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Wellens Syndrome

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101. Subtle Dynamic T-waves, Followed by LAD Occlusion and Arrest

, less than 0.010 ng/mL) She ended up doing fine and in the next few days was discharged home in good condition. Smith comment: T-wave inversion such as seen in the first ECG can be seen with active non-transmural ischemia. We usually see this sort of T-wave inversion AFTER chest pain has resolved and, in that case, it is called "Wellens' syndrome," and implies that when the patient had pain the LAD was occluded, but that it spontaneously reperfused and resulted in "reperfusion" T-wave inversion (...) the patient had only just become pain free, it would be better to get one 20 minutes later to see how the ECG changes. Thanks Although subtle — the history and clearly biphasic T waves in V2-thru-V4 of the initial ECG in this case should strongly suggest WellensSyndrome until proven otherwise. The clinical importance of WellensSyndrome is the very high correlation this type of ECG finding has with a tight LAD lesion. As emphasized by Dr. Smith — specific conditions should be established before

2017 Dr Smith's ECG Blog

102. CBT may help reduce anxiety and depression in people with diabetes, but standardised approach needed

to three times that of the general population (Anderson, Freedland et al. 2001). Anxiety also occurs in around 14% of people with diabetes, and 40% show elevated levels of sub-syndromal anxiety (Smith, Beland et al. 2013). One might suggest that a major factor linking all mental disorders is mental distress , which can similarly significantly impair those suffering chronic physical illnesses. Ameliorating mental distress may well be where CBT makes its mark and transcends its utility across (...) (Wellen and Hotamisligil 2005), a hypothesis might begin to form as to CBT’s potential benefit on not only the mental distress related to a chronic disease, but also potentially the disease processes behind it. Enter this new systematic review and meta-analysis by Uchendu and Blake (2017), which was published recently in the journal Diabetic Medicine. Mental distress can affect all people with a chronic illness, and CBT might help. Methods The researchers took a systematic review and meta-analytic

2017 The Mental Elf

103. Echocardiography, even (or especially) with Speckle Tracking, can get you in trouble.

exam and expert interpretation. 5. This case does not demonstrate it, but a wall motion abnormality may disappear after spontaneous reperfusion ( ). 6. Patients with transient occlusion may manifest only transient STEMI on ECG. Subsequent troponins may be all negative and subsequent formal echo may be normal. . Posted by Steve Smith at Labels: , , , , Reactions: 8 comments: Alswiss This confirms that the typical Wellens-morphology do happen "only" in 15-20% of the anterior riperfusion-cases (de (...) Zwaan 1981-1989): right ? merci dr Smith ! Al Al, That would only be confirmed if I were showing a next day ECG, which I did not do here and I don't have (but maybe could find). It often takes longer for the Wellens' waves to appear, and they are also dependent on the amount of infarct. If very small, there may be no T-wave inversion, though usually when Troponin I is > 1.0 ng/mL, Wellens' waves appear. Thanks! Steve Great as always. I would say that i see hypokinesis on the anterior septum

2017 Dr Smith's ECG Blog

104. Chest pain, ST elevation, and negative serial trops: normal variant ("early repol"). Right?

as ''ST elevation'' in lead V1 to V4? And, if it was LAD spontaneously lysed from 100% to 80%, why there was no reperfusion T waves like the mechanism of Wellen's syndrome? Thanks again for presenting this case! Allen, It spontaneously lysed from 100% to 80%, and did so fast enough that there was no myocardial necrosis (no elevated troponin). Wellens' waves only occur when there is some infarction, often very little. But with no troponin elevation, one does not expect Wellens' waves. STeve Would cath (...) ! The physicians were alarmed by this and realized they may have dodged a bullet. They took the patient to the cath lab and found an 80% thrombotic LAD lesion. It was stented. This patient (and his physicians) were very lucky. Had this patient not spontaneously reperfused, he would have lost his entire anterior wall, and possibly died. It is dangerous to rely only on troponins for the diagnosis of acute coronary syndrome! Learning Points: 1. Not all ischemic ST elevation results in elevated troponin 2

2017 Dr Smith's ECG Blog

105. Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death

and acronyms ACC American College of Cardiology ACE angiotensin-converting enzyme ACS acute coronary syndrome AF atrial fibrillation AGNES Arrhythmia Genetics in the Netherlands AHA American Heart Association AMIOVIRT AMIOdarone Versus Implantable cardioverter-defibrillator: Randomized Trial in patients with non-ischaemic dilated cardiomyopathy and asymptomatic non-sustained ventricular tachycardia ARB angiotensin II receptor blocker ARVC arrhythmogenic right ventricular cardiomyopathy AV atrio-ventricular (...) AVID Antiarrhythmic drugs Versus Implantable Defibrillator BrS Brugada Syndrome CAD coronary artery disease CARE-HF CArdiac REsynchronization – Heart Failure CASH Cardiac Arrest Study Hamburg CAST Cardiac Arrhythmia Suppression Trial CAT CArdiomyopathy Trial CHD congenital heart disease CI confidence interval CIDS Canadian Implantable Defibrillator Study CMR cardiac magnetic resonance COMPANION Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure CPG Committee for Practice

