© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
Compensated cardiac hypertrophy: arrhythmogenicity and the new myocardial phenotype. I. Fibrosis
aU127-INSERM, Hôpital Lariboisière, 41 Bd de la Chapelle, 75475 Paris Cedex, France
bService de Cardiologie B, Hôpital Bichat, Paris, France
* Corresponding author. Tel.: +33 (1) 42858065; fax: +33 (1) 48742315.
The high incidence of arrhythmias in compensated cardiac hypertrophy is related to two independently regulated components—fibrosis and the adaptational phenotypic changes in membrane proteins linked to cardiac hypertrophy, and fibrosis. During the regression of hypertensive cardiopathy in middle-aged spontaneously hypertensive rats, the roles of cardiac hypertrophy and fibrosis can be analysed separately, revealing that both correlate independently with arrhythmias. In an experimental model of myocardial infarction it is possible to prevent arrhythmias with propranolol at the same time as cardiac hypertrophy, despite ventricular fibrosis. Fibrosis would appear to create arrhythmias both by anatomical uncoupling and by a re-entry mechanism generated by the zig-zag propagation of the transverse waveform. Triggered activity and automaticity depend on the membrane phenotype of the cardiocyte. They also play an important role, which is aggravated by myocardial heterogeneity.
KEYWORDS Arrhythmias; Hypertrophy; Propranolol; Fibrosis; Heart failure
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
E. Anter and D. J. Callans Pharmacological and Electrical Conversion of Atrial Fibrillation to Sinus Rhythm Is Worth the Effort Circulation, October 6, 2009; 120(14): 1436 - 1443. [Full Text] [PDF] |
||||
![]() |
B. Burstein and S. Nattel Atrial Fibrosis: Mechanisms and Clinical Relevance in Atrial Fibrillation J. Am. Coll. Cardiol., February 26, 2008; 51(8): 802 - 809. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Pandya, H.-S. Kim, and O. Smithies Fibrosis, not cell size, delineates beta-myosin heavy chain reexpression during cardiac hypertrophy and normal aging in vivo PNAS, November 7, 2006; 103(45): 16864 - 16869. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. M. Wolf, I. P. G. Moskowitz, S. Arno, D. M. Branco, C. Semsarian, S. A. Bernstein, M. Peterson, M. Maida, G. E. Morley, G. Fishman, et al. Somatic events modify hypertrophic cardiomyopathy pathology and link hypertrophy to arrhythmia PNAS, December 13, 2005; 102(50): 18123 - 18128. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Fenning, G. Harrison, R. Rose'meyer, A. Hoey, and L. Brown L-Arginine attenuates cardiovascular impairment in DOCA-salt hypertensive rats Am J Physiol Heart Circ Physiol, October 1, 2005; 289(4): H1408 - H1416. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Milliez, X. Girerd, P.-F. Plouin, J. Blacher, M. E. Safar, and J.-J. Mourad Evidence for an increased rate of cardiovascular events in patients with primary aldosteronism J. Am. Coll. Cardiol., April 19, 2005; 45(8): 1243 - 1248. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Lopez, R. Querejeta, A. Gonzalez, E. Sanchez, M. Larman, and J. Diez Effects of loop diuretics on myocardial fibrosis and collagen type I turnover in chronic heart failure J. Am. Coll. Cardiol., June 2, 2004; 43(11): 2028 - 2035. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Tsybouleva, L. Zhang, S. Chen, R. Patel, S. Lutucuta, S. Nemoto, G. DeFreitas, M. Entman, B. A. Carabello, R. Roberts, et al. Aldosterone, Through Novel Signaling Proteins, Is a Fundamental Molecular Bridge Between the Genetic Defect and the Cardiac Phenotype of Hypertrophic Cardiomyopathy Circulation, March 16, 2004; 109(10): 1284 - 1291. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Patel, S. F. Nagueh, N. Tsybouleva, M. Abdellatif, S. Lutucuta, H. A. Kopelen, M. A. Quinones, W. A. Zoghbi, M. L. Entman, R. Roberts, et al. Simvastatin Induces Regression of Cardiac Hypertrophy and Fibrosis and Improves Cardiac Function in a Transgenic Rabbit Model of Human Hypertrophic Cardiomyopathy Circulation, July 17, 2001; 104(3): 317 - 324. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Baillard, P. Mansier, P. V. Ennezat, L. Mangin, C. Medigue, B. Swynghedauw, and B. Chevalier Converting Enzyme Inhibition Normalizes QT Interval in Spontaneously Hypertensive Rats Hypertension, September 1, 2000; 36(3): 350 - 354. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Wolk Arrhythmogenic mechanisms in left ventricular hypertrophy Europace, January 1, 2000; 2(3): 216 - 223. [Abstract] [PDF] |
||||
![]() |
E. Macchi, M. Cavalieri, D. Stilli, E. Musso, S. Baruffi, G. Olivetti, P. R. Ershler, R. L. Lux, and B. Taccardi High-density epicardial mapping during current injection and ventricular activation in rat hearts Am J Physiol Heart Circ Physiol, November 1, 1998; 275(5): H1886 - H1897. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Lee, G. Morley, Q. Huang, A. Fischer, S. Seiler, J. W. Horner, S. Factor, D. Vaidya, J. Jalife, and G. I. Fishman Conditional lineage ablation to model human diseases PNAS, September 15, 1998; 95(19): 11371 - 11376. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. T. Weber Monitoring Vascular Sclerosis in Hypertension : A New Window of Opportunity Circulation, August 11, 1998; 98(6): 498 - 500. [Full Text] [PDF] |
||||





