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Citations: 1-69
Database: Ovid MEDLINE(R) <1996 to February Week 2 2004>
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Citation <1>
Unique Identifier
9636339
Authors
O'Connor FG. Kugler JP. Oriscello RG.
Institution
Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA.
Title
Sudden death in young athletes: screening for the needle in a haystack.[see
comment][erratum appears in Am Fam Physician 1999 Feb 1;59(3):540]. [Review]
[31 refs]
Comments
Comment in: Am Fam Physician. 1998 Nov 15;58(8):1760-1; PMID: 9835851
Source
American Family Physician. 57(11):2763-70, 1998 Jun.
Abstract
Nontraumatic sudden death in young athletes is always disturbing, as apparently
invincible athletes, become, without warning, victims of silent heart disease. Despite
public perception to the contrary, sudden death in young athletes is exceedingly rare.
It most commonly occurs in male athletes, who have estimated death rates nearly
fivefold greater than the rates of female athletes. Congenital cardiovascular disease is
the leading cause of non-traumatic sudden athletic death, with hypertrophic
cardiomyopathy being the most common cause. Screening athletes for disorders
capable of provoking sudden death is a challenge because of the low prevalence of
disease, and the cost and limitations of available screening tests. Current
recommendations for cardiovascular screening call for a careful history and physical
examination performed by a knowledgeable health care provider. Specialized testing
is recommended only in cases that warrant further evaluation. [References: 31]
Citation <2>
Unique Identifier
9835851
Authors
Holmes PS. Kerle KK. Seto CK.
Title
Sickle cell trait and sudden death in athletes.[comment].
Comments
Comment on: Am Fam Physician. 1998 Jun;57(11):2763-70; PMID: 9636339
Source
American Family Physician. 58(8):1760-1, 1998 Nov 15.
Citation <3>
Unique Identifier
10740158
Authors
Kinoshita N. Mimura J. Obayashi C. Katsukawa F. Onishi S. Yamazaki H.
Institution
Sports Medicine Research Center, Keio University, Japan. [email protected]
Title
Aortic root dilatation among young competitive athletes: echocardiographic
screening of 1929 athletes between 15 and 34 years of age.
Source
American Heart Journal. 139(4):723-8, 2000 Apr.
Abstract
BACKGROUND: Aortic dilatation can be lethal for young competitive athletes. The
prevalence among athletes is not known, however, and thus a reasonable approach to
early recognition remains uncertain. METHODS AND RESULTS: Echocardiograms
of 1929 normotensive athletes 15 to 34 years of age were analyzed. Five (0.26%)
athletes had aortic dilatation; 4 of the 5 played basketball. This made the prevalence
of aortic dilatation 0.96% (4 of 415) among basketball and volleyball players, who
represented a population of especially tall athletes. Tallness aside, only 2 of the 5
athletes had features of Marfan syndrome. Among the athletes without aortic
dilatation, the relation between body surface area and aortic root dimension was
nonlinear and best described with a quadratic regression model. Athletes with aortic
dilatation fell well outside the 95% confidence interval. CONCLUSION: Because a
higher incidence of aortic dilatation is to be anticipated among very tall athletes,
inclusion!
of echocardiography in screening before participation in certain sports should be
considered.
Citation <4>
Unique Identifier
8752203
Authors
Comfort SR. Curry RC Jr. Roberts WC.
Institution
Department of Medicine, Orlando General Hospital, Florida, USA.
Title
Sudden death while playing tennis due to a tear in ascending aorta (without
dissection) and probable transient compression of the left main coronary artery.
Source
American Journal of Cardiology. 78(4):493-5, 1996 Aug 15.
Citation <5>
Unique Identifier
10392228
Authors
Futterman LG. Lemberg L.
Institution
Department of Medicine, University of Miami School of Medicine, Fla., USA.
Title
Commotio cordis: sudden cardiac death in athletes.
Source
American Journal of Critical Care. 8(4):270-2, 1999 Jul.
Abstract
Commotio cordis due to blunt trauma to the precordium is a rare cause of death in
young athletes, occurring less frequently than all of the other athletics-related deaths.
Several measures, such as the use of safety baseballs and the use of chest protectors,
can help protect young athletes from commotio cordis. In general, sudden cardiac
death in athletes is receiving increasing attention from the public as a result of recent
deaths of high-profile athletes. Sudden cardiac death, however, is rare, with an
estimated 1 out of 200,000 high school athletes at risk each year. However, the
personal, physiological, and cardiovascular benefits of athletics far outweigh the risks.
Therefore, the message to parents is to allow their children to participate in athletics
because the benefits far outweigh the risks.
Citation <6>
Unique Identifier
9662112
Authors
Lesauskaite V. Valanciute A.
Institution
Kaunas Medical Academy, Institute of Cardiology, Lithuania.
Title
Causes of sudden cardiac death in young athletes: the role of hypoperfusion.
Source
American Journal of Forensic Medicine & Pathology. 19(2):157-61, 1998 Jun.
Abstract
The role of hypoperfusion in cases of sudden cardiac death of young athletes is
discussed. The coronary index, a ratio of the coronary caliber and the myocardial
mass, was estimated from postmortem coronary angiograms. The coronary index
reflects the degree of myocardial blood supply. In each case, a decrease in the
coronary index, in combination with fibrosis and necrosis of the myocardium, was
revealed. We suggest that recurring myocardial necrosis developed as a result of
hypoperfusion of the hypertrophic myocardium during physical overload.
Citation <7>
Unique Identifier
12464814
Authors
Byard RW. James RA. Gilbert JD.
Institution
Forensic Science, Aldeaide, South Australia. [email protected]
Title
Childhood sporting deaths.
Source
American Journal of Forensic Medicine & Pathology. 23(4):364-7, 2002 Dec.
Abstract
Exercise-induced collapse and sudden death are unusual in childhood. For this
reason, a study was undertaken of a series of 12 cases of sudden death in childhood
occurring during physical exertion associated with sporting activities. The age range
was 7 to 16 years (mean 12.3 years, M:F ratio 5:1). Deaths resulted from trauma
associated with the sporting activity, from an idiosyncratic response to exertion, or
from exacerbation of a known underlying disease. Trauma was directly fatal (n = 4:
vascular trauma in 1, head injury in 2, drowning in 1), exacerbated an underlying
medical condition (n = 1: hypertrophic obstructive cardiomyopathy), or followed
collapse from underlying organic disease (n = 1: drowning in epilepsy). Deaths after
exertion occurred when there was an unexpected response to underlying occult
disease (n = 4: aortic stenosis in 1, cerebral arteriovenous malformation in 1,
hypertrophic obstructive cardiomyopathy in 1, coronary atherosclerosis in 1) or to
preex!
isting known disease (n = 2: surgically corrected transposition of the great vessels in
1, asthma in 1). The fatal episodes often resulted from a complex interplay of a
variety of factors, including physical exertion, possible trauma, and underlying
organic disease. Testing of other family members may be indicated in cases where a
rare, possibly familial, disease is found. Evaluation of cases required descriptions of
activities before death, information from the medical history of the deceased, and
detailed findings from the autopsy.
Citation <8>
Unique Identifier
12604991
Authors
Fornes P. Lecomte D.
Institution
Institute of Forensic Medicine of Paris, and Department of Forensic Sciences,
Medical School Cochin Port-Royal, University of Paris, Paris, France.
[email protected]
Title
Pathology of sudden death during recreational sports activity: an autopsy study of 31
cases.[see comment].
Comments
Comment in: Am J Forensic Med Pathol. 2003 Sep;24(3):309; PMID: 12960672
Source
American Journal of Forensic Medicine & Pathology. 24(1):9-16, 2003 Mar.
Abstract
A growing number of people are involved in recreational physical activity. It is
therefore not uncommon for a medical examiner to encounter sports-related sudden
deaths and to be faced with the legal implications. The authors examined the clinical
and cardiac pathologic patterns in 31 persons who died suddenly during sports
activities and underwent autopsy at the Institute of Forensic Medicine of Paris
between 1991 and 2001. Twenty-nine male subjects, ranging in age from 7 to 57 years
(mean 30 years) and two female subjects, 8 and 60 years old, died suddenly during
sports activities. The sports involved were various, with running the most frequent: 13
cases. Cardiomyopathies (10 cases) and coronary artery disease (9 cases) were the
most frequent causes of deaths. Despite the severity of lesions, only 4 subjects had a
known cardiovascular disease. In conclusion, with regard to prevention, efforts should
be continued to improve the sensitivity and specificity of diagnostic too!
ls and screening strategies. In this regard, medicolegal autopsies should be
systematically performed in cases of sudden death during sports activities, because
they provide accurate and useful information for a better knowledge of sports-related
mortality.
Citation <9>
Unique Identifier
12960672
Authors
Koehler SA. Ladham S. Shakir A. Wecht CH.
Title
Pathology of sudden death during recreational sports activity.[comment].
Comments
Comment on: Am J Forensic Med Pathol. 2003 Mar;24(1):9-16; PMID: 12604991
Source
American Journal of Forensic Medicine & Pathology. 24(3):309, 2003 Sep.
Citation <10>
Unique Identifier
9934429
Authors
Basilico FC.
Institution
Center for Sports Cardiology, New England Baptist Hospital, Boston,
Massachusetts, USA.
Title
Cardiovascular disease in athletes. [Review] [70 refs]
Source
American Journal of Sports Medicine. 27(1):108-21, 1999 Jan-Feb.
Abstract
As a physician, coach, or trainer, we see athletes as healthy, physically fit, and able
to tolerate extremes of physical endurance. It seems improbable that such athletes
may have, on occasion, underlying life-threatening cardiovascular abnormalities.
