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Atrial Ultrastructural Remodeling. Introduction:Atrial structural and electrophysiologic changes occur during atrial tachycardia. The role of high ventricular rate in these processes remains to be established.Methods and Results:Six goats were subjected to 4 weeks of rapid atrioventricular (AV) pacing at an atrial and ventricular rate of 240 beats/min, resulting in development of congestive heart failure. In another five goats, AV block was created. These goats then were subjected to 4 weeks of atrial pacing, also at 240 beats/min while the ventricular rate was kept low and regular at 80 beats/min (A-paced). Pacing was interrupted only for measurement of atrial effective refractory period and right atrial diameter. The ultrastructure of both atria was examined by light and electron microscopy, including quantification of the percentage of atrial extracellular matrix (%ECM). A group of six goats served as controls. In the AV-paced group, severe structural remodeling occurred in the atria, including severe loss of sarcomeres, glycogen accumulation, disruption of sarcoplasmic reticulum, and appearance of numerous small mitochondria and nuclei with homogeneously distributed chromatin. In contrast, structural changes were virtually absent in the atria of A-paced goats. Only a redistribution of nuclear chromatin and the appearance of numerous mitochondria were observed. The ultrastructure was normal in control animals. The%ECM was increased in AV-paced goats (29%) compared to A-paced animals (18%) and controls (17%) (P<0.05). Finally, right atrial diameter increased by 51% in AV-paced goats but was unchanged in A-paced goats (P<0.05). In both experimental groups, atrial effective refractory period shortened during pacing.Conclusion:Structural remodeling during chronic atrial tachycardia is related to the concomitant presence of a high ventricular rate and hence the occurrence of congestive heart failure rather than a high atrial rate. Electrical remodeling can occur in the absence of significant structural changes.(J Cardiovasc Electrophysiol, Vol. 15, pp. 1167-1174, October 2004) [ABSTRACT FROM AUTHOR]

It is well known that atrial tachycardia causes atrial electrical remodeling, characterized by shortening of atrial effective refractory periods (AERPs) and loss of physiological adaptation of AERP to rate. However, the nature and time course of changes in ventricular effective refractory periods (VERP) caused by rapid rates are to be established. After being instrumented with epicardial electrodes on both atria and both ventricles nine goats were subjected to 1 week of rapid AV pacing with a rate of 240 beats/min and an AV delay of 100 ms. Pacing was only interrupted for measurement of left and right AERPs and VERPs at three basic cycle lengths (BCL) of 400 ms, 300 ms, and 200 ms during sinus rhythm in the conscious animal. Left and right AERPs decreased at all BCLs, reaching minimum values after 3 days (right AERP at RCL of 400 ms, 96 ± 16 ms after 3 days vs 144 ± 16 ms at baseline, P < 0.05). In contrast, both left and right VERPs did not change at any BCL. This study demonstrates a difference between the atria and ventricles with respect to tachycardia induced changes in refractoriness. [ABSTRACT FROM AUTHOR]

Introduction: Atrial fibrillation (AF) and congestive heart failure (CHF) are two clinical entities that often coincide. Our aim was to establish the influence of concomitant high ventricular rate and consequent development of CHF on electrical remodeling and dilation during atrial tachycardia. Methods and Results: A total of 14 goats was studied. Five goats were subjected to 3:1 AV pacing (A-paced group, atrial rate 240 beats/min, ventricular rate 80 beats/min). Nine goats were subjected to rapid 1:1 AV pacing (AV-paced group, atrial and ventricular rates 240 beats/min). During 4 weeks, right atrial (RA) and left ventricular (LV) diameters were measured during sinus rhythm. Atrial effective refractory periods (AERP) and Inducibility of AF were assessed at three basic cycle lengths (BCL). After 4 weeks of rapid AV pacing, RA and LV diameters had increased to 151% and 113% of baseline, whereas after rapid atrial pacing alone, these parameters were unchanged. Right AERP (157 ± 10 msec vs 144 ± 16 msec at baseline with BCL of 400 msec in the A-paced and AV-paced group, respectively) initially decreased in both groups, reaching minimum values within 1 week. Subsequently, AERP partially recovered in AV-paced goats, whereas AERP remained short in A-paced goats (79 ± 7 msec vs 102 ± 12 msec after 4 weeks; P < 0.05). Left AERP demonstrated a similar time course. Inducibility of AF increased in both groups and reached a maximum during the first week in both groups, being 20% and 48% in the A-paced and AV-paced group, respectively. Conclusion: Nature and time course of atrial electrical remodeling and dilation during atrial tachycardia are influenced by concurrent high ventricular rate and consequent development of CHF. [ABSTRACT FROM AUTHOR]