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• W1938269320 abstract "HomeCirculationVol. 132, No. 22Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 14: Sickle Cell Trait Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBEligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 14: Sickle Cell TraitA Scientific Statement From the American Heart Association and American College of Cardiology Barry J. Maron, MD, FACC, Chair, Kevin M. Harris, MD, FACC, Paul D. Thompson, MD, FAHA, FACC, E. Randy Eichner, MD and Martin H. Steinberg, MDon behalf of the American Heart Association Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology, Council on Cardiovascular Disease in the Young, Council on Cardiovascular and Stroke Nursing, Council on Functional Genomics and Translational Biology, and the American College of Cardiology Barry J. MaronBarry J. Maron Search for more papers by this author , Kevin M. HarrisKevin M. Harris Search for more papers by this author , Paul D. ThompsonPaul D. Thompson Search for more papers by this author , E. Randy EichnerE. Randy Eichner Search for more papers by this author and Martin H. SteinbergMartin H. Steinberg Search for more papers by this author and on behalf of the American Heart Association Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology, Council on Cardiovascular Disease in the Young, Council on Cardiovascular and Stroke Nursing, Council on Functional Genomics and Translational Biology, and the American College of Cardiology Originally published2 Nov 2015https://doi.org/10.1161/CIR.0000000000000250Circulation. 2015;132:e343–e345Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2015: Previous Version 1 IntroductionSickle cell trait (SCT), in which a normal hemoglobin gene and an abnormal mutated β-globin sickle gene (HbS) are inherited, occurs in 8% of blacks in the United States (0.08% of nonblacks).1,2 SCT has been regarded as a benign condition that generally does not expose affected people to health risks, although for many years it has also been recognized as a potential cause of death in military training recruits during vigorous and intense physical exertion.3 More recently, evidence has been assembled proposing SCT as a cause of sudden death in competitive athletes, usually during training and conditioning.4,5 In 2010, the National Collegiate Athletic Association (NCAA) mandated SCT screening (with solubility testing) for all student-athletes in division I sports (division II, 2012; division III, 2013). In addition, all newborns have been routinely tested for SCT shortly after birth since 1987 in accordance with a National Institutes of Health recommendation.1,6 Much of the controversy regarding SCT and athletes has focused on mandatory screening measures for the genetic defect, an issue that we have not addressed in this statement.That SCT can be responsible for lethal sudden collapse,7 including on the athletic field, is based on evidence from the forensic-based US National Sudden Death in Athletes Registry4,8,9 and other databases,10 as well as numerous case reports and considerable expert experience acquired in athletic venues.5 The epidemiology and characterization of SCT-related events in athletes are evolving. A large experience from the US Sudden Death in Athletes Registry documented SCT-associated collapse and death in 0.9% of 2462 athletes. This outcome occurred in 3.3% of the blacks in the registry.4 Ages of the victims were 12 to 22 years, and 90% were male. Events were most common in college football players during conditioning drills.A distinctive clinical presentation has emerged that involves gradual deterioration over several minutes. Symptoms include cramping, dyspnea, muscle pain and severe weakness, and fatigue and exhaustion, provoked by vigorous physical exertion, often with sequential brief bursts of sustained maximal physical activity (eg, interval training). Events typically occur early in the training season or after periods of deconditioning, often in ambient temperatures ≥80°, at high altitude, or associated with development of rhabdomyolysis.4,11–14 Notably, this scenario is in striking contrast to collapse caused by cardiovascular disease with ventricular tachyarrhythmias, which is typically virtually instantaneous.8,9Although the pathophysiology and clinical determinants of death in people with SCT participating in intense exercise are not fully understood, cardiovascular collapse likely occurs under conditions that (in laboratory studies) promote HbS polymerization and erythrocyte sickling. These include hyperthermia, dehydration, acidosis, and hypoxemia.11–14 It is possible that with intense exercise, a cascade of events ensues under unpredictable circumstances that recreates some of the laboratory conditions that lead to HbS polymerization and erythrocyte sickling, thereby triggering vascular occlusion, endothelial damage, and impaired muscular blood flow.12–16 This exertional sickling scenario could promote rhabdomyolysis and disseminated intravascular coagulation, which in turn could lead to hyperkalemia, lactic acidosis, worsening hypoxia, impaired cardiac and renal function, and lethal arrhythmias. However, widespread sickling in the heart and other organs identified at autopsy does not itself represent definitive evidence for SCT-related death, because postmortem HbS polymerization and erythrocyte