Regular physical activity promulgates cardiovascular fitness and lowers the risk of
cardiac disease. However, under intense physical exertion and with a substrate of
significant cardiac disease--whether congenital or acquired--athletes may succumb to
sudden cardiac death. The deaths of high-profile athletes receive much attention
through the national news media, but there are also deaths of other athletes. With
repetitive, intense physical exercise, the heart undergoes functional and morphologic
changes. Knowledge of those changes may help one identify cardiovascular
abnormalities that can cause sudden death from the heart known as an "athlete's
heart." This article will review cardiovascular diseases that may limit an athlete'!
s participation in sports and that may put an athlete at risk for sudden cardiac death. It
also reviews the extent and limitations of the cardiovascular preparticipation
screening examination. Team physicians, coaches, and trainers must understand the
process of evaluation of a symptomatic athlete that may indicate significant cardiac
abnormalities. Finally, guidelines to determine eligibility of athletes with
cardiovascular disease to return to sports will be reviewed. [References: 70]
Citation <11>
Unique Identifier
11304649
Authors
Somberg JC.
Institution
Rush-Presbyterian-St. Luke's Medical Center, Rush University, Chicago, IL, USA.
Title
Sudden death in athletes.
Source
American Journal of Therapeutics. 7(6):399-403, 2000 Nov.
Citation <12>
Unique Identifier
10223306
Authors
Larsson E. Wesslen L. Lindquist O. Baandrup U. Eriksson L. Olsen E. Rolf C.
Friman G.
Institution
Department of Pathology, Uppsala University, Uppsala Hospital, Sweden.
Title
Sudden unexpected cardiac deaths among young Swedish orienteers--morphological
changes in hearts and other organs.
Source
APMIS. 107(3):325-36, 1999 Mar.
Abstract
During the years 1979-1992 an accumulation of sudden unexpected cardiac deaths
(SUD) occurred among young Swedish orienteers. A reevaluation of material saved
from 16 autopsies was undertaken. Myocarditis was most frequent. It was found in
different stages in the majority of cases, indicating subacute or chronic disease with
ongoing reparative processes. There were severe morphological changes in all cases.
All but one showed a picture of fibrosis and unspecific hypertrophy and/or
degenerative changes in myocytes. The hearts were classified into three groups (A-C),
based on the morphological picture of the retrieved heart tissue and the macroscopic
description. Group A comprised five cases in which areas with active myocarditis
combined with areas of healing or healed myocarditis widely distributed in the left
ventricle were the only morphological changes found. Group B comprised four cases
demonstrating foci of myocarditis in different stages in the left ventricle and chang!
es resembling those found in arrhythmogenic right ventricular dysplasia (ARVD),
including degenerative changes with fibrosis and fatty infiltration located in either
ventricle. Group C comprised the remaining seven cases. In none of the cases were
coronary artery or valvular anomalies present, nor significant coronary sclerosis or
changes outside the heart that could cause SUD.
Citation <13>
Unique Identifier
9183244
Authors
Siegel AJ.
Title
Relative risk of sudden cardiac death during marathon running.[comment].
Comments
Comment on: Arch Intern Med. 1996 Nov 11;156(20):2297-302; PMID: 8911236
Source
Archives of Internal Medicine. 157(11):1269-70, 1997 Jun 9.
Citation <14>
Unique Identifier
10463922
Authors
Luke LC.
Title
Having advanced resuscitation facilities at end of marathons does not guarantee
survival.[comment].
Comments
Comment on: BMJ. 1999 May 8;318(7193):1285-6; PMID: 10231271
Source
BMJ. 319(7209):581, 1999 Aug 28.
Citation <15>
Unique Identifier
9429003
Authors
Sharma S. Whyte G. McKenna WJ.
Institution
Department of Cardiovascular Sciences, St George's Hospital Medical School,
London, United Kingdom.
Title
Sudden death from cardiovascular disease in young athletes: fact or fiction?.
[Review] [86 refs]
Source
British Journal of Sports Medicine. 31(4):269-76, 1997 Dec.
Citation <16>
Unique Identifier
10786871
Authors
Pedoe DT.
Institution
Cardiac Department, St Bartholomew's Hospital, London, United Kingdom.
Title
Sudden cardiac death in sport--spectre or preventable risk?.
Source
British Journal of Sports Medicine. 34(2):137-40, 2000 Apr.
Citation <17>
Unique Identifier
10953896
Authors
Quigley F.
Institution
Oakacre, Ballineen, Co, Cork, Ireland. [email protected]
Title
A survey of the causes of sudden death in sport in the Republic of Ireland.
Source
British Journal of Sports Medicine. 34(4):258-61, 2000 Aug.
Abstract
BACKGROUND: Sudden death in sport is rare, but when it occurs the effects are
devastating. There have not been any reports to date describing the frequency and
causes of sudden death in sport in the Republic of Ireland. AIM: To describe the
incidence, possible causes, associated factors, and pathological findings in people
who died while exercising in the Republic of Ireland in the 10 year period from
January 1987 to December 1996. METHODS: All 49 regional coroners in the
Republic of Ireland were approached and details on all cases of sudden death in sport
from 1 January 1987 to 31 December 1996 were requested. A questionnaire was used
to document age, sex, participating sport, previous symptoms, previous medical
investigations, circumstances of death, and main pathological finding in all reported
cases. RESULTS: Of the 49 coroners surveyed, 45 replied. A total of 51 cases of
sudden death in sport were identified. The median age was 48 (range 15-78). Fifty of
the deaths were!
of men. Golf was the most popular participating sport. In 42 cases, the pathological
cause of death was atherosclerotic coronary artery disease. CONCLUSIONS: This is
the first time the incidence of sudden death in sport in the Republic of Ireland has
been described. The main cause of death in all age groups was atherosclerotic
coronary artery disease.
Citation <18>
Unique Identifier
12547737
Authors
Pigozzi F. Spataro A. Fagnani F. Maffulli N.
Institution
Sports Medicine Unit, University Institute of Movement Sciences (IUSM), Plazza
Lauro de Bosis, 6-00194 Rome, Italy.
Title
Preparticipation screening for the detection of cardiovascular abnormalities that may
cause sudden death in competitive athletes.
Source
British Journal of Sports Medicine. 37(1):4-5, 2003 Feb.
Citation <19>
Unique Identifier
11984027
Authors
Maron BJ.
Institution
Cardiovascular Research Division, Minneapolis Heart Institute Foundation,
Minneapolis, MN 55407, USA. [email protected]
Title
The young competitive athlete with cardiovascular abnormalities: causes of sudden
death, detection by preparticipation screening, and standards for disqualification.
[Review] [24 refs]
Source
Cardiac Electrophysiology Review. 6(1-2):100-3, 2002 Feb.
Citation <20>
Unique Identifier
12497946
Authors
Thiene G. Basso C. Corrado D.
Institution
Istituto di Anatomia Patologica Universita degli Studi Via A Gabelli, 61, 35121
Padova. [email protected]
Title
Sudden death in the young and in the athlete: causes, mechanisms and prevention.
[Review] [42 refs]
Source
Cardiologia. 44 Suppl 1(Pt 1):415-21, 1999 Dec.
Citation <21>
Unique Identifier
8724552
Authors
Maron BJ.
Institution
Cardiovascular Research Division, Minneapolis Heart Institute Foundation,
Minnesota, USA.
Title
Triggers for sudden cardiac death in the athlete. [Review] [97 refs]
Source
Cardiology Clinics. 14(2):195-210, 1996 May.
Abstract
Sudden death on the athletic field is usually due to underlying cardiovascular
disease. Coronary artery disease is most common in older athletes, and a variety of
congenital cardiovascular malformations predominate in young competitive athletes.
Of these lesions, the most common in North America is hypertrophic
cardiomyopathy. A variety of coronary artery anomalies are next in frequency, with
the most important being anomalous origin of left main coronary artery from the
anterior sinus of Valsalva. [References: 97]
Citation <22>
Unique Identifier
9276171
Authors
Lewis JF.
Institution
Department of Medicine, University of Florida Health Science Center, Gainesville,
USA.
Title
Considerations for racial differences in the athlete's heart and related cardiovascular
disease. [Review] [64 refs]
Source
Cardiology Clinics. 15(3):485-91, 1997 Aug.
Abstract
Athletic training is often associated with modest increases in left ventricular
chamber size, wall thickness, and mass, which appear to be related to the level and
intensity of training as well as the type of activity performed. It appears that for given
levels and types of training, some individuals show more marked morphologic
changes. It has been speculated that the cardiac alterations that occur with athletic
conditioning may be due, in part, to genetic factors that exist independent of training.
Related to this issue is the possibility that racial (or biologic) differences in cardiac
response to exercise may also exist. This article reviews the available data that
address racial differences in the cardiac response to exercise and to left ventricular
pressure overload and the implications of these findings. [References: 64]
Citation <23>
Unique Identifier
9276170
Authors
Maron BJ.
Institution
Cardiovascular Research Division, Minneapolis Heart Institute Foundation,
Minnesota, USA.
Title
Risk profiles and cardiovascular preparticipation screening of competitive athletes.
[Review] [75 refs]
Source
Cardiology Clinics. 15(3):473-83, 1997 Aug.
Abstract
There has been heightened interest in the design and role of preparticipation
screening for high school and college athletes. An American Heart Association
consensus panel, composed of cardiovascular specialists and other physician experts
having extensive clinical experience with athletes of all ages as well as a legal expert,
assessed the benefits and limitations of preparticipation screening for early detection
of cardiovascular abnormalities in competitive athletes. The panel addressed costefficiency and feasibility issues as well as the medicolegal implications of screening;
and developed consensus recommendations and guidelines for the most prudent,
practical, and effective screening procedures and strategies. [References: 75]
Citation <24>
Unique Identifier
9276168
Authors
Virmani R. Burke AP. Farb A. Kark JA.
Institution
Department of Cardiovascular Pathology, Armed Forces Institute of Pathology,
Washington, DC, USA.
Title
Causes of sudden death in young and middle-aged competitive athletes. [Review]
[79 refs]
Source
Cardiology Clinics. 15(3):439-66, 1997 Aug.
Abstract
The incidence of sudden death in athletes is low. Some pathologic conditions may
predispose to sudden death during exercise in young athletes. In older individuals,
exercise may trigger terminal arrhythmias in patients with severe coronary
atherosclerosis. Screening programs with a history and a physical examination are
recommended for high school and collegiate sports participants. For older individuals
who are likely to have undetected or overt coronary heart disease and are exercising
for physical fitness, caution regarding the level of activity and type of symptoms that
are frequently associated with coronary disease may help prevent sudden death.
