Editorials |
From the Beth Israel Deaconess Medical Center, Cardiovascular Division, Department of Medicine, and Harvard Medical School, Boston, Mass.
Correspondence to Richard L. Verrier, PhD, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Harvard-Thorndike Electrophysiology Institute, Harvard Institutes of Medicine, 77 Avenue Louis Pasteur, Room 223, Boston, MA 02115. E-mail rverrier@bidmc.harvard.edu
See related article, pages 7683
Key Words: myocardial infarction nerve growth factor nerve sprouting neural remodeling sympathetic nerve ventricular arrhythmia
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Although the concept of remodeling is well established with respect to heart muscle, the importance of a restructuring of cardiac innervation, or "rewiring," after myocardial infarction (MI) has only recently received due attention. Pioneering contributions in this regard have emerged from the laboratories of Zipes1 and Chen.26 Recently, Cao, Chen, and coworkers25 provided evidence implicating nerve sprouting in ventricular arrhythmogenesis and potentially sudden cardiac death (SCD). These investigators reported a significant correlation between increased sympathetic nerve density as reflected in immunocytochemical markers with history of arrhythmias including ventricular tachycardia and SCD in native hearts of human transplant recipients with severe heart failure.3 Their observations suggested an association between postinjury sympathetic nerve density and susceptibility to life-threatening ventricular arrhythmias in these patients. In a canine post-MI model, they demonstrated that induction of nerve sprouting by infusion of nerve growth factor (NGF) into the left stellate ganglion (LSG) resulted in increased incidence of ventricular tachycardia and fibrillation.4 Significantly, the predisposition to arrhythmias was again linked to immunocytochemical evidence of a heterogeneous pattern of sympathetic reinnervation. In a similar conscious canine model, the group reported the frequent occurrence before ventricular tachycardia (VT) of visible T-wave alternans,5 a noninvasive marker of risk for ventricular arrhythmias in the post-MI population.7,8 More recently, Liu et al6 demonstrated in rabbits that hypercholesterolemia induces proarrhythmic neural and myocardial remodeling. Nerve sprouting and sympathetic hyperinnervation were associated with dispersion of repolarization, changes in calcium currents, and increased ventricular fibrillation incidence. Collectively, this evidence indicates that heterogeneous remodeling and hyperadrenergic
This article has been cited by other articles:
![]() |
J. J. Goldberger and R. Passman Implantable Cardioverter-Defibrillator Therapy After Acute Myocardial Infarction The Results Are Not Shocking. J. Am. Coll. Cardiol., November 24, 2009; 54(22): 2001 - 2005. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. L. Lujan, Y. Chen, and S. E. DiCarlo Paraplegia increased cardiac NGF content, sympathetic tonus, and the susceptibility to ischemia-induced ventricular tachycardia in conscious rats Am J Physiol Heart Circ Physiol, May 1, 2009; 296(5): H1364 - H1372. [Abstract] [Full Text] [PDF] |
||||
![]() |
T.-M. Lee, M.-S. Lin, and N.-C. Chang Effect of pravastatin on sympathetic reinnervation in postinfarcted rats Am J Physiol Heart Circ Physiol, December 1, 2007; 293(6): H3617 - H3626. [Abstract] [Full Text] [PDF] |
||||
|
Circulation Research Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2004 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |