Abstract
Objective
The purpose of this study is to explore the left atrium (LA) electrophysiologic abnormalities in atrial fibrillation (AF) patients detected during sinus rhythm and to determine the relationship between the type of AF and the electrophysiologic substrate in the LA.
Methods
Eighty patients with AF (30 paroxysmal AF, 22 persistent AF, and 28 long-standing AF) and 20 age- and sex-matched patients with left-sided accessory pathway were prospectively studied. High-density three-dimensional electroanatomic mapping was performed during sinus rhythm in LA, which was divided into six segments for regional analysis. Mean bipolar voltage, low voltage zone (LVZ) distribution, LA activation time, and electrogram complexity were assessed.
Results
The LA mean voltage was 3.67 ± 0.68 mV in no AF group, 2.16 ± 0.63 mV in the paroxysmal, 1.81 ± 0.36 mV in the persistent, and 1.48 ± 0.34 mV in the long-standing AF patients (P < 0.001). The total LA activation time was 75.3 ± 5.4 ms in no AF, 89.7 ± 12.3 ms in paroxysmal AF, 104.9 ± 6.1 ms in persistent AF, and 115.6 ± 12.1 ms in the long-standing AF patients, respectively (P < 0.001). With the progression of AF, there was a higher incidence of LVZ detection and increased prevalence of complex electrograms with 95 % of complex electrograms in areas with the bipolar voltage ≤ 1.3 mV in persistent and long-standing AF patients.
Conclusion
Patients with AF have abnormal electrophysiologic substrate in sinus rhythm characterized by lower mean bipolar voltage, more prevalent complex electrograms, and longer LA activation time. This substrate progresses parallel to progression of AF type.
Similar content being viewed by others
References
Kistler, P. M., Sanders, P., Fynn, S. P., Stevenson, I. H., Spence, S. J., Vohra, J. K., et al. (2004). Electrophysiologic and electroanatomic changes in the human atrium associated with age. Journal of the American College of Cardiology, 44, 109–116.
Healey, J. S., Baranchuk, A., Crystal, E., Morillo, C. A., Garfinkle, M., Yusuf, S., et al. (2005). Prevention of atrial fibrillation with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: A meta-analysis. Journal of the American College of Cardiology, 45, 1832–1839.
Sanders, P., Morton, J. B., Davidson, N. C., Spence, S. J., Vohra, J. K., Sparks, P. B., et al. (2003). Electrical remodeling of the atria in congestive heart failure: Electrophysiological and electroanatomic mapping in humans. Circulation, 108, 1461–1468.
Verheule, S., Wilson, E., Everett, T., Shanbhag, S., Golden, C., & Olgin, J. (2003). Alterations in atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation. Circulation, 107, 2615–2622.
Corradi, D., Callegari, S., Benussi, S., Maestri, R., Pastori, P., Nascimbene, S., Bosio, S., et al. (2005). Myocyte changes and their left atrial distribution in patients with chronic atrial fibrillation related to mitral valve disease. Human Pathology, 36, 1080–1089.
He, X., Gao, X., Peng, L., Wang, S., Zhu, Y., Ma, H., et al. (2011). Atrial fibrillation induces myocardial fibrosis through angiotensin II type 1 receptor-specific Arkadia-mediated downregulation of Smad 7. Circulation Research, 108, 164–175.
Kawara, T., Derksen, R., de Groot, J. R., Coronel, R., Tasseron, S., Linnenbank, A. C., et al. (2001). Activation delay after premature stimulation in chronically diseased human myocardium relates to the architecture of interstitial fibrosis. Circulation, 104, 3069–3075.
Spach, M. S., & Dolber, P. C. (1986). Relating extracellular potentials and their derivatives to anisotropic propagation at a microscopic level in human cardiac muscle: Evidence for electrical uncoupling of side-to-side fiber connections with increasing age. Circulation Research, 58, 356–371.
Verma, A., Wazni, O. M., Marrouche, N. F., Martin, D. O., Kilicaslan, F., Minor, S., et al. (2005). Pre-existent left atrial scarring in patients undergoing pulmonary vein antrum isolation: An independent predictor of procedural failure. Journal of the American College of Cardiology, 45, 285–292.