[References: 79]
Citation <25>
Unique Identifier
10423663
Authors
Basso C. Corrado D. Thiene G.
Institution
Department of Pathology University of Padua Medical School, Padua, Italy.
Title
Cardiovascular causes of sudden death in young individuals including athletes.
[Review] [55 refs]
Source
Cardiology in Review. 7(3):127-35, 1999 May-Jun.
Abstract
From 1978 to 1993 in the Veneto region, we collected 200 cases of sudden death in
the young (</=35 years). Sudden death was cerebral in 15 cases (7.5%), respiratory in
10 (5%), and cardiovascular in 163 (81.5%), whereas it remained unexplained in 12
cases (6%). Among cardiovascular sudden death, obstructive coronary atherosclerosis
accounted for 23% of cases, arrhythmogenic right ventricular cardiomyopathy for
12.5%, mitral valve prolapse for 10%, conduction system abnormalities for 10%,
congenital coronary artery anomalies for 8.5%, myocarditis for 7.5%, hypertrophic
cardiomyopathy for 5.5%, aortic rupture for 5.5%, dilated cardiomyopathy for 5%,
nonatherosclerotic-acquired coronary artery disease for 3.5%, postoperative
congenital heart disease for 3%, aortic stenosis for 2%, pulmonary embolism for 2%,
and other causes for 2%. Cardiac arrest remained unexplained in 6% of the cases.
Specific pathology and pathogenetic mechanisms of each disease were investigated
and correla!
ted with clinical signs and symptoms in detail. A large spectrum of cardiovascular
disorders, both congenital and acquired, may represent the organic substrate of sudden
death in the young. The underlying abnormality is frequently concealed and
discovered only at postmortem examination. Most of the diseases, although
asymptomatic, are potentially detectable during life with proper imaging tests.
[References: 55]
Citation <26>
Unique Identifier
12085972
Authors
Firoozi S. Sharma S. Hamid MS. McKenna WJ.
Institution
Department of Cardiological Sciences, St George's Hospital Medical School,
London, UK. [email protected]
Title
Sudden death in young athletes: HCM or ARVC?.
Source
Cardiovascular Drugs & Therapy. 16(1):11-7, 2002 Jan.
Abstract
Sudden non-traumatic death in young athletes is due to underlying
congenital/inherited cardiac diseases in over 80% of cases. The two commonest
conditions leading to sudden cardiac death in athletes below the age of 25 years are
hypertrophic cardiomyopathy (HCM) and arrhythmogenic right ventricular
cardiomyopathy (ARVC). Hypertrophic cardiomyopathy is caused by mutations in
genes, which code for sarcomeric contractile proteins. It can present with symptoms
such as palpitation, presyncope or syncope. In a small number of cases, sudden death
is the first clinical manifestation of the condition. It is well established that HCM
accounts for over half of all cases sudden cardiac death in young individuals below 25
years of age. The management of HCM broadly encompasses symptom control,
familial evaluation and the prevention of sudden death. Arrhythmogenic right
ventricular cardiomyopathy, similarly, is a genetic disorder of the heart muscle and
leads to symptoms such as palpitati!
on and syncope and more rarely sudden death. The diagnosis of ARVC is most likely
underestimated due to the lack of a single diagnostic test and subtle morphological
changes in some cases. The diagnosis is based on clinical and family history and noninvasive investigations. The physiological adaptations seen in some athletes, as a
response to physical training, may resemble phenotypically mild forms HCM and
ARVC. Therefore, a diagnostic algorithm enabling this differentiation would be of
importance especially bearing in mind the consequences of a misdiagnosis.
Citation <27>
Unique Identifier
8772711
Authors
Maron BJ. Thompson PD. Puffer JC. McGrew CA. Strong WB. Douglas PS.
Clark LT. Mitten MJ. Crawford MH. Atkins DL. Driscoll DJ. Epstein AE.
Institution
Office of Scientific Affairs, American Heart Association, Dallas, TX 75231-4596,
USA.
Title
Cardiovascular preparticipation screening of competitive athletes. A statement for
health professionals from the Sudden Death Committee (clinical cardiology) and
Congenital Cardiac Defects Committee (cardiovascular disease in the young),
American Heart Association.
Source
Circulation. 94(4):850-6, 1996 Aug 15.
Citation <28>
Unique Identifier
10200904
Authors
Weiner HR.
Institution
Robert E. Norris Health Center, University of Wisconsin-Milwaukee, WI 53211,
USA.
Title
Preventing sudden death in student athletes.
Source
Comprehensive Therapy. 25(3):151-4, 1999 Mar.
Abstract
Cardiac death in athletes younger than 35 is almost always associated with
congenital malformations, of which hypertrophic cardiomyopathy is most common.
This article proposes a screening history and physical examination for these
conditions.
Citation <29>
Unique Identifier
11124716
Authors
Link MS. Wang PJ. Estes NA 3rd.
Institution
The Cardiac Arrhythmia Service, New England Medical Center, Tufts University
School of Medicine, Boston, Massachusetts, USA. [email protected]
Title
Ventricular arrhythmias in the athlete. [Review] [76 refs]
Source
Current Opinion in Cardiology. 16(1):30-9, 2001 Jan.
Abstract
Life-threatening ventricular arrhythmias in the athlete nearly always occur in the
presence of structural heart disease. In the last few years, 2 new causes of lifethreatening arrhythmias have been described in patients with normal hearts-that of the
Brugada syndrome and that of commotio cordis. Non-life-threatening premature
ventricular beats and even nonsustained ventricular tachycardia are not rare, and
although usually benign, can be secondary to cardiomyopathies. Athletes with
symptoms of syncope, especially if exertional, warrant a complete evaluation. The
treatment of athletes and other individuals with life-threatening ventricular
arrhythmias has been revolutionized by the implantable cardioverter defibrillator, a
device that affords excellent protection from sudden death. Defining those athletes
who would benefit from the implantable defibrillator is not always clear. Furthermore,
participation in competitive athletics for athletes with life-threatening arrhythmias!
or structural heart disease known to put the athlete at risk for life-threatening
arrhythmias is usually prohibited. [References: 76]
Citation <30>
Unique Identifier
9784970
Authors
Maron BJ.
Institution
Minneapolis Heart Institute Foundation, Minn., USA.
Title
Heart disease and other causes of sudden death in young athletes. [Review] [148
refs]
Source
Current Problems in Cardiology. 23(9):477-529, 1998 Sep.
Citation <31>
Unique Identifier
12831714
Authors
Glorioso J Jr. Reeves M.
Institution
Family Practice Residency Program, Tripler Army Medical Center, MCHK-FMR, 1
Jarrett White Road, Tripler AMC, HI 96859-5000, USA. [email protected]
Title
Marfan syndrome: screening for sudden death in athletes. [Review] [36 refs]
Source
Current Sports Medicine Reports. 1(2):67-74, 2002 Apr.
Abstract
Marfan syndrome is a common, preventable cause of sudden cardiac death in the
athlete. It is an autosomal-dominant disorder of connective tissue with variable
penetration that affects multiple organ systems. Aortic root aneurysm rupture or
dissection is the most common cause of sudden death. A directed family and personal
history, in addition to a search for characteristic physical stigmata, can optimize the
screening of athletes during the preparticipation evaluation. Athletes who have
pertinent findings on the preparticipation evaluation should undergo further diagnostic
evaluation. Echocardiography is essential to rule out cardiovascular involvement in
those suspected of having Marfan syndrome, and should be mandated when positive
pertinent family or personal history is elicited or when cardiac abnormalities are
detected. Fortunately, due to characteristic historic and clinical findings, Marfan
syndrome can be detected early, allowing appropriate treatment and ultimately !
prevention of sudden death in affected athletes. [References: 36]
Citation <32>
Unique Identifier
12831662
Authors
Schulze-Bahr E. Monnig G. Eckardt L. Wedekind H. Wichter T. Breithardt G.
Institution
Department Molekular-Kardiologie, Institut fur Arterioskleroseforschung an der
Westfalischen, Wilhelms-Universitat Munster, Domagkstrasse 3, D-48149 Munster,
Germany. [email protected]
Title
The long QT syndrome: considerations in the athletic population. [Review] [41 refs]
Source
Current Sports Medicine Reports. 2(2):72-8, 2003 Apr.
Abstract
In athletes, ventricular arrhythmias and sudden cardiac death are rare and
unpredictable events. Often, an underlying heart disease is present, but pre-existing
clinical signs or symptoms may not be recognized. Primary electrical disorders (such
as the long QT syndrome) are rarely present in athletes but, so far, are a considerable
reason for disqualification from sport activity. These disorders are mostly inherited,
and patients should be referred to a cardiologist with special experience. Through the
efforts of molecular genetics and cellular electrophysiology, an increasing
understanding of the underlying mechanisms of arrhythmogenesis is being gathered.
During the past decade, evidence has grown that establishing accurate genetic
diagnoses and dissection of molecular disease mechanisms can have an impact on
prognosis, and help direct therapy in a range of cardiovascular diseases. Further
achievements in the areas of clinical and molecular research, improvement of
medical!
education, and expansion of genotyping facilities will facilitate the correct and
immediate identification of affected patients. [References: 41]
Citation <33>
Unique Identifier
9621845
Authors
Reisdorff EJ. Prodinger RJ.
Institution
Michigan State University, Ingham Regional Medical Center, Lansing, USA.
Title
Sudden cardiac death in the athlete. [Review] [52 refs]
Source
Emergency Medicine Clinics of North America. 16(2):281-94, 1998 May.
Abstract
The sudden unexpected death of an athlete is a disturbing and tragic event. Sudden
cardiac death in the young athlete is caused primarily by cardiomyopathies and
nonatherosclerotic coronary artery abnormalities; in the mature athlete, the most
prevalent cause of sudden cardiac death is atherosclerotic coronary disease. The job of
the emergency physician is to resuscitate those who succumb to ventricular
dysrhythmias during exercise and to screen patients for potential risk of sudden
cardiac death when they present with warning symptoms such as syncope.
