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Wellens Syndrome

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141. Obesity 2.0: More Than Just the Extra Weight

. 7. Goldfine AB, Silver R, Aldhahi W, et al. Use of salsalate to target inflammation in the treatment of insulin resistance in type 2 diabetes. Clin Transl Sci. 2008;1(1):36-43. 8. Kintscher U, Hartge M, Hess K, et al. T-lymphocyte infiltration in visceral adipose tissue: a primary event in adipose tissue inflammation and the development of obesity-mediated insulin resistance. Arterioscler Thromb Vasc Biol. 2008;28(7):1304-1310. 9. Wellen KE, Hotamisligil GS. Obesity-induced inflammatory changes (...) Clin Invest. 2006;116(7):1793-1801. 13. Gonzalez-Gay MA, De Matias JM, Gonzalez-Juanatey C, et al. Anti-tumor necrosis factor-alpha blockade improves insulin resistance in patients with rheumatoid arthritis. Clin Exp Rheumatol. 2006;24(1):83-86. 14. Stanley TL, Zanni MV, Johnsen S, et al. TNF-alpha antagonism with etanercept decreases glucose and increases the proportion of high molecular weight adiponectin in obese subjects with features of the metabolic syndrome. J Clin Endocrinol Metab. 2011;96

2012 Clinical Correlations

142. Management of Atrial Fibrillation

Through Pacing 8.4 Upstream Therapy 8.4.1 Angiotensin-converting Enzyme Inhibitors and Angiotensin Receptor Blockers 8.4.2 Statins 8.4.3 Polyunsaturated Fatty Acids and Aldosterone Antagonist 9 Management – Special Populations xiv9.1 Post-Operative AF 9.1.1 Prevention Of Post-operative AF 9.1.2 Treatment of Post-operative AF 9.2 Acute Coronary Syndrome 9.3 Wolff-Parkinson-White (WPW) Pre-excitation Syndromes 9.3.1 Sudden Death And Risk Stratification 9.4 Hyperthyroidism 9.5 Pregnancy 9.6 Hypertrophic (...) to stroke and thromboembolism in AF (See Table 1, Page 1). Only antithrombotic therapy has been shown to reduce AF-related deaths. 6 > Stroke in AF is often severe and results in long-term disability or death. Approximately 20% of stroke is due to AF and undiagnosed ‘silent AF’ is a likely cause of some ‘cryptogenic’ strokes. 2,7 Paroxysmal AF carries the same stroke risk as permanent or persistent AF. 8 AF also account for one-third of all admissions for cardiac arrhythmias. Acute Coronary Syndrome

2012 Ministry of Health, Malaysia

143. 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 (...) it. Until then, I would recommend a close caution on these asymptomatic patients, to keep them, just that, asymptomatic. Dr. Bond is a second year resident at NYU Langone Medical Center Faculty peer reviewed by Steven Fowler,MD, Department of Medicine (Cardiology), NYU Langone Medical Center Image courtesy of Wikimedia Commons References: [i] Wellens HJ. Early Repolarization Revisited. N Engl J Med May 8, 2008. 358:2063-2065. [ii] Haïssaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest

2011 Clinical Correlations

144. Dynamic T-wave inversions in the setting of left bundle branch block. (PubMed)

Dynamic T-wave inversions in the setting of left bundle branch block. We illustrate the case a patient with left bundle branch block (LBBB) and electrocardiogram (ECG) changes consistent with those described in Wellens' syndrome. The characteristic ECG findings of Wellens' syndrome identify patients who have a particularly high rate of important coronary events in the near future, however these findings have previously been described only in the setting of normal conduction. A review of Wellens (...) ' syndrome, its criteria and pathophysiology, and its proposed appearance in the setting of LBBB is presented.Copyright © 2016 Elsevier Inc. All rights reserved.

2016 American Journal of Emergency Medicine

145. Low-grade inflammation and the brain

observational studies and experimental studies using the model of administration of lipopolysaccharide (a component of bacterial shell) in humans. She also assesses more specifically the role of inflammation in fatigue and motivational changes, two symptoms that are highly sensitive to inflammation and may explain the psychiatric vulnerability of obese patients. References Wellen, K.E. and G.S. Hotamisligil, Obesity-induced inflammatory changes in adipose tissue. J Clin Invest, 2003. 112 :1785-8. Dantzer, R (...) ., Depression and inflammation: an intricate relationship. Biol Psychiatry, 2012. 71 : p. 4-5. Parkitny, L., et al., Inflammation in complex regional pain syndrome: a systematic review and meta-analysis. Neurology, 2013. 80 :106-17. Dantzer, R., et al., From inflammation to sickness and depression: when the immune system subjugates the brain. Nat Rev Neurosci, 2008. 9 :46-56. Capuron, L. and A.H. Miller, Immune system to brain signaling: neuropsychopharmacological implications. Pharmacol Ther, 2011. 130

