Participation of atrial specialized conduction pathways in atrial flutter.

Pastelín, Gustavo; Méndez, Rafael; Moe, Gordon K.

doi:10.1161/01.res.42.3.386

Cited by 43 publications

(7 citation statements)

References 39 publications

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“…Their maps suggest that an area of depressed conduction at the area of the tuberculum intervenosum was the pathologic substrate for atrial flutter. We also failed to find evidence for the suggestion made by Pastelin et al 24 that the so-called specialized internodal pathways play an important role in the genesis and maintenance of circus movement flutter.…”

Section: Discussioncontrasting

confidence: 98%

Intra-atrial reentry as a mechanism for atrial flutter induced by acetylcholine and rapid pacing in the dog.

Allessie¹,

Lammers²,

Bonke³

et al. 1984

Circulation

267

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In the isolated blood-perfused canine heart we produced episodes of rapid atrial flutter by continuous infusion of acetylcholine and rapid pacing. The spread of excitation during atrial flutter was mapped with the aid of two endocavitary mapping electrodes containing 960 leads and recording from 192 different sites simultaneously. The flutter maps clearly showed that intra-atrial reentry was the mechanism responsible for the arrhythmia. However, the localization and size of the intra-atrial circuits differed from case to case even in the same heart. The orifices of the venae cavae or the atrioventricular ring did not serve as a central anatomic obstacle for circus movement. We also failed to identify a special role of the intemodal pathways in the formation of the loop. Instead, the intra-atrial circuits could be found everywhere, provided sufficient atrial mass was available to accommodate the circuit. The diameter of the circuits varied between 1.5 and 3 cm at a cycle length between 65 and 155 msec. The average conduction velocity of the circulating impulse varied between 60 and 80 cm/sec. Spontaneous termination of atrial flutter frequently occurred and was based on local conduction block in a narrow part of the circuit. Another interesting aspect of these studies is the finding that during continuous circus movement of the impulse, the amount of myocardium that is activated may vary considerably. This marked periodicity in excited tissue mass during atrial flutter could adequately explain the continuously undulating baseline or typical sawtoothlike F waves as seen in the surface electrocardiogram during atrial flutter. Circulation 70, No. 1, 123-135, 1984. THE EXACT MECHANISMS underlying atrial flutter in human beings are still unknown. Detailed clinical studies with intracavitary and intraesophageal leads and programmed electrical stimulation have not resulted in the identification of a single mechanism of human atrial flutter. The results of some studies were explained by assuming the presence of an ectopic focus of abnormal impulse formation, -5 whereas other investigations point to a circus movement involving a large part of the atria.3' 61 Extensive epicardial mapping of the atria in patients with atnal flutter who are subjected to cardiac surgery could be an excellent and direct way to evaluate this condition. However, such studies have been scarce and do not yet allow general conclusions. 12

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Section: Discussioncontrasting

confidence: 98%

Intra-atrial reentry as a mechanism for atrial flutter induced by acetylcholine and rapid pacing in the dog.

Allessie¹,

Lammers²,

Bonke³

et al. 1984

Circulation

267

View full text Add to dashboard Cite

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“…This could correspond to initially left-sided location of the earliest pacemaker described by Kamino and associates (17,23) and, later on, the ring-like shape of the sinus venosus (30) that serves as a pacemaker. Normally, this activity is ultimately reorganized to the rightsided node, but occasional persistence of pacemaking tissues on the left side, including the orifice of the pulmonary vein(s), was attributed to atrial arrhythmias (31).…”

Section: Discussionmentioning

confidence: 99%

Changes in activation sequence of embryonic chick atria correlate with developing myocardial architecture

