GENERAL CARDIOLOGY: The athlete's heart

Oakley, D.

doi:10.1136/heart.86.6.722

Cited by 45 publications

(23 citation statements)

References 19 publications

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“…ECG can often be abnormal in well-trained athletes Sudden cardiac death in athletes Bille et al 13 [ 4,41,[95][96][97], wi th patterns resembling th ose found in cardiovascular diseases such as HCM, which is the origin of many false positives. Despite this disadvantage, it is still considered a valuable screening tool because of its high negative predictive value and its low cost.…”

Section: Discussionmentioning

confidence: 99%

Sudden cardiac death in athletes: the Lausanne Recommendations

Bille

Figueiras

Schamasch

et al. 2006

European Journal of Cardiovascular Prevention & Rehabilitat

214

190

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Objectives This study reports on sudden cardiac death (SCD) in sport in the literature and aims at achieving a generally acceptable preparticipation screening protocol (PPSP) endorsed by the consensus meeting of the International Olympie Committee (IOC). Background The sudden death of athletes under 35 years engaged in competitive sports is a well-known occurrence; the incidence is higher in athletes ( ~ 2/1OO000 per year) than in non-athletes (2.5: 1 ), and the cause is cardiovascular in over 90%.Methods A systematic review of the literature identified causes of SCD, sex, age, underlying cardiac disease and the type of sport and PPSP in use. Methods necessary to detect pre-existing cardiac abnormalities are discussed to formulate a PPSP for the Medical Commission of the IOC.Results SCD occurred in 1101 (1966-2004) reported cases in athletes under 35 years, 50% had congenital anatomical heart disease and cardiomyopathies and 10% had early-onset atherosclerotic heart disease. Forty percent occurred in athletes un der 18 years, 33% under 16 years; the female/male ratio was 1 /9. SCD was reported in almost ail sports; most frequently involved were soccer (30%), basketball (25%) and running (15%). The PPSP were of varying quality and content. The IOC consensus meeting accepted the proposed Lausanne Recommendations based on this research and expert opinions (http://multimedia.olympic.org/pdf/en_report_886.pdf). Conclusion SCD occurs more frequently in young athletes, even those under the age of 18 years, than expected and is predominantly caused by pre-existing congenital cardiac abnormalities. Premature atherosclerotic disease forms another important cause in these young adults. A generally acceptable PPSP has been achieved by the IOC's acceptance of the Lausanne Recommendations. Eur J Cardiovasc Prev Rehabil 13:000-000

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Section: Discussionmentioning

confidence: 99%

Sudden cardiac death in athletes: the Lausanne Recommendations

Bille

Figueiras

Schamasch

et al. 2006

European Journal of Cardiovascular Prevention & Rehabilitat

214

190

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“…37,38 However, not all forms of cardiac hypertrophy are necessarily pathological, as athletic conditioning can stimulate heart growth without deleterious consequence, ie, a physiological type of cardiac hypertrophy. 39 The observed G-CSF-induced hypertrophy cannot be simply explained as a compensatory response because the hypertrophic reaction was more pronounced in G-CSFtreated hearts, which showed less severe heart failure than was seen in the untreated hearts. In the present study, moreover, we detected increased activation of both Akt and Stat3, ie, increased levels of phospho-Akt and phospho-Stat3, in the G-CSF-treated hearts.…”

Section: Beneficial Effect Of G-csf On Cardiomyopathic Hamsters and Tmentioning

confidence: 99%

Autophagic Cardiomyocyte Death in Cardiomyopathic Hamsters and Its Prevention by Granulocyte Colony-Stimulating Factor

