Reperfusion arrhythmias were described from the first trials of intracoronary thrombolysis for myocardial infarction. The prevalence of ventricular fibrillation during intravenous thrombolysis is low (< 7%) and comparable to that observed with classical treatment. Holter recording shows that ventricular tachycardia and accelerated idioventricular rhythms occur in over 80% of cases. These arrhythmias are generally well tolerated and do not require specific therapy. A bradycardia-hypotension syndrome is observed in about a quarter of reperfused patients, nearly always in inferior wall infarction. It normally resolves spontaneously or after atropine or vascular filling. Reperfusion is associated with a clearcut increase in the number of episodes of arrhythmia. Some arrhythmias such as sustained ventricular tachycardia, early accelerated idioventricular rhythms (occurring in the first 6 hours) or the bradycardia-hypotension syndrome may be considered as non-invasive criteria of reperfusion. More severe ischemia and sudden reperfusion favour the arrhythmogenicity of reperfusion in the animal. Recent data suggest that this may be the case in the clinical context. In some uncontrolled studies, lidocaine, betablockers and aspirin did not affect the prevalence of the arrhythmias. Preliminary trials indicate that flunarizine and captopril may reduce the incidence of reperfusion arrhythmias in man. Ventricular arrhythmias and myocardial stunning could be the result of sa single phenomenon (the extent of the ischemic lesions or reperfusion lesions). Studies currently under way should clarify the relationship between the incidence of arrhythmias, the severity of stunning and myocardial recovery. Protocols evaluating therapeutic interventions on the reperfusate should include Holter monitoring.