Podcasts about ctpa

The JournalFeed podcast for the week of July 31 to August 4th, 2023.These are summaries from just 2 of the 5 article we cover every week! For access to more, please visit JournalFeed.org for details about becoming a member.Monday Spoon Feed:In a retrospective study of 331 low risk acute pulmonary embolism patients, concerning CTPA findings were not associated with adverse clinical outcomes.Thursday Spoon Feed:In this individual patient data meta-analysis, researchers found that a positive clinician gestalt was associated with a three times higher risk of pulmonary embolism (PE) compared to negative gestalt.

Panel: Pramod Chandru and Shreyas Iyer.Case Summary: 61-year-old male presenting with 2 distinct episodes of shortness of breath, chest pain, and associated presyncope.   Asymptomatic by the time of arrival to the emergency department.   ECG and observations at triage were unremarkable.  No recent travel or recent major surgeries.  Initial troponin and serial troponin were 80ng/L.   D-dimer was ordered given static troponin and the nature of symptoms: 0.58.  Although this D-dimer was negative when age-adjusted, a V/Q scan was pursued as the patient was not felt to fit a ‘low risk' pre-test probability for PE (IV contrast shortage dictated V/Q over CTPA).  Bilateral segmental pulmonary PE identified on V/Q scan with mild right heart strain evident on subsequent CTPA and TTE.   Key Discussion Points: If a case does not follow the usual ‘pattern' of your initial diagnosis, consider alternate aetiologies.  There are many tools available for risk-stratifying PE including PERC, age-adjusted D-dimer, and the YEARS diagnostic pathway. However, the way in which to appropriately utilize these tools is nuanced.   A paper published in JAMA in December 2021 demonstrates some ways in which these tools can be used together (see first reference below).   The PESI score (even prior to definitive diagnosis) can be useful to risk stratify patients with possible PE and help determine their disposition.   Take-Home Points: Pre-test probability is incredibly important, particularly in entities such as PE where only highly invasive imaging modalities are diagnostic.  Having a structured approach to protect yourself from your own mistakes is extremely important (such as a hypothesis and hypothesis testing approach).  References & Background Reading:  Effect of a Diagnostic Strategy Using an Elevated and Age-Adjusted D-Dimer Threshold on Thromboembolic Events in Emergency Department Patients With Suspected Pulmonary Embolism: A Randomized Clinical Trial. JAMA. 2021 Dec 7;326(21):2141-2149. doi: 10.1001/jama.2021.20750.  Thiruganasambandamoorthy, V., Stiell, I.G., Sivilotti, M.L. et al. Risk stratification of adult emergency department syncope patients to predict short-term serious outcomes after discharge (RiSEDS) study. BMC Emerg Med 14, 8 (2014). https://doi.org/10.1186/1471-227X-14-8. Crane SD, Risk stratification of patients with syncope in an accident and emergency department Emergency Medicine Journal 2002;19:23-27. Almulhim KN. The Characteristics of Syncope-Related Emergency Department Visits: Resource Utilization and Admission Rate Patterns in Emergency Departments. Cureus. 2022 Feb 8;14(2):e22039. doi: 10.7759/cureus.22039. PMID: 35340474; PMCID: PMC8913182.  Iwuji K, Almekdash H, Nugent KM, Islam E, Hyde B, Kopel J, Opiegbe A, Appiah D. Age-Adjusted D-Dimer in the Prediction of Pulmonary Embolism: Systematic Review and Meta-analysis. J Prim Care Community Health. 2021 Jan-Dec;12:21501327211054996. doi: 10.1177/21501327211054996. PMID: 34814782; PMCID: PMC8640977.  Schouten HJ, Geersing GJ, Koek HL, et al. Diagnostic accuracy of conventional or age-adjusted D-dimer cut-off values in older patients with suspected venous thromboembolism: systematic review and meta-analysis. 2012. In: Database of Abstracts of Reviews of Effects (DARE): Quality-assessed Reviews [Internet]. York (UK): Centre for Reviews and Dissemination (UK); 1995-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK133492/. Franco-Moreno AI, Bustamante-Fermosel A, Ruiz-Giardin JM, Muñoz-Rivas N, Torres-Macho J, Brown-Lavalle D. Utility of probability scores for the diagnosis of pulmonary embolism in patients with SARS-CoV-2 infection: A systematic review. Rev Clin Esp (Barc). 2023 Jan;223(1):40-49. doi: 10.1016/j.rceng.2022.07.004. Epub 2022 Sep 22. PMID: 36241500; PMCID: PMC9492501.  Christ M, Geier F, Popp S, Singler K, Smolarsky A, Bertsch T, Müller C, Greve Y. Diagnostic and prognostic value of high-sensitivity cardiac troponin T in patients with syncope. Am J Med. 2015 Feb;128(2):161-170.e1. doi: 10.1016/j.amjmed.2014.09.021. Epub 2014 Oct 15. PMID: 25447619.  Lindner G, Pfortmueller CA, Funk GC, Leichtle AB, Fiedler GM, Exadaktylos AK. High-Sensitive Troponin Measurement in Emergency Department Patients Presenting with Syncope: A Retrospective Analysis. PLoS One. 2013 Jun 18;8(6):e66470. doi: 10.1371/journal.pone.0066470. PMID: 23823330; PMCID: PMC3688899.  Music/Sound Effects: ENGINE by Alex-Productions | https://onsound.eu/, Music promoted by https://www.free-stock-music.com, Creative Commons / Attribution 3.0 Unported License (CC BY 3.0), https://creativecommons.org/licenses/by/3.0/deed.en_US.  Feel It by MBB feat. JV Saxx | https://soundcloud.com/mbbofficial, https://www.instagram.com/JVSAXX/, Music promoted by https://www.free-stock-music.com, Creative Commons / Attribution-ShareAlike 3.0 Unported (CC BY-SA 3.0), https://creativecommons.org/licenses/by-sa/3.0/deed.en_US. Lakeside by Scandinavianz | https://soundcloud.com/scandinavianz, Music promoted by https://www.free-stock-music.com, Creative Commons / Attribution 3.0 Unported License (CC BY 3.0), https://creativecommons.org/licenses/by/3.0/deed.en_US.  Ocean Love by LiQWYD | https://www.liqwydmusic.com, Music promoted by https://www.free-stock-music.com, Creative Commons / Attribution 3.0 Unported License (CC BY 3.0), https://creativecommons.org/licenses/by/3.0/deed.en_US. Nostalgic Marshmallows by Arthur Vyncke | https://soundcloud.com/arthurvost, Music promoted by https://www.free-stock-music.com, Creative Commons / Attribution-ShareAlike 3.0 Unported (CC BY-SA 3.0), https://creativecommons.org/licenses/by-sa/3.0/deed.en_US. Sound effects from https://www.free-stock-music.com. Promotional Video (Soundtrack):Pina Colada by Scandinavianz | https://soundcloud.com/scandinavianz,Music promoted by https://www.free-stock-music.com, Creative Commons / Attribution 3.0 Unported License (CC BY 3.0), https://creativecommons.org/licenses/by/3.0/deed.en_US.Disclaimer:Please be advised that the individual views and opinions expressed in this recording strive to improve clinical practice, are our own, and do not represent the views of any organization or affiliated body. Therapies discussed are general and should not be a substitute for an individualized assessment from a medical professional.Thank you for listening!Please send us an email to let us know what you thought.You can contact us at westmeadedjournalclub@gmail.com.You can also follow us on Facebook, Instagram, and Twitter!See you next time!~

Hosts Denise Dente and Jessica Quick of Buzz Beaute are joined this week by Carys Smith, Regulatory Information Officer at the CTPA, The Cosmetic, Toiletry, and Perfumery Association. She discusses different claims, how they are regulated, and how brands and retailers can stay in compliance.Instagram: https://www.instagram.com/beautybizshow/See omnystudio.com/listener for privacy information.

