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Wellens Syndrome

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161. It is Far too Early for a Requiem for Unstable Angina

had chest pain just prior to arrival in the ED, but it resolved prior to physician evaluation. He did use cocaine a few days prior. He had blood pressures in the 170/100 range. Here is his initial ECG: There is terminal T-wave inversion in V2-V5, highly suggestive of "Wellens' syndrome." Patient had pain, is pain free, has intact R-waves, and terminal T-wave inversion (Wellens' Pattern A) There was no further pain, but a second ECG was recorded 1 hour later: There is some evolution of T-wave (...) inversion (V3 has a deeper negative deflection), increasing suspicion for Wellens' syndrome. The ED was concerned about "Wellens' pattern," and gave aspirin, clopidogrel, and heparin. He was not given anything for his blood pressure. He was admitted to the hospital. The consultants were very worried as well, and discussed angiogram vs. stress test in the morning. Comment: when a patient has cardiac ischemia and is hypertensive, the blood pressure should be controlled. There are many choices. One

2014 Dr Smith's ECG Blog

162. Anterior STEMI?

% of black men and 1% of black women had this finding. 1 of 5099 white patients had it. Aside from an 8.8% incidence (9 of 109) black males aged 17-19, it was evenly distributed by age group. I have reviewed these 101 ECGs, and what strikes me is: 1. There is a relatively short QT interval (QTc < 425ms) (this case would be an exception!) 2. The leads with T-wave inversion often have very distinct J-waves. 3. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which (...) they are V2-V4) 4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', ). 5. The leads with T-wave inversion (left precordial) usually have some ST elevation 6. Right precordial leads often have ST elevation typical of classic early repolarization 7. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves 8. The T-wave inversion in leads V4-V6 is preceded by high R-wave amplitude 9. II, III, and aVF also frequently have T-wave inversion. Posted

2014 Dr Smith's ECG Blog

163. Waxing and Waning Chest Pain

in by troponins, the infarct related artery is closed about 25-30% of the time. These patients have higher biomarkers, worse LV function, and higher mortaility than patients whose artery is open. 1. Wang T et al. Am Heart J 2009;157(4):716-23. 2. From AM, et al. Am J Cardiol 2010;106(8):1081-5. 3. Pride YB et al. JACC: Cardiovasc Interventions 2010; 3(8):806-11. Lessons : 1. Wellens' syndrome has analogous findings in the inferior and/or lateral walls. 2. T-wave changes of the posterior wall record (...) Waxing and Waning Chest Pain Dr. Smith's ECG Blog: Waxing and Waning Chest Pain Tuesday, April 8, 2014 A male in his 50s presented with Chest pain on and off during the day. At the time of presentation, he had only some jaw pain. An ECG was recorded: What do you think? There are inferior and lateral T-wave inversions (reperfusion T-waves, analogous to Wellens' waves which were described in the LAD distribution, V2-V4, but this also applies also to other coronary distributions). There is also ST

2014 Dr Smith's ECG Blog

164. Unstable Angina: Dr. Braunwald asks if it is time for a Requiem

to the waiting room with a "normal" EKG who later coded in the waiting room. This is also where the ST elevation showed up in your second EKG... Yes, but this is a common nonspecific finding in ECGs with deep S-waves. In first ecg there is t wave inversion, is it Wellen's t wave Or if during pain if this ecg recorded than what is importance of t wave inversion in this case? The T-wave inversion is very nonspecific. It does not look like Wellens'. Also, Wellens' is a syndrome, not an ECG finding: Typical

2014 Dr Smith's ECG Blog

165. A Non STEMI that needs the cath lab now.

now The diagnosis is acute MI, but not STEMI. There is slight ST elevation in lead III with reciprocal ST depression in aVL. The T-wave is inverted in III, indicating reperfusion (what I like to call "inferior Wellens' syndrome). There is no Q-wave, so this is unlikely to be old MI, and more likely to be acute NonSTEMI of the inferior wall. I saw these ECGs, and since there was no immediate urgency, allowed the resident to manage it without any comment. However, he did not see the abnormality (...) ischemia, when the primary ECG manifestation is ST elevation with reciprocal ST depression, and when it is ST depression due to subendocardial ischemia, with reciprocal ST elevation Thanks for the explanation , Prehospital ECG shows "slight ST elevation in lead III with reciprocal ST depression in aVL. The T-wave is inverted in III, indicating reperfusion (what I like to call "inferior Wellens' syndrome)" as you mentioned in blog. Sir, is there is subtle ST depression in lead V2 in same ECG along

