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Epidemiology of SCD in Athletes

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Mahesh J. Patel, MD

Mahesh J. Patel, MD

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  • Sudden cardiac death (SCD) in a young athlete commonlybrings to the forefront the many gaps in knowledgeregarding how to predict and prevent these rare tragicevents.1–3 Although the number of athletic sudden deaths isrelatively small, with 100 to 150 competitive deaths duringsports in the United States annually, they represent animportant and emotionally charged public health issue, perhapsout of proportion to the relative risks of other pediatricdeaths
  • Born and raised in Beaver County, Pennsylvania(All of his accomplishments were achieved before the three-point line was introduced to NCAA basketball, and despite being unable to play varsity as a freshman under then-NCAA rules.[1]) One of the youngest players ever inducted into the Naismith Memorial Basketball Hall of Fame, Maravich was cited by the Hall as "perhaps the greatest creative offensive talent in history".[2] In an April 2010 interview, Hall of Fame player John Havlicek said "the best ball-handler of all time was (Pete) Maravich.”consequence of a previously undetected congenital heart defect. (June 22, 1947 – January 5, 1988
  • Born and raised in Beaver County, Pennsylvania(All of his accomplishments were achieved before the three-point line was introduced to NCAA basketball, and despite being unable to play varsity as a freshman under then-NCAA rules.[1]) One of the youngest players ever inducted into the Naismith Memorial Basketball Hall of Fame, Maravich was cited by the Hall as "perhaps the greatest creative offensive talent in history".[2] In an April 2010 interview, Hall of Fame player John Havlicek said "the best ball-handler of all time was (Pete) Maravich.”consequence of a previously undetected congenital heart defect. (June 22, 1947 – January 5, 1988
  • Postmortem examination of a former professional basketball player revealed an abnormal heart, most notably a single coronary artery. The literature on single coronary arteries is briefly reviewed, and the possible mechanism which caused the patient's condition is considered. This case is particularly unusual because of the patient's profession, which is so physically demanding.Maravich's Heart Defect May Have Been ReparableFebruary 04, 1988|ALLAN PARACHINI | Times Staff WriterEmailShareThe rare heart defect that killed basketball star Pete Maravich might have been repaired by an operation like common bypass surgery if his complaints of intense shoulder and chest pain in the last six months of his life had led to a thorough examination, according to doctors who reviewed coroner's documents released Wednesday.And while physicians who reviewed the 16-page file agreed the detailed coroner's findings are consistent with previous disclosures of the strange cause of the basketball star's death Jan. 5, several experts said they were still puzzled by how, under the circumstances, Maravich could have ever played basketball--let alone star for a decade in the National Basketball Assn.Several doctors suggested that the highly unusual total absence of one of the major arteries to Maravich's heart may have obscured the possibility his heart tissue had also been damaged by any of a variety of factors.They range from latent weakening resulting from years of excessive drinking--behavior to which Maravich himself alludes in a recently published biography--or an undiagnosed viral infection."This is a really bizarre case," said Dr. Frank Litvack, a cardiology diagnostic expert at Cedars-Sinai Medical Center, who reviewed the full documentary file. He said the heart defect may occur in only between 1 in 100,000 to 1 in 1 million patients.Maravich was 40 when he died. He collapsed after playing in a pickup game at a Pasadena church and died shortly after paramedics rushed him to a local hospital.Tests of Maravich's blood and stomach contents for the presence of alcohol and a wide variety of other drugs, including cocaine, were completely negative, the coroner's written report confirmed."Usually patients like this don't go on for 40 years. They don't make it that long," said Dr. Paul Thompson, a sudden death expert at Brown University in Rhode Island who reviewed the Maravich autopsy file Wednesday."The problem with the diagnosis," said Dr. Thomas Klitzner, a UCLA specialist in pediatric cardiology and the way heart rhythm disturbances lead to sudden death, "is how did he play basketball for all those years in the NBA?"Litvack, who reviewed the full documentary file, said damage to Maravich's heart tissue "is not explained purely by the coronary anomaly."He said, "It is difficult to know why he would have (the damage found in the heart muscle.) It could be anything from a previous viral infection to drinking."The file, which comprises the official, written