Emotions can influence our behaviors quite directly. When you are proud of your kids, emotions might help you celebrate and share your joy, and encourage your children to continue on a path to success. When you are ashamed of your kids, they might interfere with your ability to be as supportive as your child needs you to be. Susan Bauerfeld, PhD is a licensed clinical psychologist in private practice in Wilton, CT. Bringing a combination of skills and experience with CBT, attachment theory, neuropsychology, cognitive remediation, coaching and parenting her 3 wonderful, challenging boys, she is an ardent proponent of facilitating change through education, understanding, skill development and practice. She offers workshops, psychotherapy and guidance for parents looking to strengthen their relationships and effectiveness with their children, and ADHD coaching for teens and adults. Dr. Bauerfeld holds an MA and PhD from Fairleigh Dickinson University, a BA from Trinity College and is a member of APA, CTPA, CHADD and Phi Beta Kappa. Ten Tips for Calm and Confident Parenting of Complex Kids Parenting complex kids can be difficult, even mind-numbing at times. In this FREE Guide you'll find clear, quick guidance to help you calm the chaos and more confidently prepare your child for greater independence and success! Learn techniques parents all over the world are using to reduce friction and (believe it!) rediscover the joy of parenting. Listen to this bonus episode from the archives of ImpactParents with Dr. Susan Bauerfeld about how emotions influence behavior and how to manage them. Here is what was covered on this special archival episode: Shift from shame and blame to a more productive approach Tackling the real challenge, rather than focusing on the threat Problem-solving from your frontal lobe, and overcoming the “Amygdala hijack” Connect with Dr. Bauerfeld: Website:  https://susanbauerfeld.com/   Learn more about your ad choices. Visit megaphone.fm/adchoices

CardioNerds (Amit and Dan) join join Dr. Andrew Dicks (Vascular medicine physician at Prisma Health, former fellow at Mass General Vascular) and Dr. Prateek Sharma (Vascular interventional & medicine fellow at MGH) for an ice-cold drinks at the Esplanade in Boston, MA to discuss a case about a patient who developed a pulmonary embolism and masterfully discuss the diagnosis and management of of pulmonary emboli. Dr. Ido Weinberg (Director, Vascular Medicine Fellowship at MGH) provides the ECPR for this episode. Case Abstract: A 59-year-old Spanish-speaking man with no significant past medical history presents after falling 15-20 feet from a ladder and landing on his back. He was found to have an L1 fracture and left radial fracture and underwent T12-L2 fusion with neurosurgery on hospital day 1 and ORIF of left radial fracture with orthopedic surgery on hospital day 2. On hospital day 5, he develops acute onset tachycardia with HR in the 130s bpm with new O2 requirement associated with mild shortness of breath at rest without any chest discomfort. His labs were notable for an elevated troponin and proBNP. He underwent CTPA which demonstrated acute bilateral occlusive pulmonary emboli (PE) extending in the right and left main pulmonary arteries. TTE demonstrated right ventricle dilation. The patient was started on a heparin infusion and a PE response team (PERT) meeting was held to discuss treatment options. Given recent surgery, use of thrombolytic therapy was felt to be too risky and thus he was taken for percutaneous thrombectomy in the cath lab. PA pressure prior to intervention was 51/21 mmHg. The patient underwent suction thromboembelectomy with the Flow Triever device with extraction of thrombus and improvement in PA pressure to 19/11 mmHg. He was treated with anticoagulation thereafter and discharged home two days after the procedure. Jump to: Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Acute bilateral occlusive and nonocclusive pulmonary emboli extending from the right and left main pulmonary arteries to the lobar and segmental arteries of all the lobes.  Moderate right heart strain including the right atrium and the right ventricle. RV/LV ratio > 1.0. Right ventricular cavity is dilated (RV size at the base measures to 45mm). Right ventricular systolic function is moderately decreased. Right ventricular free wall is hypokinetic with sparing of the right ventricular apex consistent with acute right ventricular strain Pulmonary angiography demonstrated extensive proximal bilateral PEs Caption: Post-procedure TTE demonstrated resolution of RV strain with normalization of RV size and function. Episode Schematics & Teaching Pearls While there are markers to suggest PE, such as ECG findings or evidence of RV dilatation, a PE cannot be confirmed without imaging.Elevation of cardiac biomarkers and evidence of RV dysfunction are used to risk stratify PE, not the degree of thrombus burden or locale of thrombus.Enoxaparin is the preferred anticoagulant to initiate at time of PE diagnosis if comorbidities allow.Optimal treatment of intermediate risk PE remains uncertain as there is little data about long-term outcomes. Aggressive treatment should be used judiciously and chosen on a case-by-case basis.PE response teams (PERT) allow for multidisciplinary expert opinion in the face of scarce evidence to determine what is felt to be the best management strategy. Notes 1. What is a PERT team and why is it helpful? We have several tools and approaches for the management of PE. There are also many subspecialities involved in the care of patients with PE, including vascular medicine,

The JournalFeed podcast for the week of April 25-29, 2022. These are summaries from just 2 of the 5 article we cover every week! For access to more, please visit JournalFeed.org for details about becoming a member. CTPA Incidentals Spoon Feed: Computed tomography pulmonary angiography (CTPA) yields an alternative diagnosis to pulmonary embolism (PE) in ~40% of patients with a negative PE study. Alternative diagnoses are more likely to occur in patients with increased age and in patients referred from the hospital setting (ICU or inpatient unit). Headache Nerve Blocks Spoon Feed: Peripheral nerve blocks may help achieve symptomatic improvement in our primary headache patients, but we are still far off with research supporting it as a first-line intervention.

Theme: Pulmonary Embolism.Participants: Dr Bristi Roy (respiratory physician), Dr Vanessa Wong (respiratory advanced trainee), Dr Arwen Morath (emergency physician), Dr Pramod Chandru, Kit Rowe, and Caroline Tyers.   Discussion:van der Pol, L., Tromeur, C., Bistervels, I., Ni Ainle, F., van Bemmel, T., & Bertoletti, L. et al. (2019). Pregnancy-Adapted YEARS Algorithm for Diagnosis of Suspected Pulmonary Embolism. New England Journal Of Medicine, 380(12), 1139-1149. https://doi.org/10.1056/nejmoa1813865.Presenter: Dr Vanessa Wong (respiratory advanced trainee at Westmead Hospital). Summary: PE is a leading cause of maternal death in pregnant women.  However, the radiation exposure to both mother and foetus involved in the diagnosis of PE remains a complex issue.  This is a multi-centre prospective study that utilised the YEARS algorithm (published several years prior) and a D-dimer to predict PE in pregnant women presenting with suspected PE.  The study was conducted over a 5-year period from October 2013 to May 2019.  It looked at pregnant women over the age of 18 years that had been referred to ED or the obstetric ward with concerns for potential PE.   The YEARS algorithm focuses on the 3 elements of the Well's criteria considered to be the highest yield (being clinical signs of DVT, haemoptysis, and PE as the most likely diagnosis).   As part of the algorithm, those patients with clinical signs of DVT underwent a doppler US and were commenced on anticoagulation (and presumed to have a PE) if this was positive for DVT.   PE was excluded in those patients without any of the YEARS criteria and with a D-dimer less than 1.0.   PE was also excluded in those who had 1-3 of the YEARS criteria and a D-dimer < 0.5, while those with 1-3 of the YEARS criteria and a D-dimer > 0.5 went on to have a CTPA to look for PE.  The primary outcome was the cumulative incidence of symptomatic VTE on objective testing during a 3 month follow-up period.   The secondary outcome was the proportion of patients in whom CTPA was not indicated to safely exclude PE.   There were 510 pregnant women recruited into the study (46% of whom were in the third trimester of pregnancy) with 12 being excluded   Of the 498 patients included, 4 had signs and symptoms of DVT with a positive doppler ultrasound.  20 patients of the remaining 494 were diagnosed with PE as part of the pathway.  During follow-up, one popliteal DVT was diagnosed, and no patient had PE.  CTPA was avoided in 195 patients (39%).   Take-Home Points: This provides a framework for assessing patients, particularly in the first and second trimesters of pregnancy (and may aid in safely excluding PE without CTPA for low-risk patients).  However, in high-risk patients, pursuing a scan remains the most appropriate approach.   References: van der Hulle T, Cheung WY, Kooij S, et al. Simplified diagnostic management of suspected pulmonary embolism (the YEARS study): a prospective, multicentre, cohort study. Lancet 2017;390:289-297. Credits:This episode was produced by the ­­­­Emergency Medicine Training Network 5 with the assistance of Dr Kavita Varshney and, Deepa Dasgupta. Music/Sound Effects Dusk by MusicbyAden | https://soundcloud.com/musicbyaden, Music promoted by https://www.free-stock-music.comCreative Commons Attribution-ShareAlike 3.0 Unported, https://creativecommons.org/licenses/by-sa/3.0/deed.en_US. It's Time by Jay Someday | https://soundcloud.com/jaysomeday, Music promoted by https://www.free-stock-music.comCreative Commons Attribution 3.0 Unported License, https://creativecommons.org/licenses/by/3.0/deed.en_US. Magic by Savfk | https://www.youtube.com/savfkmusic, Music promoted by https://www.free-stock-music.com, Attribution 4.0 International (CC BY 4.0), https://creativecommons.org/licenses/by/4.0/. My Old East Coast by Vendredi feat. Melanie | https://soundcloud.com/vendrediduo, Music promoted by https://www.free-stock-music.com, Creative Commons Attribution 3.0 Unported License, https://creativecommons.org/licenses/by/3.0/deed.en_US. Nightswim by Scandinavianz | https://soundcloud.com/scandinavianz, Music promoted by https://www.free-stock-music.com, Creative Commons Attribution 3.0 Unported License, https://creativecommons.org/licenses/by/3.0/deed.en_US. Sound effects from https://www.free-stock-music.com. Tropical Fever by LiQWYD & Luke Bergs | https://www.liqwydmusic.com, https://soundcloud.com/bergscloud, Music promoted by https://www.free-stock-music.com, Creative Commons Attribution-ShareAlike 3.0 Unported, https://creativecommons.org/licenses/by-sa/3.0/deed.en_US. Thank you for listening!Please send us an email to let us know what you thought.You can contact us at westmeadedjournalclub@gmail.com.You can also follow us on Facebook, Instagram, and Twitter!See you next time,Caroline, Kit, Pramod, Samoda, and Shreyas.~

I attended my first NR/CTPA World Championship earlier this month in Montpelier, Ohio and had a fantastic time. Because I had such a great time, I called up the RC Monster Truck race director, Eric Krush, to talk with him about the event.  Hope you enjoy it and put it on the calendar for next year!   Check out the NR/CTPA at their website http://nrctpa.org/

It's the JournalFeed Podcast for the week of August 16-20, 2021. We cover detecting central vertigo on exam, silver nitrate for recurrent epistaxis, cerebral venous thrombosis, spotting RV dysfunction in PE on CT, and D-dimer in pregnancy.

