Introduction
There has been a reduction in the incidence of post MI VSR because of
primary PCI. Anterior MI is more likely to cause apical or anterior
septal defects, and inferior or lateral MI is more likely to cause basal
or posterior septal defects (1) .
The incidence of post-infarction VSR is reported as 1–2% after AMI.
However, the incidence may be recently decreased with early
interventions after AMI including thrombolytic therapy, primary PCI, and
urgent CABG. The timing to develop post-MI VSD is variable, in a few
hours up to 2 weeks (average time of 2–4 days). It is usually
associated with complete occlusion of a single coronary artery with poor
collateral vessels. About 2/3 of post-infarction VSDs are located in the
antero-apical septum, while the remaining in posterior septum, from left
anterior artery (LAD) and dominant right coronary artery (RCA) or
circumflex artery (Cx) occlusions. The natural history of untreated VSR
is extremely poor. The early development of congestive heart failure
(CHF) leading to cardiogenic shock is the primary cause of death.
Ventricular dysfunction may be left or right, depending on the territory
infracted and the location of VSR. Especially in posterior infarct,
significant mitral valve regurgitation (MR) can play an important role
in the development of heart failure, resulting in elevated left
ventricular end-diastolic pressure (LVEDP) and pulmonary edema. The
degree of left-to-right shunt depends on the size of the VSD and
pressure gradient across the septum. If the shunt is large, the normally
compliant right ventricle (RV) will not tolerate the sudden increase in
load, and the development of significant RV failure. As a result, severe
biventricular failure is not uncommon in patients with post-infarction
VS (5) .