2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities

Tracy, Cynthia M.; Darbar, Dawood; DiMarco, John P.; Dunbar, Sandra B.; Estes, N.A. Mark; Ferguson, T. Bruce; Hammill, Stephen C.; Karasik, Pamela; Link, Mark S.; Marine, Joseph E.; Schoenfeld, Mark H.; Shanker, Asheesh; Silka, Michael J.; Stevenson, Lynne Warner; Stevenson, William G.; Varosy, Paul D.; Epstein, Andrew E.; Ellenbogen, Kenneth A.; Freedman, Roger A.; Gettes, Leonard S.; Gillinov, A. Marc; Gregoratos, Gabriel; Hayes, David L.; Hlatky, Mark A.; Newby, L. Kristin; Page, Richard L.; Sweeney, Michael O.; Anderson, Jeffrey L.; Jacobs, Alice K.; Halperin, Jonathan L.; Albert, Nancy M.; Creager, Mark A.; DeMets, David L.; Ettinger, Steven M.; Guyton, Robert A.; Hochman, Judith S.; Kushner, Frederick G.; Ohman, E. Magnus; Yancy, Clyde W.

doi:10.1016/j.jtcvs.2012.08.032

Cited by 43 publications

(11 citation statements)

References 68 publications

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“…They have been successfully used for more than 50 years with continuous refinement (1), but are limited in some instances by complications ranging from inadequate autonomic support to lead fracture, infections, and adverse cardiac remodeling (2, 3). Biological pacemakers—that is, pacemakers that are created by cell or gene therapy—have been developed with the ultimate goal of replacing electronic devices.…”

Section: Introductionmentioning

confidence: 99%

Biological pacemaker created by minimally invasive somatic reprogramming in pigs with complete heart block

Dawkins²,

Cho³

et al. 2014

Sci. Transl. Med.

161

170

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Somatic reprogramming by reexpression of the embryonic transcription factor T-box 18 (TBX18) converts cardiomyocytes into pacemaker cells. We hypothesized that this could be a viable therapeutic avenue for pacemaker-dependent patients afflicted with device-related complications, and therefore tested whether adenoviral TBX18 gene transfer could create biological pacemaker activity in vivo in a large-animal model of complete heart block. Biological pacemaker activity, originating from the intramyocardial injection site, was evident in TBX18-transduced animals starting at day 2 and persisted for the duration of the study (14 days) with minimal backup electronic pacemaker use. Relative to controls transduced with a reporter gene, TBX18-transduced animals exhibited enhanced autonomic responses and physiologically superior chronotropic support of physical activity. Induced sinoatrial node cells could be identified by their distinctive morphology at the site of injection in TBX18-transduced animals, but not in controls. No local or systemic safety concerns arose. Thus, minimally invasive TBX18 gene transfer creates physiologically relevant pacemaker activity in complete heart block, providing evidence for therapeutic somatic reprogramming in a clinically relevant disease model.

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Section: Introductionmentioning

confidence: 99%

Biological pacemaker created by minimally invasive somatic reprogramming in pigs with complete heart block

Dawkins²,

Cho³

et al. 2014

Sci. Transl. Med.

161

170

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“…[126][127][128][129] In 2012, an ACC Foundation/AHA/Heart Rhythm Society (HRS) task force updated guidelines for device-based therapy of cardiac rhythm abnormalities. 130 Patients with CHD were not a specifically included subgroup, but it is likely that many aspects of the recommendations are relevant to the CHD population, despite the absence of data. Similar caution must be applied in regard to extrapolation, as discussed above in terms of HF therapies.…”

Section: -113mentioning

confidence: 99%

“…Conventional approaches for device implantation can be used per available consensus guideline statements for determining indications for pacemaker, ICD, and CRT, including the 2012 ACC Foundation/ AHA/HRS update on device-based therapy. 130,132 The key challenge in the management of obstructive defects in CHD is determining the timing of intervention.…”

