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Although heavy physical exercise, and psychological stress that produces similar physiological responses, may trigger a cardiac event in the immediate (within one hour) postexertion period,1 ,2 there is prospective evidence that the relative risk of sudden cardiac death and non-fatal myocardial infarction occurring during this period is reduced in individuals who exercise regularly.2 ,3 The intensity of the exercise required to induce this protection, as well as the time course of this protection, are subjects of ongoing debate3 ,4; the conclusion that “the protective effect of exercise requires continued exertion”3 implies that the duration of the protection is relatively short lived. The mechanisms of this risk reduction remain unclear but include an increase in baroreflex sensitivity (and increased vagal activity that is antifibrillatory5) and favourable effects on other risk factors.6
Both exercise training7 and right ventricular pacing8 ,9 confer significant protection against coronary artery occlusion induced ventricular fibrillation in conscious7 and anaesthetised8 ,9 dogs. Similar to the protection associated with ischaemic preconditioning (defined as the protective effect of brief coronary artery occlusions against the consequences of a subsequent more prolonged period of ischaemia), the protection is demonstrable immediately after, or even during,7 the pacing or exercise period but is lost shortly afterwards.9 Of potential clinical interest is the more recent finding that the protection associated with both ischaemic preconditioning and cardiac pacing, returns 20–24 hours after the initial stimulus, a phenomenon that has been described as the second window of protection10 or delayed myocardial protection.11 In pacing studies, protection is again lost 48 hours after the stimulus8 but can be regained if the pacing stimulus is repeated.12 Under these conditions, …