Myocardial rupture is a more common cause of death after infarction than is generally appreciated.1 It complicates about 3% of all myocardial infarctions and is the cause of death in about 17% of fatal infarcts. Myocardial rupture can involve the LV wall, the septum and the papillary muscles and occurs in proportion to the amount of muscle at risk with a ratio of about 10:2:1. Rupture of the LV wall is almost always immediately fatal and is the cause of death in about 13% (75% of 17%) of all fatal infarcts, as
“electromechanical dissociation”.

The minority who rupture only through the septum (loosely known as post-infarct VSD) may be saved by surgery. The hospital mortality for surgical repair is probably 40% (without reporting bias – but there is surgical selection and natural selection – most have had to survive transfer to a surgical centre). The mortality is close to 100% without surgery. Favourable features are younger age, anterior rather than inferior infarcts, more surviving left and right ventricular myocardium, and functioning kidneys. There was a vogue for holding these patients on a balloon pump to operate on them when the infarcted tissue is better able to take stitches. It is a long wait before there is any material advantage, and any benefit in reported figures of percentage operative survival was due to loss of patients along the way. If you are going to operate on these cases, it is probably a case of the sooner the better.

Current data would suggest that concomitant coronary artery bypass grafting does little to improve mortality rates from surgical post-infarct VSD.2

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