Molecular and cellular aspects of re-entrant arrhythmias.

Abstract

In recent years it has become evident that myocardial tissue undergoes remodeling in diseased states such as myocardial infarction and hypertrophy which affects membrane channels, cell-to-cell coupling as well as the connective tissue matrix. Although the detailed mechanisms of ventricular arrhythmias in ventricular hypertrophy are not known, studies carried out by computer simulations or high resolution mapping of electrical activity have suggested a complex interaction between changing ionic currents at the level of the cell membranes, altered cell-to-cell coupling and altered macroscopie-structure. The present report summarises these recent developments and their potential relevance for arrhythmogenesis.