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2015 European Society of Cardiology

106. A young woman with altered mental status and hypotension

blockers Here is a followup ECG: The patient had an initial troponin of 0.100 ng/mL, which could easily have been mistaken for acute coronary syndrome, but a D dimer was measured and was 2000. CTPA confirmed pulmonary emboli. The patient was NOT on a beta blocker. Learning Points: Learn the morphology of acute right heart strain vs. Wellens' T-wave inversions here: Use point of care ultrasound to confirm ECG findings of PE, OMI, etc. Posted by Pendell at Labels: , Reactions: 4 comments: excellent (...) hours later could only detect "mild RV strain" at that time. She was admitted to the ICU. Hypercoagulability workup has thus far been unrevealing. Case 2 Here are 2 ECGs recorded from one patient with pulmonary embolism just this week. The patient had sudden chest pain and SOB: Notice again the T-wave inversion in V1-V3 AND lead III. The T-wave inversion is domed, which is different from Wellens' This ECG is deceptive because there is no tachycardia, which is unusual in a patient who is not on beta

2019 Dr Smith's ECG Blog

107. A 40-something healthy male with transient chest squeezing

showed no WMA. First troponin was 0.042 ng/mL (elevated above 99th %-ile URL of 0.030 ng/mL). 1.5 hours later, this ECG was recorded: Still normal Several more were recorded, with no change. This was recorded at 8 hours: There is the beginning of terminal T-wave inversion in V2 . This is Wellens' syndrome, but, in Wellens', you don't always get an ECG recorded during pain as we do here. This shows that a patient with Wellens' had OMI at the time of their pain and that the T-wave inversion of Wellens (...) is identical between A and B. The artifact affects WCT and thus the changes seen in the chest leads in A are likely also artifactual, including the finding of TQRSD. It is interesting that no T wave inversion is present after NTG when the patient is pain free, considering Wellens syndrome, which is beautifully shown in the later ECGs. /Thomas @ Thomas Lindow — THANK YOU for your excellent comments! I expand upon determining which lead is most likely the source of artifact in the very next Blog post (from

2019 Dr Smith's ECG Blog

108. Do you understand these T-wave inversions?

involved in Wellens syndrome, which is simply the name given to reperfusion of anterior wall OMI when the patient is in the pain free state of reperfusion and has not yet lost the anterior wall (requires persistent R-waves to be classic Wellens syndrome). This pattern occurs in any wall of the heart, whichever wall is currently reperfused from a prior occlusion. On this note, "type A" and "type B" Wellens are useless distinctions that arose before we realized that reperfusion is a progression (...) of findings starting with terminal T-wave inversions ("type A") and progressing to full T-wave inversions ("type B"). My analogy for this misunderstanding of Wellens syndrome that I tell my residents is this: "Imagine you were an alien looking through a microscope and you discovered Earth. You zoom in to a city and look at a single street and you see humans, which happens to be a woman walking with her small child. You watch them for a few hours and then report your findings to your fellow aliens: you

2019 Dr Smith's ECG Blog

109. How to Read an ECG

of change, where evolution, indeed, stops? Could we blame the end of evolution on administrators? A peculiar element of ECG interpretation is the appearance of completely ‘new’ diseases within the last decade or so – syndromes that were allegedly not around when those more wizened of us trained. Wellen syndrome, ST elevation in aVR, Brugada syndrome, Spodick sign etc, as though these pathophysiological conditions have recently materialised out of nowhere. Where were they before? What did clinicians make (...) to remember his poetry – consider the epithet ‘ ’. Dawn is only ever rosy-fingered, and is mentioned 20 times in the Odyssey. See? Actually, when it comes to it, perhaps you are correct after all… ‘How to…’ An Instruction manual for those in Critical Care How to Read an ECG About Michelle Johnston Lives for teaching and loves clinical work, but with social media, she is like the syndromic cousin in the corner who gets brought out and patted on the head once in a while. | | | | Reader Interactions Leave

2018 Life in the Fast Lane Blog

110. Atypical Electrocardiographic Presentations in Need of Primary Percutaneous Coronary Intervention. (PubMed)

risk, ECG patterns of acute coronary syndrome, often associated with coronary occlusion or critical stenosis. After screening 997 studies, we identified the following distinct "STEMI equivalent" ECG patterns: Wellens' syndrome, de Winter sign, hyperacute T waves, left bundle branch block-including paced rhythm-and right bundle branch block. For each pattern, a brief summary of the existing evidence, together with the sensitivity, specificity, and positive predictive value-whenever available (...) -are presented. In conclusion, prompt recognition of "STEMI equivalent" ECG patterns is crucial for every physician or paramedic dealing with acute coronary syndrome patients in the emergency department or the prehospital setting, as misinterpretation of those high risk presentations can lead to reperfusion delays and worse outcomes.Copyright © 2019 Elsevier Inc. All rights reserved.