Chang, S. L., Tai, C. T., Lin, Y. J., Wongcharoen, W., Lo, L. W., Tuan, T. C., Udyavar, A. R., Chang, S. H., Tsao, H. M., Hsieh, M. H., Hu, Y. F., Chen, Y. J., & Chen, S. A. (2007). Biatrial substrate properties in patients with atrial fibrillation. Journal of Cardiovascular Electrophysiology, 18, 1134–1139.
Stiles, M. K., John, B., Wong, C. X., Kuklik, P., Brooks, A. G., Lau, D. H., Dimitri, H., et al. (2009). Paroxysmal atrial fibrillation is associated with abnormal atrial substrate: Characterizing the “second factor”. Journal of the American College of Cardiology, 53, 1182–1191.
Teh, A. W., Kistler, P. M., Lee, G., Medi, C., Heck, P. M., Spence, S. J., et al. (2012). Electroanatomic remodeling of the left atrium in paroxysmal and persistent atrial fibrillation patients without structural heart disease. Journal of Cardiovascular Electrophysiology, 23, 232–238.
Marcus, G. M., Yang, Y., Varosy, P. D., Ordovas, K., Tseng, Z. H., Badhwar, N., et al. (2007). Regional left atrial voltage in patients with atrial fibrillation. Heart Rhythm, 4, 138–144.
Assayag, P., Carre, F., Chevalier, B., Delcayre, C., Mansier, P., & Swynghedauw, B. (1997). Compensated cardiac hypertrophy: Arrhythmogenicity and the new myocardial phenotype. I. Fibrosis. Cardiovascular Research, 34, 439–444.
Silver, M. A., Pick, R., Brilla, C. G., Jalil, J. E., Janicki, J. S., & Weber, K. T. (1990). Reactive and reparative fibrillar collagen remodeling in the hypertrophied rat left ventricle: Two experimental models of myocardial fibrosis. Cardiovascular Research, 24, 741–747.
Huang, J. L., Tai, C. T., Lin, Y. J., Ting, C. T., Chen, Y. T., Chang, M. S., et al. (2006). The mechanisms of an increased dominant frequency in the left atrial posterior wall during atrial fibrillation in acute atrial dilatation. Journal of Cardiovascular Electrophysiology, 17, 178–188.
Lellouche, N., Buch, E., Celigoj, A., Siegerman, C., Cesario, D., De Diego, C., et al. (2007). Functional characterization of atrial electrograms in sinus rhythm delineates sites of parasympathetic innervation in patients with paroxysmal atrial fibrillation. Journal of the American College of Cardiology, 50, 1324–1331.
Miyamoto, K., Tsuchiya, T., Narita, S., Yamaguchi, T., Nagamoto, Y., Ando, S., et al. (2009). Bipolar electrogram amplitudes in the left atrium are related to local conduction velocity in patients with atrial fibrillation. Europace, 11, 1597–1605.
Ju, W., Yang, B., Chen, H., Zhang, F., Zhai, L., Cao, K., et al. (2011). Localized reentry as a novel type of the proarrhythmic effects of linear ablation in the left atrium. Pacing and Clinical Electrophysiology, 34, 919–926.
Boldt, A., Wetzel, U., Lauschke, J., Weigl, J., Gummert, J., Hindricks, G., et al. (2004). Fibrosis in left atrial tissue of patients with atrial fibrillation with and without underlying mitral valve disease. Heart, 90, 400–405.
Luo, M. H., Li, Y. S., & Yang, K. P. (2006). Fibrosis of collagen I and remodeling of connexin 43 in atrial myocardium of patients with atrial fibrillation. Cardiology, 107, 248–253.
Eckstein, J., Verheule, S., de Groot, N. M., Allessie, M., & Schotten, U. (2008). Mechanisms of perpetuation of atrial fibrillation in chronically dilated atria. Progress in Biophysics and Molecular Biology, 97, 435–451.
Lau, D. H., Psaltis, P. J., Mackenzie, L., Kelly, D. J., Carbone, A., Worthington, M., et al. (2011). Atrial remodeling in an ovine model of anthracycline-induced nonischemic cardiomyopathy: Remodeling of the same sort. Journal of Cardiovascular Electrophysiology, 22, 175–182.
Verheule, S., Sato, T., Everett, T., Engle, S. K., Otten, D., Rubart-von der Lohe, M., et al. (2004). Increased vulnerability to atrial fibrillation in transgenic mice with selective atrial fibrosis caused by overexpression of TGF-beta1. Circulation Research, 94, 1458–1465.
