A common mechanism in the protective effects of preconditioning, cardiac pacing and physical exercise against ischemia and reperfusion-induced arrhythmias

Ischemic preconditioning results not only in a reduction in myocardial ischemic damage, but also in a marked suppression of those ventricular arrhythmias that result from a more prolonged period of ischemia and reperfusion insult. This protection is time-dependent and occurs in two distinct phases. There is an ‘early phase’ which is apparent immediately after the preconditioning stimulus but fades quickly (within 1 h to 2 h), and a ‘delayed protection phase’ in which the antiarrhythmic protection reappears 20 h to 24 h later. In both phases, the intensity of protection largely depends on the nature of the preconditioning stimulus. This can be ischemia resulting from brief coronary artery occlusions, cardiac pacing or vigorous physical exercise. Both cardiac pacing and exercise results in a marked reduction in the incidence and severity of ischemia and reperfusion-induced ventricular arrhythmias 24 h later. Although the precise mechanisms of the delayed protection that results from cardiac pacing and exercise are not yet fully understood, there is some evidence that similar endogenous protective substances (such as bradykinin, prostanoids and nitric oxide), as with ischemic preconditioning, play a pivotal trigger and mediator role in this anti-arrhythmic protection.