Arrhythmogenic mechanisms in left ventricular hypertrophy

An important mechanism contributing to the high mortality and sudden death in patients with left ventricular hypertrophy (LVH) is ventricular arrhythm ia. Part of the risk is associated with the pro-arrhythmic electrophysiolog ical phenotype of the hypertrophied myocardium. The most consistently obser ved abnormality is prolongation of the action potential duration and refrac toriness. which sets the stage for arrhythmias based on early or delayed af terdepolarizations and triggered activity. In addition, non-uniform prolong ation of the action potential in LVH may be pro-arrhythmic by leading to in creased dispersion of repolarization or refractoriness and favouring re-ent ry. The occurrence of delayed afterdepolarization-induced triggered activit y and other ventricular arrhythmias are also related to the impaired abilit y to handle intracellular calcium due to changes in the density of ryanodin e receptors and the Ca2+-ATPase of the sarcoplasmic reticulum. Slowing and fractionation of ventricular conduction, creating the conditions for micro- reentry and arrhythmogenesis, are characteristic of severe LVH. as is the e xpression of the I-f current (which may be a source of increased automatici ty). The pro-arrhythmic potential of LVH is also related to the presence of coex isting 'extrinsic' factors. The most important and pro-arrhythmic associati on of LVH is that with myocardial ischaemia. Other conditions include neuro endocrine factors, ventricular wall stress or electrolyte disturbances. The electrophysiological mechanisms of the interactions between these 'extrins ic' factors and LVH have not been fully elucidated. Further research into t hese mechanisms is required and may have important implications for our und erstanding of the mechanisms of cardiac arrhythmias in LVH and the appropri ate use of antiarrhythmic drug therapy. (Europace 2000; 2: 216-223) (C) 200 0 The European Society of Cardiology.