**5. Pathophysiology**

The pathophysiology reflects two different types of defects. The first, a simple rupture, is a direct through-and-through defect that is typically located anteriorly when associated with a LAD territory infarct. Alternatively, complex defects are believed to result from tracking of blood as it dissects thru the septum with left ventricular entry sites remote from right ven‐ tricular exit sites – these tracks then enlarge over time due to the pressure gradient between the left and right ventricle. Obviously, with unpredictable injury to the septum, there can be a combination of the 2 different pathologies. Multiple defects are found in 5-11% of cases and emphasized the need for a complex pre-operative and intra-operative assessment of all pathways to insure a complete repair [18] and the observation that most defects are proba‐ bly larger than they initially appear. Incomplete closure of residual or secondary defects can account for post-operative recurrences. Transmural infarcts can be quite extensive with de‐ fects developing to several centimeters in diameter and can often involve extensive areas of the left ventricular free wall and potentially the annular structures of the mitral valve. For complex defects, as blood dissects through the necrotic myocardium there can be further ex‐ pansion and damage with loss of cellular integrity. With local cellular destruction there is fragmentation with degeneration of myocytes with enzymatic digestion and destruction. In patients who survive the acute presentation, up to 66% develop chronic ventricular aneur‐ ysms and a third will have significant functional mitral regurgitation from the secondary ef‐ fects on the ventricular free wall.

Interestingly, and clearly an area of further study, the pathologic consequences and out‐ comes of surgery of anterior and posterior defects are different in ways beyond what can be explained by the varying degree of shunting. Autopsy studies have shown that anterior PI-VSDs were associated with 33% of the LV and only 10% of the RV being infarcted, while posterior defects were associated with only 20% of the LV and 33% of the RV being infarcted [15]. Particularly considering the acute pressure/volume overload and associated RV failure, it becomes understandable why posterior based defects are associated with a worse prognosis.
