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Wellens Syndrome

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121. Collection of Breath and Sweat to Identify Indicators of Hypoglycemia

. Information provided by (Responsible Party): Steven J. Russell, MD, PhD, Massachusetts General Hospital Study Details Study Description Go to Brief Summary: Breath and sweat samples will be collected at intervals throughout the visit, with increased frequency during hypoglycemia. Collaborators with the MITRE Corporation will perform analyses on these samples to identify any relationships between volatile organic compounds in breath and sweat and hypoglycemia. Condition or disease Intervention/treatment (...) 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 participation. History of hypoglycemic seizures (grand mal) or coma

2018 Clinical Trials

122. Case Report: Diffuse T wave inversions as initial electrocardiographic evidence in acute pulmonary embolism Full Text available with Trip Pro

inversions with serial troponin elevation. There was initial concern for Wellen's syndrome but was finally diagnosed as acute PE. This case underscores the necessity of vigilance and a lower threshold for PE work up even in patients presenting as acute coronary syndrome. (...) Case Report: Diffuse T wave inversions as initial electrocardiographic evidence in acute pulmonary embolism Acute pulmonary embolism (PE) is a life-threatening condition and is typically diagnosed by a combination of symptoms, clinical signs and imaging. Electrocardiogram may be helpful in diagnosis, and the most widely described pattern of occurrence is the so-called S 1Q 3T 3 pattern. Here, we describe the case of an African-American male who presented with typical chest pain, diffuse T wave

2018 F1000Research

123. ACC/AAP/AHA/ASE/HRS/SCAI/SCCT/SCMR/SOPE 2014 Appropriate Use Criteria for Initial Transthoracic Echocardiography in Outpatient Pediatric Cardiology

Campbell et al. -,2014:-–- AUC for Pediatric Echocardiography 9 Downloaded From: http://content.onlinejacc.org/ on 09/29/2014TABLE 7 Systemic Disorders Indication Appropriate Use Rating 62. Cancer without chemotherapy M (5) 63. Prior to or during chemotherapy in cancer A (8) 64. Sickle cell disease and other hemoglobinopathies A (8) 65. Connective tissue disorder such as Marfan, Loeys Dietz, and other aortopathy syndromes A (9) 66. Suspected connective tissue disorder A (7) 67. Clinically (...) at high risk for cardiovascular involvement, including but not limited to diabetes, systemic hypertension, obesity, stroke, and peripheral vascular disease R (2) 97. Genetic disorder at high risk for cardiovascular involvement A (7) 98. Marfan or Loeys Dietz syndrome A (7) 99. Connective tissue disorder other than Marfan or Loeys Dietz syndrome M (6) 100. Congenital left-sided heart lesion, including but not limited to mitral stenosis, left ventricular out?ow tract obstruction, bicuspid aortic valve

2014 Society for Cardiovascular Angiography and Interventions

124. Atrial Fibrillation: Guidelines For Management of Patients With

Noncardiac Illness .. e49 7.7. Pulmonary Disease: Recommendations e49 7.8. WPW and Pre-Excitation Syndromes: Recommendations e49 7.9. Heart Failure: Recommendations .. e50 7.10. Familial (Genetic) AF: Recommendation... e51 7.11. Postoperative Cardiac and Thoracic Surgery: Recommendations e51 8.EVIDENCE GAPS AND FUTURE RESEARCH DIRECTIONS .. e52 REFERENCES .. e52 APPENDIX 1 Author Relationships With Industry and Other Entities (Relevant) ... e66 APPENDIX 2 Reviewer Relationships With Industry and Other (...) . . e13 2.2.3.1. Atrial Tachycardia Remodeling e13 2.2.3.2. In?ammation and Oxidative Stress e13 2.2.3.3. The Renin-Angiotensin-Aldosterone System e13 2.2.3.4. Risk Factors and Associated Heart Disease e13 3.CLINICAL EVALUATION: RECOMMENDATION . ... e14 3.1. Basic Evaluation of the Patient With AF ... e14 3.1.1. Clinical History and Physical Examination . ... e14 3.1.2. Investigations ... e14 3.1.3. Rhythm Monitoring and Stress Testing ... e15 4.PREVENTION OF THROMBOEMBOLISM ... e15 4.1. Risk-Based

