**3. Clinical presentation**

The incidence of PI-VSD has decreased considerably over the years with advances in myocardial reperfusion strategies. Historically, up to 5% of all myocardial infractions were associated with mechanical complications such free-wall rupture, papillary muscle rupture, and PI-VSD (Agnihotri, 2008). With current treatment algorithms that advocate early and aggressive attempts at revascularization of the acute ischemic myocardial – such as thrombolytic therapy, early percutanous interventions with coronary stenting (PCI), and, less frequently, emergent coronary artery bypass surgery (CABG) – the overall incidence has dropped significantly. Large multi-centers studies evaluating the pathophysiologies of acute myocardial infarctions have shown a current incidence of approximately 0.2% of all AMI. With delays in therapies, or late clinical presentation, and the resulting increase in myocardial damage, this incidence increases up to 2%. Despite the relatively low risk of developing a PI-VSD, it account for a disproportionally high risk of mortality. Over 5% of all early deaths after AMI are attributed directly to the pathophysiologic complications of PI-VSD (Poulsen, 2008).

The timing of the development of a PI-VSD can be quite variable with the average time to clinical presentation is between 2 and 4 days, however presentation can be as few as a few hours after AMI or as long as several weeks.

Patient risk factors include gender, with men at a greater risk than women (3:2 ratio), increasing age, and current smoking history. The mean age of presentation in GUSTO was 62.5 years and ranged from 44 to 81 years (Crenshaw, 2000).