The beauty industry has faced a challenging year, shaped by the ongoing COVID-19 crisis, regulatory changes under Brexit and incoming sustainability legislation at EU level. But industry has learned so much and remains innovative and driven in its approach to gain ground and grow in 2021, says CTPA chief Dr Emma Meredith.

The beauty industry has faced a challenging year, shaped by the ongoing COVID-19 crisis, regulatory changes under Brexit and incoming sustainability legislation at EU level. But industry has learned so much and remains innovative and driven in its approach to gain ground and grow in 2021, says CTPA chief Dr Emma Meredith.

REFERÊNCES1.Offringa A, Montijn R, Singh S, Paul M, Pinto YM, Pinto-Sietsma SJ. The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin-angiotensin system. Eur Heart J Cardiovasc Pharmacother. 2020.2.Santamarina MG, Boisier D, Contreras R, Baque M, Volpacchio M, Beddings I. COVID-19: a hypothesis regarding the ventilation-perfusion mismatch. Crit Care. 2020;24(1):395.3.Merrill JT, Erkan D, Winakur J, James JA. Emerging evidence of a COVID-19 thrombotic syndrome has treatment implications. Nat Rev Rheumatol. 2020.4.Teuwen LA, Geldhof V, Pasut A, Carmeliet P. COVID-19: the vasculature unleashed. Nat Rev Immunol. 2020;20(7):389-91.5.Potus F, Mai V, Lebret M, Malenfant S, Breton-Gagnon E, Lajoie AC, et al. Novel insights on the pulmonary vascular consequences of COVID-19. Am J Physiol Lung Cell Mol Physiol. 2020;319(2):L277-L88.6.Varga Z, Flammer AJ, Steiger P, Haberecker M, Andermatt R, Zinkernagel AS, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet. 2020;395(10234):1417-8.7.Ackermann M, Verleden SE, Kuehnel M, Haverich A, Welte T, Laenger F, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-8.8.McGonagle D. Immune Mechanisms of Pulmonary Intravascular Coagulopathy in COVID-19 Pneumonia. lancet Rheumatol. 2020.9.Perricone C, Bartoloni E, Bursi R, Cafaro G, Guidelli GM, Shoenfeld Y, et al. COVID-19 as part of the hyperferritinemic syndromes: the role of iron depletion therapy. Immunol Res. 2020;68(4):213-24.10.Long B, Brady WJ, Koyfman A, Gottlieb M. Cardiovascular complications in COVID-19. Am J Emerg Med. 2020;38(7):1504-7.11.Price LC, McCabe C, Garfield B, Wort SJ. Thrombosis and COVID-19 pneumonia: the clot thickens! Eur Respir J. 2020;56(1).12.Parry AH, Wani AH, Yaseen M, Dar MI. Demystifying pulmonary vascular complications in severe coronavirus disease-19 pneumonia (COVID-19) in the light of clinico-radiologic-pathologic correlation. Thromb Res. 2020.13.Polak SB, Van Gool IC, Cohen D, von der Thusen JH, van Paassen J. A systematic review of pathological findings in COVID-19: a pathophysiological timeline and possible mechanisms of disease progression. Mod Pathol. 2020.14.von der Thusen J, van der Eerden M. Histopathology and genetic susceptibility in COVID-19 pneumonia. Eur J Clin Invest. 2020:e13259.15.Behzad S, Aghaghazvini L, Radmard AR, Gholamrezanezhad A. Extrapulmonary manifestations of COVID-19: Radiologic and clinical overview. Clin Imaging. 2020;66:35-41.16.Qanadli SD, Beigelman-Aubry C, Rotzinger DC. Vascular Changes Detected With Thoracic CT in Coronavirus Disease (COVID-19) Might Be Significant Determinants for Accurate Diagnosis and Optimal Patient Management. AJR Am J Roentgenol. 2020;215(1):W15.17.Moreira BL, Santana PRP, Zanetti G, Marchiori E. COVID-19 and acute pulmonary embolism: what should be considered to indicate a computed tomography pulmonary angiography scan? Rev Soc Bras Med Trop. 2020;53:e20200267.18.Oudkerk M, Kuijpers D, Oudkerk SF, van Beek EJ. The vascular nature of COVID-19. Br J Radiol. 2020:20200718.19.Lang M, Som A, Mendoza DP, Flores EJ, Reid N, Carey D, et al. Hypoxaemia related to COVID-19: vascular and perfusion abnormalities on dual-energy CT. Lancet Infect Dis. 2020.20.Grillet F, Behr J, Calame P, Aubry S, Delabrousse E. Acute Pulmonary Embolism Associated with COVID-19 Pneumonia Detected by Pulmonary CT Angiography. Radiology. 2020:201544.21.Poyiadji N, Cormier P, Patel PY, Hadied MO, Bhargava P, Khanna K, et al. Acute Pulmonary Embolism and COVID-19. Radiology. 2020:201955.22.Lang M. Pulmonary Vascular Manifestations of COVID-19 Pneumonia. Radiol Cardiothorac Imaging. 2020.23.Kaminetzky M. Pulmonary Embolism on CTPA in COVID-19 Patients. Radiol Cardiothorac Imaging. 2020.24.Thachil J, Srivastava A. SARS-2 Coronavirus-Associated Hemostatic Lung Abnormality in COVID-19: Is It Pulmonary Thrombosis or Pulmonary Embolism? Semin Thromb Hemost. 2020.25.Grillet F, Behr J, Calame P, Aubry S, Delabrousse E. Acute Pulmonary Embolism Associated with COVID-19 Pneumonia Detected with Pulmonary CT Angiography. Radiology. 2020;296(3):E186-E8.26.Saba L, Sverzellati N. Is COVID Evolution Due to Occurrence of Pulmonary Vascular Thrombosis? J Thorac Imaging. 2020.27.E C. Pulmonary Thromboembolism in COVID-19: Venous Thromboembolism or Arterial Thrombosis? Radiol Cardiothorac Imaging. 2020.28.Provencher S, Potus F, Bonnet S. COVID-19 and the pulmonary vasculature. Pulm Circ. 2020;10(3):2045894020933088.

