New Scope of the Document Although reports on cardiovascular screening efficacy have predominantly involved populations of adolescents and young adults participating in competitive athletics, the ...context of the present discussion is intentionally (and necessarily) much more expansive. ...it is underscored that the present report is not limited in scope to universal mass screening for athlete populations but importantly includes considerations for screening large, young, and truly general populations (school-aged, 12-25 years old, of both sexes) with respect to relevant logistical, ethical, legal, and societal issues (e.g., in the United States or other countries or communities of various sizes, in schools, or in regional or military populations).
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
The American Heart Association recognizes the importance of physically active lifestyles to the health and well-being of children and adults with congenital heart defects. Counseling of patients with ...congenital heart defects should emphasize the importance of daily physical activity and decreasing sedentary behavior as appropriate for the patient’s clinical status. The suggested practices are based on relevant research regarding the benefits of physical activity for healthy children and adults, because research on physical activity among patients with congenital heart defects is lacking. There is no evidence regarding whether or not there is a need to restrict recreational physical activity among patients with congenital heart defects, apart from those with rhythm disorders. It is important to recognize that most patients with congenital heart defects are relatively sedentary and that the physical and psychosocial health benefits of physical activity are important for this population, which is at risk for exercise intolerance, obesity, and psychosocial morbidities. Therefore, counseling to encourage daily participation in appropriate physical activity should be a core component of every patient encounter.
The purpose of this statement is to address the state of evidence on the routine use of pulse oximetry in newborns to detect critical congenital heart disease (CCHD).
A writing group appointed by the ...American Heart Association and the American Academy of Pediatrics reviewed the available literature addressing current detection methods for CCHD, burden of missed and/or delayed diagnosis of CCHD, rationale of oximetry screening, and clinical studies of oximetry in otherwise asymptomatic newborns. MEDLINE database searches from 1966 to 2008 were done for English-language papers using the following search terms: congenital heart disease, pulse oximetry, physical examination, murmur, echocardiography, fetal echocardiography, and newborn screening. The reference lists of identified papers were also searched. Published abstracts from major pediatric scientific meetings in 2006 to 2008 were also reviewed. The American Heart Association classification of recommendations and levels of evidence for practice guidelines were used. In an analysis of pooled studies of oximetry assessment performed after 24 hours of life, the estimated sensitivity for detecting CCHD was 69.6%, and the positive predictive value was 47.0%; however, sensitivity varied dramatically among studies from 0% to 100%. False-positive screens that required further evaluation occurred in only 0.035% of infants screened after 24 hours.
Currently, CCHD is not detected in some newborns until after their hospital discharge, which results in significant morbidity and occasional mortality. Furthermore, routine pulse oximetry performed on asymptomatic newborns after 24 hours of life, but before hospital discharge, may detect CCHD. Routine pulse oximetry performed after 24 hours in hospitals that have on-site pediatric cardiovascular services incurs very low cost and risk of harm. Future studies in larger populations and across a broad range of newborn delivery systems are needed to determine whether this practice should become standard of care in the routine assessment of the neonate.
Background
Changes in energy substrate metabolism are first responders to hemodynamic stress in the heart. We have previously shown that hexose‐6‐phosphate levels regulate mammalian target of ...rapamycin (mTOR) activation in response to insulin. We now tested the hypothesis that inotropic stimulation and increased afterload also regulate mTOR activation via glucose 6‐phosphate (G6P) accumulation.
Methods and Results
We subjected the working rat heart ex vivo to a high workload in the presence of different energy‐providing substrates including glucose, glucose analogues, and noncarbohydrate substrates. We observed an association between G6P accumulation, mTOR activation, endoplasmic reticulum (ER) stress, and impaired contractile function, all of which were prevented by pretreating animals with rapamycin (mTOR inhibition) or metformin (AMPK activation). The histone deacetylase inhibitor 4‐phenylbutyrate, which relieves ER stress, also improved contractile function. In contrast, adding the glucose analogue 2‐deoxy‐d‐glucose, which is phosphorylated but not further metabolized, to the perfusate resulted in mTOR activation and contractile dysfunction. Next we tested our hypothesis in vivo by transverse aortic constriction in mice. Using a micro‐PET system, we observed enhanced glucose tracer analog uptake and contractile dysfunction preceding dilatation of the left ventricle. In contrast, in hearts overexpressing SERCA2a, ER stress was reduced and contractile function was preserved with hypertrophy. Finally, we examined failing human hearts and found that mechanical unloading decreased G6P levels and ER stress markers.
Conclusions
We propose that glucose metabolic changes precede and regulate functional (and possibly also structural) remodeling of the heart. We implicate a critical role for G6P in load‐induced mTOR activation and ER stress.
The purpose of this statement is to address the state of evidence on the routine use of pulse oximetry in newborns to detect critical congenital heart disease (CCHD).
A writing group appointed by the ...American Heart Association and the American Academy of Pediatrics reviewed the available literature addressing current detection methods for CCHD, burden of missed and/or delayed diagnosis of CCHD, rationale of oximetry screening, and clinical studies of oximetry in otherwise asymptomatic newborns. MEDLINE database searches from 1966 to 2008 were done for English-language papers using the following search terms: congenital heart disease, pulse oximetry, physical examination, murmur, echocardiography, fetal echocardiography, and newborn screening. The reference lists of identified papers were also searched. Published abstracts from major pediatric scientific meetings in 2006 to 2008 were also reviewed. The American Heart Association classification of recommendations and levels of evidence for practice guidelines were used. In an analysis of pooled studies of oximetry assessment performed after 24 hours of life, the estimated sensitivity for detecting CCHD was 69.6%, and the positive predictive value was 47.0%; however, sensitivity varied dramatically among studies from 0% to 100%. False-positive screens that required further evaluation occurred in only 0.035% of infants screened after 24 hours.