2014 American College of Cardiology

125. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation Full Text available with Trip Pro

: Recommendations e240 7.5. Hyperthyroidism: Recommendations e241 7.6. Acute Noncardiac Illness e241 7.7. Pulmonary Disease: Recommendations e242 7.8. WPW and Pre-Excitation Syndromes: Recommendations e242 7.9. Heart Failure: Recommendations e243 7.10. Familial (Genetic) AF: Recommendation e244 7.11. Postoperative Cardiac and Thoracic Surgery: Recommendations e244 Evidence Gaps and Future Research Directions e244 References e245 Appendix 1. Author Relationships With Industry and Other Entities (Relevant) e258 (...) of different practice patterns and patient populations on the treatment effect and relevance to the ACC/AHA target population to determine whether the findings should inform a specific recommendation. The ACC/AHA practice guidelines are intended to assist clinicians in clinical decision making by describing a range of generally acceptable approaches to the diagnosis, management, and prevention of specific diseases or conditions. The guidelines attempt to define practices that meet the needs of most

2014 American Heart Association

126. HRS/ACC/AHA Expert Consensus Statement on the Use of Implantable Cardioverter-Defibrillator Therapy in Patients Who Are Not Included or Not Well Represented in Clinical Trials Full Text available with Trip Pro

. In addition, no levels of evidence are provided because there are no randomized controlled trials that have been specifically designed to address the clinical conditions posed by this document. The recommendations are largely based on subgroup analysis of randomized clinical trials, retrospective studies, analyses of large registries, and expert opinion. Similarly, this document does not use the same methodology as an Appropriate Use Criteria document. For this consensus document, the writing group (...) mortality by a reduction in SCD in patients with nonischemic heart disease who have an LVEF ≤30%–35%, are NYHA Class II or III, are receiving chronic optimal medical therapy, and who have reasonable expectation of survival with good functional status for more than 1 year. 2008 ACC/AHA/HRS Guidelines for Device-Based Therapy ICD therapy is indicated in patients who are survivors of cardiac arrest due to VF or hemodynamically unstable sustained VT after evaluation to define the cause of the event

2014 American Heart Association

127. Royal Flying Doctor Service Western Operations Clinical manual part 1.Clinical guidelines

with treatment ? Antisocial, explosive or impulsive personality traits or personality disorders In addition patients suffering delirium and dementia in particular may be worsened by unfamiliar environment and night-time conditions. Escalation of care: 1. Ensure during pre-flight assessment that adequate history for warning signs and risk factors taken. 2. Ensure adequate pre-flight sedation including adequate antipsychotics for patients suffering from psychotic illness. 3. Doctor accompaniment 4. Additional (...) (Paediatric) 5 1.5 The Deteriorating Patient 7 2 CARDIOVASCULAR 1 2.1 Acute Coronary Syndromes 1 2.2 Acute Pulmonary Oedema 6 2.3 Cardiac Arrhythmias 8 3 ENDOCRINE 1 3.1 Diabetic Ketoacidosis 1 3.2 Hypoglycaemia 3 3.3 Hypocalcaemia 5 4 GASTROINTESTINAL 1 4.1 Acute Pancreatitis 1 4.2 Haematemesis and Melaena 3 4.3 Intestinal Obstruction 5 5 GENITOURINARY 1 5.1 Acute / Chronic Renal Failure 1 6 INFECTIOUS DISEASES 1 6.1 Bacterial Meningitis 1 6.2 Meningococcal Infection 3 6.3 Tuberculosis 5 6.4 Meliodosis 6

