ABSTRACT
Sudden cardiac death can result from physiological facilitators acting on myocyte substrates that trigger lethal arrhythmias (Campbell 1991; Willich et al. 1993). Cardiac substrates for arrhythmias can be anatomical, functional, and/or electrophysiological abnormalities of cardiomyocytes (Campbell 1991; Willich et al. 1993). For example, damaged myocardium or altered cardiac electrical activity, such as QT interval prolongation, can serve as substrates for triggered, life-threatening arrhythmias and sudden cardiac death (Kloner and Jennings 2001; Fallavollita et al. 2005; Pizzuto et al. 2006). Although earlier studies indicate that
seizure activity may cause myocyte damage (Woodruff et al. 2003; Brobbey and Ravakhah 2004; Stollberger and Finsterer 2004; Parvulescu-Codrea et al. 2006) and cardiac electrical dysfunction, including QT interval prolongation (Brotherstone et al. 2009; Surges et al. 2010; Isik et al. 2011; Seyal et al. 2011) in patients, the contributions of seizures to generation of arrhythmogenic substrates have not been fully elucidated. This chapter describes our studies using animal models of SE and epilepsy to evaluate the effects of seizures on cardiac myocyte damage and cardiac electrical activity.
