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.
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.
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