REFERÊNCES1.Offringa A, Montijn R, Singh S, Paul M, Pinto YM, Pinto-Sietsma SJ. The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin-angiotensin system. Eur Heart J Cardiovasc Pharmacother. 2020.2.Santamarina MG, Boisier D, Contreras R, Baque M, Volpacchio M, Beddings I. COVID-19: a hypothesis regarding the ventilation-perfusion mismatch. Crit Care. 2020;24(1):395.3.Merrill JT, Erkan D, Winakur J, James JA. Emerging evidence of a COVID-19 thrombotic syndrome has treatment implications. Nat Rev Rheumatol. 2020.4.Teuwen LA, Geldhof V, Pasut A, Carmeliet P. COVID-19: the vasculature unleashed. Nat Rev Immunol. 2020;20(7):389-91.5.Potus F, Mai V, Lebret M, Malenfant S, Breton-Gagnon E, Lajoie AC, et al. Novel insights on the pulmonary vascular consequences of COVID-19. Am J Physiol Lung Cell Mol Physiol. 2020;319(2):L277-L88.6.Varga Z, Flammer AJ, Steiger P, Haberecker M, Andermatt R, Zinkernagel AS, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet. 2020;395(10234):1417-8.7.Ackermann M, Verleden SE, Kuehnel M, Haverich A, Welte T, Laenger F, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-8.8.McGonagle D. Immune Mechanisms of Pulmonary Intravascular Coagulopathy in COVID-19 Pneumonia. lancet Rheumatol. 2020.9.Perricone C, Bartoloni E, Bursi R, Cafaro G, Guidelli GM, Shoenfeld Y, et al. COVID-19 as part of the hyperferritinemic syndromes: the role of iron depletion therapy. Immunol Res. 2020;68(4):213-24.10.Long B, Brady WJ, Koyfman A, Gottlieb M. Cardiovascular complications in COVID-19. Am J Emerg Med. 2020;38(7):1504-7.11.Price LC, McCabe C, Garfield B, Wort SJ. Thrombosis and COVID-19 pneumonia: the clot thickens! Eur Respir J. 2020;56(1).12.Parry AH, Wani AH, Yaseen M, Dar MI. Demystifying pulmonary vascular complications in severe coronavirus disease-19 pneumonia (COVID-19) in the light of clinico-radiologic-pathologic correlation. Thromb Res. 2020.13.Polak SB, Van Gool IC, Cohen D, von der Thusen JH, van Paassen J. A systematic review of pathological findings in COVID-19: a pathophysiological timeline and possible mechanisms of disease progression. Mod Pathol. 2020.14.von der Thusen J, van der Eerden M. Histopathology and genetic susceptibility in COVID-19 pneumonia. Eur J Clin Invest. 2020:e13259.15.Behzad S, Aghaghazvini L, Radmard AR, Gholamrezanezhad A. Extrapulmonary manifestations of COVID-19: Radiologic and clinical overview. Clin Imaging. 2020;66:35-41.16.Qanadli SD, Beigelman-Aubry C, Rotzinger DC. Vascular Changes Detected With Thoracic CT in Coronavirus Disease (COVID-19) Might Be Significant Determinants for Accurate Diagnosis and Optimal Patient Management. AJR Am J Roentgenol. 2020;215(1):W15.17.Moreira BL, Santana PRP, Zanetti G, Marchiori E. COVID-19 and acute pulmonary embolism: what should be considered to indicate a computed tomography pulmonary angiography scan? Rev Soc Bras Med Trop. 2020;53:e20200267.18.Oudkerk M, Kuijpers D, Oudkerk SF, van Beek EJ. The vascular nature of COVID-19. Br J Radiol. 2020:20200718.19.Lang M, Som A, Mendoza DP, Flores EJ, Reid N, Carey D, et al. Hypoxaemia related to COVID-19: vascular and perfusion abnormalities on dual-energy CT. Lancet Infect Dis. 2020.20.Grillet F, Behr J, Calame P, Aubry S, Delabrousse E. Acute Pulmonary Embolism Associated with COVID-19 Pneumonia Detected by Pulmonary CT Angiography. Radiology. 2020:201544.21.Poyiadji N, Cormier P, Patel PY, Hadied MO, Bhargava P, Khanna K, et al. Acute Pulmonary Embolism and COVID-19. Radiology. 2020:201955.22.Lang M. Pulmonary Vascular Manifestations of COVID-19 Pneumonia. Radiol Cardiothorac Imaging. 2020.23.Kaminetzky M. Pulmonary Embolism on CTPA in COVID-19 Patients. Radiol Cardiothorac Imaging. 2020.24.Thachil J, Srivastava A. SARS-2 Coronavirus-Associated Hemostatic Lung Abnormality in COVID-19: Is It Pulmonary Thrombosis or Pulmonary Embolism? Semin Thromb Hemost. 2020.25.Grillet F, Behr J, Calame P, Aubry S, Delabrousse E. Acute Pulmonary Embolism Associated with COVID-19 Pneumonia Detected with Pulmonary CT Angiography. Radiology. 2020;296(3):E186-E8.26.Saba L, Sverzellati N. Is COVID Evolution Due to Occurrence of Pulmonary Vascular Thrombosis? J Thorac Imaging. 2020.27.E C. Pulmonary Thromboembolism in COVID-19: Venous Thromboembolism or Arterial Thrombosis? Radiol Cardiothorac Imaging. 2020.28.Provencher S, Potus F, Bonnet S. COVID-19 and the pulmonary vasculature. Pulm Circ. 2020;10(3):2045894020933088.

REFERENCES1.Offringa A, Montijn R, Singh S, Paul M, Pinto YM, Pinto-Sietsma SJ. The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin-angiotensin system. Eur Heart J Cardiovasc Pharmacother. 2020.2.Santamarina MG, Boisier D, Contreras R, Baque M, Volpacchio M, Beddings I. COVID-19: a hypothesis regarding the ventilation-perfusion mismatch. Crit Care. 2020;24(1):395.3.Merrill JT, Erkan D, Winakur J, James JA. Emerging evidence of a COVID-19 thrombotic syndrome has treatment implications. Nat Rev Rheumatol. 2020.4.Teuwen LA, Geldhof V, Pasut A, Carmeliet P. COVID-19: the vasculature unleashed. Nat Rev Immunol. 2020;20(7):389-91.5.Potus F, Mai V, Lebret M, Malenfant S, Breton-Gagnon E, Lajoie AC, et al. Novel insights on the pulmonary vascular consequences of COVID-19. Am J Physiol Lung Cell Mol Physiol. 2020;319(2):L277-L88.6.Varga Z, Flammer AJ, Steiger P, Haberecker M, Andermatt R, Zinkernagel AS, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet. 2020;395(10234):1417-8.7.Ackermann M, Verleden SE, Kuehnel M, Haverich A, Welte T, Laenger F, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-8.8.McGonagle D. Immune Mechanisms of Pulmonary Intravascular Coagulopathy in COVID-19 Pneumonia. lancet Rheumatol. 2020.9.Perricone C, Bartoloni E, Bursi R, Cafaro G, Guidelli GM, Shoenfeld Y, et al. COVID-19 as part of the hyperferritinemic syndromes: the role of iron depletion therapy. Immunol Res. 2020;68(4):213-24.10.Long B, Brady WJ, Koyfman A, Gottlieb M. Cardiovascular complications in COVID-19. Am J Emerg Med. 2020;38(7):1504-7.11.Price LC, McCabe C, Garfield B, Wort SJ. Thrombosis and COVID-19 pneumonia: the clot thickens! Eur Respir J. 2020;56(1).12.Parry AH, Wani AH, Yaseen M, Dar MI. Demystifying pulmonary vascular complications in severe coronavirus disease-19 pneumonia (COVID-19) in the light of clinico-radiologic-pathologic correlation. Thromb Res. 2020.13.Polak SB, Van Gool IC, Cohen D, von der Thusen JH, van Paassen J. A systematic review of pathological findings in COVID-19: a pathophysiological timeline and possible mechanisms of disease progression. Mod Pathol. 2020.14.von der Thusen J, van der Eerden M. Histopathology and genetic susceptibility in COVID-19 pneumonia. Eur J Clin Invest. 2020:e13259.15.Behzad S, Aghaghazvini L, Radmard AR, Gholamrezanezhad A. Extrapulmonary manifestations of COVID-19: Radiologic and clinical overview. Clin Imaging. 2020;66:35-41.16.Qanadli SD, Beigelman-Aubry C, Rotzinger DC. Vascular Changes Detected With Thoracic CT in Coronavirus Disease (COVID-19) Might Be Significant Determinants for Accurate Diagnosis and Optimal Patient Management. AJR Am J Roentgenol. 2020;215(1):W15.17.Moreira BL, Santana PRP, Zanetti G, Marchiori E. COVID-19 and acute pulmonary embolism: what should be considered to indicate a computed tomography pulmonary angiography scan? Rev Soc Bras Med Trop. 2020;53:e20200267.18.Oudkerk M, Kuijpers D, Oudkerk SF, van Beek EJ. The vascular nature of COVID-19. Br J Radiol. 2020:20200718.19.Lang M, Som A, Mendoza DP, Flores EJ, Reid N, Carey D, et al. Hypoxaemia related to COVID-19: vascular and perfusion abnormalities on dual-energy CT. Lancet Infect Dis. 2020.20.Grillet F, Behr J, Calame P, Aubry S, Delabrousse E. Acute Pulmonary Embolism Associated with COVID-19 Pneumonia Detected by Pulmonary CT Angiography. Radiology. 2020:201544.21.Poyiadji N, Cormier P, Patel PY, Hadied MO, Bhargava P, Khanna K, et al. Acute Pulmonary Embolism and COVID-19. Radiology. 2020:201955.22.Lang M. Pulmonary Vascular Manifestations of COVID-19 Pneumonia. Radiol Cardiothorac Imaging. 2020.23.Kaminetzky M. Pulmonary Embolism on CTPA in COVID-19 Patients. Radiol Cardiothorac Imaging. 2020.24.Thachil J, Srivastava A. SARS-2 Coronavirus-Associated Hemostatic Lung Abnormality in COVID-19: Is It Pulmonary Thrombosis or Pulmonary Embolism? Semin Thromb Hemost. 2020.25.Grillet F, Behr J, Calame P, Aubry S, Delabrousse E. Acute Pulmonary Embolism Associated with COVID-19 Pneumonia Detected with Pulmonary CT Angiography. Radiology. 2020;296(3):E186-E8.26.Saba L, Sverzellati N. Is COVID Evolution Due to Occurrence of Pulmonary Vascular Thrombosis? J Thorac Imaging. 2020.27.E C. Pulmonary Thromboembolism in COVID-19: Venous Thromboembolism or Arterial Thrombosis? Radiol Cardiothorac Imaging. 2020.28.Provencher S, Potus F, Bonnet S. COVID-19 and the pulmonary vasculature. Pulm Circ. 2020;10(3):2045894020933088.

Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast, summary and backstage pass to the journal and its editors. I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: I'm Dr. Greg Hundley, the director of the Pauley Heart Center at VCU health in Richmond, Virginia. Dr. Carolyn Lam: Oh, Greg. Today we have a special episode focused on COVID‐19 pandemic, something that has just affected us so severely worldwide, it really needs no introduction. Why are we doing a special issue? Well, I think it very quickly got recognized that patients with cardiovascular disease do seem predisposed to severe COVID‐19 syndrome, and that these patients can have an acute COVID‐19 cardiovascular syndrome, in fact. We're going to be talking all about this in a series of interviews about the syndrome, the clinical presentations, what this implies for management. Is the pulmonary embolism involved in the pathophysiology of all of it? And what are ways that we should use to monitor or even screen these patient?, For example, what's the role of troponins? Dr. Greg Hundley: Yes, Carolyn. I am excited, just as well as you, and our first paper today is from Dr. Leslie Cooper, from the Mayo Clinic. He's really done a nice review describing the disease process and the management of acute COVID‐19 and the cardiovascular syndromes. Dr. Greg Hundley: Leslie, we'd like to welcome you to Circulation on the Run and just to get started, I'm wondering, could you tell us a little bit about the genesis of your paper and then also perhaps some of the mechanism, how does this virus affect our systems and promote cardiovascular disease? Dr. Leslie Cooper: In mid‐March as the COVID, crisis was taking off in this country, I was on a telephone call with Dr. [Biykem] Bozkurt and [Dr. Mark] Drazner, from Texas. We realized that there was a terrific need for clinicians to have an overview of how to manage the COVID‐19 impact on the heart. There was also, at that point, very little clinical data about the mechanisms and what the real pathogenesis was. We set about and the rapidly put together the available world's literature. That is what was ultimately published here in Circulation about two weeks ago. Dr. Greg Hundley: Tell us a little bit about that mechanism. Dr. Leslie Cooper: It became apparent that there is not one specific mechanism. We initially thought that like the Coxsackie viruses, this could be a direct cardiac damage, but clinically as we reviewed the literature, it became clear that it's more systemic. The older patients who have preexisting cardiac disease, hypertension, coronary disease, other risk factors, such as diabetes or obesity have a much greater risk of cardiac involvement and the consequences of that cardiac involvement are very substantial. Dr. Leslie Cooper: In addition, when you get a profound cytokine storm from the systemic infection, that can depress cardiac function. A combination, in individuals, of cytokine mediated damage from systemic inflammation, stress induced cardiomyopathy, as you would see in takotsubo, as well as hypoxia and perhaps increased pressures in the lung from, as Carolyn mentioned, pulmonary emboli, and finally direct viral damage. Viruses can infect macrophages in the heart. There is a growing body of literature that there can be a direct effect independent of the systemic infection. The answer is there are multiple factors each of which may have its own therapeutic target. Dr. Carolyn Lam: Oh, I love the way you explained that so clearly Leslie, and in fact, this is really bringing back sweet memories of when I was training under you at Mayo Clinic. I won't say how many years ago, but there comes the question, you know so much about myocarditis, in general, and a different viral myocarditis. Could you maybe tell us a little bit about how this one may or may not differ and also how this impacts management? Dr. Leslie Cooper: The coronaviruses have a very different mechanism of cell entry and propagation. It does not appear that this particular infection in the heart is causing the kind of antigen specific immune reaction that you see classically with a Coxsackie virus. We're not seeing necessarily a lot of auto‐antibody, molecular mimicry. We're not seeing a lot of T‐cell infiltrate. We are seeing some infection of macrophages, and it's not yet clear how many of those were infected peripherally and then migrated to the heart. The histology is quite different and the acute damage is therefore, more subtle. You're not seeing sheets of lymphocytes and the targeted therapies would not be necessarily directed at those cells. Dr. Leslie Cooper: Having said that, inflammation more broadly, for example, anti‐IL‐6, anti‐IL‐1 type, anti‐cytokine mechanisms are currently under evaluation in clinical trials, and they may be quite meaningful. Quite meaningful in the setting of the systemic inflammation. When you compare this to a SARS and other coronavirus infections, I'd like to say, we have known that occasionally a coronavirus can cause myocarditis, for 40 years. It's simply not very common. It predisposes the individual or makes the particular virus more cardiovirulent at this point. Dr. Carolyn Lam: All listeners, you have to get ahold of this beautiful paper. As Greg was actually suggesting a little bit earlier, they're this beautiful figure that you have to refer to that shows a management pathway and considerations. Also, very lovely illustrations of potential mechanisms. Leslie, could you also let us know then, in the overall management, not just treatment, where is the place then, for things like myocardial biopsy? Dr. Leslie Cooper: I think you have to start with the clinical presentation. COVID‐19 as a syndrome, and SARS‐CoV‐2 as a virus, can present with multiple cardiac syndromes. The first would be ST segment elevation, like myocardial infarction with normal coronary arteries. In that setting, it may be microvascular obstruction, or it could be myocarditis or stress cardiomyopathy, perhaps in a younger person who doesn't have risk factors. Dr. Leslie Cooper: Can also present with a primary cardiomyopathy, a heart failure presentation, shortness of breath, systolic dysfunction. And finally it can present as a pericardial effusion, not the most common presentation, but it's important to realize that just like other viruses, this can cause an epicardial or pericardial inflammation. Dr. Leslie Cooper: Management really depends on the clinical syndrome and I'd emphasize guideline‐directed medical management. If it's an arrhythmia, a ventricular tachycardia or heart block, manage that per the current guidelines. The same is true for systolic heart failure. Dr. Leslie Cooper: In addition, I would say that since most patients with COVID infection do not have cardiac involvement, you should first treat the whole patient. First, see the clinical syndrome. What is the dominant problem? Is it a lung problem? Is it kidneys? Then, if there is a cardiac manifestation, we recommend starting with a troponin. If the troponin is elevated, proceed to a point of care echo. Dr. Leslie Cooper: We do want to minimize exposure of allied health staff and physicians to the virus. We do not recommend multimodality imaging or heart biopsy upfront. Having said that, if the patient has substantial left ventricular systolic dysfunction, and they're already in the cath lab, because you're excluding coronary disease, our paper does recommend that you consider an endomyocardial biopsy to find the mechanism of left ventricular dysfunction. Dr. Greg Hundley: Very good, Leslie. Dr. Greg Hundley: Could you close this out, a little bit about therapy when we have patients with this severe hypertension, respiratory abnormalities requiring ventilation, and then also these devastating cardiovascular effects. Are we looking at anti‐inflammation is primarily the target as opposed to antiviral therapy? Dr. Leslie Cooper: Right now, there are a couple of clinical pearls. Number one, as in all cardiogenic shock, you don't have... Sinus tachycardia is not a therapeutic target. You may need that because of low stroke volume. You want to allow when it's compensatory for the tachycardia. Once you've treated with guideline directed therapy, the arrhythmias and the cardiomyopathy appropriately, specific mechanistic interventions, such as antiviral therapy or anticytokine therapy should be given within the context of a clinical trial, wherever possible. Dr. Leslie Cooper: Our article recommends that if you have access to a clinical trial and in this country, the convalescent plasma trial, is up and running. Mayo is leading that for the country. It's available at approximately 600 sites. We would recommend, first of all, enrollment in a trial because we then will understand the mechanisms and the best treatment. If you don't have access, it really depends on the clinical syndrome and how sick the patient is. Patients who are less sick have been treated with things like hydroxychloroquine. People who are more sick, we move on to a convalescent plasma and anticytokine therapy such as tocilizumab. Dr. Greg Hundley: Very good. Well, Leslie, we want to thank you for sharing this wonderful review with us at Circulation. We feel very privileged to have the opportunity to publish this and also to share it with our readership. Again, thank you for all of your frontline work at the Mayo clinic and helping participate in trials and things of this nature to combat this terrible disease. Dr. Leslie Cooper: Thank you so much. Dr. Carolyn Lam: Greg, from acute COVID‐19 cardiovascular syndrome to now, all about troponins. I am so, so thrilled that Dr. Nicholas Mills is here with us, not only our associate editor, but also corresponding author of the next paper. He's from University of Edinburgh in UK. Nick, I love the question that you asked in your title, "Are troponins an ally or a foe in the fight against COVID?" Explain, please. Dr. Nicholas Mills: I strongly believe that they can be an ally, but I recognize amongst cardiologists and clinicians around the world that are grappling with this new condition, that the use of biomarkers can be contentious. We're still learning very much about this condition and how it affects the heart. Therefore, it's difficult to provide very clear guidelines. It's how you interpret the cardiac biomarkers in this condition. The reason I feel strongly that they can be an ally is, they're easy to measure, they're cheap, and you don't require a direct patient contact to obtain the result of the test. It gives us some fundamental information about whether the heart is involved or not. Dr. Greg Hundley: Nick, can you tell us which biomarkers do you favor and is it high sensitivity troponin? Is it regular troponin? For our listeners in many different hospitals across the world, what would you suggest? Dr. Nicholas Mills: The evidence that has that merged very rapidly over the last few weeks and months suggests that our range of cardiac markers have very, very high prediction for poor outcome. Whether that's predicting a patient that might deteriorate and require admission to an intensive care unit for ventilation, or develop complications such as acute kidney injury or death. Dr. Nicholas Mills: There are a number of biomarkers that look very useful for predicting the course of a patient. The strongest, in most studies, is cardiac troponin. I think it's because we do have such sensitive assays now. High sensitive assays are such a fabulous way of getting a barometer of your heart health. The heart of course, is a fairly fundamental organ. If this condition is going to affect to any other organ out with the lungs. If it's the heart, you're going to be in trouble. I think high sensitive troponins, in particular, give us such exquisite information about the systemic complications of this virus that they are perhaps above all other markers, the most useful for predicting outcomes. Now, that clinical question goes beyond that. We need to understand how this virus is affecting the heart and whether we can intervene in any shape or form in response to these results in order to try and improve the course for these patients. That is a more challenging question. Dr. Greg Hundley: Nick, you've got a wonderful figure and we just heard from Leslie Cooper about the different cardiovascular disorders. Once we have elevation or experience, we see elevation in a patient with a biomarker, whether that be high sensitivity, proponent, BNP, et cetera. How does that point us in a direction of where our next move is, clinically, to combat this disease process in patients? Dr. Nicholas Mills: I think the first thing to say is that biomarkers do need to be interpreted in the clinical context and to understand that the pre‐test probability of having underlying structural chronic disease in your patient who presents with COVID‐19. That will very much influence your interpretation. If you think about the spectrum of conditions that you might see, and in fact, that we are seeing, there are a number that I would highlight. In particular, we know from many years of looking after patients with bacterial or viral pneumonia, that the pro inflammatory state of those conditions in patients who are vulnerable, older, and have underlying coronary heart disease is a really powerful risk factor for acute coronary syndrome and type one myocardial infarction. Dr. Nicholas Mills: Often in ventilated patients or patients who have clearly an alternative diagnosis, these important conditions, which are treatable, are overlooked. I think in considering the potential causes of myocardial injury of these patients, we should not overlook the probability that vulnerable patients have triggered acute cornea events in the context of their illness. Dr. Nicholas Mills: The other group that I think are really important are type two myocardial infarcts. They are an increasingly well‐recognized group of patients with the use of high sensitive tests in critical care units around the world. In the context of profound hypoxia or hypotension in sepsis, it gives the clinician managing the patient an idea about the vulnerability of the patient and their susceptibility and risk. I think that is also important. Dr. Nicholas Mills: Then, I think there's a separate group of conditions that are a direct consequence of the exposure to coronavirus and the clinical syndrome of COVID‐19. We are seeing case reports and have our own experience locally, of patients who develop myocarditis in this condition. I think it is rare, but it is real. When it occurs, it can be particularly severe and associated with prothrombotic complications. The other conditions that we are seeing are stress cardiomyopathies in relation to profound breathlessness, and that is not uncommon. Dr. Nicholas Mills: We are trying to systematically scan our more critically unwell patients in the intensive care unit to look for evidence of cardiomyopathy. Dr. Nicholas Mills: The final group that I would highlight is in those that are more severely unwell. Right ventricular dysfunction as a cost of either prothrombotic changes or of ARDS itself, is a really important observation that an elevated cardiac biomarker may be the first clue that that patient is developing cardiac decompensation. Although there's a range of different, important underlying conditions and the biomarker in itself cannot differentiate between these, I think recognizing that the patient is at risk of these underlying cardiac artery disease is an important first step. Dr. Carolyn Lam: Nick, really nicely explained. I'm going to read one of the lines from, I think, one of the concluding paragraphs from your paper, because it's really interesting. "Clinicians must recognize that troponin is not a test for myocardial infarction and it never was." Now, that's very interesting. I know in many ways you've explained it in what you said earlier, but could you maybe just end by hammering home what you meant there? Dr. Nicholas Mills: Myocardial infarction is a clinical diagnosis. It is not a test, one test. It's a combination of clinical features, a variety of different tests that help you arrive at that final diagnosis. Unfortunately, when troponin was introduced into clinical practice a number of years ago, as a replacement for CKMB, it became a sort of de facto. This is the test we use to differentiate people with myocardial infarction, without it, and that has become perpetuated in our clinical practice. Dr. Nicholas Mills: As the technologies move forward and we've developed really high sensitive tests that allow us to measure proponent accurately in almost all patients, it's become abundantly clear that it is a marker of heart injury in a very wide range of clinical conditions. We need to almost unlearn that original teaching, but this was a marker used exclusively to rule in and rule out myocardial infarction and embrace it as a test that tells us about your heart health and how it is affected in a wide range of conditions. Dr. Nicholas Mills: For me, it's never really been high sensitivity troponin in any way, a test exclusively of myocardial infarction. I use it very widely. I always find it informative in the clinical setting in order to guide decisions that I make for my patients. In a patient with ischemic chest pain and an elevated troponin, the default is, this is a type one myocardial infarction until proven otherwise. In all other settings, this is evidence of acute myocardial injury. Some careful consideration is required to determine what the mechanism is that underpins that. Dr. Carolyn Lam: There, you heard it, ladies and gentlemen. That kind of wisdom is going to last beyond COVID‐19. Thank you so much, Nick, for joining us today. That was awesome. Dr. Nicholas Mills: Pleasure. Dr. Greg Hundley: Well, listeners, now we're going to switch and talk a little bit about pulmonary emboli and to introduce that topic. We have Dr. Sophie Susan from Lille, France, who has performed a study in France, looking for this disorder. Dr. Greg Hundley: Welcome Sophie. I was wondering, could you start us off, tell us a little bit about the background for your study, the hypothesis and the question you were going to address, and then what was the study population and some of your results? Dr. Sophie Susan: I work in Lille University Hospital, which is in the North of France. During the early days of March, we had the first patients with COVID‐19 and we were very surprised. High number of patients with sudden aggravation of the respiratory symptoms. We were suspecting high numbers of, I would rather say pulmonary thrombi or pulmonary embolisms. We looked back to medical records of patients admitted in our institution last year, in the same period of time, to look at the frequency of these pulmonary embolism or pulmonary thrombi. We also looked at all the patients admitted for influenza, ARDS in our institution last year. Dr. Sophie Susan: What we observed is that there was a higher frequency of pulmonary embolism during COVID‐19. We observed 22 patients. At the moment we sent the [Research] Letter to Circulation. That means 20% of patients admitted in ICU. And by comparison, there were only 6% of patients in the same period of time in ICU last year. To be sure to avoid any bias in the data collection, we looked also at the CTPA, the angiograms, of the angiography of those patients. We observed that in influenza patients, they were much more investigation with CTPA than in COVID‐19 patients. Despite this higher number of CTPA perform, they were less pulmonary embolism or thrombi identified. Our conclusion was at that moment, that there was an awareness on the new increase frequency in thrombotic pulmonary complications in COVID‐19 patients. Dr. Greg Hundley: Thank you so much, Sophie. You've got a beautiful table in your article. Were there any particular patient characteristics that you could identify in this patient population that you think may make patients predisposed to this? Dr. Sophie Susan: Yes, we were very surprised in my region. My area is a metabolic area and we were very surprised to observe the high number of obese patients in our ICU. There was a publication from our group on the subject. We looked at the BMI of those patients and on our table, you can see that almost all of them were above 25, and the large majority about 30 BMI. They were also all receiving thromboprophylaxis at baseline at the entrance in ICU. Although all the patients were at least receiving 40 milligrams of Heparin, or even more, and some of them were also on their particular levels of low molecular weight or unfractionated heparin therapy. Dr. Carolyn Lam: That is a very important point that you just made, that some of these patients, or a lot of them, had background prophylaxis already. Sophie, could you end by telling us how have these results perhaps influence your management? Or what do you think are the implications? Dr. Sophie Susan: It's a difficult question. The first issue is that regarding the population admitted in ICU, we've got a lot of weight patients and there are no current guidelines adapting thromboprophylaxis to weight. The first question was that 40 milligram of heparin is good for everyone. Do we need to increase this regimen in obese patients? Dr. Sophie Susan: There was a proposal of ESC two years ago, and we adapted these proposals for COVID‐19 patients. We do believe that 40 milligrams of heparin is not enough for patients in ICU, for overweight patients in ICU. So for a BMI above 30, we think that we should increase the regimen of low molecular weight or unfractionated heparin. That's the first point. Dr. Sophie Susan: We've got also, a disease that is random, very difficult sometimes to perform CTPA, difficult, to move patients to those exams. Sometimes we've got to give a probabilistic treatment and in case of acute worsening of the respiratory status and in particular, in case of repositioning patients, when they are under high‐positive and expiratory pressure, sometimes they get sudden aggravation. We must think about probabilistic therapeutic approach with heparin on those patients. That's the two main conclusions we made for the adaptation of protocols. Dr. Carolyn Lam: Well, thank you so much, Sophie. I really am so grateful that you published this work here at Circulation. You very, very, fairly pointed out what you found. I thought that your inclusion of the control groups was really the best that we could do, and therefore your data represent the best available evidence for a very important question that we've all been asking. Are these patients at higher risk of pulmonary embolism? Dr. Carolyn Lam: Thank you so much for sharing that with us. Dr. Sophie Susan: Thank you very much for the invitation. Dr. Carolyn Lam: What an amazing series of papers that we have on COVID‐19. Guess what? These three that we talked about today are not the only ones. We really strongly encourage you to look at ahajournals.org/coronavirus where you can see many more papers published in Circulation, relevant to COVID‐19 as well as some commentary from experts on the front lines. Dr. Carolyn Lam: Thank you very much, once again, everyone for joining us today. Dr. Greg Hundley: Have a great week. Dr. Greg Hundley: This program is copyright, the American Heart Association, 2020  