Sedmera

Wessels²,

Trusk³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Changes in activation sequence of embryonic chick atria correlate with developing myocardial architecture. Am J Physiol Heart Circ Physiol 291: H1646 -H1652, 2006. First published May 5, 2006 doi:10.1152/ajpheart.01007.2005.-To characterize developmental changes in impulse propagation within atrial musculature, we performed high-speed optical mapping of activation sequence of the developing chick atria using voltage-sensitive dye. The activation maps were correlated with detailed morphological studies using scanning electron microscopy, histology, and whole mount confocal imaging with three-dimensional reconstruction. A preferential pathway appeared during development within the roof of the atria, transmitting the impulse rapidly from the right-sided sinoatrial node to the left atrium. The morphological substrate of this pathway, the bundle of Bachman, apparent from stage 29 onward, was a prominent ridge of pectinate muscles continuous with the terminal crest. Further acceleration of impulse propagation was noted along the ridges formed by the developing pectinate muscles, ramifying from the terminal crest toward the atrioventricular groove. In contrast, when the impulse reached the interatrial septum, slowing was often observed, suggesting that the septum acts as a barrier or sink for electrical current. We conclude that these inhomogeneities in atrial impulse propagation are consistent with existence of a specialized network of fast-conducting tissues. The purpose of these preferential pathways appears to be to assure synchronous atrial activation and contraction rather than rapid impulse conduction between the sinoatrial and atrioventricular nodes. chick embryo; optical mapping; conduction system; internodal pathways; pectinate muscles THE SPECIALIZED CONDUCTION tissues mediate coordinated propagation of electrical activity through the adult vertebrate heart. Although the ventricular component of the conduction system (His bundle, bundle branches, and Purkinje fibers) is relatively well characterized (reviewed in Ref. 14), controversy persists about the existence and even definition of specialized fastconducting tissues within the atria (21). Inhomogeneities in conduction properties of atrial tissues are widely recognized and are believed to be largely due to structural characteristics (18). The morphological substrate of so-called internodal conduction tracts (20) is less well defined, since these bundles do not satisfy the criteria set for specialized ventricular conduction tissues (1).Atrial conduction in adult human and animal hearts is well studied. Excitation starts in the sinoatrial node (or sinus venosus in the lower vertebrates) and propagates across the atrial roof in a generally radial manner, described as "waves produced when a stone is dropped into still water" (26). These "waves" are not perfectly concentric, since there are numerous "holes" in the atria where the veins enter (21), and spread of impulse appears to be faster along the main bundles of the pectinate muscles (2, 10, 26). In particu...

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“…Moreover, the risk of developing atrial fibrillation increases in patients with obesity and MeS [5] , [6] , [7] . Atrial fibrillation is the most common tachyarrhythmia associated with an increased morbidity and mortality [7] , [8] , [9] .…”

Section: Introductionmentioning

confidence: 99%

“…The precise mechanisms through which MeS causes atrial fibrillation are not completely understood, but the syndrome has been associated with electrical remodeling of the atrium and sinoatrial (SA) node [8] , [10] ; specifically, an increase in action potential duration and changes in the refractory period, as well as changes in the passive electrical properties in both tissues [11] , [12] , [13] .…”

Section: Introductionmentioning

confidence: 99%

Metabolic Syndrome Remodels Electrical Activity of the Sinoatrial Node and Produces Arrhythmias in Rats

et al. 2013

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In the last ten years, the incidences of metabolic syndrome and supraventricular arrhythmias have greatly increased. The metabolic syndrome is a cluster of alterations, which include obesity, hypertension, hypertriglyceridemia, glucose intolerance and insulin resistance, that increase the risk of developing, among others, atrial and nodal arrhythmias.The aim of this study is to demonstrate that metabolic syndrome induces electrical remodeling of the sinus node and produces arrhythmias. We induced metabolic syndrome in 2-month-old male Wistar rats by administering 20% sucrose in the drinking water. Eight weeks later, the rats were anesthetized and the electrocardiogram was recorded, revealing the presence of arrhythmias only in treated rats. Using conventional microelectrode and voltage clamp techniques, we analyzed the electrical activity of the sinoatrial node.We observed that in the sinoatrial node of “metabolic syndrome rats”, compared to controls, the spontaneous firing of all cells decreased, while the slope of the diastolic depolarization increased only in latent pacemaker cells. Accordingly, the pacemaker currents If and Ist increased. Furthermore, histological analysis showed a large amount of fat surrounding nodal cardiomyocytes and a rise in the sympathetic innervation. Finally, Poincaré plot denoted irregularity in the R-R and P-P ECG intervals, in agreement with the variability of nodal firing potential recorded in metabolic syndrome rats.We conclude that metabolic syndrome produces a dysfunction SA node by disrupting normal architecture and the electrical activity, which could explain the onset of arrhythmias in rats.

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Participation of atrial specialized conduction pathways in atrial flutter.

Cited by 43 publications

References 39 publications

Intra-atrial reentry as a mechanism for atrial flutter induced by acetylcholine and rapid pacing in the dog.

Intra-atrial reentry as a mechanism for atrial flutter induced by acetylcholine and rapid pacing in the dog.

Changes in activation sequence of embryonic chick atria correlate with developing myocardial architecture

Metabolic Syndrome Remodels Electrical Activity of the Sinoatrial Node and Produces Arrhythmias in Rats

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