2014 Dr Smith's ECG Blog

166. Management of recent-onset atrial fibrillation and flutter in the emergency department

Fibrillation Guidelines Committee c DOI: ---- Figure 1 A management strategy for patients with recent-onset AF/AFL. ---- Figure 2 Electrocardiogram of rapid ventricular preexcitation (Wolff-Parkinson-White syndrome) during atrial fibrillation. Note very rapid (up to 300 bpm) irregular wide QRS complexes. Hide Pane Expand all Collapse all Article Outline Abstract Atrial fibrillation (AF) is the most common arrhythmia managed by emergency physicians. There is increasing evidence that most patients (...) , associated cardiac conditions, current antiarrhythmic agents, anticoagulation and current INR level, rhythm on most recent ECG, and risk of thromboembolism per the CHADS 2 [ C ongestive Heart Failure, H ypertension, A ge, D iabetes, S troke/Transient Ischemic Attack] score (see Table 1 and Therapies for Prevention of Stroke and Vascular Events). AF may be related to acute, temporary causes including alcohol use (eg, “holiday heart syndrome”), myocardial ischemia or infarction, myocarditis or pericarditis

2010 CPG Infobase

167. Chest pain and Transient ST Elevation

, or disappearance of the S wave in leads with an Rs configuration )" They gave him nitro and morphine and his pain resolved. The ED ECG is below, 27 minutes after the prehospital ECG, and few minutes after resolution of pain. Pretty much normal The ED physician activated the cath lab and the cardiologists were in disagreement but took the patient to the cath lab. He had a 95% thrombotic LAD that was stented. Troponin I peaked at 2.4 ng/ml. Here is his 30 hour ECG: Sinus with PVC. Classic Wellens' syndrome ECG (...) This is a great demonstration of something I have promoted for years, but without proof : That Wellens' syncdrome is the result of the aftermath of spontaneously reperfused LAD occlusion that went unrecorded during the episode of pain. This idea is supported by these characteristics of Wellens' syndrome: 1. Wellens' syndrome is always after resolution of pain 2. There are always preserved R-waves 3. The LAD is always open, or there is good colllateral flow 4. The T-wave inversion of Wellens' is identical

2013 Dr Smith's ECG Blog

168. Man in his 60's with very subtle ECG and pain not controlled with medical therapy

overlooked by any ED physician. What are the subtle changes you found in this ECG? The subtle findings are best seen in III and aVF: especially aVF, with an ST segment that goes down then up Do you think the regional wall abnormality found in the distal septum is responsible for the early injury pattern(minor STE + increased T wave amp)in lead II? I don't think that is related, and I'm not certain there are significant findings in lead II, although I grant that the T-wave is a bit large. in wellen's (...) syndrome the resolution of pain should not be lead us to say that " theres nothing or it's gastric reflux". i think a key point is that whenever the pain goes off the ekg manifesations should do the same. i noticed that in V1 there's inverted T wave and it's associatedd with an inverted T wave in III, should some one put on top of differential diagnostic the possibility of Pulmonary Embolism ? Dr lotfi bensekrane. Both symptoms and EKG need to resolve. There are studies showing dynamic ST segments

2013 Dr Smith's ECG Blog

169. A Tough ECG, But Learn From It!

-elevation acute coronary syndromes undergoing diagnostic angiography Am Heart J 2009;157(4):716-23. 2. From AM, Best PJM, Lennon RJ, Rihal CS, Prasad A. Acute Myocardial Infarction Due to Left Circumflex Artery Occlusion and Significance of ST-Segment Elevation. Amercan Journal of Cardiology 2010;106(8):1081-5. 3. Sorajja P, Gersh BJ, Cox DA, et al. Impact of delay to angioplasty in patients with acute coronary syndromes undergoing invasive management: analysis from the ACUITY (Acute Catheterization (...) and Urgent Intervention Triage strategY) trial. J Am Coll Cardiol 2010;55(14):1416-24. 4. Pride YB, Tung P, Mohanavelu S, et al. Angiographic and Clinical Outcomes Among Patients With Acute Coronary Syndromes Presenting With Isolated Anterior ST-Segment Depression: A TRITON–TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis In Myocardial Infarction 38) Substudy Journal of the American College of Cardiology: Cardiovascular

2013 Dr Smith's ECG Blog

170. 24 yo woman with chest pain: Is this STEMI? Pericarditis?

infarct. At cath, the culprit was a proximal LAD lesion (open, with TIMI-3 flow)! It had embolized to the distal LAD, which was a "type III" or "wraparound" LAD supplying the inferor wall. So this was an antero-infero-lateral MI. The proximal lesion was stented and the distal was treated with antiplatelet and antithrombotic therapy. The next day she has reperfusion T-waves in the anterior leads, as well as inferior and lateral leads: Looks like Wellens' syndrome in anterior leads, because (...) leads. Chest X-ray confirmed absence of Boerhaave's syndrome. Some might suspect pericarditis in a young person with diffuse ST elevation. However, you diagnose pericarditis at your peril! I believe pericarditis is over diagnosed, even in the literature, and that many cases assumed to be pericarditis in the past would not be proved to be Acute MI. This is conjecture based on many cases that I have seen, not based on peer-reviewed evidence. Furthermore, in our study of benign inferior ST elevation vs