results of the autopsy and other post-mortem tests, confirms that Maravich completely lacked one of the major arteries supplying oxygen-rich blood to the tissue of his heart.The documents also revealed for the first time that Maravich had complained of chest pain in the final six months of his life. Previous reports had indicated he also complained of intense pain in his right shoulder.The combination of chest and shoulder pain, said doctors questioned by The Times, could have led to the ordering of a treadmill stress test on Maravich, in which the test subject walks on a treadmill while instruments monitor heart function.Maravich's personal physician, Dr. William Mitchell, of Covington, La., did not respond to calls seeking reaction to the autopsy details.Thompson said chest and shoulder pain in a 40-year-old man are always potential danger signs that should be taken as a possible warning of heart problems.Thompson and Dr. Jeffrey Isner, a Tufts University specialist in heart disease processes who has reviewed the Maravich case with Los Angeles County Coroner's Office officials, agreed that the treadmill stress test could have produced results that would lead doctors to order additional tests that would have discovered the strange inherited anomaly in Maravich's heart.The only procedure that could have definitively diagnosed Maravich is a procedure called cardiac catheterization in which a wire is introduced into the arteries while X-ray machinery, assisted by dye injected into the blood, projects pictures of the organs on a television screen. The catheterization procedure is commonly used to determine if bypass surgery is necessary.Maravich's defect could probably have been repaired by an operation almost identical to common bypass surgery.The entire blood supply to Maravich's heart had been supplied, the autopsy file indicated, by a narrow shunt-like vessel that ran circuitously across Maravich's heart from the right to left side.The natural shunt was never able to supply adequate amounts of blood, resulting in gradual deterioration of the muscle in Maravich's heart, enlargement of the heart and development of fiber-like growths in the tissue, the coroner concluded.
  • Sudden cardiac death (SCD) associated with athletic activity is a rare but devastating event. Victims are usually young and apparently healthy, but many have underlying cardiovascular disease that is not diagnosed until after the event. As a result, there is great interest in detecting such abnormalities early, and then defining appropriate activity restrictions for affected individuals to minimize the risk of SCD.
  • SCD is a very real public health issue and personal issue fornot only the athlete, but also for the nonathlete. SCD in ayoung individual is devastating. Appropriate measures ofprevention and treatment are critical. However, based on thebest available evidence, it is evident that measures conclusivelyeffective in reducing athletic SCD remain unknown.Nearly all available data are limited by their observationalnature. Standard definitions of competitive athletes and athleticsudden death are needed. Robust national registries ofathletic sudden death are also essential. Randomized trials ofscreening and restriction prospectively collecting cost andoutcomes data are needed. The ethics of selectively screeningathletes for cardiovascular conditions that predispose to SCDwithout broader screening of the nonathletic population meritcareful consideration. Additional studies are needed to evaluatethe long-term consequences of athletic restriction. Theconsiderable controversy related to many of the issues regardingathletic sudden death stems from the lack of evidence toresolve them. Experience indicates that when there is disagreementamong experts, there is a dearth of reliable data.The best available data indicate that the total number ofathletic deaths is relatively small. Furthermore, provenstrategies to prevent athletic sudden death are not currentlyavailable. Based on these considerations, the most reasonedapproach currently is advancing the available evidenceby obtaining data from appropriately designedstudies rather than prematurely advancing well-intendedyet unproven strategies.
  • the first systematic investigation of the health consequences of physcial inactivity was published around this time- British epidemiologist Jeremy Morris published a landmark article in Lancet in 1953, which suggested a strong relationship between physical inactivity and CV disease. - he compared heart attack rates of bus drivers vs. conductors in a double decker buses. Drivers sat 90% shift and conductors climbed about 600 stairs a day. - conductors had more than 50% less heart attacks. Follow-up studies indicated that these results were independednt of body type.- he corroborated these findings by comparing postal workers, those who delivered mail by walking andbicycling vs. the post office clerks and telephone operators.