[References: 52]
Citation <34>
Unique Identifier
8781830
Authors
Wesslen L. Pahlson C. Lindquist O. Hjelm E. Gnarpe J. Larsson E. Baandrup U.
Eriksson L. Fohlman J. Engstrand L. Linglof T. Nystrom-Rosander C. Gnarpe H.
Magnius L. Rolf C. Friman G.
Institution
Department of Infectious Diseases, Uppsala University Hospital, Denmark.
Title
An increase in sudden unexpected cardiac deaths among young Swedish orienteers
during 1979-1992.[see comment].
Comments
Comment in: Eur Heart J. 1996 Jun;17(6):810-2; PMID: 8781814
Source
European Heart Journal. 17(6):902-10, 1996 Jun.
Abstract
BACKGROUND: Sixteen cases of sudden unexpected cardiac death, 15 males and
one female, are known to have occurred among young Swedish orienteers from 1979
to 1992, of which seven cases occurred between 1989 and 1992. This is considered to
be indicative of an increased death rate. RESULTS: Histopathological evaluation
showed myocarditis in a higher than expected proportion of cases. In one such case,
which we studied before the sudden unexpected death occurred, the victim had
suffered a Chlamydia pneumoniae infection verified by serology, and a nucleotide
sequence was found in the heart and lung by means of the polymerase chain reaction
(PCR) that hybridized with a probe specific for that organism. Male Swedish
orienteers do not, however, seem to have an increased rate of exposure to this agent.
No further sudden unexpected deaths among young orienteers have occurred over the
past 3.5 years. At the beginning of that period, attempts were made to modify training
habits and att!
itudes.
Citation <35>
Unique Identifier
8781814
Authors
Willems S.
Title
Sudden cardiac death in young athletes: orienteering on Chlamydia
pneumoniae?[comment].
Comments
Comment on: Eur Heart J. 1996 Jun;17(6):902-10; PMID: 8781830
Source
European Heart Journal. 17(6):810-2, 1996 Jun.
Citation <36>
Unique Identifier
10329096
Authors
Tabib A. Miras A. Taniere P. Loire R.
Institution
Department of Pathology, L.Pradel Hospital, Lyon, France.
Title
Undetected cardiac lesions cause unexpected sudden cardiac death during occasional
sport activity. A report of 80 cases.
Source
European Heart Journal. 20(12):900-3, 1999 Jun.
Abstract
The retrospective analysis of 1500 forensic autopsies after sudden cardiac death
showed that 80 (77 men, three women) had died following sport, for which they had
been inadequately trained. The chosen sport (both dynamic and static), and the cardiac
pathology discovered during autopsy make it possible to divide the population into
two groups. Group 1 were those under 30 years of age (27 cases) engaged in jogging,
gymnastics, rugby, tennis and boxing who suffered from hypertrophic
cardiomyopathy (29.6%), arrhythmogenic right ventricular cardiomyopathy (25.9%),
non-atherosclerotic (14. 8%), aortic stenosis (7.4%), atrial septal defect (3.7%),
stenosing coronary atherosclerosis (3.7%), and structural abnormalities of the His
bundle (3.7%). Group 2 were those over 30 years of age (53 cases), engaged in
swimming, cycling, jogging and football. The cardiac lesions responsible were
stenosing atherosclerotic coronary disease (49%), non-atherosclerotic coronary
disease (1.8%), hypert!
rophic cardiomyopathy (20%), obstructive cardiomyopathy (4.8%), structural
abnormalities of the His bundle (7.4%), myocardic bruise scar (4%), and
arrhythmogenic right ventricular cardiomyopathy (3. 7%). In both groups, dilated
cardiomyopathy occurred with identical frequency (11%).Conclusions The lesions
discovered are the same as those identified in professional athletes, when the body
tries to avoid mortal rhythmic decompensation in the case of an over-loading volume
and tension during an ill-adapted effort. Forensic autopsy should establish these
anomalies because the transmissible genetic characteristics of some of them could
underline the need for check-ups in other members of the family. Copyright 1999 The
European Society of Cardiology.
Citation <37>
Unique Identifier
8960437
Authors
Dickerman RD. McConathy WJ. Schaller F. Zachariah NY.
Title
Cardiovascular complications and anabolic steroids. [Review] [6 refs]
Source
European Heart Journal. 17(12):1912, 1996 Dec.
Citation <38>
Unique Identifier
12807837
Authors
Firoozi S. Sharma S. McKenna WJ.
Institution
Department of Cardiological Sciences, St George's Hospital Medical School,
London, UK.
Title
Risk of competitive sport in young athletes with heart disease. [Review] [25 refs]
Source
Heart (British Cardiac Society). 89(7):710-4, 2003 Jul.
Abstract
The majority of sudden deaths in young athletes occur in the context of underlying
inherited or genetic cardiac disorders. The evaluation of every athlete regarding
underlying cardiac disease is impractical and therefore needs to be targeted at those
who are at a higher risk. A practical approach would be to channel efforts towards
athletes with cardiac symptoms, those with a family history of inherited cardiac
disease, and those with a family history of premature sudden death. There are
potential pitfalls in the evaluation of young athletes using non-invasive tests when
making the distinction between physiological adaptations to exercise and cardiac
pathology. Physicians evaluating young athletes need to be aware of the spectrum of
physiological adaptations and to be familiar with conditions responsible for sudden
death in this population. [References: 25]
Citation <39>
Unique Identifier
11156285
Authors
Burtscher M. Pachinger O. Mittleman MA. Ulmer H.
Institution
Department of Sport Science, University of Innsbruck, Austria.
[email protected]
Title
Prior myocardial infarction is the major risk factor associated with sudden cardiac
death during downhill skiing.
Source
International Journal of Sports Medicine. 21(8):613-5, 2000 Nov.
Abstract
More than 90% of all sudden cardiac deaths (SCDs) during downhill skiing, the most
popular winter sport world-wide, are attributed to men over the age of 34. However,
no data exist on additional risk factors and triggers for SCD related to downhill
skiing. Therefore risk factor profiles of 68 males who died from SCD during downhill
skiing were compared to those of 204 matched controls. Skiers who suffered SCD had
much more frequently prior myocardial infarction (MI) (41% vs. 1.5%; p<0.001),
hypertension (50% vs. 17%; p<0.001), known coronary heart disease (CHD) without
prior MI (9% vs. 3%; p=0.05) and were less engaged in strenuous exercise (4% vs.
15%; p<0.05) when compared to controls. Multivariate analyses even enhanced the
importance of these risk factors. Downhill skiing is considered to be a serious trigger
for SCD especially in skiers with prior MI but also for those with hypertension,
known CHD without prior MI, or insufficient adaptation to strenuous exercise. Skiin!
g-related increased sympathetic activity might well disturb the autonomic balance
with subsequent arrhythmias and/or may increase cardiac work and platelet
aggregability with possible plaque rupture and coronary thrombosis. Therefore
adaptation to high intensity exercise and therapeutic interventions or abstinence from
skiing in certain cases should be considered for downhill skiers at high risk.
Citation <40>
Unique Identifier
8903257
Authors
Kerle KK. Runkle GP.
Title
Sickle cell trait and sudden death in athletes.[comment].
Comments
Comment on: JAMA. 1996 Jul 17;276(3):199-204; PMID: 8667563
Source
JAMA. 276(18):1472, 1996 Nov 13.
Citation <41>
Unique Identifier
8667563
Authors
Maron BJ. Shirani J. Poliac LC. Mathenge R. Roberts WC. Mueller FO.
Institution
Division of Cardiovascular Research, Minneapolis Heart Institute Foundation, MN
55407, USA.
Title
Sudden death in young competitive athletes. Clinical, demographic, and pathological
profiles.[see comment].
Comments
Comment in: JAMA. 1996 Nov 13;276(18):1472; PMID: 8903257
Source
JAMA. 276(3):199-204, 1996 Jul 17.
Abstract
OBJECTIVE: To develop clinical, demographic, and pathological profiles of young
competitive athletes who died suddenly. DESIGN: Systematic evaluation of clinical
information and circumstances associated with sudden deaths; interviews with family
members, witnesses, and coaches; and analyses of postmortem anatomic,
microscopic, and toxicologic data. PARTICIPANTS AND SETTING: A total of 158
sudden deaths that occurred in trained athletes throughout the United States from
1985 through 1995 were analyzed. MAIN OUTCOME MEASURES--Characteristics
and probable cause of death. RESULTS: Of 158 sudden deaths among athletes, 24
(15%) were explained by noncardiovascular causes. Among the 134 athletes who had
cardiovascular causes of sudden death, the median age was 17 years (range, 12-40
years), 120 (90%) were male, 70 (52%) were white, and 59 (44%) were black. The
most common competitive sports involved were basketball (47 cases) and football (45
cases), together accounting for 68% of s!
udden deaths. A total of 121 athletes (90%) collapsed during or immediately after a
training session (78 cases) or a formal athletic contest (43 cases), with 80 deaths
(63%) occurring between 3 PM and 9 PM. The most common structural
cardiovascular diseases identified at autopsy as the primary cause of death were
hypertrophic cardiomyopathy (48 athletes [36%]), which was disproportionately
prevalent in black athletes compared with white athletes (48% vs 26% of deaths; P =
.01), and malformations involving anomalous coronary artery origin (17 athletes
[13%]). Of 115 athletes who had a standard preparticipation medical evaluation, only
4 (3%) were suspected of having cardiovascular disease, and the cardiovascular
abnormality responsible for sudden death was correctly identified in only 1 athlete
(0.9%). CONCLUSIONS: Sudden death in young competitive athletes usually is
precipitated by physical activity and may be due to a heterogeneous spectrum of
cardiovascular disease, most co!
mmonly hypertrophic cardiomyopathy. Preparticipation screening appeared to be of
limited value in identification of underlying cardiovascular abnormalities.
Citation <42>
Unique Identifier
12902362
Authors
Maron BJ. Poliac LC. Ashare AB. Hall WA.
Title
Sudden death due to neck blows among amateur hockey players.