Cruelty Free est une appellation qui garantit au consommateur que son produit est 100% sans cruauté. C’est à dire aucun produit fini ou ingrédient qui le compose ne doit avoir été testé sur les animaux. Les fournisseurs doivent fournir une attestation confirmant qu'ils ne pratiquent pas l'expérimentation animale et la marque accepte d'être contrôlée à tout moment par un organisme indépendant. Parmi les nombreux labels Cruelty Free présents sur le marché, Leaping Bunny et Cruelty Free de PETA sont les plus stricts. Ces labels garantissent que la marque ne commercialise pas en Chine et qu'aucun produit ou ingrédient qui les compose n'est testé sur les animaux. Parmi les marques dites "sûres" ont peut par exemple citer Lush, l'une des maisons les plus emblématiques dans le domaine, ou encore Urban Decay ou Too Faced. Coline du blog Et pourquoi pas Coline et ambassadrice de The Body Shop, marque engagée de longue date contre toute expérimentation animale, explique : "Il y a des contrôles, des preuves à fournir qu'à aucun moment, aucun ingrédient ni produit n'a été testé sur les animaux et cela remonte évidemment jusqu'aux fournisseurs. Ce qui est certain par contre, c'est que les marques Cruelty Free doivent parfois renoncer à certains ingrédients pour pouvoir créer leurs produits. Malgré le fait qu'elles arrivent à prouver qu'un ingrédient est inoffensif pour la santé via des méthodes alternatives, les résultats peuvent être refusés par les règles européennes". Angélique, auteure du Blog Glam&Conscious a quant à elle sa propre technique: "Pour m'assurer qu'une marque est Cruelty Free, je la contacte et lui demande si ses ingrédients ou ses produits finis sont testés et si elle vend en Chine. Cela demande du temps et des recherches mais heureusement, sur Internet, on apprend vite quand une marque se fait racheter ou qu'elle se lance sur le marché chinois. Des blogueuses très engagées ont également établi des listes qui peuvent servir de référence". La solution pour être sûre d'éviter les produits testés sur les animaux serait donc de privilégier des marques bio et naturelles qui contiennent peu de substances chimiques, et acheter que des produits aux labels exigeants. Certaines consommateurs et consommatrices, encore plus exigeantes, n'arrêtent pas leur sélection à l'appellation Cruelty Free: elles souhaitent également s'assurer que les produits qu'elles achètent sont vegan, c'est à dire sans aucune substance d'origine animale : ni miel, ni lait, ni kératine… la liste est longue. Selon Chris Flower, directeur général de la CTPA (association cosmétique britannique), plus de 200 méthodes alternatives ont été développées et validées par l'OCDE (l'Organisation pour la coopération et le développement économiques) comme les tests sur des cornées optiques synthétiques (plutôt que de réaliser des tests directement dans les yeux des rongeurs). Bien que controversé chez les défenseurs de la cause animale, le géant mondial de la cosmétique L'Oréal effectue certains de ses tests sur des peaux reconstruites à Lyon à EpiSkin, le premier centre mondial d'évaluation prédictive de l'industrie cosmétique. See acast.com/privacy for privacy and opt-out information.