  • the first systematic investigation of the health consequences of physcial inactivity was published around this time- British epidemiologist Jeremy Morris published a landmark article in Lancet in 1953, which suggested a strong relationship between physical inactivity and CV disease. - he compared heart attack rates of bus drivers vs. conductors in a double decker buses. Drivers sat 90% shift and conductors climbed about 600 stairs a day. - conductors had more than 50% less heart attacks. Follow-up studies indicated that these results were independednt of body type.- he corroborated these findings by comparing postal workers, those who delivered mail by walking andbicycling vs. the post office clerks and telephone operators. Sudden cardiac death (SCD) is rare, but may occur during physical activity [49,50]. The risk of SCD in athletes is discussed separately. (See "Risk of sudden cardiac death in athletes".)The increase in risk is seen in both men and women. In the Physicians' Health Study of 21,481 males followed for 12 years, the absolute risk of SCD during any one episode of vigorous exercise was low (one death per 1.51 million episodes of exercise) [51]. In the Nurses' Health Study of 69,693 women, the absolute risk was even lower, with one death per 36.5 million hours of exertion [52]. The risk of cardiac arrest is less or may not be increased at all if there is habitual, heavy leisure-time physical activity, as noted in both the Physicians' Health Study and the Nurses' Health Study [51,52]. Mechanisms of SCD in those who exercise include coronary artery disease, arrhythmias (especially ventricular tachycardia and ventricular fibrillation), structural heart disease, and myocarditis [53]. Causes of SCD in people who exercise can be divided according to age [49]. SCD is generally a result of atherosclerotic coronary artery disease in those over age 35 years. It is more likely to be due to congenital abnormalities such as hypertrophic cardiomyopathy, coronary anomalies, or to myocarditis in younger individuals. (See "Overview of sudden cardiac arrest and sudden cardiac death", section on 'Exercise'.)Because the increase in risk of SCD during or just after activity is low, the long-term health benefits of exercise outweigh the risks in patient with and without established heart disease [54]. MechanismsMalignant arrhythmia such as VT or VF. Exercise training can induce changes in cardiac structure that create arrhythmic substrateThe immediate physiologic demands of intense exercise can also trigger malignant arrhythmias.Myocardial infarctionSudden cardiac death (SCD) is rare but may occur during exercise.Physicians' Health Study21,481 males followed for 12 yearsabsolute risk: one death per 1.51 million episodes of exerciseNurses' Health Study69,693 womenabsolute risk: one death per 36.5 million hours of exertion
  • Causes of death in the US population aged 1 to 21 years. Injury, homicide, and suicide dwarf the number of sudden deaths in athletes. SCD indicates sudden cardiac death. Data from the Centers for Disease Control and Prevention (http://webappa.cdc.gov/sasweb/ncipc/leadcaus10.html).100 to 150 competitive deaths duringsports in the United States annuallyOn average, every 3 days in the United States a competitiveathlete experiences a SCD, and many of these deaths arenationally noted.However, this same intense media speculationis not given to a nonathlete who experiences SCD orindeed to a competitive athlete who has SCD off the athleticfield.What about riscd in non-athletes – poorly undrestood or deaths outside exercise time in athletesAtletes are healthyBut Rare eventRank order – causes ofr deathLink Circ 2012
  • Figure 1. Number of cardiovascular (CV), trauma-related, and other sudden death events in 1866 young competitive athletes, tabulated by year.Background—Sudden deaths in young competitive athletes are highly visible events with substantial impact on thephysician and lay communities. However, the magnitude of this public health issue has become a source of controversy.Methods and Results—To estimate the absolute number of sudden deaths in US competitive athletes, we have assembleda large registry over a 27-year period using systematic identification and tracking strategies. A total of 1866 athletes whodied suddenly (or survived cardiac arrest), 196 years of age, were identified throughout the United States from 1980to 2006 in 38 diverse sports. Reports were less common during 1980 to 1993 (576 [31%]) than during 1994 to 2006(1290 [69%], P0.001) and increased at a rate of 6% per year. Sudden deaths were predominantly due to cardiovasculardisease (1049 [56%]), but causes also included blunt trauma that caused structural damage (416 [22%]), commotiocordis (65 [3%]), and heat stroke (46 [2%]). Among the 1049 cardiovascular deaths, the highest number of events ina single year was 76 (2005 and 2006), with an average of 66 deaths per year (range 50 to 76) over the last 6 years; 29%occurred in blacks, 54% in high school students, and 82% with physical exertion during competition/training, whereasonly 11% occurred in females (although this increased with time; P0.023). The most common cardiovascular causeswere hypertrophic cardiomyopathy (36%) and congenital coronary artery anomalies (17%).Conclusions—In this national registry, the absolute number of cardiovascular sudden deaths in young US athletes wassomewhat higher than previous estimates but relatively low nevertheless, with a rate of 100 per year. These data arerelevant to the current debate surrounding preparticipation screening programs with ECGs and also suggest the need forsystematic and mandatory reporting of athlete sudden deaths to a national registry. (Circulation. 2009;119:1085-1092.)