Source
JAMA. 290(5):599-601, 2003 Aug 6.
Citation <43>
Unique Identifier
10735397
Authors
Pfister GC. Puffer JC. Maron BJ.
Institution
Cardiovascular Research Division, Minneapolis Heart Institute Foundation, Minn
55407, USA.
Title
Preparticipation cardiovascular screening for US collegiate student-athletes.[see
comment].
Comments
Comment in: JAMA. 2000 Aug 23-30;284(8):957; author reply 958; PMID:
10944631, Comment in: JAMA. 2000 Aug 23-30;284(8):958; PMID: 10944632
Source
JAMA. 283(12):1597-9, 2000 Mar 22-29.
Abstract
CONTEXT: Sudden death in young competitive athletes due to unsuspected
cardiovascular disease has heightened interest in preparticipation screening.
OBJECTIVE: To assess screening practices for detecting potentially lethal
cardiovascular diseases in college-aged student-athletes. DESIGN, SETTING, AND
PARTICIPANTS: A total of 1110 National Collegiate Athletic Association member
colleges and universities were surveyed between 1995 and 1997, with 879 (79%)
responding to the questionnaire. MAIN OUTCOME MEASURES: Information on the
administration and scope of the preparticipation screening process was obtained from
the team physician or athletic director; preparticipation screening forms were
evaluated for content and compared with 12 items recommended by the 1996
American Heart Association (AHA) consensus panel screening guidelines.
RESULTS: Preparticipation screening was a requirement at 855 (97%) of 879
schools, was performed on campus at 713 schools (81 %), and was required a!
nnually by 446 schools (51 %). Team physicians were responsible for examinations at
603 (85%) of 713 schools with on-campus screening, although 135 of these schools
(19%) also approved nurse practitioners and 244 schools (34%) allowed athletic
trainers to perform examinations. Of the history and physical examination screening
forms analyzed from 625 institutions, only 163 schools (26%) had forms that
contained at least 9 of the recommended 12 AHA screening guidelines and were
judged to be adequate, whereas 150 (24%) contained 4 or fewer of these parameters
and were considered to be inadequate. Smaller Division III schools were more likely
than larger Division I schools to have inadequate screening forms (30% vs 14%;
P<.001). Relevant items that were omitted from more than 40% of the screening
forms included history of exertional chest pain, dyspnea, or fatigue; familial heart
disease or premature sudden death; and physical stigmata or family history of Marfan
syndrome. CONCLUS!
ION: The preparticipation screening process used by many US colleges and
universities may have limited potential to detect (or raise the suspicion of)
cardiovascular abnormalities capable of causing sudden death in competitive studentathletes.
Citation <44>
Unique Identifier
10338239
Authors
Deady B. Innes G.
Institution
Royal Columbian Hospital New Westminster, BC, Canada.
Title
Sudden death of a young hockey player: case report of commotio cordis.
Source
Journal of Emergency Medicine. 17(3):459-62, 1999 May-Jun.
Abstract
Despite the use of protective gear, a 15-year-old hockey player died when he was
struck in the chest by a puck. This is the fifth recorded hockey death related to socalled commotio cordis, that is, blunt chest injury without myocardial structural
damage. In light of inadequacies of commercial chest protectors currently in use for
hockey, the authors hope to educate players and coaches about the danger of blocking
shots with the chest. Physicians should be aware that commotio cordis represents a
distinctive pathological condition, in the event of which immediate recognition,
precordial thump, CPR, and defibrillation are potentially lifesaving. Appropriate
medical supervision at amateur hockey games, 911 telephone access, and on-site
automated external defibrillators are issues that deserve careful consideration.
Citation <45>
Unique Identifier
9610969
Authors
Neuman TS. Jacoby I. Bove AA.
Institution
Hyperbaric Medicine Center and Department of Emergency Medicine, University of
California Medical Center, San Diego, USA.
Title
Fatal pulmonary barotrauma due to obstruction of the central circulation with air.
Source
Journal of Emergency Medicine. 16(3):413-7, 1998 May-Jun.
Abstract
Cardiac arrest in cases of barotraumatic arterial gas embolism (AGE) is usually
ascribed to reflex dysrhythmias secondary to brainstem embolization or secondary to
coronary artery embolization. Several case reports suggest that obstruction of the
central circulation (i.e., the heart, pulmonary arteries, aorta, and arteries to the head
and neck) may play a role in the pathogenesis of sudden death in victims of
pulmonary barotrauma. We report three consecutive cases of fatal AGE in patients in
whom chest roentgenograms demonstrated confluent air lucencies filling the central
vascular bed, the heart, and great vessels. In none of the victims was there evidence
by history or at autopsy that the intravascular gas was iatrogenically introduced. Total
occlusion of the central vascular bed with air is a mechanism of death in some victims
of AGE, and resuscitation efforts for such patients should take this possibility into
consideration.
Citation <46>
Unique Identifier
12570951
Authors
Link MS. Maron BJ. Wang PJ. VanderBrink BA. Zhu W. Estes NA 3rd.
Institution
Center for the Cardiovascular Evaluation of Athletes and the Cardiac Arrhythmia
Service, New England Medical Center, Tufts University School of Medicine, Boston,
Massachusetts, USA. [email protected]
Title
Upper and lower limits of vulnerability to sudden arrhythmic death with chest-wall
impact (commotio cordis).
Source
Journal of the American College of Cardiology. 41(1):99-104, 2003 Jan 1.
Abstract
OBJECTIVES: In an animal model of commotio cordis, sudden death with chestwall impact, we sought to systematically evaluate the importance of impact velocity
in the generation of ventricular fibrillation (VF) with baseball chest-wall impact.
BACKGROUND: Sudden cardiac death can occur with chest-wall blows in
recreational and competitive sports (commotio cordis). Analyses of clinical events
suggest that the energy of impact is often not of unusual force, although this has been
difficult to quantify. METHODS: Juvenile swine (8 to 25 kg) were anesthetized,
placed prone in a sling to receive chest-wall strikes during the vulnerable time
window during repolarization for initiation of VF with a baseball propelled at 20 to 70
mph. RESULTS: Impacts at 20 mph did not induce VF; incidence of VF increased
incrementally from 7% with 25 mph impacts, to 68% with chest impact at 40 mph,
and then diminished at >/=50 mph (p < 0.0001). Peak left ventricular pressure
generated by the chest bl!
ow was related to the incidence of VF in a similar Gaussian relationship (p < 0.0001).
CONCLUSIONS: The energy of impact is an important variable in the generation of
VF with chest-wall impacts. Impacts at 40 mph were more likely to produce VF than
impacts with greater or lesser velocities, suggesting that the predilection for commotio
cordis is related in a complex manner to the precise velocity of chest-wall impact.
Citation <47>
Unique Identifier
14662260
Authors
Williams RG. Chen AY.
Title
Identifying athletes at risk for sudden death.[comment].
Comments
Comment on: J Am Coll Cardiol. 2003 Dec 3;42(11):1959-63; PMID: 14662259
Source
Journal of the American College of Cardiology. 42(11):1964-6, 2003 Dec 3.
Citation <48>
Unique Identifier
8800121
Authors
Maron BJ. Poliac LC. Roberts WO.
Institution
Cardiovascular Research Division, Minneapolis Heart Institute Foundation,
Minnesota 55407, USA.
Title
Risk for sudden cardiac death associated with marathon running.[see comment].
Comments
Comment in: J Am Coll Cardiol. 1997 Jan;29(1):224; PMID: 8996321
Source
Journal of the American College of Cardiology. 28(2):428-31, 1996 Aug.
Abstract
OBJECTIVES: This analysis was performed to quantitatively assess the relative
risks, associated with underlying cardiovascular disease, incurred in the course of
intense competitive sports. BACKGROUND: Sudden cardiac death during athletic
activities is a highly visible event, and controversy persists regarding the true risks
associated with participation in sports. METHODS: The prevalence of sudden death
was assessed in two systematically tabulated groups of endurance runners competing
in the annual Marine Corps (1976 to 1994) and Twin Cities (1982 to 1994)
marathons, held over a cumulative 30-year period. RESULTS: A total of 215,413
runners completed the races, and four exercise-related sudden deaths occurred, each
due to unsuspected structural cardiovascular disease. Three deaths occurred during the
race (after 15 to 24 miles [24 to 38.4 km]) and the other immediately after its
completion. The ages were 19 to 58 years (average 37), and three were men. Three of
the sudden d!
eaths were due to atherosclerotic coronary artery disease (narrowing of two or three
vessels) and one to anomalous origin of the left main coronary artery from the right
sinus of Valsalva. None of the four runners had prior documentation of heart disease
or experienced prodromal symptoms, and two had previously completed three
marathon races each. The overall prevalence of sudden cardiac death during the
marathon was only 0.002%, strikingly lower than for several other variables of risk
for premature death calculated for the general U.S. population. CONCLUSIONS:
Although highly trained athletes such as marathon runners may harbor underlying and
potentially lethal cardiovascular disease, the risk for sudden cardiac death associated
with such intense physical effort was exceedingly small (1 in 50,000) and as little as
1/100th of the annual overall risk associated with living, either with or without heart
disease. The low risk for sudden death identified in long-distance runners !
from the general population suggests that routine screening for cardiovascular disease
in such athletic populations may not be justifiable.
Citation <49>
Unique Identifier
10807452
Authors
Basso C. Maron BJ. Corrado D. Thiene G.
Institution
Department of Pathology, University of Padua Medical School, Italy.
Title
Clinical profile of congenital coronary artery anomalies with origin from the wrong
aortic sinus leading to sudden death in young competitive athletes.[see comment].
[Review] [47 refs]
Comments
Comment in: J Am Coll Cardiol. 2001 Nov 1;38(5):1587-8; PMID: 11691551,
Comment in: J Am Coll Cardiol. 2001 Oct;38(4):1269-70; author reply 1270-1;
PMID: 11587030
Source
Journal of the American College of Cardiology. 35(6):1493-501, 2000 May.