2016 Body in Mind blog

146. Chest pain with giant global T wave inversions and extreme QT prolongation. (PubMed)

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

147. Can pain be a classically conditioned response?

not tap in? Frédéric Wellens, pht says How about this ste5e says Hi All, A test that I find is positive on the more extreme FM patients is that I ask them to observe as I press on myself where they describe their worst pain. For the most severe FM patients they will report that they experience their pain worsening as I press on me. Sometimes they report that this pain stays worse for some time. Some learn to wince when they just see my thumb. I have never touched them. This forms a good starting point (...) theory. People respond to an internal “threat” (pain) exactly as they respond to an external one – the ANS does not understand the distinction – it only recognises that the mind is distressed. And in chronic pain/central sensitisation. It’s not the pain that is conditioned – it’s the distress. Decondition the distress and the pain either disappears on its own, or it becomes more easily treatable. Frédéric Wellens, pht says John, would you be more in agreement with the possibility that a particular

2016 Body in Mind blog

148. ECG of the Week - 6th June 2016 - Interpretation

therapy was maximised and staged further intervention was planned for the RCA lesion. More on Wellen's Check out: Dr Smith's ECG Blog Articles Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens' syndrome. Am J Emerg Med. 2002 Nov;20(7):638-43. PMID: Full text Mead NE, O'Keefe KP. Wellen's syndrome: An ominous EKG pattern. J Emerg Trauma Shock. 2009 Sep-Dec; 2 (3) : 206–208. Full text . References / Further Reading Life in the Fast Lane Textbook C han TC, Brady (...) ) QRS - Normal (100ms) QT - 440ms Segments: Nil significant change Additional: Deep T wave inversion leads V1-3 & aVL Prominent T waves III, aVF, V6 Interpretation: Wellen's pattern Deep T wave inversion leads V1-3 aVL inversion consistent with ACS What happened ? The patient had an angiogram which showed: Left main: Normal LAD: 80% mid stenosis Cx: 40% stenosis RCA: 60% proximal & 90% mid stenosis The LAD lesion was stented and subsequent echo showed only mild LV systolic dysfunction. Medical

2016 ECG of the Week blog

149. 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

150. A warning sign. (PubMed)

symptom resolution showed biphasic T wave inversions in V2 and V3 which prompted an emergent coronary angiogram that revealed 90% occlusion of the proximal LAD. The immediate recognition of Wellens' pattern lead to emergent coronary revascularization and prevention of acute myocardial infarction in our patient. Clinicians should be aware of this syndrome so that prompt invasive therapy can be done to avoid evolution into MI and subsequent left ventricular dysfunction.Copyright © 2016 European

2016 European journal of internal medicine

151. Dock’s murmur in LAD stenosis

recently [3]. Echocardiography was also useful in ruling out aortic regurgitation as a cause of the murmur. References Dock W, Zoneraich S. A diastolic murmur arising in a stenosed coronary artery. Am J Med. I967;42:6I7-619. Sangster JF, Oakley CM. Diastolic murmur of coronary artery stenosis. Br Heart J. 1973;35:840-4. Stankovic I, Kafedzic S, Putnikovic B, Neskovic AN. An Echocardiographic Illustration of the Dock’s Murmur in a Patient With Wellens Syndrome. Can J Cardiol. 2015 Dec 29. pii: S0828

2016 Cardiophile MD blog

152. 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

153. 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

154. 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

155. A 30 year old African American with Chest pain and T-wave Inversion

. The worry here was that it was Wellens' syndrome. BTWI has a comparatively short QT. My hand-measured, Bazett-corrected QTc in both of them is 415 ms. The apparent increase on the 2nd is because the raw QT is longer, but is limited by the correction. Wellens' is generally (but not always!) longer. The giveaways are the tall R-waves in the affected leads, with minimal S-waves, and the presence of J-waves, especially in V3-V6 on the second ECG. U-waves are a common feature of early repolarization, which