2014 Clinical Practice Guidelines Portal

128. Exercise Standards for Testing and Training Full Text available with Trip Pro

, and during this time additional purposes for testing have evolved. Exercise testing now is used widely for the following: Detection of coronary artery disease (CAD) in patients with chest pain (chest discomfort) syndromes or potential symptom equivalents Evaluation of the anatomic and functional severity of CAD Prediction of cardiovascular events and all-cause death Evaluation of physical capacity and effort tolerance Evaluation of exercise-related symptoms Assessment of chronotropic competence (...) isometric or resistance exercise. A normal increase in HR during exercise is ≈10 bpm per metabolic equivalent (MET). Moreover, the HR response is generally continuous with increasing workload. An accelerated HR response to standardized submaximal workloads is observed after prolonged bed rest, indicating that physical conditioning also plays a role in the HR response, which also can change in response to anemia, metabolic disorders, variable vascular volume or peripheral resistance, or ventricular

2013 American Heart Association

129. 2013 ACC/AHA Guideline for the Management of ST-Elevation Myocardial Infarction - Focused Update

to determine whether the ?ndings should inform a speci?c recommendation. The ACCF/AHA practice guidelines are intended to assist healthcare providers in clinical decision making by describ- ing a range of generally acceptable approaches to the diag- nosis, management, and prevention of speci?c diseases or conditions. The guidelines attempt to de?ne practices that meet the needs of most patients in most circumstances. The ultimate judgment regarding care of a particular patient must be made (...) . Approach to Noninfarct Artery Disease. . . .e117 12.7. Prevention of SCD .e117 12.8. Prevention of HF .e117 References .e118 Appendix 1. Author Relationships With Industry and Other Entities (Relevant) .e135 Appendix 2. Reviewer Relationships With Industry and Other Entities (Relevant) .e138 Appendix 3. Abbreviation List .e140 Preamble The medical profession should play a central role in evalu- ating the evidence related to drugs, devices, and procedures for the detection, management, and prevention

2013 Society for Cardiovascular Angiography and Interventions

130. Clinical Practice Guidelines for Antimicrobial Prophylaxis in Surgery Full Text available with Trip Pro

Director and Associate Professor, Division of Infectious Diseases, School of Medicine, JHU. Search for other works by this author on: Maureen K. Bolon, M.D., M.S. Associate Professor of Medicine, Division of Infectious Diseases, Feinberg School of Medicine, Northwestern University, Chicago, IL. Search for other works by this author on: Douglas N. Fish, Pharm.D., FCCM, FCCP, BCPS Professor and Chair, Department of Clinical Pharmacy, University of Colorado, Anschultz Medical Campus, and Clinical (...) Specialist, Critical Care/Infectious Diseases, Department of Pharmacy Services, University of Colorado Hospital, Aurora. Search for other works by this author on: Lena M. Napolitano, M.D., FACS, FCCP, FCCM Professor of Surgery and Division Chief, Acute Care Surgery, Trauma, Burn, Critical Care, Emergency Surgery, and Associate Chair of Surgery, Critical Care, Department of Surgery, and Director, Surgical Critical Care, University of Michigan Health System, Ann Arbor. Search for other works by this author

2013 Infectious Diseases Society of America

131. Developing and Sustaining Nursing Leadership

, they are inspiring a collaborative approach to patient care. When nurses clarify information for patients and their families, they are promoting a greater understanding of their illness and ensuring patients are empowered to make informed decisions about their care (Patrick et al., 2011). The conceptual model developed in the original leadership guideline is still relevant, although we have made a few changes to reflect current evidence related to healthy work environments (refer to page 8 for a more detailed

2013 Registered Nurses' Association of Ontario

132. Do patients with LBBB and STEMI, when reperfused, develop T-wave inversion (reperfusion T-waves)?

. Smith SW . Validation of the Modified Sgarbossa Rule for Diagnosis of STEMI in the Presence of Left Bundle Branch Block. American Heart Journal 170(6):1255-1264; December 2015. Before the case, a few comments: Pendell and I just published a case report of a patient with left bundle branch block who presented with chest pain that then resolved. His ED ECG showed his baseline LBBB, with no evidence of MI. Over the ensuing hours, he developed classic T-wave inversion of Wellens' syndrome (...) , but in the context of LBBB! Troponins were then positive, and the angiogram revealed a 99% LAD lesion with thrombus. The case demonstrates that Wellens' syndrome can occur in the context of LBBB. Here is a link to the case report: Though Wellens' syndrome was described in the LAD territory, I have shown cases demonstrating that it occurs in any coronary distribution. That is to say, that reperfusion results in terminal T-wave inversion even if the involved territory is the inferior or the lateral wall. Today's