We bring you pearls from the American College of Emergency Physicians (ACEP) 2018 Scientific Assembly in San Diego, CA. In this episode we highlight: Myths in diagnostic imaging Torsion ultrasound is insensitive CTPA for PE is not perfect. There are false positives AND false negatives Myths in pediatrics Response to antipyretics does NOT make viral infection more likely Juice in kids with gastroenteritis is a great way to rehydrate them Kids don't have to wait 24 hours on antibiotics for strep throat before returning to school, if they got 50 mg/kg amoxicillin prior to 5pm the night before, they're fine Thanks for listening! Jeremy Faust and Lauren Westafer

In Part 1 of Pulmonary Embolism Challenges in Diagnosis Drs. Helman, Lang and DeWit discussed a workup algorithm using PERC and Wells score, the bleeding risk of treated pulmonary embolism, pearls in decision making on whether or not to work up a patient for pulmonary embolism, how risk factors contribute to pretest probability, the YEARS criteria and age-adjusted D-dimer. In this Part 2 we answer questions such as: what are the important test characteristics of CTPA we need to understand? Which patients with subsegmental pulmonary embolism should we treat? When should we consider VQ SPECT? What is the best algorithm for the work up of pulmonary embolism in pregnant patients? How best should we implement pulmonary embolism diagnostic decision tools in your ED? and many more… The post Ep 114 Pulmonary Embolism Challenges in Diagnosis 2 – Imaging, Pregnancy, Subsegmental PE appeared first on Emergency Medicine Cases.

Venous thromboembolism (VTE) is one of the most preventable complications in hospitalised patients. Critically ill patients are at risk of VTE due to coexisting of multiple risk factors but, at the same time, often at risk of bleeding. Though not common, fatal pulmonary embolism (PE) continues to occur [1] – due to the alignment of failures (or ‘holes’) in each defensive layer according to the Swiss cheese model [2]. Tackling this is not easy because the pattern of the ‘holes’ in each layer of the cheese is different between patients and, to complicate the matter further, both the size and location of the ‘holes’ also change with time in each individual patient.  In brief, fatal PE occurs due to one of the three failures – failure to prevent, failure to diagnose and failure to treat (aggressively). It is well established that anticoagulants are very effective in reducing VTE. The golden rule to reduce the size of the ‘holes’ in prevention is to use a multimodal approach, with anticoagulants as a key player. The bottom line is that any anticoagulants, even at a reduced dose, is better than no anticoagulant. Judging bleeding risk to determine when anticoagulant prophylaxis can be safely initiated solely based on INR or aPTT is a last century practice. As for diagnosing PE in the critically ill, computed tomography pulmonary angiography (CTPA) is the practical gold standard. While contrast-induced-nephropathy (CIN) is real and critically ill patients are certainly at risk, the benefits of a CTPA will almost always outweigh the risk of CIN when intensivists suspect their patients may have PE (or when the pre-test probability is >10-15%)[3,4]. Immediate aggressive systemic anticoagulation is pivotal in confirmed PE. It is better to aim at a higher aPTT (80-100s) target than a lower one (e.g. 60-80s) as soon as possible to avoid clot propagation which may lead to requiring even higher risk therapies, such as thrombolysis, extracorporeal membrane oxygenation (ECMO) or surgical embolectomy. For those unfortunate few individuals who continue to deteriorate despite systemic anticoagulation, the options ‘to lyse, suck, use ECMO, or remove’ are endless; but in reality the choice is often limited by what expertise is most available at the time of crisis.    Finally, the controversial issue of using inferior vena cava filters as a primary VTE prophylaxis in patients with contraindications to anticoagulants will be discussed, including the results of our recently completed randomized controlled trial [5].    References:  [1] Ho KM, Burrell M, Rao S, Baker R. Incidence and risk factors for fatal pulmonary embolism   after major trauma: a nested cohort study. Br J Anaesth 2010;105:596-602.  [2] Reason J. Human error: models and management. BMJ 2000; 320: 768-70.  [3] Ho KM. Balancing the risks and benefits of using emergency diagnostic radiocontrast studies to diagnose life-threatening illness in critically ill patients: a decision analysis. Anaesth Intensive Care 2016;44:724-8.  [4] Ho KM, Harahsheh Y. Predicting contrast-induced nephropathy after CT pulmonary angiography in the critically ill: a retrospective cohort study. J Intensive Care 2018;6:3.  [5] Ho KM, Rao S, Honeybul S, Zellweger R, Wibrow B, Lipman J, Holley A, Kop A, Geelhoed E, Corcoran T. Detailed assessment of benefits and risks of retrievable inferior vena cava filters on patients with complicated injuries: the da Vinci multicentre randomised controlled trial study protocol. BMJ Open 2017;7:e016747. 

