**3. Clinical Presentation**

The incidence of PI-VSD has decreased dramatically over the years with advances in myo‐ cardial reperfusion and early revascularization strategies. Historically, up to 5% of AMI were associated with mechanical complications such free-wall ruptures, papillary muscle rupture, and PI-VSD [1]. With advanced in therapies that advocate early and aggressive at‐ tempts at reperfusion of the acute ischemic myocardial – such as thrombolytic therapy, early percutaneous interventions with coronary stenting (PCI), and, rarely, emergent coronary ar‐ tery bypass surgery (CABG) – the overall presentation of mechanical complications, such as PI-VSD, has decreased significantly. Large multi-center studies evaluating the pathophysiol‐ ogies of acute myocardial infarctions have shown a current incidence of approximately 0.2% of all AMI. In patients who present late or in whom there is a delay in therapy and there is a resulting increase in myocardial damage, this incidence increases up to 2%. Despite the low risk of developing a PI-VSD, it accounts for a disproportionally high mortality rate. Five per‐ cent of all early deaths after AMI are attributed directly to the complications of PI-VSD [36].

The timing of the development of a PI-VSD can be quite variable. The average time to clini‐ cal presentation is between 2 and 4 days. However, some patients can present as early as a few hours after AMI or as long as several weeks.

Risk factors include gender, with men at a greater risk than women (3:2 ratio), increasing age, and current smoking history. In the GUSTO trial, the mean age of presentation with a PI-VSD was 62.5 years and ranged from 44 to 81 years [13].