2017 Dr Smith's ECG Blog

133. Chest Pain, LBBB, and a ratio that does not quite meet the Modified Sgarbossa Criteria

my interpretation. Here is my response: "V3 is suspicious for excessive discordance. I would say it does not look like an acute STEMI, but I could be wrong." The patient received thrombolytic therapy. An angiogram was done after thrombolysis : It showed moderate diffuse coronary disease and no thrombus . LAD: mid segment moderate disease OM: mid segment moderate lesion. OM2: ostial moderate lesion Ramus: moderate mid segment lesion RCA: diffuse disease mid to distal, moderate lesion The angiogram (...) was considered to be "negative" for a culprit. An ECG was repeated: LBBB is resolved. There is T-wave inversion in V2 and V3 highly suggestive of Wellens' waves This represents LAD reperfusion An echo was done : There were septal, apical, and anterior wall motion abnormalities. Troponins --(high sensitivity troponin I BiomerieuxVIDAS TNHS): 99% reference = 19 ng/L (%CV = 7% at this level) LoD = 2 ng/L Initial : 13 ng/L (detectable, but still below the 99%) Followup : 38 ng/L (above the 99

2017 Dr Smith's ECG Blog

134. A 30-something woman with chest pain and h/o pulmonary hypertension due to chronic pulmonary emboli

in right-sided lead V1 is only seen with RVH in adults when RVH is marked, and/or with end-stage pulmonary disease; and/or when there is pulmonary hypertension. No one single ECG finding is diagnostic of RVH — but rather it is a combination of findings in the right clinical setting that makes the diagnosis. As per Dr. Smith — the only definitive finding in support of RVH on this tracing is RV “strain” (ie, the prominent anterior T wave inversion). That said, there are other subtle indicators consistent (...) for a predominant R wave in lead V1 would miss many cases in which RVH was present. Finally, as noted — PE should be ruled out (as was done), given the anterior T wave inversion as seen here. It’s always instructive to review the many variant patterns of ECG RVH — Thanks to Dr. Smith for presenting. Thanks, Ken! Could the last ecg in this post have Wellen's warning? The last ECG is a down up T-wave, not an up-down T-wave. It could look like that in either posterior MI or hypokalemia. But not Wellens'. See

2017 Dr Smith's ECG Blog

135. Right precordial ST depression in a patient with chest pain

tall, peaked, anterior T waves, which we call "posterior reperfusion T-waves" or Wellens' syndrome of the posterior wall.(7) Authors in the past have confused acutely occluded posterior MI (which may have either upright or inverted T-waves) with, on the other hand, prolonged or reperfused posterior MI (both of which do indeed have upright T-waves). Is there a tall R-wave in right precordial leads in acute posterior STEMI? Similarly, a tall R-wave in V1 or V2 is not a feature of acute posterior (...) as ST elevation in lead V8: they are opposite! The magnitude may be different, but the direction should be opposite. If it is not, then the state of the artery may have changed. References 1. Wang T, Zhang M, Fu Y, et al. Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non–ST-elevation acute coronary syndromes undergoing diagnostic angiography Am Heart J 2009;157:716-23 2. Matetzky S, Friemark D, Feinberg MS, et al. Acute myocardial infarction