2013 Dr Smith's ECG Blog

171. Activate the Cath Lab?

. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which they are V2-V4) 4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', ). 5. The leads with T-wave inversion (left precordial) usually have some ST elevation 6. Right precordial leads often have ST elevation typical of classic early repolarization (not in this case) 7. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves (as here) 8. The T-wave (...) inversion in leads V4-V6 is preceded by high R-wave amplitude (as here) 9. II, III, and aVF also frequently have T-wave inversion. --In this case, the ST elevation in also not high (less than the ) --The T-waves are not upright, so if this is MI as in Wellens' syndrome, the pain should be resolved. Acute and ongoing occlusion should have an upright T-wave. Recognizing this requires some experience and seeing many such cases. Posted by Steve Smith at Labels: , Reactions: 2 comments: Or when i am not sure

2013 Dr Smith's ECG Blog

172. Middle Aged Male with Chest Pain and Previous MI

of occluded proximal circumflex near the ostium of the first obtuse marginal where the previous stent had been placed. The maximum troponin I was 80 ng/ml. Here is the post-PCI ECG: Notice the tall and large precordial T-waves. These are what I call . They are the analog of Wellens' T-waves and if recorded from the posterior wall would look like Wellens' T-waves. But because the leads are over the anterior wall, then they are large and upright, rather than inverted! Opiates in Acute Coronary Syndrome

2013 Dr Smith's ECG Blog

173. Male in his 40's with chest pain.

-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. Outcome : This time, the troponin was positive [which one would expect when there is not just resolution of STE, but also T-wave inversion (Wellens')]. The patient underwent coronary angiography, which (...) , and the ECG was interpreted as early repolarization. A bedside echocardiogram reportedly showed no wall motion abnormality. A repeat ECG was recorded: Here, V2-V5 have less ST elevation and the T-waves are smaller. It appears normal, and different from the presenting ECG. An application of the equation has equivocal results depending on whether the STE60V3 is measured at 1.5 or 2.0 mm. Nevertheless, the change shows that the previous ECG was indeed due to acute coronary syndrome (ACS). This was not seen

2013 Dr Smith's ECG Blog

174. Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis

definition of 90 vs. 100). The QRS was measured by the computer at 117 ms (but to my eye is normal) There is an rSr' in V1, and if the QRS really is long, this is an incomplete RBBB (I don't think it is long). Computerized QTc is 435 ms. There is abnormal T-wave inversion in leads V2-V5, suggestive of ischemia. There is another finding which suggests the diagnosis. The ECG differential includes Wellens' syndrome and pulmonary embolism. Here is her previous ECG from 2 months prior: There is sinus rhythm (...) at a normal rate (75). There is abnormal T-wave inversion in lead V2 only now, but the S1Q3T3 (the finding which suggests PE) is here also. So is this just baseline T-wave inversion? Wellens'? Pulmonary embolism? First, the increased heart rate should always sway you towards PE. Wellens' syndrome implies open arteries, perfusion of the myocardium, and the patient uncommonly has tachycardia. Baseline T-wave inversion is an unlikely explanation because there is extension out to V5. PE is very likely

2012 Dr Smith's ECG Blog

175. Benign T-wave Inversion: view video or read text

. The leads with T-wave inversion often have very distinct J-waves. 3. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which they are V2-V4) 4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', ). 5. The leads with T-wave inversion (left precordial) usually have some ST elevation 6. Right precordial leads often have ST elevation typical of classic early repolarization 7. The T-wave inversion in leads V4-V6 is preceded (...) it to be BTWI. Wellens' syndrome. Note the evolution from A to C. It begins with terminal T-wave inversion (biphasic) in lead V2, later extends to V3 and V4, and still later becomes deep and symmetric and only then extends to V6. There was a critical LAD stenosis. In this case I do not know what the computerized QTc was. This is taken from an article I wrote in EM Clinics of North America 2006;24(1):53-89. Posted by Steve Smith at Labels: , , Reactions: 16 comments: Dr. Smith, in the 5 examples of BTWI