Burstein, B., Qi, X. Y., Yeh, Y. H., Calderone, A., & Nattel, S. (2007). Atrial cardiomyocyte tachycardia alters cardiac fibroblast function: A novel consideration in atrial remodeling. Cardiovascular Research, 76, 442–452.
Ausma, J., Litjens, N., Lenders, M. H., Duimel, H., Mast, F., Wouters, L., et al. (2001). Time course of atrial fibrillation-induced cellular structural remodeling in atria of the goat. Journal of Molecular and Cellular Cardiology, 33, 2083–2094.
Avitall, B., Bi, J., Mykytsey, A., & Chicos, A. (2008). Atrial and ventricular fibrosis induced by atrial fibrillation: Evidence to support early rhythm control. Heart Rhythm, 5, 839–845.
Goette, A., Honeycutt, C., & Langberg, J. J. (1996). Electrical remodeling in atrial fibrillation, time course and mechanisms. Circulation, 94, 2968–2974.
Fynn, S. P., Todd, D. M., Hobbs, W. J., Armstrong, K. L., Fitzpatrick, A. P., & Garratt, C. J. (2002). Clinical evaluation of a policy of early repeated internal cardioversion for recurrence of atrial fibrillation. Journal of Cardiovascular Electrophysiology, 13, 135–141.
Hirayama, Y., Atarashi, H., Kobayashi, Y., Horie, T., Iwasaki, Y., Maruyama, M., et al. (2005). Angiotensin-converting enzyme inhibitor therapy inhibits the progression from paroxysmal atrial fibrillation to chronic atrial fibrillation. Circulation Journal, 69, 671–676.
Madrid, A. H., Bueno, M. G., Robollo, J. M., Marín, I., Peña, G., Bernal, E., et al. (2002). Use of irbesartan to maintain sinus rhythm in patients with long-lasting persistent atrial fibrillation: A prospective and randomized study. Circulation, 106, 331–336.
Marchlinski, F. E., Callans, D. J., Gottlieb, C. D., & Zado, E. (2000). Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation, 101, 1288–1296.
Mahnkopf, C., Badger, T. J., Burgon, N. S., Daccarett, M., Haslam, T. S., Badger, C. T., et al. (2010). Evaluation of the left atrial substrate in patients with lone atrial fibrillation using delayed-enhanced MRI: Implications for disease progression and response to catheter ablation. Heart Rhythm, 7, 1475–1481.
Jadidi, A. S., Duncan, E., Miyazaki, S., Lellouche, N., Shah, A. J., Forclaz, A., et al. (2012). Functional nature of electrogram fractionation demonstrated by left atrial high-density mapping. Circulation. Arrhythmia and Electrophysiology, 5, 32–42.
Saghy, L., Callans, D. J., Garcia, F., Lin, D., Marchlinski, F. E., Riley, M., et al. (2012). Is there a relationship between complex fractionated atrial electrograms recorded during atrial fibrillation and sinus rhythm fractionation? Heart Rhythm, 9, 181–188.
Fundings
This work was supported by the Program for Development of Innovative Research Team in the First Affiliated Hospital of Nanjing Medical University, People’s Republic of China (IRT-004) and the Project of National Scientific Fund Committee (81070156), People’s Republic of China
Competing interests
None
Author information
Authors and Affiliations
Corresponding author
Additional information
Drs. Yazhou Lin and Bing Yang contributed equally to literature search, data collection, data analysis, data interpretation, and writing. Dr. Fermin Garcia contributed to data analysis and data interpretation. Drs. Weizhu Ju, Fengxiang Zhang, Hongwu Chen, and Jinbo Yu contributed to data collection. Dr. Kejiang Cao was responsible for data interpretation. Drs. David Callans and Francis Marchlinski were responsible for study design and language polishing. Dr. Minglong Chen was the corresponding author who contributed to the conception and study design, writing, and final approval of the version to be submitted.
Authors Yazhou Lin and Bing Yang had equal contribution to this work.
Rights and permissions
About this article
Cite this article
Lin, Y., Yang, B., Garcia, F.C. et al. Comparison of left atrial electrophysiologic abnormalities during sinus rhythm in patients with different type of atrial fibrillation. J Interv Card Electrophysiol 39, 57–67 (2014). https://doi.org/10.1007/s10840-013-9838-y
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s10840-013-9838-y