Short on time but hungry for knowledge? Curbsiders’ Journal Club gives you the speedy article analysis you crave. We provide brief summaries of recent research and news items in the field of internal medicine, so you can save time and stay on top of the literature. On this episode, we were joined by Kashlak Memorial’s very own Chair of Medicine, Dr. Robert Centor AKA @medrants on Twitter or “Uncle Bob” to the Curbsider Crew. This month’s topics include: estimating atherosclerotic cardiovascular disease risk, whether CT pulmonary angiography (CTPA) effectively rules out pulmonary embolism, discharging low risk patients with pulmonary embolism from the ED, metformin and risk of acidosis in patients with CKD, treating opioid use disorder after a nonfatal overdose, Canagliflozin and renal protection in type 2 diabetes, screening for diabetes among patients below age 40, and the association between nose-picking and staphylococcus. ACP members can claim free CME-MOC at acponline.com/curbsiders (goes live 0900 EST on podcast release date). Join our mailing list to receive a PDF copy of our show notes every Monday! And hey, while you’re here, consider rating us on iTunes and leaving a review. The Curbsiders thank you! Thoughts on the Journal Club series? Article or guest nominations? Compliments or complaints? You can reach us at thecurbsiders@gmail.com. We are also on Facebook, Instagram, and Twitter: @thecurbsiders.   Credits: Written by: Christopher J Chiu MD, Sarah Phoebe Roberts MPH Producers: Christopher J Chiu MD, Sarah Phoebe Roberts MPH Editor: Matthew Watto MD Hosts: Christopher J Chiu MD, Stuart Brigham MD, Paul Williams MD, and Matthew Watto MD Guest: Robert Centor MD Time stamps: 00:00 Disclaimer and Intro to Curbsiders Journal Club 04:00 Dr. Centor's Pick of the Week 06:10 Clinical Implications of the Revised Pooled Cohort Equations 12:10 Negative Predictive Value in CTPA for VTE 18:34 Can low risk patients with PE be discharged from the ED? 23:03 Is Metformin associated with Lactic Acidosis in those with low eGFR? 28:45 How do medications for opioid use disorder affect mortality after non-fatal overdose? 36:44 Canagliflozin and Renal Protection 43:00 Performance of USPSTF screening criteria for diabetes 46:08 Stuart on Nose picking 50:00 Chiu Bites: Infectious ties and physical attire 53:50 Outro Tags: atherosclerotic, cardiovascular, disease, risk, CT, pulmonary, angiography, CTPA, embolism, ED, metformin, acidosis, CKD, treatment, opioid, use, disorder, oud, mat, overdose, canagliflozin, renal, diabetes, screening, nose-picking, staphylococcus, ACP, CME, MOC, assistant, care, doctor, education, family, FOAM, FOAMim, FOAMed, health, hospitalist, hospital, internal, internist, meded, medical, medicine, nurse, practitioner, professional, primary, physician, resident, student

See if you can get to the correct answers before James Cassidy does in the third and final part of Naomi Laskar's interactive teaching video on causes of chest pain you might see when covering the wards. Really useful things to know in the middle of the night when there's no-one else around!

Naomi Laskar puts James Cassidy through his paces again in the second case of chest pain you are likely to come across as an F1/intern on a surgical or other ward. See if you can get the right answers before James in this interactive teaching video. All the benefits of small group teaching without the pain!

In this first ever episode of the Journal Jam podcast, a collaboration between EM Cases, Academic Life in EM and The Annals of Emergency Medicine's Global Emergency Medicine Journal Club, Teresa Chan and I, along with Jeff Kline, Jonathan Kirschner, Anand Swaminathan, Salim Rezaie and Sam Shaikh from ALiEM, discuss the potential for Age Adjusted D-dimer to rule out pulmonary embolism in low risk patients over the age of 50. We discuss 4 key questions about the ADJUST-PE Study from JAMA in March 2014 including: Would you order a CTPA on a 60 year old woman with an age adjusted D-dimer of 590 ng/L? The problem until now has been that the older the patient, the more likely the D-dimer is to be positive whether they have a PE or not, so many of us have thrown the D-dimer out the window in older patients and go straight to CTPA, even in low risk patients. If you are a risk averse doc, this strategy will lead to over-utilization of resources, huge costs, length of stay, radiation effects etc; and if you're not so risk averse, then you might decide not to work up the low risk older patient at all and miss clinically important PEs. expert peer reviewFor all the questions discussed on this podcast, the original Google Hangout interview from which this podcast was based, and the crowd sourced opinions from around world, visit the ALiEM website. Many thanks to all the talented people who made this podcast possible. Together, we're smarter! The post Journal Jam 1: Age Adjusted D-dimer with Jeff Kline and Jonathan Kirschner appeared first on Emergency Medicine Cases.

In this first ever episode of the Journal Jam podcast, a collaboration between EM Cases, Academic Life in EM and The Annals of Emergency Medicine's Global Emergency Medicine Journal Club, Teresa Chan and I, along with Jeff Kline, Jonathan Kirschner, Anand Swaminathan, Salim Rezaie and Sam Shaikh from ALiEM, discuss the potential for Age Adjusted D-dimer to rule out pulmonary embolism in low risk patients over the age of 50. We discuss 4 key questions about the ADJUST-PE Study from JAMA in March 2014 including: Would you order a CTPA on a 60 year old woman with an age adjusted D-dimer of 590 ng/L? The problem until now has been that the older the patient, the more likely the D-dimer is to be positive whether they have a PE or not, so many of us have thrown the D-dimer out the window in older patients and go straight to CTPA, even in low risk patients. If you are a risk averse doc, this strategy will lead to over-utilization of resources, huge costs, length of stay, radiation effects etc; and if you’re not so risk averse, then you might decide not to work up the low risk older patient at all and miss clinically important PEs. expert peer reviewFor all the questions discussed on this podcast, the original Google Hangout interview from which this podcast was based, and the crowd sourced opinions from around world, visit the ALiEM website. Many thanks to all the talented people who made this podcast possible. Together, we're smarter! The post Journal Jam 1: Age Adjusted D-dimer with Jeff Kline and Jonathan Kirschner appeared first on Emergency Medicine Cases.

Objectives: The objective of this study was to determine whether automated quantification of lung perfused blood volume (PBV) in dual-energy computed tomographic pulmonary angiography (DE-CTPA) can be used to assess the severity and regional distribution of pulmonary hypoperfusion in emphysema. Materials and Methods: We retrospectively analyzed 40 consecutive patients (mean age, 67 13] years) with pulmonary emphysema, who have no cardiopulmonary comorbidities, and a DE-CTPA negative for pulmonary embolism. Automated quantification of global and regional pulmonary PBV was performed using the syngo Dual Energy application (Siemens Healthcare). Similarly, the global and regional degrees of parenchymal hypodensity were assessed automatically as the percentage of voxels with a computed tomographic density less than -900 Hounsfield unit. Emphysema severity was rated visually, and pulmonary function tests were obtained by chart review, if available. Results: Global PBV generated by automated quantification of pulmonary PBV in the DE-CTPA data sets showed a moderately strong but highly significant negative correlation with residual volume in percentage of the predicted residual volume (r = -0.62; P = 0.002; n = 23) and a positive correlation with forced expiratory volume in 1 second in percentage of the predicted forced expiratory volume in 1 second (r = 0.67; P < 0.001; n = 23). Global PBV values strongly correlated with diffusing lung capacity for carbon monoxide (r = 0.80; P < 0.001; n = 15). Pulmonary PBV values decreased with visual emphysema severity (r = -0.46, P = 0.003, n = 40). Moderate negative correlations were found between global PBV values and parenchymal hypodensity both in a per-patient (r = -0.63; P G 0.001; n = 40) and per-region analyses (r = -0.62; P < 0.001; n = 40). Conclusions: Dual-energy computed tomographic pulmonary angiography allows simultaneous assessment of lung morphology, parenchymal density, and pulmonary PBV. In patients with pulmonary emphysema, automated quantification of pulmonary PBV in DE-CTPA can be used for a quick, reader-independent estimation of global and regional pulmonary perfusion, which correlates with several lung function parameters.

11/17/2008 | Part 2 of 3. Discussion of technique for performing CTPA