strain Studies have shown raised troponin's in marathon runners ACS Environmental illness Hypothermia Hyperthermia Hyponatraemia SIADH Water ingestion Hypoglycaemia Takotsubo References / Further (...) but normothermic on arrival to the Emergency Department (36 C/ 96.8 F) Click to enlarge  Rate: 78 bpm Rhythm: Regular Sinus rhythm Axis: Normal Intervals: PR - Normal QRS - Normal QT - 440ms (QTc Bazette 465 ms) Additional: ST Elevation (1mm) leads V1-3 No ST depression T wave inversion leads I, aVL, V1-6 Interpretation: Features suggestive of ACS Pain-free patient on arrival to ED Only complained of dysponea DDx: ? Reperfusion / Wellen's ? Cardiomyopathy What happened ? Following urgent cardiology consult

2017 ECG of the Week blog

173. A 25 year old with Epigastric Discomfort, Worse Supine, Better Sitting Up.

sitting up. Here is his initial ECG, with pain and diaphoresis: It is really quite normal. When I first saw it, I did not know the patient still had pain, and I responded on FB: "This is normal. However, the sharp downturn of the T-wave in V4-V5 suggests possible development of Wellens' waves, but is nonspecific. The T-wave flattening in limb leads is non specific. " However, with ongoing pain, these are unlikely to be vestigial Wellens' waves. He was given NTG and Morphine and pain was improved (...) amplitude V4 = 9 mm formula = 25.839 (greater than 23.4 is all but diagnostic of LAD occlusion) The patient was taken for angiogram. Here is the report: Here is the post reperfusion ECG Typical reperfusion T-waves, identical to Wellen's waves (Wellens' waves represent reperfusion!) Learning Points: 1. Young People can have myocardial infarction 2. Though positional pain lowers the likelihood that chest pain is MI, it does not eliminate it! 3. Always get serial ECGs. 4. Pay attention to even slightly

2016 Dr Smith's ECG Blog

174. Biphasic T-waves in a Middle-Aged Male with Vomiting

of view can we say that Wellens' waves are the evolution of an early ST elevation? Thanks in advance. Wellens' waves are reperfusion T-waves. When STEMI is reperfused, one of the first signs of reperfusion is the downward turn of the end of the T-wave. In Wellen's syndrome, there is absence of recording during chest pain, when one would have found STEMI. The artery reperfuses, the pain goes away, and the first recording you get is the terminal T-wave inversion. If you wait longer, you'll get pattern B (...) Biphasic T-waves in a Middle-Aged Male with Vomiting Dr. Smith's ECG Blog: Biphasic T-waves in a Middle-Aged Male with Vomiting Thursday, November 10, 2016 One of our residents texted me this ECG and was worried about Wellens' waves. A middle-aged male presented with vomiting. Here was the initial ED ECG: What do you think? Here is my response: Wellen's waves are always Up-Down T-waves, not Down-Up T-waves as here. Down-Up T-waves in V2 and V3 have only two causes: 1) posterior MI with some

2016 Dr Smith's ECG Blog

175. Chest pain with giant global T wave inversions and extreme QT prolongation. (Abstract)

Chest pain with giant global T wave inversions and extreme QT prolongation. Negative T waves in electrocardiography have been widely studied. We presents a case of Wellens' syndrome which is a pattern of global inverted T waves with QT prolongation on ECG due to transient proximal LAD occlusion and pointed out other differential diagnosis.Copyright © 2016 Elsevier Inc. All rights reserved.