Section: Device Therapymentioning

confidence: 99%

“…131 Because device implantation in those with CHD can be technically challenging, these procedures are best performed at a CHD center by an electrophysiologist or cardiac surgeon with expertise in CHD. The 2012 ACC Foundation/AHA/HRS task force 130 update on device-based therapy forms a basic primer for medical device use in adults and children with HF and states the following:…”

mentioning

confidence: 99%

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Chronic Heart Failure in Congenital Heart Disease

Stout¹,

Broberg²,

Book³

et al. 2016

Circulation

287

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“…1 Patients with symptomatic bradycardia not responsive to other measures such as deconditioning or the withholding of nonessential medications that are contributing to the bradycardia may need to be treated with a permanent pacemaker, although this is very rarely needed in the athlete. 2,3 Recommendations 1. Athletes with sinus bradycardia, sinus exit block, sinus pauses, and sinus arrhythmia without symptoms can participate in all competitive athletic activities unless otherwise excluded by underlying structural heart disease or other arrhythmias (Class I; Level of Evidence C).…”

Section: Circulationmentioning

confidence: 99%

Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 9: Arrhythmias and Conduction Defects

Zipes¹,

Link²,

Ackerman³

et al. 2015

Circulation

Self Cite

129

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A broad range of variations in heart rates and rhythms, specific cardiac arrhythmias, and atrioventricular (AV) and intraventricular conduction disturbances are observed in athletes. Although most are common among nonathletes as well, the special circumstances and pressures related to athletic performance demand a high level of attention. The distinction between normal variants, often exaggerated by the specific physiology of the conditioned athlete, and arrhythmias that may be symptomatic or life-threatening may be significant challenges. Bradycardia Sinus BradycardiaSinus bradycardia, defined as a sinus rate <60 beats per minute (bpm), is common in the athlete.1 Generally, it is attributed to enhanced vagal tone caused by conditioning and is thus physiological. Occasionally, heart rates can be as slow as 30 to 40 bpm at rest in the highly conditioned athlete and decrease to <30 bpm during sleep. Some athletes with marked sinus bradycardia will exhibit periods of low atrial or junctional escape rhythms with rates of 40 to 60 bpm. This is a normal phenomenon, and these will become suppressed with exercise-induced increases in the sinus rate.Evaluation of the athlete with sinus bradycardia includes a careful history to determine whether the athlete has symptoms related to the bradycardia. In addition, physical examination and an ECG are warranted, with selective use of additional tests such as an echocardiogram and exercise stress test if underlying structural heart disease is suggested. Stress testing can also be used to verify a normal rate response to exercise, if judged to be necessary. The same approach applies to the sinus arrhythmia commonly observed in the athlete. Generally, asymptomatic sinus pauses or sinus arrest (<3 seconds) are not considered clinically significant unless accompanied by symptoms. Pauses of longer duration may fall within the spectrum of physiological responses to athletic conditioning; however, when accompanied by symptoms, sinus bradycardia, The American Heart Association and the American College of Cardiology make every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.The Preamble and other Task Force reports for these proceedings are available online at http://circ.ahajournals.org (Circulation. 2015;132:e256-e261; e262-e266; e267-e272; e273-e280; e281-e291; e292-e297; e298-e302; e303-e309; e310-e314; e326-e329; e330-e333; e334-e338; e339-e342; e343-e345; and e346-e349).This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on June 24, 2015, and the American Heart Association Executive Committee on July 22, 2015, and by the American College of Cardiology Board of Trustees and Ex...

show abstract

2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities

Cited by 43 publications

References 68 publications

Biological pacemaker created by minimally invasive somatic reprogramming in pigs with complete heart block

Biological pacemaker created by minimally invasive somatic reprogramming in pigs with complete heart block

Chronic Heart Failure in Congenital Heart Disease

Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 9: Arrhythmias and Conduction Defects

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