2012 Dr Smith's ECG Blog

176. Chest pain in an 80 year old: What is the diagnosis?

continued and this repeat ECG was recorded at 1652: There is slightly more ST elevation A 3rd ECG was recorded at 1720: There is still more ST elevation and the T-waves are larger. At this point, the cath lab was activated. Angiogram revealed an acutely occluded saphenous vein graft to the LAD which was opened with PCI. Here is the post cath ECG: Now there are T-wave inversion analogous to Wellens' syndrome. These are reperfusion T-waves, also seen in I and aVL, indicating involvement of the lateral (...) go clinical,always dig deeper, as that chest pain the patient was having had to arise from some coronary pathology old or new. Dan I think there is a hint of Wellens Syndrome with slight biphasic T waves in V2-V4 suggesting obstruction to LAD. H/o CABG obscures the reliability. what do you think? Great ECG though!! I think you're being tricked by a U-wave, which follows. Also, Wellens' only occurs with an open artery. It is a result of reperfusion. Nice observation, though. Steve Smith good case

2012 Dr Smith's ECG Blog

177. Subtle Anterior Transient Injury Pattern, Not Appreciated, LAD occlusion spontaneously reperfused

the patient's baseline ECG, but we can't know for certain. The peak troponin I was 0.9 ng/ml. It is interesting that the ECG did not evolve any T-wave inversion, as might be commonly seen with Wellens' syndrome. This goes to show that not all brief LAD occlusions result in Wellens' pattern of reperfusion T-waves. This was called by the interventionalist and cardiologists a "Non STEMI." Had the ECG findings not been seen in the ED, no one would ever have known that STEMI was missed. Posted by Steve Smith (...) the initial 12-lead ECG in the detection of injury and ischemia in patients with acute coronary syndromes (ACS) during the initial ED evaluation of patients with chest pain. METHODS: A prospective observational study was performed in 1,000 patients with chest pain who were admitted to a university teaching hospital and who underwent continuous ST-segment monitoring with SECG during the initial ED evaluation. The initial ECG was obtained on presentation, and SECG readings were obtained at least every 20

2012 Dr Smith's ECG Blog

178. Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death

with depressed ST takeoff) Previously published in: Harrigan (Ed.). The ECG in Emergency Medicine. Smith SW and Whitwam W. The ECG in Acute Coronary Syndromes. EM Clinics of N Am 24(1):53-89; Feb 2006] With no more overt STEMI, and (through bad thinking and "Nah, couldn't be ") I thought that there must have been some mistake in recording the first ECG. At worst, if it was a STEMI, I thought that it is reperfused. I cancelled the cath lab activation for the team that would have to come in from home. (Today I (...) would have unequivocally interpreted leads V2 and V3 as LAD occlusion). At 1942, the patient started becoming hypotensive, so I recorded another ECG at 1946: Need I say more? Obvious anterior STEMI. Previously published in: Harrigan (Ed.). The ECG in Emergency Medicine. Smith SW and Whitwam W. The ECG in Acute Coronary Syndromes. EM Clinics of N Am 24(1):53-89; Feb 2006 I activated the cath lab again at 1946, so that I had caused a 17 minute delay by cancelling. He went to the cath lab, had an LAD

2012 Dr Smith's ECG Blog

179. What is the rhythm? And is there new left bundle branch block (LBBB)?

ventricular focus. Dr. Wellens popularized this criteria and Dr. Marriott referred to it as the "Philadelphia clue". (2,3) Reference/Source: 1.) Marriott HJL. Practical Electrocardiography. 8th ed. Baltimore: Williams & Wilkins, 1988, p. 277, 329, & 373. 2.) Marriott HJL. Marriott’s Manual in Electrocardiography. 1st ed. Naples: Trinity Press, 1999, p. 101 3.) http://heart.bmj.com/content/86/5/579.full I like your blog... thanks. What do you think about ST change in aVr? Was this meaningful or reciprocal (...) something? Steve Smith Anonymous The above ECG record looks rather at the rhythm of the atrioventricular junction, carried out with the accompanying left bundle branch block - this is demonstrated by the retrograde P <100 ms wave for the QRS syndrome. Thanks for the blog Dr. Smith. A great inspiration to learn ECGs : ) and a favourite now world over. Dr. Smith, how do you figure that the P wave is upright in lead II ?? It could be inverted and produce the same curve in lead II if it came a touch earlier

2012 Dr Smith's ECG Blog

180. Stuttering thrombus in the LAD, dynamic hyperacute T-waves, Q-waves, full resolution at 3 months

than 0.04): QTc 447 ms. T-waves continue to diminish. Q-wave in V2, V3. Just before cath, time = 240 minutes: QTc 447 ms. T-waves very diminished now Here is a composite of V4-V6 from previous to prehospital to ED: 2 hours after LAD intervention (80% stenosis with hazy LAD thrombus): QTc 450. T-waves begin to invert. If this was the first ECG you had recorded in the ED, it would be Wellens' syndrome. Next Day . Troponin I peaked at 2.28 mcg/L. The septum, anterior wall, and apex are akinetic

2011 Dr Smith's ECG Blog

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