Skip Navigation

Europace 2000 2(3):216-223; doi:10.1053/eupc.2000.0110
© 2000 by European Society of Cardiology
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (7)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Wolk, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wolk, R.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

REVIEW

Arrhythmogenic mechanisms in left ventricular hypertrophy

R. Wolk

Department of Cardiology, Medical Centre for Postgraduate Education Warsaw, Poland

An important mechanism contributing to the high mortality and sudden death in patients with left ventricular hypertrophy (LVH) is ventricular arrhythmia. Part of the risk is associated with the pro-arrhythmic electrophysiological phenotype of the hypertrophied myocardium. The most consistently observed abnormality is prolongation of the action potential duration and refractoriness, which sets the stage for arrhythmias based on early or delayed afterdepolarizations and triggered activity. In addition, non-uniform prolongation of the action potential in LVH may be pro-arrhythmic by leading to increased dispersion of repolarization or refractoriness and favouring re-entry. The occurrence of delayed afterdepolarization-induced triggered activity and other ventricular arrhythmias are also related to the impaired ability to handle intracellular calcium due to changes in the density of ryanodine receptors and the Ca2+-ATPase of the sarcoplasmic reticulum. Slowing and fractionation of ventricular conduction, creating the conditions for micro-reentry and arrhythmogenesis, are characteristic of severe LVH, as isthe expression of the Ifcurrent (which may be a source of increased automaticity).

The pro-arrhythmic potential of LVH is also related to the presence of coexisting ‘extrinsic’ factors. The most important and pro-arrhythmic association of LVH is that with myocardial ischaemia. Other conditions include neuroendocrine factors, ventricular wall stress or electrolyte disturbances. The electrophysiological mechanisms of the interactions between these ‘extrinsic’ factors and LVH have not been fully elucidated. Further research into these mechanisms is required and may have important implications for our understanding of the mechanisms of cardiac arrhythmias in LVH and the appropriate use of antiarrhythmic drug therapy.

Key Words: Sudden death, hypertrophy, arrhythmias, ischaemia

Correspondence: Dr Robert Wolk, Department of Cardiology, Postgraduate Medical School, Grochowski Hospital, Grenadierow 51/59, 04-073 Warsaw, Poland.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
R. Wolk
Calcineurin, myocardial hypertrophy, and electrical remodeling
Cardiovasc Res, February 1, 2003; 57(2): 289 - 293.
[Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.