2019 American Journal of Cardiology

111. Comprehensive geriatric care in hospitals: the role of inpatient geriatric consultation teams

to develop recommendations for the patients’ care plan. 12 • Implementing. If geriatric syndromes or care problems are identified, appropriate evidence-based interventions need to be implemented. 11 The CGA-care process was evaluated by robust meta-analysis 12, 14 that showed beneficial effects compared with conventional care: decreased hospital mortality, higher proportion of hospitalised patients returning to home, improved cognitive functioning. Acute geriatric units remain the gold standard

2015 Belgian Health Care Knowledge Centre

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

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 (...) . 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

2016 Dr Smith's ECG Blog

113. 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

114. 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 I would do it. In a future case, you may not be so confident, so you would get serial ECGs and order an immediate, emergency, contrast echo by an expert. OK? Steve Anonymous Same problem here Dr.Smith, we don't have a cath lab and while my attendings understand that this is a LAD problem, they are not willing to thrombolyse, not only De Winter's but also Wellen's, which are considered STEMI equivalents. They prefer to send the patient to another shop 2hours away from ours. How do you think

2016 Dr Smith's ECG Blog

115. 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

116. 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

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

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 (...) Formula now = 19.971 (clearly normal) More evidence that the presenting ECG represents LAD occlusion. Here is the subsequent formal echo: The estimated left ventricular ejection fraction is 67 %. Normal estimated left ventricular ejection fraction . Left ventricular hypertrophy concentric . Regional wall motion abnormality-anterior hypokinetic. Here is the next day ECG: There was such rapid and complete reperfusion that no reperfusion T-waves (Wellen's waves) did not evolve. This is somewhat unusual

2016 Dr Smith's ECG Blog

118. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia

tachycardia, junctional tachycardia, multifocal atrial tachycardia, paroxysmal supraventricular tachycardia, permanent form of junctional reciprocating tachycardia, pre-excitation, pregnancy, quality of life, sinoatrial node, sinus node reentry, sinus tachycardia, supraventricular tachycardia, supraventricular arrhythmia, tachycardia, tachyarrhythmia, vagal maneuvers (Valsalva maneuver ), and Wolff-Parkinson-White syndrome . Additionally, the GWC reviewed documents related to supraventricular tachycardia (...) (SVT) previously published by the ACC, AHA, and Heart Rhythm Society (HRS). References selected and published in this document are representative and not all-inclusive. An independent ERC was commissioned to perform a systematic review of key clinical questions, the results of which were considered by the GWC for incorporation into this guideline. The systematic review report on the management of asymptomatic patients with Wolff-Parkinson-White (WPW) syndrome is published in conjunction

2015 American Heart Association

119. 2015 ACC/AHA/HRS Advanced Training Statement on Clinical Cardiac Electrophysiology (A Revision of the ACC/AHA 2006 Update of the Clinical Competence Statement on Invasive Electrophysiology Studies, Catheter Ablation, and Cardioversion)

. Evolution of CCEP 1525 1.2.2. Levels of Training 1525 1.2.3. Methods for Determining Procedural Numbers 1525 2. General Standards 1526 2.1. Faculty 1526 2.2. Facilities 1526 2.3. Equipment 1526 2.4. Ancillary Support 1526 3. Training Components 1526 3.1. Didactic Program 1526 3.2. Clinical Experience 1527 3.3. Hands-On Procedural Experience 1527 3.4. Diagnosis and Management of Emergencies and Complications 1527 3.5. Diagnosis and Management of Rare Clinical Conditions and Syndromes 1528 3.6. Research (...) and Scholarly Activity 1528 4. Training Requirements 1528 4.1. Development and Evaluation of Core Competencies 1528 4.2. Number of Procedures and Duration of Training 1528 4.3. Diagnostic Testing 1537 4.3.1. Noninvasive Diagnostic Tests 1537 4.3.2. Invasive Electrophysiological Evaluation 1538 4.4. Arrhythmia Types and Syndromes 1538 4.4.1. Pathophysiological Basis of Cardiac Arrhythmias/Basic Electrophysiology 1538 4.4.2. Inherited Arrhythmia Syndromes and Genetic Testing 1538 4.4.3. Bradyarrhythmias 1538

2015 American Heart Association

120. Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 4: Congenital Heart Disease

) sports (Class IIb; Level of Evidence C) . Elevated Pulmonary Vascular Resistance in CHD Patients with pulmonary vascular disease and CHD are at risk of sudden death during sports activity. In those with shunts (commonly septal defects or complex CHD), cyanosis is usually present at rest (Eisenmenger syndrome) and worsens with exercise. Most of these patients self-limit their activity, and they should not participate in competitive sports, with the exception of low-intensity (class IA) sports (...) death with exercise have been reported with severe cases. Risk stratification for exercise-related arrhythmias remains imprecise for this anomaly. In patients for whom there is also evidence of Wolff-Parkinson-White syndrome or in whom a defibrillator has been implanted, the recommendations found in Task Force 9 should be respected as well. Note that the recommendations below apply both before and after surgical plication and are based on the degree of valve regurgitation and existence

2015 American Heart Association

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