Invited Review ArticleFibrosis and Cardiac Arrhythmiasde Jong, Sanne MSc*; van Veen, Toon A B PhD*; van Rijen, Harold V M PhD*; de Bakker, Jacques M T PhD*†‡Author Information From the *Department of Medical Physiology, University Medical Center, Utrecht, The Netherlands; †Department of Experimental Cardiology, Heart Failure Research Center, Amsterdam, The Netherlands; and ‡Interuniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands. Received for publication July 27, 2010; accepted November 18, 2010. The authors report no conflicts of interest. Reprints: Jacques M. T. de Bakker, PhD, Academic Medical Center, Department of Experimental Cardiology, Meibergdreef 9, 1105AZ Amsterdam, The Netherlands (e-mail:firstname.lastname@example.org). Journal of Cardiovascular Pharmacology: June 2011 - Volume 57 - Issue 6 - p 630-638 doi: 10.1097/FJC.0b013e318207a35f Buy Metrics Abstract In this review article about fibrosis and arrhythmias, we show that the amount of collagen, a normal element of the heart muscle, increases with age and in heart disease. The relation between fibrosis and electrophysiological parameters such as conduction, fractionation of electrograms, abnormal impulse initiation as well as arrhythmogenicity is discussed. Next to the amount of fibrosis, we offer data suggesting that collagen texture too plays a role in conduction slowing and arrhythmia vulnerability. Data are shown revealing that fibrosis can also be induced by reduced sodium channel and connexin43 expression. Finally contrast-enhanced magnetic resonance to detect fibrosis and ventricular tachycardia vulnerability in a noninvasive way as well as a reduction of fibrosis and arrhythmogenicity by inhibition of the renin-angiotensin-aldosterone system is discussed. © 2011 Lippincott Williams & Wilkins, Inc.