Irregular Micro-motion Period Measurement: Reentry Boosters as a Case Study
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The mechanisms responsible for active cardiac arrhythmias are generally divided into two major categories: (1) enhanced or abnormal impulse formation and (2) reentry. Reentry can be subdivided into three subcategories: (1) circus movement, (2) reflection, and (3) Phase 2 reentry. Reentry occurs when a propagating impulse fails to die out after normal activation of the heart and persists to re-excite the heart after expiration of the refractory period. Evidence implicating reentry as a mechanism of cardiac arrhythmias stems back to the turn of the century. Amplification of intrinsic electrical heterogeneities provides the substrate responsible for developing Phase 2 and circus movement reentry, which underlie ventricular tachycardia in the long QT and Brugada syndromes.
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In five patients, bundle of His electrograms were recorded during right ventricular pacing at various cycle lengths. In all patients, as the cycle length of stimulation was decreased, the pattern of retrograde conduction proceeded from 1:1 retrograde conduction to retrograde Wenckebach with or without manifest reentry, to retrograde Wenckebach cycles with concealed reentry. The requisite condition for reentry was a critical retrograde A-V nodal delay. During retrograde Wenckebach cycles, reentry could be either concealed or manifest. Concealed reentry resulted in typical or ordinary Wenckebach cycles on the surface electrocardiogram and manifest reentry resulted in ventricular echo beats. Depending upon the cycle length of stimulation, reentry could be concealed on the surface electrocardiogram but manifest on the His bundle electrogram recording. Concealed reentry could be manifest by turning off the stimulator at the appropriate time in the cardiac cycle while manifest reentry could be concealed by changing the cycle length of stimulation. Reentry with collision of wavefronts within the A-V node or proximal His-Purkinje conduction system explains why the last ventricular impulse is not conducted to the atria during ordinary Wenckebach cycles.
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Reentry corridor defines an reentry zone where the vehicle can fulfill flying mission and reenter the Earth safely,which is an important part of reentry trajectory optimization,reentry design and fly mission.In this paper,Chapman assumptions and dynamics model of reentry are introduced,and reentry corridor of vehicle from space is studied.The important points effecting reentry corridor boundary are introduced,the result proves the effectiveness of the analysis.
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Reentry within the right bundle branch which, to our knowledge is a hitherto undescribed mechanism of His‐Purkinje reentry in man, was elicited during programmed right ventricular stimulation. Electrophysiologic analysis excluded atrioventricular nodal reentry. His bundle reentry, reentry involving both bundle branches, and intraventricular micro‐reentry.
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It is well known that the reentry or circus movement is one of important mechanisms underlying the generation of arrhythmias. This is recently clasified into three category such as ordered reentry which means circus movement in an anatomically defined pathway, random reentry which means circus movement without the involvement of an anatomic obstracle and reflected reentry which does not require the reentrant circuit. In this article I describe some recent progress in studies on designed to present the characteristics of the circus movement. On the theoretical considerations, the reentry has been regularly explained for by terms such as conduction velocity (V), refractory period (R) and length of circuit (L). Basic contribution of appearance of reentry in heart tissue needs the following conditions : (1) slow conduction (2) shortening of refractory period and (3) existence of unidirectional block. The reflected reentry which does not require the circuitous pathway and unidirectional block complexed the conception of reentry itself. On the other hand, experimental technique used to investigate mechanism of arrhythmias including simulations were developed to document the spread of activation in the heart tissues. Simultaneous multi-recordings display the sequence of reentry in pathological conditions. However, direct evidence of reentry is very rare in clinical fields. Moreover, there is no complete methods distinguishing reentry from other mechanism such as abnormal automaticity. The progress in this field is expected.
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We have studied the dynamics of reentry inside the SAN. We have found that reentry is unstable at high intercellular conductance. Rotating reentry induces a slow migrating crescent-shaped functional block near the boundary of the SAN. An abnormal conduction from atrial tissue into the SAN occurs after decay of the reentry. ACh increases lifespan of the reentry in the SAN.
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