  • Circ Arrhythm Electrophysiol. 2014 Mar 1. [Epub ahead of print]Etiologies of Sudden Cardiac Death in National Collegiate Athletic Association Athletes.Harmon KG1, Drezner JA, Maleszewski JJ, Lopez-Anderson M, Owens D, Prutkin JM, Asif IM, Klossner D, Ackerman MJ.Author information AbstractBACKGROUND: -The etiology of sudden cardiac death (SCD) in college athletes has not been defined by systematic case identification.METHODS AND RESULTS: -45 cases of SCD were identified in National Collegiate Athletic Association (NCAA) athletes from 2004 - 2008 based on an internal reporting system and review of media reports. Autopsy reports were reviewed and adjudicated by a multi-disciplinary panel. Cause of death could be reasonably determined in 36 cases. 3 athletes had no autopsy, 5 autopsy reports could not be obtained, and 1 autopsy had insufficient information to determine cause of death. The most common finding at death was a structurally normal heart or autopsy-negative sudden unexplained death (11, 31%), followed by coronary artery abnormalities (5, 14%), dilated cardiomyopathy (3, 8%), myocarditis related (3, 8%), aortic dissection (3, 8%), and idiopathic left ventricular hypertrophy (LVH)/possible hypertrophic cardiomyopathy (HCM) (3, 8%). There was one case each (3%) of HCM, arrhythmogenic right ventricular cardiomyopathy, long QT syndrome, commotiocordis, and Kawasaki's disease. There was one case of death in a sickle cell positive athlete who also had LVH. The adjudicated diagnosis agreed with the official pathology report in only 59% of cases.CONCLUSIONS: -Unexplained death with a structurally normal heart is the most common finding after suspected SCD in NCAA athletes. HCM is infrequently seen, and conclusions in autopsy reports may not accurately reflect the pathologic findings. Standardized protocols for cardiovascular autopsies in athletes are needed, including post-mortem genetic testing, particularly in autopsy-negative cases.KEYWORDS: Background—The true incidence of sudden cardiac death (SCD) in US athletes is unknown. Current estimates are based largely on case identification through public media reports and estimated participation rates. The purpose of this study was to more precisely estimate the incidence of SCD in National Collegiate Athletic Association (NCAA) student-athletes and assess the accuracy of traditional methods for collecting data on SCD. Methods and Results—From January 2004 through December 2008, all cases of sudden death in NCAA student-athletes were identified by use of an NCAA database, weekly systematic search of public media reports, and catastrophic insurance claims. During the 5-year period, there were 273 deaths and a total of 1 969 663 athlete participant-years. Of these 273 deaths, 187 (68%) were due to nonmedical or traumatic causes, 80 (29%) to medical causes, and 6 (2%) to unknown causes. Cardiovascular-related sudden death was the leading cause of death in 45 (56%) of 80 medical cases, and represented 75% of sudden deaths during exertion. The incidence of SCD was 1:43 770 participants per year. Among NCAA Division I male basketball players, the rate of SCD was 1:3100 per year. Thirty-nine (87%) of the 45 cardiac cases were identified in the NCAA database, only 25 (56%) by use of public media reports, and 9 (20%) from catastrophic claims data. Conclusions—SCD is the leading medical cause of death and death during exercise in NCAA student-athletes. Current methods of data collection underestimate the risk of SCD. Accurate assessment of SCD incidence is necessary to shape appropriate health policy decisions and develop effective strategies for prevention.
  • Among the 36 cases (80%) where the cause of death could be reasonably determined(Figure 1), the most common finding was AN-SUD (11, 31%) followed by coronary arteryabnormalities (5, 14%), dilated cardiomyopathy (3, 8%), myocarditis related (3, 8%), aorticdissection (3, 8%), and idiopathic left ventricular hypertrophy (LVH)/possible HCM (3, 8%).There was one case each (3%) of HCM, arrhythmogenic cardiomyopathy (ARVC), commotiocordis, and Kawasaki disease. There was one case of death in a sickle cell positive athlete whoalso had LVH. Toxicology screens were available for all autopsies and were negative or noncontributory.
  • The precise frequency with which theseevents occur in the United States remains unclear because ofthe absence of athletic death registries (and indeed any SCDregistry) with mandatory reporting requirements.
  • high school or college athletes. Masters sports are organized forms of competition specifically designed for older athletes. Such sports programs primarily include apparently normal and healthy individuals over the age of 35, although many participants are greater than 50 or 60 years of age.A recreational athlete is between the definition of the physically active person and the competitive athlete. They are physically active, however, they may or may not train at the same intensity level that a competitive athlete would (i.e. someone who is on the bowling team once a week or someone who plays on a basketball league at the local Y with their friends once a week). Recreational athletes may or may not meet the recommended guidelines for physical activity, which is comprised of at least 30 minutes of moderate physical activity most days of the week or at least 20 minutes of vigorous physical activity at least 3 days out of the week, depending if other exercise activity is incorporated during the week. The weekend warrior is someone who decides to squeeze in their physical activity only 1-2 days a week, normally on the weekend, while remaining relatively inactive the rest of the week. Weekend warriors generally do not meet the criteria of being regularly active and do not meet the current recommended guidelines for physical activity.
  • BACKGROUNDApproximately 2 million people participate in long-distance running races in the UnitedStates annually. Reports of race-related cardiac arrests have generated concernabout the safety of this activity.METHODSWe assessed the incidence and outcomes of cardiac arrest associated with marathonand half-marathon races in the United States from January 1, 2000, to May 31, 2010.We determined the clinical characteristics of the arrests by interviewing survivorsand the next of kin of nonsurvivors, reviewing medical records, and analyzing postmortemdata.RESULTSOf 10.9 million runners, 59 (mean [°¿SD] age, 42°¿13 years; 51 men) had cardiac arrest(incidence rate, 0.54 per 100,000 participants; 95% confidence interval [CI], 0.41 to0.70). Cardiovascular disease accounted for the majority of cardiac arrests. The incidencerate was significantly higher during marathons (1.01 per 100,000; 95% CI,0.72 to 1.38) than during half-marathons (0.27; 95% CI, 0.17 to 0.43) and among men(0.90 per 100,000; 95% CI, 0.67 to 1.18) than among women (0.16; 95% CI, 0.07 to0.31). Male marathon runners, the highest-risk group, had an increased incidenceof cardiac arrest during the latter half of the study decade (2000–2004, 0.71 per100,000 [95% CI, 0.31 to 1.40]; 2005–2010, 2.03 per 100,000 [95% CI, 1.33 to 2.98];P = 0.01). Of the 59 cases of cardiac arrest, 42 (71%) were fatal (incidence, 0.39 per100,000; 95% CI, 0.28 to 0.52). Among the 31 cases with complete clinical data,initiation of bystander-administered cardiopulmonary resuscitation and an underlyingdiagnosis other than hypertrophic cardiomyopathy were the strongest predictorsof survival.CONCLUSIONSMarathons and half-marathons are associated with a low overall risk of cardiac arrestand sudden death. Cardiac arrest, most commonly attributable to hypertrophiccardiomyopathy or atherosclerotic coronary disease, occurs primarily among malemarathon participants; the incidence rate in this group increased during the pastdecade.
  • FabriceNdalaMuamba (born 6 April 1988) is a retired professional footballer who played for Arsenal, Birmingham City and Bolton Wanderers as a central midfielder. Born in Zaire (now the Democratic Republic of the Congo), Muamba moved to England at the age of 11, and subsequently played for the England under-21 team.Muamba began his career in 2002, joining Arsenal's youth academy. After three years, he turned professional in 2005. He made his debut for Arsenal in the League Cup, but played only one other professional match for the club. Following a loan spell with Birmingham City, he made the move permanent in 2007. He stayed with Birmingham City for one additional year, and left after making more than 70 appearances and making his England under-21 debut while with the team. He joined Bolton Wanderers in 2008.In March 2012, Muamba suffered a cardiac arrest during a televised FA Cup match between Bolton and Tottenham Hotspur, from which he recovered despite his heart having stopped for more than an hour. Following medical advice, he announced his retirement from professional football in August 2012.