Currently, CCHD is not detected in some newborns until after their hospital discharge, which results in significant morbidity and occasional mortality. Furthermore, routine pulse oximetry performed on asymptomatic newborns after 24 hours of life, but before hospital discharge, may detect CCHD. Routine pulse oximetry performed after 24 hours in hospitals that have on-site pediatric cardiovascular services incurs very low cost and risk of harm. Future studies in larger populations and across a broad range of newborn delivery systems are needed to determine whether this practice should become standard of care in the routine assessment of the neonate.
Protecting the Heart of the American Athlete Lawless, Christine E., MD, FACC, FACSM; Asplund, Chad, MD, FACSM; Asif, Irfan M., MD ...
Journal of the American College of Cardiology,
11/2014, Volume:
64, Issue:
20
Journal Article
Peer reviewed
Open access
The American College of Cardiology (ACC) Sports and Exercise Cardiology Section convened the "Think Tank to Protect the Heart of the American Athlete and Exercising Individual" on October 18, 2012, ...in Washington, DC.\n Asif University of Tennessee Family and Sports Medicine--Assistant Professor; Fellowship Director, Sports Medicine None None None None None None Ron Courson University of Georgia--Senior Associate Athletic Director None None None None None None Michael S. Emery Carolina Cardiology Consultants None None None None None None Anthon R, Fuisz Medstar Washington Hospital Center-Director, Cardiac MRI None None None None None None Richard J. Kovacs Krannert Institute of Cardiology-Professor of Clinical Medicine Biomedical Systems Insight Pharmaceuticals Theravancedagger Xenoport None None Biotie (DSMB) Eli Lilly (DSMB)dagger Cook Incorporated Med Institutedagger None Silvana M. Lawrence Baylor College of Medicine--Associate Professor, Department of Pediatrics, Section of Cardiology None None None None None None Benjamin D. Levine Institute for Exercise and Environmental Medicine None None None None None Defendant, 2013, Postural Orthostatic Tachycardia Syndrome Mark S. Link Tufts Medical Center None None None None None None Matthew W. Martinez Lehigh Valley Health Network None None None None None None G. Paul Matherne University of Virginia Health Sciences Center-Division Chief of Pediatric Cardiology None None None None None None Brian Olshansky University of Iowa Hospitals-Professor of Medicine Arrhythmia Grand Roundslow * BioControl Boehringer Ingleheim Boston Scientific (guidant) Combined Medicare Medicaid Services Daiichi Sankyo Gerson Lehman Medtronicdagger Sanofi Aventis None None Amarin (DSMB) Boston Scientific (DSMB) Sanofi Aventis (DSMB) Boston Scientific Executive Health Resourcesdagger Thompson Reuterslow * Defendant, 2013 Event Monitors Third Party, 2012, Cardiac Arrest William O. Roberts University of Minnesota Medical School-Professor, Department of Family Medicine and Community Health None None None None None None Lisa Salberg Hypertrophic Cardiomyopathy Association-Chief Executive Officer None None None None None None Victoria L. Vetter Children's Hospital of Philadelphia Division of Cardiology-Professor of Pediatrics None None None None None None Robert A. Vogel University of Colorado-Professor of Medicine Pritikin Longevity Center National Football Leaguedagger None None Sanofidagger None None Jim Whitehead American College of Sports Medicine-Executive Vice President/Chief Executive Officer * This table represents all relationships of committee members with industry and other entities that were reported by authors, including those not deemed to be relevant to this document, at the time this document was under development.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
It was investigated how A
1
‐adenosine receptor overexpression alters the effects of carbachol on force of contraction and beating rate in isolated murine atria. Moreover, the influence of pertussis ...toxin on the inotropic and chronotropic effects of adenosine and carbachol in A
1
‐adenosine receptor overexpressing atria was studied.
Adenosine and carbachol alone exerted negative inotropic and chronotropic effects in electrically driven left atrium or spontaneously beating right atrium of wild‐type mice.
These effects were abolished or reversed by pre‐treatment of animals with pertussis toxin which can interfere with signal transduction through G‐proteins.
Adenosine and carbachol exerted positive inotropic but negative chronotropic effects in atrium overexpressing A
1
‐adenosine receptors from transgenic mice.
The positive inotropic effects of adenosine and carbachol were qualitatively unaltered whereas the negative chronotropic effects were abolished or reversed in atrium overexpressing A
1
‐adenosine receptors after pre‐treatment by pertussis toxin.
Qualitatively similar effects for adenosine and carbachol were noted in the presence of isoprenaline, β‐adrenoceptor agonist.
It is concluded that overexpression of A
1
‐adenosine receptors also affects the signal transduction of other heptahelical, G‐protein coupled receptors like the M‐cholinoceptor in the heart. The chronotropic but not the inotropic effects of adenosine and carbachol in transgenic atrium were mediated
via
pertussis toxin sensitive G‐proteins.
British Journal of Pharmacology
(2003)
138
, 209–217. doi:
10.1038/sj.bjp.0705012
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