sickling are an expected consequence of the diminished oxygen environment at death.These considerations have advanced specific precautionary recommendations for targeted and tailored measures during training for athletes with SCT to enhance the prevention of sudden death.15,16 These precautions, which can also benefit all athletes, include more gradual conditioning at the beginning of the training season (or after periods of deconditioning) with attention to modifying pace, providing adequate rest and hydration during conditioning drills, and promoting a high index of suspicion to immediately cease physical activity should muscle weakness, cramping or pain, fatigue, and disproportionately excessive dyspnea occur.Indeed, collapse of an athlete with SCT is a medical emergency that requires support of vital signs, administration of supplemental oxygen, intravenous hydration, possibly cooling to protect against fulminating rhabdomyolysis, and likely rapid transport to a medical facility. A metabolic insult with lactic acidosis, hyperkalemia, and hypocalcemia can lead to pulseless electrical activity, so that the effectiveness of external defibrillation in this clinical setting is unpredictable. Such modified conditioning strategies and surveillance are now widely used by athletic trainers and coaching staffs in college athletic programs to prevent SCT-related complications and catastrophes.SCT should now be included among the myriad of nontraumatic risks of sports participation capable of leading to the demise of some susceptible athletes, the vast majority of whom are black.RecommendationsRecognition of SCT status is not itself a justification for disqualification from competitive sports (Class I; Level of Evidence C).Recommended preventive strategies (including adequate rest and hydration) should be performed to minimize the likelihood of an event occurring on the athletic field in a person known to have SCT (Class I; Level of EvidenceB).It is critical to be prospectively aware of acute emergency medical strategies should suspicion of an emerging event arise in an athlete known to have SCT (Class I; Level of Evidence C).Particular caution should be exercised for athletes known to have SCT who are competing or training in high environmental temperatures or at extreme altitude (Class I; Level of Evidence C).DisclosuresWriting Group DisclosuresWriting Group MemberEmploymentResearch GrantOther Research SupportSpeakers’ Bureau/HonorariaExpert WitnessOwnership InterestConsultant/Advisory BoardOtherBarry J. MaronMinneapolis Heart Institute FoundationNoneNoneNoneNoneNoneNoneNoneE. Randy EichnerUniversity of OklahomaNoneNoneNoneNoneNoneNoneNoneKevin M. HarrisMinneapolis Heart Institute FoundationNoneNoneNoneNoneNoneNoneNoneMartin H. SteinbergBoston UniversityNoneNoneNoneNoneNoneNoneNonePaul D. ThompsonHartford HospitalNoneNoneNoneNoneNoneNoneNoneThis table represents the relationships of writing group members that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure Questionnaire, which all members of the writing group are required to complete and submit. A relationship is considered to be “significant” if (a) the person receives $10 000 or more during any 12-month period, or 5% or more of the person’s gross income; or (b) the person owns 5% or more of the voting stock or share of the entity, or owns $10 000 or more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant” under the preceding definition.Reviewer DisclosuresReviewerEmploymentResearch GrantOther Research SupportSpeakers’ Bureau/HonorariaExpert WitnessOwnership InterestConsultant/Advisory BoardOtherMichelle A. GrenierUniversity of MississippiNoneNoneNoneNoneNoneNoneNonePranav KansaraChristiana Care Health SystemNoneNoneNoneNoneNoneNoneNoneMark S. KindyMedical University of South CarolinaNoneNoneNoneNoneNoneNoneNoneThis table represents the relationships of reviewers that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure Questionnaire, which all reviewers are required to complete and submit. A relationship is considered to be “significant” if (a) the person receives $10 000 or more during any 12-month period, or 5% or more of the person’s gross income; or (b) the person owns 5% or more of the voting stock or share of the entity, or owns $10 000 or more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant” under the preceding definition.FootnotesThe American Heart Association and the American College of Cardiology make every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on June 24, 2015, and the American Heart Association Executive Committee on July 22, 2015, and by the American College of Cardiology Board of Trustees and Executive Committee on June 3, 2015.The American Heart Association requests that this document be cited as follows: Maron BJ, Harris KM, Thompson PD, Eichner ER, Steinberg MH; on behalf of the American Heart Association Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology, Council on Cardiovascular Disease in the Young, Council on Cardiovascular and Stroke Nursing, Council on Functional Genomics and Translational Biology, and the American College of Cardiology. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: Task Force 14: sickle cell trait: a scientific statement from the American Heart Association and American College of Cardiology. Circulation. 