  • SCD is a very real public health issue and personal issue fornot only the athlete, but also for the nonathlete. SCD in ayoung individual is devastating. Appropriate measures ofprevention and treatment are critical. However, based on thebest available evidence, it is evident that measures conclusivelyeffective in reducing athletic SCD remain unknown.Nearly all available data are limited by their observationalnature. Standard definitions of competitive athletes and athleticsudden death are needed. Robust national registries ofathletic sudden death are also essential. Randomized trials ofscreening and restriction prospectively collecting cost andoutcomes data are needed. The ethics of selectively screeningathletes for cardiovascular conditions that predispose to SCDwithout broader screening of the nonathletic population meritcareful consideration. Additional studies are needed to evaluatethe long-term consequences of athletic restriction. Theconsiderable controversy related to many of the issues regardingathletic sudden death stems from the lack of evidence toresolve them. Experience indicates that when there is disagreementamong experts, there is a dearth of reliable data.The best available data indicate that the total number ofathletic deaths is relatively small. Furthermore, provenstrategies to prevent athletic sudden death are not currentlyavailable. Based on these considerations, the most reasonedapproach currently is advancing the available evidenceby obtaining data from appropriately designedstudies rather than prematurely advancing well-intendedyet unproven strategies.
  • SCD is a very real public health issue and personal issue fornot only the athlete, but also for the nonathlete. SCD in ayoung individual is devastating. Appropriate measures ofprevention and treatment are critical. However, based on thebest available evidence, it is evident that measures conclusivelyeffective in reducing athletic SCD remain unknown.Nearly all available data are limited by their observationalnature. Standard definitions of competitive athletes and athleticsudden death are needed. Robust national registries ofathletic sudden death are also essential. Randomized trials ofscreening and restriction prospectively collecting cost andoutcomes data are needed. The ethics of selectively screeningathletes for cardiovascular conditions that predispose to SCDwithout broader screening of the nonathletic population meritcareful consideration. Additional studies are needed to evaluatethe long-term consequences of athletic restriction. Theconsiderable controversy related to many of the issues regardingathletic sudden death stems from the lack of evidence toresolve them. Experience indicates that when there is disagreementamong experts, there is a dearth of reliable data.The best available data indicate that the total number ofathletic deaths is relatively small. Furthermore, provenstrategies to prevent athletic sudden death are not currentlyavailable. Based on these considerations, the most reasonedapproach currently is advancing the available evidenceby obtaining data from appropriately designedstudies rather than prematurely advancing well-intendedyet unproven strategies.

Transcript

  • 1. The Epidemiology of Sudden Cardiac Death in Athletes Mahesh J. Patel, MD Assistant Professor Preventive & Rehabilitative Cardiology Duke Heart Center
  • 2. • Starred in college at Louisiana State University • All-time leading college scorer with an average of 44.2 pts/game • Played for 3 NBA teams • Forced into retirement at age 32 due to knee problems. • Inducted into the NBA Hall of Fame. • Sudden cardiac death (SCD) at age 40 during a recreational game of basketball Pete Maravich
  • 3. • Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) refer to the sudden cessation of cardiac activity with hemodynamic collapse, typically due to sustained ventricular tachycardia/ventricular fibrillation. • The event is referred to as SCA (or aborted SCD) if an intervention (eg, defibrillation) or spontaneous reversion restores circulation, and the event is called SCD if the patient dies. • However, the use of SCD to describe both fatal and nonfatal cardiac arrest persists by convention. Sudden Cardiac Death
  • 4. Coronary Anomaly & Cardiomyopathy
  • 5. Young vs. Older Athlete
  • 6. • SCD risks with vigorous intensity exercise • SCD risks in young athletes • SCD risks in masters & recreational athletes • Strategies to reduce risks of SCD Outline
  • 7. Blair JAMA 1989 0 1 2 3 4 5 6 7 8 9 10 1st 2nd 3rd 4th 5th Women Men Increasing cardiopulmonary fitness RR of CV Death Athletes & CV Mortality
  • 8. Mittleman NEJM 1993 Habitual vigorous exercise lowers CV risks 107 20 9 2 Patients engaging in vigorous exertion ( ≥ 6 METS ) within one hour before MI
  • 9. Vigorous intensity exercise can increase risk of sudden cardiac death (SCD) Physicians' Health Study 21,481 males - absolute risk: one death per 1.51 million episodes of vigorous exercise Nurses' Health Study 69,693 women - absolute risk: one death per 36.5 million hours of exertion
  • 10. Link Circulation 2012 How common is sudden death in young, competitive US athletes ? 100 to 150 competitive deaths during sports in the United States annually. On average, every 3 days in the United States a competitive athlete experiences a SCD.
  • 11. Maron Circulation 2009 Young Athletes Registry - 1866 athlete deaths - 38 sports - 56% CV causes - 3% commotio cordis - From 2001-2006, incidence of SCD was 0.61 / 100,000 person-yrs (assuming 10.9 million participants/yr)
  • 12. Maron Circulation 2009 Causes of SCD in 690 confirmed events over 27 years CAUSE # of CASES PERCENTAGE 1) Hypertrophic cardiomyopathy (HCM) 251 36 % 2) Coronary artery anomalies 119 17 % 3) Possible HCM 57 8 % 4) Myocarditis 41 6 % 5) Arrhythmogenic RV cardiomyopathy 30 4 % 6) Ion channelopathies 25 4 % 7) Mitral valve disease 24 3 % 8) LAD myocardial bridge 23 3 % 9) Coronary artery disease 23 3 % 10) Aortic rupture 10 1 %
  • 13. - 273 athlete deaths - 1.97 participant-years - 16% CV events - From 2004-2008, incidence of SCD was 2.3 / 100,000 person-yrs Sudden Death in NCAA 2004 – 2008 Harmon Circulation 2011
  • 14. CAUSE # of CASES PERCENTAGE 1) Autopsy Negative –sudden unexplained death 11 31% 2) Coronary artery anomalies 5 14% 3) Dilated cardiomyopathy 3 8% 4) Myocarditis 3 8% 5) Aortic dissection 3 8% 6) Possible HCM 3 8% 7) HCM 1 3% 8) Arrhythmogenic cardiomyopathy 1 3% 9) Commotio cordis 1 3% 10) Kawasaki disease 1 3% Causes of SCD in 36 confirmed events in NCAA from 2004 - 2008 Harmon Circ: Arrythmia & EP 2014
  • 15. Link Circulation 2012 Wide variation in SCD incidence rates
  • 16. Corrado JAMA 2006 Incidence of SCD & Screening Strategies 3.5 1.0
  • 17. • Younger athletes • Masters athletes • Recreational athletes The Heterogeneity of Athletes
  • 18. Myerburg Circulation 2007 Age-related risks of SCD
  • 19. Marijon Circulation 2011 Sports-related SCD in General Population in France
  • 20. Marijon Circulation 2011 Prevalence of SCD by Sports Type in France
  • 21. Exercise is like a Drug
  • 22. 0 5 10 15 20 * d * PercentChangePeakVO2 Inactive Low Dose Moderate Low Dose Vigorous High Dose Vigorous Duscha CHEST 2005 Early detection & treatment of traditional CV risk factors - Sedentary individuals with traditional CV risk factors
  • 23. O’Connor JAMA 2009 Moderate intensity exercise training (60-70% of heart rate reserve) was related to 15% reduction in CV mortality or HF hospitalization in pts with HFrEF Exercise & Heart Failure High prevalence of evidenced based therapies such as beta blockers and ace inhibitors
  • 24. Other evidenced-based therapies
  • 25. Resuscitation Strategies
  • 26. • While exercise training lowers the overall risk of CV death, vigorous exercise in athletes can increase the risks of SCD in susceptible individuals. • SCD in young athletes is a rare event and those at risk typically have uncommon CV diseases, such as HCM and coronary anomalies. • SCD in masters and recreational athletes is much more common and those at risk for SCD typically have more common CV diseases such as CAD. Conclusions
  • 27. • The risks of SCD in athletes can be reduced through early detection and treatment of CV disease or its RF, via optimal exercise training regimens and use of other evidenced based therapies. • Rapid resuscitation strategies employed during sudden cardiac arrest in athletes are effective strategies to restore circulation and avert death. Conclusions