Abstract
OBJECTIVES: The purpose of this study is to characterize the clinical profile and
identify clinical markers that would enable the detection during life of anomalous
coronary artery origin from the wrong aortic sinus (with course between the aorta and
pulmonary trunk) in young competitive athletes. BACKGROUND: Congenital
coronary artery anomalies are not uncommonly associated with sudden death in
young athletes, the catastrophic event probably provoked by myocardial ischemia.
Such coronary anomalies are rarely identified during life, often because of insufficient
clinical suspicion. However, since anomalous coronary artery origin is amenable to
surgical treatment, timely clinical identification is crucial. METHODS: Because of
the paucity of available data characterizing the clinical profile of wrong sinus
coronary artery malformations, we reviewed two large registries comprised of young
competitive athletes who died suddenly, assembled consecutively in the U.S. and
Italy. RES!
ULTS: We reported 27 sudden deaths in young athletes, identified solely at autopsy
and due to either left main coronary artery from the right aortic sinus (n = 23) or right
coronary artery from the left sinus (n = 4). Each athlete died either during (n = 25) or
immediately after (n = 2) intense exertion on the athletic field. Fifteen athletes (55%)
had no clinical cardiovascular manifestations or testing during life. However, in the
remaining 12 athletes (45%) aged 16 +/- 7, certain clinical data were available.
Premonitory symptoms had occurred in 10, including syncope in four (exertional in
three and recurrent in two, 3 to 24 months before death) and chest pain in five
(exertional in three, all single episodes, < or =24 months before death). All
cardiovascular tests were within normal limits, including 12-lead electrocardiogram
(ECG) pattern (in 9/9), stress ECG with maximal exercise (in 6/6) and left ventricular
wall motion and cardiac dimensions by two-dimensional echocard!
iography (in 2/2). CONCLUSIONS: With regard to congenital coronary artery
anomalies of wrong aortic sinus origin in young competitive athletes, 1) standard
testing with ECG under resting or exercise conditions is unlikely to provide clinical
evidence of myocardial ischemia and would not be reliable as screening tests in large
athletic populations, 2) premonitory cardiac symptoms not uncommonly occurred
shortly before sudden death (typically associated with anomalous left main coronary
artery), suggesting that a history of exertional syncope or chest pain requires
exclusion of this anomaly. These observations have important implications for the
preparticipation screening of competitive athletes. [References: 47]
Citation <50>
Unique Identifier
8996321
Authors
Rich MW.
Title
Risk for sudden cardiac death associated with marathon running.[comment].
Comments
Comment on: J Am Coll Cardiol. 1996 Aug;28(2):428-31; PMID: 8800121
Source
Journal of the American College of Cardiology. 29(1):224, 1997 Jan.
Citation <51>
Unique Identifier
12651044
Authors
Maron BJ. Carney KP. Lever HM. Lewis JF. Barac I. Casey SA. Sherrid MV.
Institution
Minneapolis Heart Institute Foundation, 920 East 28th Street, Suite 60, Minneapolis,
MN 55407, USA. [email protected]
Title
Relationship of race to sudden cardiac death in competitive athletes with
hypertrophic cardiomyopathy.
Source
Journal of the American College of Cardiology. 41(6):974-80, 2003 Mar 19.
Abstract
OBJECTIVES: The goal of this study was to determine the impact of race on
identification of hypertrophic cardiomyopathy (HCM). BACKGROUND: Sudden
death in young competitive athletes is due to a variety of cardiovascular diseases
(CVDs) and, most commonly, HCM. These catastrophes have become an important
issue for African Americans, although HCM has been previously regarded as rare in
this segment of the U.S. population. METHODS: We studied the relationship of race
to the prevalence of CVDs causing sudden death in our national athlete registry, and
compared these findings with a representative multicenter hospital-based cohort of
patients with HCM. RESULTS: Of 584 athlete deaths, 286 were documented to be
due to CVD at ages 17 +/- 3 years; 156 (55%) were white, and 120 (42%) were
African American. Most were male (90%), and 67% participated in basketball and
football. Among the 286 cardiovascular deaths, most were due to HCM (n = 102;
36%) or anomalous coronary artery of wrong!
sinus origin (n = 37; 13%). Of the athletes who died of HCM, 42 (41%) were white,
but 56 (55%) were African American. In contrast, of 1,986 clinically identified HCM
patients, only 158 (8%) were African American (p < 0.001). CONCLUSIONS: In this
autopsy series, HCM represented a common cause of sudden death in young and
previously undiagnosed African American male athletes, in sharp contrast with the
infrequent clinical identification of HCM in a hospital-based population (i.e., by
seven-fold). This discrepancy suggests that many HCM cases go unrecognized in the
African American community, underscoring the need for enhanced clinical
recognition of HCM to create the opportunity for preventive measures to be employed
in high-risk patients with this complex disease.
Citation <52>
Unique Identifier
9857867
Authors
Maron BJ. Gohman TE. Aeppli D.
Institution
Cardiovascular Research Division, Minneapolis Heart Institute Foundation,
Minnesota 55407, USA.
Title
Prevalence of sudden cardiac death during competitive sports activities in Minnesota
high school athletes.
Source
Journal of the American College of Cardiology. 32(7):1881-4, 1998 Dec.
Abstract
OBJECTIVES: Reliable prevalence data would be useful in assessing the impact of
sudden cardiac death in young competitive athletes on the community and designing
effective preparticipation screening strategies. BACKGROUND: The frequency with
which these catastrophes occur is largely unknown. METHODS: We utilized a
circumstance unique to Minnesota in which the precise number of participants and
deaths due to cardiovascular disease could be ascertained over a substantial period of
time based on a long-standing insurance program for catastrophic injury or death,
mandatory for all student athletes engaged in interscholastic sports. RESULTS: Over
the 12-year period, 1985/1986 to 1996/1997, inclusive, three sudden deaths due to
cardiovascular disease occurred in competitive high school athletes (grades 10-12)
during competition or practice. At autopsy, 1 each proved to be due to anomalous
origin of the left main coronary artery from the right sinus of Valsalva, congenital
aortic v!
alve stenosis (with bicuspid valve) and myocarditis. All three athletes were white and
male, 16 or 17 years of age; two competed in cross-country/track and one in
basketball. During the study period there were 1,453,280 overall sports participations
and 651,695 student athlete participants among the 27 high school sports. The
calculated risk for sudden death was 1:500,000 participations and 1:217,400
participants per academic year (or 0.46/100,000, annually). Over a 3-year high school
career for a student athlete the estimated risk was 1:72,500. CONCLUSIONS: The
risk of sudden cardiac death in a population of high school student athletes was small,
in the range of one in 200,000 per year, and was higher in male athletes. The rare
occurrence of sudden cardiac death in competitive sports underlines the limitations
implicit in structuring productive and cost-effective broad-based preparticipation
screening strategies for high school athletes.
Citation <53>
Unique Identifier
14662259
Authors
Corrado D. Basso C. Rizzoli G. Schiavon M. Thiene G.
Institution
Department of Cardiology, University of Padua, Padua, Italy.
Title
Does sports activity enhance the risk of sudden death in adolescents and young
adults?[see comment].
Comments
Comment in: J Am Coll Cardiol. 2003 Dec 3;42(11):1964-6; PMID: 14662260
Source
Journal of the American College of Cardiology. 42(11):1959-63, 2003 Dec 3.
Abstract
OBJECTIVES: We sought to assess the risk of sudden death (SD) in both male and
female athletes age 12 to 35 years. BACKGROUND: Little is known about the risk of
SD in adolescents and young adults engaged in sports. METHODS: We did a 21-year
prospective cohort study of all young people of the Veneto Region of Italy. From
1979 to 1999, the total population of adolescents and young adults averaged
1,386,600 (692,100 males and 694,500 females), of which 112,790 (90,690 males and
22,100 females) were competitive athletes. An analysis by gender of risk of SD and
underlying pathologic substrates was performed in the athletic and non-athletic
populations. RESULTS: There were 300 cases of SD, producing an overall cohort
incidence rate of 1 in 100,000 persons per year. Fifty-five SDs occurred among
athletes (2.3 in 100,000 per year) and 245 among non-athletes (0.9 in 100,000 per
year), with an estimated relative risk (RR) of 2.5 (95% confidence interval [CI] 1.8 to
3.4; p < 0.0001). T!
he RR of SD among athletes versus non-athletes was 1.95 (CI 1.3 to 2.6; p = 0.0001)
for males and 2.00 (CI 0.6 to 4.9; p = 0.15) for females. The higher risk of SD in
athletes was strongly related to underlying cardiovascular diseases such as congenital
coronary artery anomaly (RR 79, CI 10 to 3,564; p < 0.0001), arrhythmogenic right
ventricular cardiomyopathy (RR 5.4, CI 2.5 to 11.2; p < 0.0001), and premature
coronary artery disease (RR 2.6, CI 1.2 to 5.1; p = 0.008). CONCLUSIONS: Sports
activity in adolescents and young adults was associated with an increased risk of SD,
both in males and females. Sports, per se, was not a cause of the enhanced mortality,
but it triggered SD in those athletes who were affected by cardiovascular conditions
predisposing to life-threatening ventricular arrhythmias during physical exercise.
Citation <54>
Unique Identifier
10341774
Authors
Young MC. Fricker PA. Thomson NJ. Lee KA.
Institution
Australian Institute of Sport, Canberra, ACT. [email protected]
Title
Sudden death due to ischaemic heart disease in young aboriginal sportsmen in the
Northern Territory, 1982-1996.
Source
Medical Journal of Australia. 170(9):425-8, 1999 May 3.
Abstract
OBJECTIVE: To estimate the incidence of sport-related sudden cardiac death due to
ischaemic heart disease (IHD) in competitive young Aboriginal sportsmen.
SETTING: Northern Territory (NT), 1982-1996. DESIGN: Retrospective case series
with cases identified from Australian Bureau of Statistics cause-of-death listings and
NT coronial autopsy records. MAIN OUTCOME MEASURES: Circumstances and
incidence of sport-related sudden cardiac deaths due to IHD; autopsy findings.
