© 2000 American Heart Association, Inc.
Integrative Physiology |
Interdependence of Modulated Dispersion and Tissue Structure in the Mechanism of Unidirectional Block
From the Heart and Vascular Research Center, MetroHealth Campus, Case Western Reserve University, Cleveland, Ohio.
Correspondence to Kenneth R. Laurita, PhD, MetroHealth Campus, Case Western Reserve University, 2500 MetroHealth Dr, Rammelkamp, 6th floor, Cleveland, Ohio 44109-1998. E-mail klaurita{at}metrohealth.org
Abstract—We previously showed that a premature stimulus can significantly alter vulnerability to arrhythmias by modulating spatial gradients of ventricular repolarization (ie, modulated dispersion). However, it is not clear if such changes in arrhythmia vulnerability can be attributed to the formation of an electrophysiological substrate for unidirectional block and what the potential role is of tissue structure in this process. Therefore, the main objective of the present study was to examine the concomitant effect repolarization gradients and tissue structure have on unidirectional block. Optical action potentials were recorded from 128 ventricular sites (1 cm2) in 8 Langendorff-perfused guinea pig hearts. Propagation was confined to the epicardial surface using an endocardial cryoablation procedure, and a 12-mm barrier with a 1.5-mm isthmus was etched with a laser onto the epicardium. A premature stimulus (S2) was delivered over a range of S1S2 coupling intervals to modulate repolarization gradients in a predictable fashion. When a second premature stimulus (S3) was delivered from the center of the isthmus, the occurrence and orientation of unidirectional block were highly dependent on repolarization gradients created by the S2 beat. In this model, a local repolarization gradient of 3.2 ms/mm was required for unidirectional block at this isthmus. In addition, the formation of unidirectional block was critically dependent on the presence of the source-sink mismatch imposed by the isthmus. These results may explain how the interplay between spatial heterogeneities of repolarization and tissue structure form a substrate for unidirectional block and reentry.
Key Words: optical mapping • source-sink mismatch • repolarization • reentry • premature stimulation
This article has been cited by other articles:
 |
|
 |
|
  S. Poelzing and D. S. Rosenbaum The Modulated Dispersion Hypothesis Confirmed in Humans Circ Arrhythm Electrophysiol, April 1, 2009; 2(2): 100 - 101. [Full Text] [PDF]
|
|
|
|
 |
|
 D. Sato, L.-H. Xie, A. A. Sovari, D. X. Tran, N. Morita, F. Xie, H. Karagueuzian, A. Garfinkel, J. N. Weiss, and Z. Qu Synchronization of chaotic early afterdepolarizations in the genesis of cardiac arrhythmias PNAS, March 3, 2009; 106(9): 2983 - 2988. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. de Diego, R. K. Pai, A. S. Dave, A. Lynch, M. Thu, F. Chen, L.-H. Xie, J. N. Weiss, and M. Valderrabano Spatially discordant alternans in cardiomyocyte monolayers Am J Physiol Heart Circ Physiol, March 1, 2008; 294(3): H1417 - H1425. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M.-J. Yang, D. X. Tran, J. N. Weiss, A. Garfinkel, and Z. Qu The pinwheel experiment revisited: effects of cellular electrophysiological properties on vulnerability to cardiac reentry Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1781 - H1790. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. R. Mills, N. Mal, F. Forudi, Z. B. Popovic, M. S. Penn, and K. R. Laurita Optical mapping of late myocardial infarction in rats Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H1298 - H1306. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. S. Chauhan, E. Downar, K. Nanthakumar, J. D. Parker, H. J. Ross, W. Chan, and P. Picton Increased ventricular repolarization heterogeneity in patients with ventricular arrhythmia vulnerability and cardiomyopathy: a human in vivo study Am J Physiol Heart Circ Physiol, January 1, 2006; 290(1): H79 - H86. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. S. Po, Y. Li, D. Tang, H. Liu, N. Geng, W. M. Jackman, B. Scherlag, R. Lazzara, and E. Patterson Rapid and Stable Re-Entry Within the Pulmonary Vein as a Mechanism Initiating Paroxysmal Atrial Fibrillation J. Am. Coll. Cardiol., June 7, 2005; 45(11): 1871 - 1877. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. S Spector Diagnosis and management of sudden cardiac death Heart, March 1, 2005; 91(3): 408 - 413. [Full Text] [PDF]
|
|
|
|
|
|
S. Poelzing and D. S. Rosenbaum Altered connexin43 expression produces arrhythmia substrate in heart failure Am J Physiol Heart Circ Physiol, October 1, 2004; 287(4): H1762 - H1770. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Miyauchi, M. C. Fishbein, and H. S. Karagueuzian Electrical current-induced atrial and pulmonary vein action potential duration shortening and repetitive activity Am J Physiol Heart Circ Physiol, July 1, 2004; 287(1): H178 - H186. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. G. Akar and D. S. Rosenbaum Transmural Electrophysiological Heterogeneities Underlying Arrhythmogenesis in Heart Failure Circ. Res., October 3, 2003; 93(7): 638 - 645. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. E. Saffitz and R. B. Schuessler Connexin-40, Bundle-Branch Block, and Propagation at the Purkinje-Myocyte Junction Circ. Res., November 10, 2000; 87(10): 835 - 836. [Full Text] [PDF]
|
|