2015 Dr Smith's ECG Blog

156. Persistent Juvenile T-wave Pattern

are the symmetric T-waves of Wellens' Pattern B syndrome: Figure 5. Note the near perfect symmetry of V2 and V3. This is NOT normal, not PJTWP. The ECG of another healthy 3 year-old, taken from Chan et al. (2) Figure 6. Notice the inverted T-waves in V1-V3 are slightly asymmetric. An example of a juvenile T wave pattern in a healthy 11 year-old male is provided in an article by Sharieff and Rao:(3) Figure 7. Here the T inversion is limited to V1 and V2; it is slightly asymmetric. Defining “persistent” juvenile (...) =a Thank you for this great post.I have a couple of questions: 1.If the pacient with the Figure 1. EKG had chest pain, wouldn't PE be on top of the differential diagnosis? (at a glance this EKG looks similar- even if for an expert there are differences) 2.Would a pacient with figure 10. EKG and recently resolved chest pain be suspected of Wellens syndrome

2015 Dr Smith's ECG Blog

157. A Middle-Age Male with Chest Pain that Recurs in the ED

you is that when the patient had arrived pain free , he had this ECG recorded: Here there is subtle terminal T-wave inversion in V2, and a bit in V3, typical of early Pattern A Wellens' waves. So the first ECG is not normal; it is " pseudonormal ." It triggered the recording of serial ECGs (sorry, not available) which showed increasing ST elevation diagnostic of LAD occlusion. So this was Wellens' syndrome, a state of spontaneous reperfusion of the LAD, manifesting with "reperfusion T-waves" and R (...) -wave preservation after an episode of closure of the LAD. Thus, the patient presents pain free after an episode of angina. The importance of Wellens' syndrome is that the artery can close off again at any moment, in which case the inverted T-waves will become upright again and look normal. This is called "pseudonormalization". The first ECG was recorded so soon after re-occlusion of the artery that this ECG shows no signs of occlusion other than pseudonormalization, which requires comparison

2015 Dr Smith's ECG Blog

158. New 40 minute lecture on T-wave Inversion

wave in both ECGs?? I think they are within normal limits 40:08 which wall is involved????????? Inferior and posterior Hi Smith, As I am about to complete my first year of residency (cardiology) I discussed T wave inversions and Wellens Syndrome with my fellow colleagues. One of my colleague is just doing a six month rotation in our Cardiology department and asked an intersting questions. With a patient with Wellens Syndrome, now pain free, after 6h from the first pain episode (...) is it possibile that the high sensible troponins stay negative? In that case (negative high sensisble troponins) should the patients be still sent to the cath lab or sent home and undergo an elective II level imaging test (RM/ TC)? My opinion on the latter is that with a pathological ECG and no clear cause (unseen/unknown wellens ECG pattern) patient should stay hospitalized. I'm interested in what you think about these two questions. Thank you for your help and congratulations on your excellent blog.

2015 Dr Smith's ECG Blog

159. Sudden Left Trapezius Pain and Syncope

or pericarditis. Another great case Steve - the reperfused ECG seems to have some 'posterior reperfusion T-waves' as well! Sam Indeed, Sam! matthias Is there any explanation for the T waves V1-V3 getting taller over the course of time? and thanks a lot for this great blog!! Matthias Yes! Posterior Reperfusion T-waves. Our paper on the topic: (...) , show them these cases. where are you in France. I occasionally come and speak in France (my favorite country) and would love to talk on subtle ECGs. Steve Smith i thankfull or u iam learning many things glad to hear it. thanks for the feedback! Stuart Hi Steve, Just yesterday I found a patient with an interesting ECG that showed what looked like early repol inferiorly, but with ST depression and TWI in aVL. He also had fairly subtle biphasic T waves in V2-3 which looked to me like Wellen's, very

2014 Dr Smith's ECG Blog

160. 45 year old with chest pain

, as seen in Figure 3. There is new T-wave inversion in I, aVL, V4-V6. There is terminal T-wave inversion (biphasic) in V2 and V3, but complicated by the U-waves seen in these leads. This T-wave inversion represents a form of Wellenssyndrome, indicating spontaneous reperfusion of a brief left anterior descending coronary occlusion. This time troponin was positive, and the patient underwent coronary angiography, which showed severe subtotal left anterior descending artery disease and 70% left main (...) to acute coronary syndrome (ACS). Remember – not all ACS has a positive troponin! When negative, it is – of course – called “unstable angina.” It usually presents with a normal or nonspecific ECG, with ST-depression, or T-wave inversion – but unstable angina may also present with transient ST-segment elevation . Perhaps more disgruntling, transient ST-elevation does not always result in a positive troponin. The ischemia may resolve so quickly that there is both no wall motion abnormality

2014 Dr Smith's ECG Blog

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