RESULTS: Between 1982 and 1996, there were eight sudden cardiac deaths due to
IHD and related to sporting activity among Aboriginal sportsmen aged 15-37 years in
the NT. Six were associated with games of Australian (rules) football. All occurred in
the Top End of the NT in the wet season, and all occurred after the first half, or within
an hour of, a game. Four of the players had macrosopic myocardial abnormalities
(hypertrophy or previous infarcts) on autopsy. The estimated incidence of IHD-related
sudden cardiac!
death among Aboriginal Australian football players in the NT was 19-24 per 100,000
player-years, compared with 0.54 per 100,000 player-years among Australian rules
footballers of similar ages in Victoria. CONCLUSIONS: Incidence of sudden cardiac
death attributable to underlying IHD was extremely high among young NT Aboriginal
Australian footballers. Prevention will best be achieved by funding culturally
appropriate long-term strategies to reduce the incidence of IHD. However, in the
short-term, community-controlled programs with education of athletes, heat-stress
reduction strategies, and cardiovascular screening should reduce the incidence of
sudden cardiac death in sport.
Citation <55>
Unique Identifier
8970136
Authors
Anonymous.
Title
Cardiovascular preparticipation screening of competitive athletes. American Heart
Association.
Source
Medicine & Science in Sports & Exercise. 28(12):1445-52, 1996 Dec.
Citation <56>
Unique Identifier
10795776
Authors
Fuller CM.
Institution
Sierra Nevada Cardiology Associates and Sierra Heart Institute, Reno, NV 89502,
USA. [email protected]
Title
Cost effectiveness analysis of screening of high school athletes for risk of sudden
cardiac death.[see comment].
Comments
Comment in: Med Sci Sports Exerc. 2000 Oct;32(10):1809-11; PMID: 11039658
Source
Medicine & Science in Sports & Exercise. 32(5):887-90, 2000 May.
Abstract
Sudden cardiac death of a high school athlete is an alarming tragedy. Three
preparticipation screening methods have been recommended to reduce its occurrence:
specific cardiovascular history and physical examination, 12-lead ECG, and twodimensional (2D) echocardiography. This study analyzes the cost effectiveness of
each of these methods. The cost to perform each test and to evaluate abnormal
screening findings were approximated. The years of life gained through detection of
athletes with potential causes of sudden cardiac death were estimated. Overall, the
approximate costs per year of life saved for the preparticipation cardiovascular
screening examinations are: specific cardiovascular history and physical examination,
$84,000; 12-lead ECG, $44,000; and 2D echocardiography, $200,000. The 12-lead
ECG is the most cost effective preparticipation cardiovascular modality of the three
currently recommended methods. Similar cost effectiveness for history and physical
examination!
or 2D echocardiography would require respectively a 2-fold increase in sensitivity or
4.5-fold decrease in cost.
Citation <57>
Unique Identifier
11039658
Authors
Fields KB.
Title
The 12-lead ECG is the most cost-effective preprecipitation cardiovascular
screen.[comment].
Comments
Comment on: Med Sci Sports Exerc. 1997 Sep;29(9):1131-8; PMID: 9309622,
Comment on: Med Sci Sports Exerc. 2000 May;32(5):887-90; PMID: 10795776
Source
Medicine & Science in Sports & Exercise. 32(10):1809-11, 2000 Oct.
Citation <58>
Unique Identifier
9309622
Authors
Fuller CM. McNulty CM. Spring DA. Arger KM. Bruce SS. Chryssos BE.
Drummer EM. Kelley FP. Newmark MJ. Whipple GH.
Institution
Sierra Nevada Cardiology Associates, Reno 89502, USA.
Title
Prospective screening of 5,615 high school athletes for risk of sudden cardiac
death.[see comment].
Comments
Comment in: Med Sci Sports Exerc. 2000 Oct;32(10):1809-11; PMID: 11039658
Source
Medicine & Science in Sports & Exercise. 29(9):1131-8, 1997 Sep.
Abstract
Sudden cardiac death among high school athletes is a very infrequent though tragic
occurrence. Despite widespread preparticipation screening for known causes of this
event, the frequency has not changed. The ECG is an acknowledged sensitive
screening tool for the common causes of sudden cardiac death in young athletes. The
specificity of the ECG in this setting is believed to be relatively low in young athletes
for which reason, in part, it is not used. We added an ECG to the usual
preparticipation screening. An echocardiogram was performed when screening was
abnormal. Outcome measures of serious or potentially serious cardiovascular
abnormalities were defined by the 16th Bethesda Conference. These abnormalities
either preclude sports participation or require further testing before approval for
participation in sports can be considered. Over 3 yr, 5,615 male and female high
school athletes were screened prospectively from 30 different high schools in northern
Nevada. Outcome!
measures were detected in 22 athletes or one per 255. Cardiac history led to detection
of outcome measures in 0 athletes, auscultation/inspection in 1/6,000 athletes, blood
pressure measurement in 1/1,000 athletes, and the ECG in 1/350 athletes. Specificity
was 97.8% for an abbreviated cardiac history and auscultation/inspection and 97.7%
for ECG. Overall, the ECG was a much more effective screening tool than cardiac
history and auscultation/inspection in detecting cardiovascular abnormalities requiring
further tests before approval for participation in sports could be given. ECG and
cardiovascular history/ausculation/inspection had similar specificity ECG was
efficiently performed on large groups of high school athletes.
Citation <59>
Unique Identifier
10709380
Authors
Phelps SE.
Institution
Department of Family Practice, Martin Army Community Hospital, Fort Benning,
GA 31905, USA.
Title
Left coronary artery anomaly: an often unsuspected cause of sudden death in the
military athlete.
Source
Military Medicine. 165(2):157-9, 2000 Feb.
Abstract
More than 300,000 cases of sudden cardiac death (SCD) occur in the United States
each year. Left coronary artery anomaly (LCAA), although rare, is second only to
hypertrophic cardiomyopathy as the most common cause of SCD associated with
structural cardiovascular abnormalities. This case illustrates SCD secondary to LCAA
in a military athlete. A 19-year-old soldier collapsed after an 8-km run. On arrival at
the emergency room, he was unresponsive and in asystole. Despite successful
resuscitation and aggressive management, the patient died the next morning. Autopsy
revealed an anomalous left coronary artery. LCAA-associated SCD is rare and usually
seen in young individuals who collapse (and/or die) while exercising. A substantial
proportion of these individuals experience prodromal symptoms of exertional chest
pain, syncope, and/or sudden collapse. Early recognition and intervention are key to
survival. Rapid, early imaging and invasive therapeutic measures leading to surgica!
l correction may be the difference between life and death.
Citation <60>
Unique Identifier
14689606
Authors
Gogbashian A.
Title
Sudden death in young athletes.[comment].
Comments
Comment on: N Engl J Med. 2003 Sep 11;349(11):1064-75; PMID: 12968091
Source
New England Journal of Medicine. 349(25):2464-5; author reply 2464-5, 2003 Dec
18.
Citation <61>
Unique Identifier
9691102
Authors
Corrado D. Basso C. Schiavon M. Thiene G.
Institution
Department of Cardiology, University of Padua, Italy.
Title
Screening for hypertrophic cardiomyopathy in young athletes.
Source
New England Journal of Medicine. 339(6):364-9, 1998 Aug 6.
Abstract
BACKGROUND: For more than 20 years in Italy, young athletes have been
screened before participating in competitive sports. We assessed whether this strategy
results in the prevention of sudden death from hypertrophic cardiomyopathy, a
common cardiovascular cause of death in young athletes. METHODS: We
prospectively studied sudden deaths among athletes and nonathletes (35 years of age
or less) in the Veneto region of Italy from 1979 to 1996. The causes of sudden death
in both populations were compared, and the pathological findings in the athletes were
related to their clinical histories and electrocardiograms. Cardiovascular reasons for
disqualification from participation in sports were investigated and follow-up was
performed in a consecutive series of 33,735 young athletes who underwent
preparticipation screening in Padua during the same period. RESULTS: Of 269
sudden deaths in young people, 49 occurred in competitive athletes (44 male and 5
female athletes; mean age, 23+/!
-7 years). The most common causes of sudden death in athletes were arrhythmogenic
right ventricular cardiomyopathy (22.4 percent), coronary atherosclerosis (18.4
percent), and anomalous origin of a coronary artery (12.2 percent). Hypertrophic
cardiomyopathy caused only 1 sudden death among the athletes (2.0 percent) but
caused 16 sudden deaths in the nonathletes (7.3 percent). Hypertrophic
cardiomyopathy was detected in 22 athletes (0.07 percent) at preparticipation
screening and accounted for 3.5 percent of the cardiovascular reasons for
disqualification. None of the disqualified athletes with hypertrophic cardiomyopathy
died during a mean follow-up period of 8.2+/-5 years. CONCLUSIONS: The results
show that hypertrophic cardiomyopathy was an uncommon cause of death in these
young competitive athletes and suggest that the identification and disqualification of
affected athletes at screening before participation in competitive sports may have
prevented sudden death.
Citation <62>
Unique Identifier
12968091
Authors
Maron BJ.
Institution
Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation,
Minneapolis, MN 55407, USA. [email protected]
Title
Sudden death in young athletes. [Review] [100 refs]
Source
New England Journal of Medicine. 349(11):1064-75, 2003 Sep 11.
Citation <63>
Unique Identifier
14681516
Authors
Ashrafian H.
Title
Sudden death in young athletes.[comment].
Comments
Comment on: N Engl J Med. 2003 Sep 11;349(11):1064-75; PMID: 12968091
Source
New England Journal of Medicine. 349(25):2464-5; author reply 2464-5, 2003 Dec
18.
Citation <64>
Unique Identifier
9632447
Authors
Link MS. Wang PJ. Pandian NG. Bharati S. Udelson JE. Lee MY. Vecchiotti
MA. VanderBrink BA. Mirra G. Maron BJ. Estes NA 3rd.
Institution
Cardiac Arrhythmia Service, Tufts-New England Medical Center, Boston, MA
02111, USA.
Title
An experimental model of sudden death due to low-energy chest-wall impact
(commotio cordis)[see comment].
