Demographics and Epidemiology of Sudden Deaths in Young Competitive Athletes: From the United States National Registry

Maron, Barry J.; Haas, Tammy S.; Ahluwalia, Aneesha; Murphy, Caleb J.; Garberich, Ross

doi:10.1016/j.amjmed.2016.02.031

Cited by 238 publications

(171 citation statements)

References 47 publications

(82 reference statements)

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“…While LV mass indexed for body surface area is lower in women, suggesting milder phenotypic expression25 (Figure 1), women are more prone to heart failure–related mortality and HCM‐related complications 26, 27. Furthermore, women with HCM have comparable rates of SCD compared with men,24, 28, 29 although they may be less exposed to arrhythmic events triggered by strenuous exercise 30, 31. As women are less likely to be diagnosed with HCM at routine medical examination, a higher index of diagnostic suspicion and lower threshold for referral to a specialist are warranted.…”

Section: Demographic Featuresmentioning

confidence: 99%

“…26,27 Furthermore, women with HCM have comparable rates of SCD compared with men, 24,28,29 although they may be less exposed to arrhythmic events triggered by strenuous exercise. 30,31 As women are less likely to be diagnosed with HCM at routine medical examination, a higher index of diagnostic suspicion and lower threshold for referral to a specialist are warranted. Little is known regarding the impact of sex hormones on the development of myocardial hypertrophy in HCM, although the older, often postmenopausal age at presentation in women with HCM support a protective role of estrogens.…”

Section: Sexmentioning

confidence: 99%

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Impact of Demographic Features, Lifestyle, and Comorbidities on the Clinical Expression of Hypertrophic Cardiomyopathy

Finocchiaro

Magavern

Sinagra

et al. 2017

JAHA

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Section: Demographic Featuresmentioning

confidence: 99%

Section: Sexmentioning

confidence: 99%

Impact of Demographic Features, Lifestyle, and Comorbidities on the Clinical Expression of Hypertrophic Cardiomyopathy

Finocchiaro

Magavern

Sinagra

et al. 2017

JAHA

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“…Hypertrophic cardiomyopathy (HCM) 4 is an extremely prevalent inherited heart disease, affecting ϳ1 in 200 individuals (5). HCM is also the most common cause of sudden cardiac death in young people (6). Clinically, HCM is characterized by left-ventricular hypertrophy, myocyte disarray, fibrosis, and diastolic dysfunction (7)(8)(9).…”

mentioning

confidence: 99%

Converter domain mutations in myosin alter structural kinetics and motor function

Gunther

Rohde

Tang

et al. 2019

Journal of Biological Chemistry

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Edited by Karen G. Fleming Myosins are molecular motors that use a conserved ATPase cycle to generate force. We investigated two mutations in the converter domain of myosin V (R712G and F750L) to examine how altering specific structural transitions in the motor ATPase cycle can impair myosin mechanochemistry. The corresponding mutations in the human ␤-cardiac myosin gene are associated with hypertrophic and dilated cardiomyopathy, respectively. Despite similar steady-state actin-activated ATPase and unloaded in vitro motility-sliding velocities, both R712G and F750L were less able to overcome frictional loads measured in the loaded motility assay. Transient kinetic analysis and stopped-flow FRET demonstrated that the R712G mutation slowed the maximum ATP hydrolysis and recovery-stroke rate constants, whereas the F750L mutation enhanced these steps. In both mutants, the fast and slow power-stroke as well as actin-activated phosphate release rate constants were not significantly different from WT. Time-resolved FRET experiments revealed that R712G and F750L populate the pre-and post-power-stroke states with similar FRET distance and distance distribution profiles. The R712G mutant increased the mole fraction in the post-power-stroke conformation in the strong actin-binding states, whereas the F750L decreased this population in the actomyosin ADP state. We conclude that mutations in key allosteric pathways can shift the equilibrium and/or alter the activation energy associated with key structural transitions without altering the overall conformation of the pre-and post-powerstroke states. Thus, therapies designed to alter the transition between structural states may be able to rescue the impaired motor function induced by disease mutations. . 4 The abbreviations used are: HCM, hypertrophic cardiomyopathy; M2␤, human ␤-cardiac myosin; MV, chicken myosin Va; DCM, dilated cardiomyopathy; FlAsH, fluorescein bis-arsenical hairpin binding dye; QSY, QSY TM 9 C5-maleimide; CaM, calmodulin; mantADP, 2Ј-deoxy-ADP labeled with N-methylanthraniloy at the 3Ј-ribose position; mant, N-methylanthraniloy; PBP-MDCC, phosphate-binding protein labeled with 7-diethylamino-3-((((2-maleimidyl)ethyl)amino)carbonyl)coumarin; (TR) 2 FRET, transient time-resolved FRET; ELC, essential light chain; PDB, Protein Data Bank. cro ARTICLE 1554 Figure 4. Actin-activated product release. Sequential mix single-turnover experiments were performed by mixing MV with ATP, aging the reaction to form the M.ADP.P i state (0.45 M), and then mixing with different concentrations of actin in the presence of MDCC-PBP (5 M ). A, the fluorescence transients were fit to a single-exponential function (phosphate burst) followed by a linear or slow exponential rise. B, the phosphate release rate constants were plotted as a function of actin concentration and fit to a hyperbolic function to estimate the maximum rate of phosphate release. C, acto-MV (0.25 M) in presence mantADP (5 M) was mixed with saturating ATP (1 mM) at 25°C to determine the ADP release rate constan...

