Fitness and the Development of Atrial Fibrillation
Author(s) -
Advay G. Bhatt,
Kevin M. Monahan
Publication year - 2015
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.115.016596
Subject(s) - atrial fibrillation , medicine , cardiology , coronary artery disease , heart failure , incidence (geometry) , optics , physics
The beneficial effect of exercise on most aspects of cardiovascular disease is well established with a salutary effect on the incidence of coronary artery disease (CAD), congestive heart failure, and premature death in those who participate in regular physical activity.1,2 This effect becomes apparent with moderate increases in activity without a defined upper limit of toxicity. For cardiac arrhythmias, atrial fibrillation (AF) in particular, the story appears more complex. In fact, only limited studies have been published on the beneficial effect of physical activity on AF, whereas a number of case-control studies have emphasized the deleterious effect of exercise when performed at sustained high levels.3,4Article see p 1827The pathophysiology of AF is highly heterogeneous and complex. Among the contributing clinical factors that lead to the development and progression of AF are advanced age, left ventricular dysfunction, valvular disease, CAD, diabetes mellitus, and hypertension.1 These physiological stressors alter the normal electrophysiological substrate of a small, rapidly conducting, uniformly repolarizing medium through fibrosis, inflammation, oxidation, and altered ion channel physiology to one adversely remodeled to support re-entry and repetitive pulmonary vein and atrial firing.5,6The extent of structural and electric remodeling of the atria generally becomes apparent only once AF is clinically established. By that point, risk factor (RF) modification may reduce the frequency and duration of AF paroxysms and theoretically may slow the progression to a more persistent pattern, but maintenance of sinus rhythm requires an ablative or pharmacological approach to make the atrial milieu less favorable for AF. Promising developments in imaging and therapeutic energy delivery to target the atrial substrate supporting AF7 have recently advanced the former, whereas antiarrhythmic drug development has been highly disappointing for longer than the last 2 decades. Despite these advances in …
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom