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Double ventricular response via dual atrioventricular nodal pathways resulting in sustained supraventricular nonreentrant tachycardia
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22.
23. 24. 25.
L. Bacharova, E.H. Estes / Journal of Electrocardiology 42 (2009) 228–232 (LIFE) Reduction in Hypertension Study. Circulation 2006;113: 1588. Horan LG. Manifest orientation: the theoretical link between the anatomy of the heart and the clinical electrocardiogram. J Am Coll Cardiol 1987;9:1049. Mashima S. Theoretical considerations on the electrocardiogram of ventricular hypertrophy. J Electrocardiol 1976;9:133. Kleber AG, Rudy J. Basic mechanisms of cardiac impulse propagation and associated arrhythmias. Physiol Rev 2004;84:431. Spach MS, Heidlage JF, Dolber PC, Barr RC. Electrophysiological effects of remodeling cardiac gap junctions and cell size. Experimental and model studies of normal cardiac growth. Circ Res 2000;86:302.
26. Spach MS, Barr RC. Effects of cardiac microstructure on propagating electrical waveforms. Circ Res 2000;86:e23. 27. Tomaselli FG, Marban E. Electrophysiological remodeling in hypertrophy and heart failure. Cardiovasc Res 1999;42:270. 28. Nattel S, Li D. Ionic remodeling in the heart. Pathophysiological significance and new therapeutic opportunities for atrial fibrillation. Circ Res 2000;87:440. 29. Akazawa H, Komuro I. Roles of cardiac transcription factors in cardiac hypertrophy. Circ Res 2003;92:1079. 30. Abildskov JA, Green LS. The recognition of arrhythmia vulnerability by body surface electrocardiographic mapping. Circulation 1987;75 (Suppl III):III-79.
Double ventricular response via dual atrioventricular nodal pathways resulting in sustained supraventricular nonreentrant tachycardia
Fig. 1
Fig. 2
Supraventricular tachycardia caused by 1:2 atrioventricular conduction (atrial rate at a cycle length of about 680 milliseconds) was observed on the esophageal electrogram (Fig. 1), and double His bundle and ventricular responses was caused by simultaneous fast and slow AV nodal pathway conduction with each atrial wave (Fig. 2). The patient underwent successful slow pathway ablation with complete disappearance of symptoms and electrocardiographic manifestations of 1:2 AV conduction. Atrial fibrillation can be erroneously diagnosed in such patients when Wenckebach periodicity is present during fast and slow AV nodal pathway conduction (J Cardiovasc Electrophysiol. 2006;17:312.). Every sinus beat with concomitant junctional premature beat resulting in a bigeminal rhythm should be considered on the differential diagnosis of such a surface ECG, but consistent HV intervals and the satisfying results of slow pathway ablation make it untenable. ESO indicates esophagus electrogram; HRA, high right atrial electrogram; His, His bundle electrogram; CSp, proximal electrogram of coronary sinus; CSm, middle electrogram of coronary sinus; CSd, distal electrogram of coronary sinus. Zhan Zhong-qun, MS, Wang Chong-quan, MD, and Dang Shu-yi, MD Shiyan, Hubei Province, China doi:10.1016/j.jelectrocard.2008.07.015
22.
23. 24. 25.
L. Bacharova, E.H. Estes / Journal of Electrocardiology 42 (2009) 228–232 (LIFE) Reduction in Hypertension Study. Circulation 2006;113: 1588. Horan LG. Manifest orientation: the theoretical link between the anatomy of the heart and the clinical electrocardiogram. J Am Coll Cardiol 1987;9:1049. Mashima S. Theoretical considerations on the electrocardiogram of ventricular hypertrophy. J Electrocardiol 1976;9:133. Kleber AG, Rudy J. Basic mechanisms of cardiac impulse propagation and associated arrhythmias. Physiol Rev 2004;84:431. Spach MS, Heidlage JF, Dolber PC, Barr RC. Electrophysiological effects of remodeling cardiac gap junctions and cell size. Experimental and model studies of normal cardiac growth. Circ Res 2000;86:302.
26. Spach MS, Barr RC. Effects of cardiac microstructure on propagating electrical waveforms. Circ Res 2000;86:e23. 27. Tomaselli FG, Marban E. Electrophysiological remodeling in hypertrophy and heart failure. Cardiovasc Res 1999;42:270. 28. Nattel S, Li D. Ionic remodeling in the heart. Pathophysiological significance and new therapeutic opportunities for atrial fibrillation. Circ Res 2000;87:440. 29. Akazawa H, Komuro I. Roles of cardiac transcription factors in cardiac hypertrophy. Circ Res 2003;92:1079. 30. Abildskov JA, Green LS. The recognition of arrhythmia vulnerability by body surface electrocardiographic mapping. Circulation 1987;75 (Suppl III):III-79.
Double ventricular response via dual atrioventricular nodal pathways resulting in sustained supraventricular nonreentrant tachycardia
Fig. 1
Fig. 2
Supraventricular tachycardia caused by 1:2 atrioventricular conduction (atrial rate at a cycle length of about 680 milliseconds) was observed on the esophageal electrogram (Fig. 1), and double His bundle and ventricular responses was caused by simultaneous fast and slow AV nodal pathway conduction with each atrial wave (Fig. 2). The patient underwent successful slow pathway ablation with complete disappearance of symptoms and electrocardiographic manifestations of 1:2 AV conduction. Atrial fibrillation can be erroneously diagnosed in such patients when Wenckebach periodicity is present during fast and slow AV nodal pathway conduction (J Cardiovasc Electrophysiol. 2006;17:312.). Every sinus beat with concomitant junctional premature beat resulting in a bigeminal rhythm should be considered on the differential diagnosis of such a surface ECG, but consistent HV intervals and the satisfying results of slow pathway ablation make it untenable. ESO indicates esophagus electrogram; HRA, high right atrial electrogram; His, His bundle electrogram; CSp, proximal electrogram of coronary sinus; CSm, middle electrogram of coronary sinus; CSd, distal electrogram of coronary sinus. Zhan Zhong-qun, MS, Wang Chong-quan, MD, and Dang Shu-yi, MD Shiyan, Hubei Province, China doi:10.1016/j.jelectrocard.2008.07.015