2016 American Journal of Emergency Medicine

176. 2 Examples of Posterior Reperfusion T-waves

and reciprocal ST depression and T-wave inversion in aVL. This is diagnostic of coronary occlusion. Figure 2d. I activated the cath lab and an occluded RCA was opened. Here is the ECG several hours after reperfusion: There are inferior and lateral reperfusion T-waves (inverted). There are large right precordial "posterior reperfusion T-waves" in lead V2 Comment If recorded on the posterior wall, the T-waves would be inverted, just like a posterior Wellens' syndrome. However, they are recorded from anterior

2015 Dr Smith's ECG Blog

177. Unstable Angina: Again, it still exists......

for an end to such testing in patients with negative troponins. That only works when the ECG is adequately interpreted. I would add that in anyone in whom you have a high suspicion based on the history, do not trust the risk scores. This patient had a very high risk story. Posted by Steve Smith at Reactions: 5 comments: Alswiss Last ECG: little T wave Inversion in III + more pronounced T wave in V2 = "little" infero-posterior Wellens's syndrome ? Thanks Dr Smith Al Yes! Sabev First ECG : Can we say (...) ECG was recorded: All ST segments have normalized. This makes the first ECG even more diagnostic of ischemia. All who were there agreed that this was acute coronary syndrome, but that the artery was open, the patient without symptoms, and that with dual antiplatelet therapy and heparin, the patient could wait until the next day for the cath lab. Next day, the patient went for angiogram and had a 95 % thrombotic occlusion of the right posterior descending artery off the RCA. All 4th generation

2015 Dr Smith's ECG Blog

178. Is this STEMI? No, it is one of the most common reasons for false cath lab activation.

syndrome, which requires R-wave preservation . Additionally, the patient denies any recent symptoms. (A true Wellen’s syndrome is observed after ischemic symptoms have resolved.) The deep S waves and ST elevation could be the result of left ventricular hypertrophy. Although R-waves may be absent in LVH, LVH has high voltage R-waves in V4-V6. So this is NOT LVH. Persistent STE after prior MI (also known as "left ventricular aneurysm morphology") This is an ECG entity that is most accurately termed (...) . He had been at the clinic for a scheduled appointment. He denied having had any chest pain, SOB, nausea, or other ischemic symptoms at any point in the day. However, records sent from the clinic indicated he had had a STEMI treated with PCI at another hospital 4 months prior. Besides a new STEMI, what can account for the ST segment elevation? The T waves are dramatically biphasic, with a steep descent, suggesting a Wellen’s pattern. The poor R wave progression, however, rules out Wellen’s

2015 Dr Smith's ECG Blog

179. Paramedics make a great call

/mL. Subsequent Echo showed EF of 56% and distal septal, anterior, apical, and anteroseptal hypokinesis (wall motion abnormality). Here are post PCI EKGs, this one at 29 minutes after arrival: You can see the beginning of terminal T-wave inversion in V2 and V3. Had there been no prior ECGs, this patient who is now pain free would be suspected of Wellens' syndrome The next one was done at 10 hours after the first: Evolving T-wave inversion, classic Wellens pattern B morphology And then the next day (...) : Full blown Wellens' Pattern B terminal T-wave inversion. Learning Points 1. This was diagnosed as a NonSTEMI. 2. The artery was occluded, or nearly so, at the time of the first ECG. 3. Serial ECGs demonstrated dynamic changes diagnostic of ACS (transient STEMI) 4. This facilitated rapid treatment of a potentially life threatening LAD thrombus. 5. This also demonstrates how Wellens' ECG morphology is a representation of the post occlusion state, after spontaneous reperfusion (although it also looks

2015 Dr Smith's ECG Blog

180. The Monitoring Study

an outpatient study testing two configurations of the bionic pancreas (bi-hormonal and insulin-only) with and without remote monitoring of hypoglycemia in 25 adult (≥ 18 years of age) subjects with type 1 diabetes in a random-order crossover study versus usual care with an insulin pump with and without remote monitoring of hypoglycemia. Condition or disease Intervention/treatment Phase Type1diabetes Device: Bihormonal Bionic Pancreas Device: Insulin Only Bionic Pancreas Other: Monitored for Hypoglycemia (...) of a presumed coronary occlusion) Abnormal EKG consistent with coronary artery disease or increased risk of malignant arrhythmia including, but not limited to, evidence of active ischemia, prior myocardial infarction, proximal LAD critical stenosis (Wellen's sign), prolonged QT interval (> 440 ms). Non-specific ST segment and T wave changes are not grounds for exclusion in the absence of symptoms or history of heart disease. A reassuring evaluation by a cardiologist after an abnormal EKG finding may allow

2016 Clinical Trials

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