Autonomic mechanisms and sudden death after abrupt coronary occlusion

In spite of recent advances in secondary prevention, sudden cardiac death h as remained a major public health problem as the majority of fatalities occ ur in subjects without a history of severe heart disease. Abrupt rapture of a vulnerable plaque resulting in thrombotic occlusion of a coronary artery is a common cause of sudden death in this population. Coronary occlusion d oes not, however, invariably lead to sudden death bur may cause acute myoca rdial infarction or exacerbation of chest pain. Extensive studies in experi mental animals and increasing clinical evidence indicate that autonomic ner vous activity has a significant role in modifying the clinical outcome. Sym pathetic hyperactivity favours the genesis of life-threatening ventricular tachyarrhythmias while vagal activation exerts an antifibrillatory effect. Strong afferent stimuli from the ischaemic myocardium impair arterial baror eflex and may lead to dangerous haemodynamic instability. Studies with a hu man angioplasty model have shown that there is wide interindividual variati on in the type and severity of autonomic reactions during the early phase o f abrupt coronary occlusion, a critical period for out-of-hospital cardiac arrest. The site of the occlusion is not a significant determinant of the r eactions, whereas the severity of a coronary stenosis, adaptation or ischae mic preconditioning, beta-blockade and gender seem to affect the autonomic reactions and occurrence of complex ventricular arrhythmias. Clinical and a ngiographic factors are, however, poor predictors of autonomic reactions in an individual patient, Recent studies have documented a hereditary compone nt for autonomic function, and genetic factors may also modify the clinical manifestations of acute coronary occlusion.