ABSTRACT
The increase in left ventricular (LV) volume after a myocardial infarction (MI) is a component of the remodelling process and it is associated with a poor clinical outcome.1 Hence, the current management strategy for ischaemic LV dysfunction has been aimed to reverse the remodelling process (i.e., reduction of LV volume) by medical and/or device therapy. To this aim, within the last decade surgical ventricular reconstruction (SVR) has gained wide acceptance between surgeons as an optional therapeutic strategy. The proposed mechanism of bene t by SVR added to coronary artery bypass grafting (CABG) lies in LV volume reduction and in the restoration of a more elliptical LV shape that in turn may improve systolic function, New York Heart Association (NYHA) functional class, and survival.2,3 In spite of the large amount of literature, however, the additional bene t of SVR to CABG remains debated.4
