We did not find any significant associations between circulating levels of CCN2 at any sampling point and infarct size, LV ejection fraction (LVEF), change in indexed LV end-diastolic volume (LVEDVi) and LV end-systolic volume (LVESVi), myocardial salvage or microvascular obstruction (MVO), respectively, neither in correlation analyses with CCN2 analysed as a continuous variable (Supplementary Table S1), nor in group analyses with CCN2 dichotomised at median value (Table 2). This evidence concerns the gene CCN2 and infarction.