Control of XXXX by @entity460 antagonism.

@entity1165 @entity7220 @entity19346 @entity1855 @entity4473 @entity714 @entity3361 @entity944 @entity299 @entity3988 @entity591 @entity8633 @entity460 @entity955 @entity741 @entity583 @entity943
In recent years @entity460 channel blockers have emerged as a new class of antiarrhythmic agents for the control of certain supraventricular and @entity943 . Electrophysiologically, they are heterogeneous but their main action is mediated through a depressant effect on the slow @entity460 channel in cardiac muscle. In isolated muscle, their actions are modulated by their reflex actions and by their interaction with the autonomic nervous system due to the nonocompetitive adrenergic blocking actions that some of the compounds exhibit. The major agents exerting antiarrhythmic actions are @entity1855 , @entity3988 , @entity4473 , @entity7220 , and @entity8633 ; the @entity19346 are devoid of significant electrophysiologic actions in vivo. @entity460 antagonists prolong intranodal conduction time, lengthen the effective and functional refractory periods in the AV node, but exert little or no effect on atrial, ventricular, His-Purkinje, or bypass tract conduction or refractoriness (except in the case of @entity8633 , which has additional electrophysiologic properties). These effects form the basis of the clinical antiarrhythmic effects of this class of agents. The most striking action is the predictable and prompt termination of reentrant supraventricular @entity591 by intravenous @entity1855 and @entity3988 and the slowing of the ventricular response in @entity955 . These agents may also be of value in the chronic control of ventricular response in @entity955 ; their role in multifocal @entity591 and other @entity591 is less well defined. @entity460 antagonists reverse ischemic @entity943 due to @entity3361 but exert little or no action in the usual forms of sustained @entity1165 associated with severe structural @entity299 . They are poor suppressants of premature ventricular contractions. Recent data have established their role in exercise-induced @entity591 occurring in the context of @entity741 ; they are also of value in @entity1165 occurring in young subjects developing @entity591 with a @entity714 with left axis deviation morphology, an @entity943 thought to be due to triggered automaticity. The role of @entity460 antagonists in reducing the incidence of @entity944 in the survivors of acute @entity583 remains uncertain.
