Dressler’s description,1> 40 years ago, of a clinical entity following an acute myocardial infarction (AMI) continues to be indelibly evoked at bedside and in the standard cardiology literature. Clinical features of this post-AMI syndrome include fever, chest pain, pericarditis, pleurisy occurring 2 to 3 weeks after the AMI, and a tendency for recurrence.2 Prior to the reperfusion era, the reported incidence of Dressler syndrome (DS) ranged from 1 to 5% of patients with AMI.2–5 The incidence of DS, however, has decreased in the reperfusion era, most likely due to the widespread use of therapy with thrombolysis6–7 and balloon angioplasty.8Supporting this, in a prospective study of 201 patients with AMI who had undergone thrombolysis, Shahar et al9found that no patient showing clinical signs of early reperfusion had DS. The only patient who developed DS in the latter study had had an extensive anterior AMI without evidence of reperfusion. Before the reperfusion era, Lichstein and colleagues10 suggested that the decreased incidence of DS was related to the modification of the treatment of patients with AMI. The use of novel therapies, such as nonsteroidal antiinflammatory agents, steroids, and salicylates, and the decreased use of oral anti-coagulants were evoked. In addition to the two mechanisms discussed above, which may account for the observed decrease in the incidence of DS,9–10 the authors propose a third hypothesis. We think that drugs that have been prescribed in previous decades as post-AMI “standard-of-care” may also play an important role in the disappearance of DS.