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This study will examine the effect of detraining as a clinical tool to prevent recurrence of lone paroxysmal atrial fibrillation (AF) and improve quality of life. Persons who engage in endurance activity with AF will be randomly assigned to undergo an 8-week period of detraining or encouraged to maintain their current level of exercise. Participants will receive a handheld device called AliveCor that can record an electrical tracing of the heart rhythm by pressing down with ones' thumbs. The amount of arrhythmia and symptoms will be recorded. The research team hypothesizes that among athletes with lone AF, an 8-week period of detraining will not affect atrial fibrillation recurrence or quality of life.
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Atrial fibrillation (AF) is the most common tachyarrhythmia amongst athletes. Atrial fibrillation is associated with poor subjective health among Masters athletes, and negatively interferes with athlete's sporting activities. The decrease in physical performance during AF episodes is attributed to the loss of atrial contribution to cardiac output related to irregular and decreased diastolic filling, and loss of sympathetic and parasympathetic control over heart rate.
There is a paucity of studies that examine the role of exercise in the treatment of atrial fibrillation among athletes. Detraining is the deliberate act of reducing volume of exercise to observe subsequent changes in cardiac indices over time or the partial or complete loss of training of induced anatomical, physiological and performance adaptions. Detraining is primarily employed as a diagnostic tool to help differentiate Athletes' heart from cardiac pathology. The role of detraining as a therapeutic modality is ill-defined and not well studied. There is a dearth of studies that examine the role of exercise in the treatment of atrial fibrillation among athletes. To date, only two observational studies (Furlanello and Hoogsteen) have suggested detraining as a potential treatment for AF among athletes. It is important to note the limitations of these studies: 1) observational study design 2) athletes were not systematically instructed to decrease exercise volume or 'detrain' 3) AF was not objectively assessed 4) pre and post measures of QOL were not recorded AF. Hoogsteen et al., surveyed 30 athletes about exercise and AF symptomatology at the time of diagnosis and 9 years later. At the time of the survey 30% of athletes noted a reduction in bouts of AF with a decrease in sporting activity. However, 43% of the athletes did not notice any relationship between reduction in activity and AF recurrence. This study was limited by the small sample size, selection bias due to symptomatic athletes responding, and AF recurrence based solely on subjective responses.
Detraining has been shown to decrease premature ventricular contractions (PVCs) and non-sustained ventricular tachycardia (NSVT) burden amongst elite athletes. After a 3-month detraining period, PVCs and NSVT decreased by eighty and ninety percent, respectively. The same group of athletes experienced a prolonged suppression of PVCs and NSVT at 1-year after retraining. While detraining is often suggested to athletes with AF, there is little evidence to support this practice. To date, only small case series and individual case reports exist.
This study aims to examine the effect of detraining as a clinical tool to prevent recurrence of lone paroxysmal AF (with no traditional AF risk factors and a structurally normal heart) and improve quality of life. Persons who engage in endurance activity with AF will be randomly assigned to undergo a 10-week period of detraining or encouraged to maintain their current level of exercise. Participants will receive a (1x 2.5 inch) handheld device called AliveCor that can record an electrical tracing of the heart rhythm by pressing down with ones' thumbs. The amount of arrhythmia and symptoms will be recorded. The research team hypothesizes that among athletes with lone AF, a 10-week period of detraining will not affect atrial fibrillation recurrence or quality of life.
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73 participants in 2 patient groups
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James McKinney, MD
Data sourced from clinicaltrials.gov
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