2017 Dr Smith's ECG Blog

136. 2 Cases of Resolved Chest Pain with Dynamic Terminal T-wave Inversion

pattern. Since Wellens' syndrome is the pain-free aftermath of an episode of chest pain associated with LAD occlusion, then at the time of active pain at which time an ECG was recorded, the ECG should have shown some evidence of STEMI, or at least of subtle acute LAD occlusion. This first ECG is a normal variant ST elevation in a young male, with high voltage . It does not represent LAD occlusion. In such a case, one should not assume a benign etiology, but use serial troponins to verify that you (...) are correct. While it is true that, on rare occasion, Wellens' syndrome may have negative serial troponins, all such cases that I have seen were with earlier generation (less sensitive) troponins. Outcome : All troponins were below the level of detection up to 16 hours after presentation. Case 2: These ECGs are classic Wellens' pattern, but also with an unusual lead V2. I saw this patient and immediately knew the diagnosis. The initial troponin I was 1.2 ng/mL (99% URL is 0.030 ng/mL). He went very

2017 Dr Smith's ECG Blog

137. A Very Elderly Male with a Fall and no Chest Pain

with Wellens' waves in V2 and V3. " My opinion was this : "There are no R-waves in V2 and V3, so it is not Wellens'. Furthermore, it can't be Wellens' syndrome even if the ECG is true Wellens' morphology: Wellens' syndrome requires that the ECG be recorded after an episode of chest pain that is now resolved. This patient had no pain at any time." I asked: "Is there a previous ECG for comparison?" (No, there was not) Continued "The QS-waves and shallow T-wave inversion are typical of a dense old transmural (...) have made me wonder whether there are q-vawes or not. Do you have any thoughts on how large the deflection would be to still call it a qs-complex? tom f very interesting, stephen GREAT case about a common primary care (as well as emergency care) issue! As per Dr. Smith, this ECG is not acute — but it most definitely suggests prior injury/infarction. In addition to lacking a history of chest pain — this tracing is not “Wellens Syndrome” because the infarction appears to have already taken place

2017 Dr Smith's ECG Blog

138. 12 Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion

involved). Case 7. A 60 year old male had resolving chest pain There is minimal ST elevation and there are subtle T-wave inversions in V2-V5 , highly suggestive of Wellens' syndrome. Is the ST Elevation normal? Very low R-wave amplitude suggests NOT. See formula here: The QTc was 380 ST Elevation at 60 ms after the J-point in lead V3 = 1.5 mm R-wave amplitude in V4 = 2.5 QRS V2 = 15.5 mm 3-variable formula = 23.4 (equals cutoff of 23.4, consistent with LAD occlusion) 4-variable formula = 18.34 (above (...) 18.2, consistent with LAD occlusion) So this, along with the resolving chest pain , appears to be a reperfusing LAD occlusion. In Wellens' syndrome, the artery is open. T-wave inversion is indicative of reperfusion of the infarct-related vessel. BP was elevated, pulse lowered to 45. He received ASA, Plavix 600mg, Heparin, and a Nitro drip. Another ECG 15 minutes later, pain free, had more T-wave inversion. Then 15 minutes after that, the pain recurred and the T-waves pseudonormalized. The ST

2017 Dr Smith's ECG Blog

139. How can you persuade your cardiologist to take a Non-STEMI patient to the cath lab emergently?

SR, Granger CB, Boden WE, et al. Early versus delayed invasive intervention in acute coronary syndromes. The New England journal of medicine 2009;360:2165-75. Posted by Steve Smith at Labels: , , Reactions: 16 comments: Hello. Great post thanks A question... Can we say that the leads v3 v4 v5 have de wellens waves suggesting LAD occlusion? Thanks. You mean de Winters, not de Wellens! de Winters waves look very similar to this and one could say they are an atypical version. Wellens waves are post (...) diffusely. This is diagnostic of ischemia. There is a Q-wave in V2 and a possible hyperacute T-wave. It is now clear the patient has acute coronary syndrome. It is not clear that there is, or is not, a complete coronary occlusion. The patient was treated with aspirin and sublingual NTG on arrival, which did not relieve his pain. Cardiology was called but they were not interested in taking the patient to the cath lab. First troponin I returned at 0.65 ng/mL. This confirms myocardial infarction. After

2017 Dr Smith's ECG Blog

140. 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

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