Miyata

Takemura

Kawase

et al. 2006

The American Journal of Pathology

112

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In UM-X7.1 hamster model of human dilated cardiomyopathy, heart failure progressively develops and causes 50% mortality by 30 weeks of age. Through ultrastructural analysis, we found that many cardiomyocytes of this model contain typical autophagic vacuoles including degraded mitochondria, glycogen granules, and myelin-like figures. In addition, ubiquitin, cathepsin D, and Rab7 were overexpressed as determined by immunoassays. Importantly, most cardiomyocytes with leaky plasma membranes were positive for cathepsin D, suggesting a direct link between autophagic degeneration and cell death. Meanwhile, cardiomyocyte apoptosis appeared insignificant. Granulocyte colony-stimulating factor (10 g/kg/ day), injected 5 days/week from 15 to 30 weeks of age, improved survival among 30-week-old hamsters (100% versus 53% in the untreated hamsters, P < 0.0001); ventricular function and remodeling, increased cardiomyocyte size, and reduced myocardial fibrosis followed by a dramatic reduction in the autophagic findings were also seen. Granulocyte colonystimulating factor also down-regulated tumor necrosis factor-␣ and increased activities of Akt signal transducer and activator of transcription-3, and matrix metalloproteinases. However, there was no clear evidence of transdifferentiation from bone marrow cells into cardiomyocytes. In conclusion, autophagic death is important for cardiomyocyte loss in the cardiomyopathic hamster, and the beneficial effect of granulocyte colony-stimulating factor acts mainly via an anti-autophagic mechanism rather than anti-apoptosis or regeneration.

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“…2,3 However, not all forms of cardiac hypertrophy are necessarily pathological, as athletic conditioning can stimulate heart growth without deleterious consequences. 4 A number of studies have been dedicated to elucidating the molecular mechanisms underlying the hypertrophic growth process of the myocardium. 5,6 One pathway that has received attention is mediated by the calcium/calmodulin-activated protein phosphatase, calcineurin (PP2B).…”

mentioning

confidence: 99%

Calcineurin/NFAT Coupling Participates in Pathological, but not Physiological, Cardiac Hypertrophy

Wilkins

Dai

Bueno

et al. 2004

Circulation Research

670

620

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Abstract-Calcineurin (PP2B) is a calcium/calmodulin-activated, serine-threonine phosphatase that transmits signals to the nucleus through the dephosphorylation and translocation of nuclear factor of activated T cell (NFAT) transcription factors. Whereas calcineurin-NFAT signaling has been implicated in regulating the hypertrophic growth of the myocardium, considerable controversy persists as to its role in maintaining versus initiating hypertrophy, its role in pathological versus physiological hypertrophy, and its role in heart failure. To address these issues, NFAT-luciferase reporter transgenic mice were generated and characterized. These mice showed robust and calcineurin-specific activation in the heart that was inhibited with cyclosporin A. In the adult heart, NFAT-luciferase activity was upregulated in a delayed, but sustained manner throughout eight weeks of pathological cardiac hypertrophy induced by pressure-overload, or more dramatically following myocardial infarction-induced heart failure. In contrast, physiological hypertrophy as produced in two separate models of exercise training failed to show significant calcineurin-NFAT coupling in the heart at multiple time points, despite measurable increases in heart to body weight ratios. Moreover, stimulation of hypertrophy with growth hormone-insulin-like growth factor-1 (GH-IGF-1) failed to activate calcineurin-NFAT signaling in the heart or in culture, despite hypertrophy, activation of Akt, and activation of p70 S6K. Calcineurin A␤ gene-targeted mice also showed a normal hypertrophic response after GH-IGF-1 infusion. Lastly, exercise-or GH-IGF-1-induced cardiac growth failed to show induction of hypertrophic marker gene expression compared with pressure-overloaded animals. Although a direct cause-and-effect relationship between NFAT-luciferase activity and pathological hypertrophy was not proven here, our results support the hypothesis that separable signaling pathways regulate pathological versus physiological hypertrophic growth of the myocardium, with calcineurin-NFAT potentially serving a regulatory role that is more specialized for maladaptive hypertrophy and heart failure.

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GENERAL CARDIOLOGY: The athlete's heart

Cited by 45 publications

References 19 publications

Sudden cardiac death in athletes: the Lausanne Recommendations

Sudden cardiac death in athletes: the Lausanne Recommendations

Autophagic Cardiomyocyte Death in Cardiomyopathic Hamsters and Its Prevention by Granulocyte Colony-Stimulating Factor

Calcineurin/NFAT Coupling Participates in Pathological, but not Physiological, Cardiac Hypertrophy

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