Mechanisms of clinical XXXX .

@entity1 @entity2917 @entity1165 @entity137 @entity591 @entity3153 @entity943
Animal data suggest that @entity943 can result from a variety of mechanisms. In clinical settings, @entity943 that are easily initiated and terminated with programmed electrical stimulation are often designated as @entity591 . However, proof of reentry is contingent upon demonstration of the entire circuit; this relation has been proposed for @entity943 associated with large circuits, such as those seen in the @entity3153 . Reentry has also been proposed as the mechanism responsible for a variety of other @entity591 , including bundle branch and @entity2917 , permanent junctional reentrant @entity591 , reentry @entity591 associated with nodoventricular Mahaim fibers and inducible atrial and @entity1165 . Documentation of triggered rhythms as the mechanism responsible for clinical @entity943 has been even more difficult. Examples of @entity943 resulting from triggered activity may include those associated with @entity137 arising from the atria, the atrioventricular junction or the ventricles. Clinical @entity943 due to triggered activity in the absence of digitalis have also been described. @entity943 that cannot be induced by electrical stimulation are presumably due to normal or abnormal automaticity. Examples of normal automaticity in the @entity1 heart are sinus rhythm and junctional and idioventricular escape rhythms. @entity591 by abnormal automaticity have seldom been investigated for the purpose of documenting the mechanism and therefore the limited data available make it difficult to draw any final conclusions.
