After an acute myocardial infarction (AMI), there are several potentially life-threatening complications: (1) Arrhythmias , (2) cardiogenic shock, (3) complete free wall ruptures which account for almost 4% of patients' deaths after AMI (33% occur within the first 24 hours, 85% within the first week ), (4) complete septal ruptures (accounting for 1% – 5% of all infarct-related deaths ), and (5) the formation of false aneurysms.
While true aneurysms typically do not require treatment, false aneurysms, or pseudoaneurysms, are the result of a complete rupture of the ventricular wall with containment of the resulting hematoma by adherent pericardium and thus have a high mortality rate. As SEAs are precursors to pseudoaneurysms with a high propensity to rupture, immediate treatment is often life-saving. Although conservative management has been reported to be successful in asymptomatic chronic SEAs [8–10], surgical treatment is still considered standard of care, especially for symptomatic acute SEAs, as in our case [9, 11–13]. The options include aneurysmectomy (resection) or aneurysmorrhaphy (patch repair) . In addition to an elevated risk of death, patients with SEAs are initially difficult to diagnose due to a lack of specific symptoms (our patient was suspected to have a pulmonary embolus). Diagnosis can be made using ultrasound, MRI, left heart catheter, or CT . Due to the high risk of rupture in combination with the difficult diagnosis, SAEs have a high mortality rate and diagnosis is often made post-mortem.
SEAs are rare; in 1,814 autopsied hearts with 1,140 MIs (in 704 hearts), only three SEAs were found (0.2% of infarcts) . Review of literature reveled 36 published cases to date. As in our case, SEAs typically occur post AMI, usually within the first few weeks. Additionally, there are reports of SEAs (1) in an avascular region without history of AMI or signs of coronary artery disease , (2) as a direct result of apicoaortic bypass , and (3) after repair of a ventricular septal rupture .