Heart failure and ischemic heart disease introduce an environment in which structural and electrical remodeling of the ventricular tissue occurs. These changes can then predispose to ventricular arrhythmias. In heart failure alone, these changes include both electrical remodeling of prolonged action potential duration (APD) and increased dispersion of refractoriness and structural remodeling that is associated with increased cell size, reduced connexin43 distribution, ion channel downregulation, and stimulation of TGF-β which can then lead to increased microfibrosis and interstitial fibrosis. Increased myocardial fibrosis can then lead to changes in cardiac fiber orientation which can then alter electrical conduction. Collectively, these changes alter the ventricular substrate which can then alter the mechanisms and characteristics of any resulting ventricular arrythmias. In this chapter we will discuss these structural changes that occur, how it effects conduction, which can ultimately lead to arrhythmias.
|Original language||English (US)|
|Title of host publication||Ventricular Arrhythmia|
|Subtitle of host publication||From Principles to Patients|
|Publisher||Nova Science Publishers, Inc.|
|Number of pages||14|
|State||Published - Feb 1 2013|
ASJC Scopus subject areas