Comments
Comment in: N Engl J Med. 1998 Jun 18;338(25):1841-3; PMID: 9632454,
Comment in: N Engl J Med. 1998 Nov 5;339(19):1398-9; author reply 1399; PMID:
9841311, Comment in: N Engl J Med. 1998 Nov 5;339(19):1398; author reply 1399;
PMID: 9841310, Comment in: N Engl J Med. 1998 Nov 5;339(19):1399; PMID:
9841312
Source
New England Journal of Medicine. 338(25):1805-11, 1998 Jun 18.
Abstract
BACKGROUND: The syndrome of sudden death due to low-energy trauma to the
chest wall (commotio cordis) has been described in young sports participants, but the
mechanism is unknown. METHODS: We developed a swine model of commotio
cordis in which a low-energy impact to the chest wall was produced by a wooden
object the size and weight of a regulation baseball. This projectile was thrust at a
velocity of 30 miles per hour and was timed to the cardiac cycle. RESULTS: We first
studied 18 young pigs, 6 subjected to multiple chest impacts and 12 to single impacts.
Of the 10 impacts occurring within the window from 30 to 15 msec before the peak of
the T wave on the electrocardiogram, 9 produced ventricular fibrillation. Ventricular
fibrillation was not produced by impacts at any other time during the cardiac cycle. Of
the 10 impacts sustained during the QRS complex, 4 resulted in transient complete
heart block. We also studied whether the use of safety baseballs, which are softer th!
an standard ones, would reduce the risk of arrhythmia. A total of 48 additional
animals sustained up to three impacts during the T-wave window of vulnerability to
ventricular fibrillation with a regulation baseball and safety baseballs of three degrees
of hardness. We found that the likelihood of ventricular fibrillation was proportional
to the hardness of the ball, with the softest balls associated with the lowest risk (two
instances of ventricular fibrillation after 26 impacts, as compared with eight instances
after 23 impacts with regulation baseballs). CONCLUSIONS: This experimental
model of commotio cordis closely resembles the clinical profile of this catastrophic
event. Whether ventricular fibrillation occurred depended on the precise timing of the
impact. Safety baseballs, as compared with regulation balls, may reduce the risk of
commotio cordis.
Citation <65>
Unique Identifier
10734649
Authors
Berul CI.
Institution
Department of Cardiology, Children's Hospital, Boston, MA 02115, USA.
Title
Cardiac evaluation of the young athlete. [Review] [11 refs]
Source
Pediatric Annals. 29(3):162-5, 2000 Mar.
Citation <66>
Unique Identifier
11986449
Authors
Link MS. Maron BJ. Wang PJ. Pandian NG. VanderBrink BA. Estes NA 3rd.
Institution
Center for the Cardiovascular Evaluation of Athletes, the Cardiac Arrhythmia
Center, New England Medical Center, Tufts University School of Medicine, Boston,
Massachusetts 02111, USA. [email protected]
Title
Reduced risk of sudden death from chest wall blows (commotio cordis) with safety
baseballs.
Source
Pediatrics. 109(5):873-7, 2002 May.
Abstract
OBJECTIVES: In an experimental model of sudden death from baseball chest wall
impact (commotio cordis), we sought to determine if sudden death by baseball impact
could be reduced with safety baseballs. BACKGROUND: Sudden cardiac death can
occur after chest wall impact with a baseball (commotio cordis). Whether softer-thanstandard (safety) baseballs reduce the risk of sudden death is unresolved from the
available human data. In a juvenile swine model, ventricular fibrillation (VF) has been
shown to be induced reproducibly by precordial impact with a 30-mph baseball 10 to
30 ms before the T-wave peak, and this likelihood was reduced with the softest safety
baseballs (T-balls). To further test whether safety baseballs would reduce the risk of
sudden death at velocities more relevant to youth sports competition, we used our
swine model of commotio cordis to test baseballs propelled at the 40-mph velocity
commonly attained in that sport. METHODS: Forty animals received up to 3 c!
hest wall impacts at 40 mph during the vulnerable period of repolarization for VF
with 1 of 3 different safety baseballs of varying hardness, and also by a standard
baseball. RESULTS: Safety baseballs propelled at 40 mph significantly reduced the
risk for VF. The softest safety baseballs triggered VF in only 11% of impacts,
compared with 19% and 22% with safety baseballs of intermediate hardness, and 69%
with standard baseballs. CONCLUSION: In this experimental model of low-energy
chest wall impact, safety baseballs reduced (but did not abolish) the risk of sudden
cardiac death. More universal use of these safety baseballs may decrease the risk of
sudden death on the playing field for young athletes.
Citation <67>
Unique Identifier
11043079
Authors
Drezner JA.
Institution
Department of Family Medicine, University of Washington School of Medicine,
Seattle, USA. [email protected]
Title
Sudden cardiac death in young athletes. Causes, athlete's heart, and screening
guidelines.[see comment]. [Review] [33 refs]
Comments
Comment in: Postgrad Med. 2001 Feb;109(2):18; PMID: 11272691
Source
Postgraduate Medicine. 108(5):37-44, 47-50, 2000 Oct.
Abstract
Sudden cardiac death of a young competitive athlete is a rare but tragic event.
Hypertrophic cardiomyopathy and coronary artery anomalies are the most frequent
causes. Most cardiovascular abnormalities go unrecognized until the time of death
owing to the lack of preceding signs or symptoms suggestive of disease. Physicians
responsible for the care of athletes should be familiar with the various causes of
sudden cardiac death, the physiologic adaptations seen in so-called athlete's heart, and
existing cardiovascular screening guidelines. The preparticipation evaluation,
although it has limitations, is the major instrument readily available for prevention of
sudden cardiac death. Effort should be made to follow established consensus
guidelines. [References: 33]
Citation <68>
Unique Identifier
11696211
Authors
Lannergard A. Fohlman J. Wesslen L. Rolf C. Friman G.
Institution
Department of Medical Sciences, Section of Infectious Diseases, Uppsala University
Hospital, Sweden.
Title
Immune function in Swedish elite orienteers.[see comment].
Comments
Comment in: Scand J Med Sci Sports. 2001 Oct;11(5):259; PMID: 11696208
Source
Scandinavian Journal of Medicine & Science in Sports. 11(5):274-9, 2001 Oct.
Abstract
During 1979-1992 an increased frequency of sudden unexpected cardiac death
(SUD) occurred among young male Swedish elite orienteers. Subacute-to-chronic
myocarditis was found in 12/16 (75%) at autopsy and Chlamydia pneumoniae, or a
cross-reacting agent, was suspected on the basis of diagnostic tests performed.
Because myocarditis is an infrequent cause of SUD and clusters of SUD are rare,
whereas Chlamydia pneumoniae infections are ubiquitous and seldom cause severe
myocarditis, 119 top ranked elite orienteers (67 males and 52 females) and 36 highly
trained male middle-distance runners and cross-country skiers, serving as controls,
underwent immunologic screening in an effort to reveal possible immune dysfunction.
Except for two orienteers and one runner/skier who showed genetic C3-deficiency or
IgA-deficiency, the results showed no significant differences between the orienteers
and controls with respect to immunoglobulin levels, complement activation,
lymphocyte subsets, in!
cluding activated T lymphocytes, and sIL-2r-alpha. IL-1 beta, IL-6, TNF-alpha, and
sCD8, tested in the orienteers only, were normal. However, IFN-gamma was
significantly higher in controls than in orienteers, who showed normal levels, whereas
the orienteers had increased sELAM-1 and sICAM-1 levels. Finally, sIL-2 receptoralpha was similarly elevated in orienteers and controls. We conclude that, with the
tests employed, no immunologic disturbance could be revealed in the orienteers that
may potentially have increased their susceptibility to myocarditis and SUD.
Citation <69>
Unique Identifier
9858396
Authors
Futterman LG. Myerburg R.
Institution
School of Medicine, University of Miami, Jackson Memorial Medical Center,
Florida, USA. [email protected]
Title
Sudden death in athletes: an update. [Review] [35 refs]
Source
Sports Medicine. 26(5):335-50, 1998 Nov.
Abstract
The athlete projects the ultimate image of well-being in the health status spectrum.
Nevertheless, exercise-related sudden cardiac death (SCD) is an uncommon, yet
tragic, occurrence. Exercise-related SCD is defined by symptoms that arise within 1
hour of participation in sport. The major mechanisms involved in exercise-related
SCD are related to haemodynamic and electrophysiological changes brought about by
exercise in the susceptible individual. Fatal arrhythmia seems to be the most common
mechanism of death. Between 1 and 5 cases of SCD per 1 million athletes occur
annually. In young athletes (<35 years old), the majority of these cases are caused by
defined and hereditary cardiovascular disorders. Among other aetiologies,
hypertrophic cardiomyopathy and coronary artery anomalies are most common in this
group. In older athletes (>35 years old), sudden death is usually associated with
atherosclerotic cardiac disease. A problem for identifying athletes at risk for SCD is
tha!
t the athlete's heart undergoes adaptive changes in response to regular physical
exercise. Alterations in cardiac function influence the physical examination, the
electrocardiogram and the echocardiogram. Because of these characteristic
'abnormalities' of the athlete's heart, it is often difficult to distinguish physiological
adaptations from pathophysiological processes. Although studies and observations
have helped to clarify the cardiovascular pathology responsible for SCD in young,
apparently healthy individuals, effective methods for preventing SCD and identifying
and screening athletes at risk remain elusive. Problems with routine comprehensive
screening of athletes include the limitations inherent in the predictive value of
available diagnostic procedures and the cost of testing large populations. The
variation from normal cardiac physiology found within the athletic population and the
rarity of SCD in athletes means that elaborate screening to determine individuals at !
risk is neither practical nor cost effective. A thorough assessment of pertinent family
and medical histories, cardiac auscultation of young athletes, evaluation of exerciseinduced symptoms and education of older athletes to the symptoms of cardiac
ischaemia are all essential to primary prevention of SCD in the athletic population.
Until reliable methods can accurately identify those athletes at risk for SCD, broad
recommendations are available to help guide the management and participation in
sports of athletes with cardiovascular disease. [References: 35]