Autonomic dysfunction and phase 2 ventricular fibrillation post myocardial infarction.

Dr Charles Murimi Mugera MSc Pharmacology Introduction The majority of the approximately 100,000 sudden cardiac deaths each year in the UK are caused by ventricular fibrillation related to ischaemia and infarction (Clements- Jewery et al., 2005; Wannamethee et al., 1995). Despite rapid advancements in the diagnosis and management of acute myocardial infarction (MI), an estimated 50% of patients die suddenly in the first hours before receiving medical attention (Lowel et al., 1993). Clinical studies indicate that the risk of sudden cardiac death is highest during the first 24 hours after an MI and diminishes thereafter (Zehender et al., 1991).The majority of these early deaths are caused by VF. Surprisingly little is known, however, about the exact time course of VF and even less about their underlying mechanisms in man. Ventricular arrhythmias post myocardial ischaemia and infarction have been extensively evaluated using animal models, and have been shown to occur in 2 distinct phases, phase 1 and phase 2 (Ravingerova et al., 1995; Clements-Jewery et al., 2005; Johnston et al., nd 1983). Animal studies have shown the 2 phase to be the more malignant arrhythmogenic period accounting for 87% of the arrhythmic deaths (Opitz et al., 1995). The relative importance of the phases of VF have not been elucidated in man and the spatial and temporal patterns of VF in man are difficult to acertain .However, the phases of VF in animal models have shown incredible similarity that cuts across all species from rodents to primates with little species variation (Curtis et al., 1987) . This evidence puts forward the elegant hypothesis that man exhibits the same biphasic susceptibility to VF (Clements-Jewery et al., 2005). 1 Cardiovascular Division King's College London the Rayne Institute St. Thomas' Hospital