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“…A third study was then published by the same team of authors in 2016, based on data of 2,046 athletes contained in the U.S. National Registry of Sudden Death in Athletes accumulated between the years 1980 and 2011. 17 Autopsyconfirmed cardiovascular diseases could be identified in 802 out 2,046 (40%) cases, mainly represented by HCM (302 out of 2,046; 14.8%), coronary arteries abnormalities (158 out 2,046; 7.7%), myocarditis (57 out of 2,046; 2.8%), ARVC (43 out of 2,046; 2.1%), and CAD (38 out of 2,046; 1.9%). The most frequently involved sports disciplines were football, basketball, baseball, and cross-country running.…”

Section: Epidemiology and Causes Of Sudden Death In Athletesmentioning

confidence: 99%

Sudden Cardiac and Noncardiac Death in Sports: Epidemiology, Causes, Pathogenesis, and Prevention

Lippi

Favaloro

Sanchís-Gomar

2018

Semin Thromb Hemost

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Although few doubts remain that physical exercise should be widely promoted for maintenance of health and fitness, the risk of adverse events such as sudden death (especially due to cardiac causes, i.e., sudden cardiac death [SCD]) during exercise remains tangible. The overall risk of sudden death in athletes is relatively low (i.e., usually comprised between 0.1 and 38/100,000 person-years), and globally comparable to that of the general population. However, up to 20% of all sudden death cases are still recorded while exercising. The most frequent underlying disorders encountered in SCD are hypertrophic cardiomyopathy and coronary artery disease (CAD), representing three quarters of all conditions. The risk related to CAD increases with aging (>35 years old), while that attributable to cardiomyopathies or fatal arrhythmias is especially frequent among young people (<35 years old). Taken together, these findings would lead to the conclusion that physical exercise may be seen as an acute trigger of myocardial ischemia or arrhythmias in some predisposed individuals. Nonetheless, the prevalence of coronary atherosclerosis seems to be higher in athletes than in sedentary subjects with comparable risk profile. On the contrary, coronary plaques in physically active subjects appear more stable, thereby attenuating the risk of rupture and subsequent myocardial ischemia. These findings, along with evidence of a considerable increase of peak coronary blood flow during exercise, make it very likely that an imbalance between oxygen demand and supply may be the most frequent cause of myocardial ischemia in athletes suffering SCD and/or cardiac arrest. Therefore, all subjects who wish to practice moderate- to high-intensity exercise are recommended to undergo preparticipation screening and annual follow-up.

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Demographics and Epidemiology of Sudden Deaths in Young Competitive Athletes: From the United States National Registry

Cited by 238 publications

References 47 publications

Impact of Demographic Features, Lifestyle, and Comorbidities on the Clinical Expression of Hypertrophic Cardiomyopathy

Impact of Demographic Features, Lifestyle, and Comorbidities on the Clinical Expression of Hypertrophic Cardiomyopathy

Converter domain mutations in myosin alter structural kinetics and motor function

Sudden Cardiac and Noncardiac Death in Sports: Epidemiology, Causes, Pathogenesis, and Prevention

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