2015;132:e343–e345.This article has been copublished in the Journal of the American College of Cardiology.Copies: This document is available on the World Wide Web sites of the American Heart Association (my.americanheart.org) and the American College of Cardiology (www.acc.org). A copy of the document is available at http://my.americanheart.org/statements by selecting either the “By Topic” link or the “By Publication Date” link. To purchase additional reprints, call 843-216-2533 or e-mail [email protected].Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines development, visit http://my.americanheart.org/statements and select the “Policies and Development” link.Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at http://www.heart.org/HEARTORG/General/Copyright-Permission-Guidelines_UCM_300404_Article.jsp. A link to the “Copyright Permissions Request Form” appears on the right side of the page.References1. Steinberg MH.In the clinic: sickle cell disease.Ann Intern Med. 2011; 155:ITC31–315. doi: 10.7326/0003-4819-155-5-201109060-01003.CrossrefMedlineGoogle Scholar2. Goldsmith JC, Bonham VL, Joiner CH, Kato GJ, Noonan AS, Steinberg MH.Framing the research agenda for sickle cell trait: building on the current understanding of clinical events and their potential implications.Am J Hematol. 2012; 87:340–346. doi: 10.1002/ajh.22271.CrossrefMedlineGoogle Scholar3. Kark JA, Posey DM, Schumacher HR, Ruehle CJ.Sickle-cell trait as a risk factor for sudden death in physical training.N Engl J Med. 1987; 317:781–787. doi: 10.1056/NEJM198709243171301.CrossrefMedlineGoogle Scholar4. Harris KM, Haas TS, Eichner ER, Maron BJ.Sickle cell trait associated with sudden death in competitive athletes.Am J Cardiol. 2012; 110:1185–1188. doi: 10.1016/j.amjcard.2012.06.004.CrossrefMedlineGoogle Scholar5. Eichner ER.Sickle cell trait in sports.Curr Sports Med Rep. 2010; 9:347–351. doi: 10.1249/JSR.0b013e3181fc73d7.CrossrefMedlineGoogle Scholar6. Bonham VL, Dover GJ, Brody LC.Screening student athletes for sickle cell trait: a social and clinical experiment.N Engl J Med. 2010; 363:997–999. doi: 10.1056/NEJMp1007639.CrossrefMedlineGoogle Scholar7. Taylor C, Kavanagh P, Zuckerman B.Sickle cell trait: neglected opportunities in the era of genomic medicine.JAMA. 2014; 311:1495–1496. doi: 10.1001/jama.2014.2157.CrossrefMedlineGoogle Scholar8. Maron BJ.Sudden death in young athletes.N Engl J Med. 2003; 349:1064–1075. doi: 10.1056/NEJMra022783.CrossrefMedlineGoogle Scholar9. Maron BJ, Doerer JJ, Haas TS, Tierney DM, Mueller FO.Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980–2006.Circulation2009; 119:1085–1092. doi: 10.1161/CIRCULATIONAHA.108.804617.LinkGoogle Scholar10. Harmon KG, Drezner JA, Klossner D, Asif IM.Sickle cell trait associated with a RR of death of 37 times in National Collegiate Athletic Association football athletes: a database with 2 million athlete-years as the denominator.Br J Sports Med. 2012; 46:325–330. doi: 10.1136/bjsports-2011-090896.CrossrefMedlineGoogle Scholar11. Admanski C.Steelers’ Ryan Clark Prominent in Sickle Cell Initiative Launch.CBSSports.com Website. 2012. http://www.cbssports.com/nfl/blog/nfl-rapidreports/20049491/steelers-ryan-clar-prominent-in-sickle-cell-initiative-launch. Accessed March 12, 2013.Google Scholar12. Jones SR, Binder RA, Donowho EMSudden death in sickle-cell trait.N Engl J Med. 1970; 282:323–325. doi: 10.1056/NEJM197002052820607.CrossrefMedlineGoogle Scholar13. Eichner ER.Sickle cell considerations in athletes.Clin Sports Med. 2011; 30:537–549. doi: 10.1016/j.csm.2011.03.004.CrossrefMedlineGoogle Scholar14. Tsaras G, Owusu-Ansah A, Boateng FO, Amoateng-Adjepong Y.Complications associated with sickle cell trait: a brief narrative review.Am J Med. 2009; 122:507–512. doi: 10.1016/j.amjmed.2008.12.020.CrossrefMedlineGoogle Scholar15. The National Athletic Trainers’ Association (NATA) releases “Sickle Cell Trait and the Athlete” consensus statement [news release]. Dallas, TX: National Athletic Trainers’ Association; June 27, 2007. http://www.nata.org/NR062107. Accessed April 17, 2012.Google Scholar16. Klossner D.2009–10 NCAA Sports Medicine Handbook. Indianapolis, IN: National Collegiate Athletic Association; 2009. http://www.ncaapublications.com/productdownloads/MD10.pdf. Accessed May 3, 2011.Google Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited ByJone P, John A, Oster M, Allen K, Tremoulet A, Saarel E, Lambert L, Miyamoto S and de Ferranti S (2022) SARS-CoV-2 Infection and Associated Cardiovascular Manifestations and Complications in Children and Young Adults: A Scientific Statement From the American Heart Association, Circulation, 145:19, (e1037-e1052), Online publication date: 10-May-2022. Lampert R and Zipes D (2018) Updated Recommendations for Athletes with Heart Disease, Annual Review of Medicine, 10.1146/annurev-med-041316-090402, 69:1, (177-189), Online publication date: 29-Jan-2018. Friedewald V (2016) Athlete Heart Clinical Guide to Cardiovascular Disease, 10.1007/978-1-4471-7293-2_14, (205-219), . December 1, 2015Vol 132, Issue 22 Advertisement Article InformationMetrics © 2015 American Heart Association, Inc.https://doi.org/10.1161/CIR.0000000000000250PMID: 26527715 Originally publishedNovember 2, 2015 KeywordsAHA Scientific Statementscardiovascular abnormalitiessickle cell traitsudden deathathletesPDF download Advertisement SubjectsStatements and Guidelines" @default.
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