Exercise stress testing in the management of ventricular tachycardias

Abstract

Exercise, whether undertaken as a pleasurable pursuit or as a clinical investigation, produces important changes in cardiovascular dynamics. Exercise stress testing has become the most important non-invasive tool for the diagnosis and prognostication of coronary artery disease. However, exercise may be arrhythmogenic. With the onset of exercise there is withdrawal of vagal tone, an increase in sympathetic tone and an increase in levels of circulating catecholamines. These effects increase the rate of phase 4 diastolic depolarisation in the sinus node and accelerate AV nodal conduction. Cardiac frequency is increased and the temporal relationship of atrial and ventricular depolarisation is optimised for that frequency. However, the electrophysiological effects of exercise are more widespread than these influences on the sinus and AV node. Increased sympathetic tone and catecholamine release promote abnormal automatic behaviour, enhance triggered automaticity and may modify myocardial and His Purkinje circuits to favour reentrant activity. Latent re-entrant arrhythmias may also be precipitated through a change in ‘trigger’ events as when etopic beat frequency is increased. Although exercise produces haemodynamic change, these probably have little or no direct bearing on arrhythmogenesis. More important is the production by exercise of regional myocardial ischaemia which in turn can create an arrhythmogenic substrate.