Background: This is a single center, observational prospective study that aimed primarily to study role of Galectin-3 (as a simple marker of inflammation and fibrosis) in prediction of the occurrence of LV remodeling after anterior ST-elevation myocardial infarction (STEMI) treated by primary percutaneous coronary intervention (pPCI) for Left anterior descending artery (LAD) or left main (LM) as infarct related artery. Patients and methods: The present study protocol yielded 2 groups of patients: First group, consists of patients found to have LVR with high galectin 3 levels at baseline and 6 months follow up after anterior STEMI treated with primary PCI to LAD or LM. Second group consists of patients found to have no LVR with low levels of galectin 3 levels at baseline and 6 months follow up after anterior STEMI treated with primary PCI to LAD or LM. Results: Baseline and 6 months EF were significantly higher in the no LVR (57±8 &55 ±8 respectively) group than the LVR group (44 ±7&37 ±8 respectively), P values were <0.001 for each. At 6-month ESV was significantly higher in the LVR group (94 ml) than the no LVR group (42 ml), P-value was <0.001. The median percent change was significantly higher in the LVR group (88.89 %) than the no LVR (5 %). EDV, the mean at 6 months was significantly higher in the LVR group (150 ml) than the no LVR group (94 ml), P-value was <0. 001.The median percent change was significantly higher in the LVR group (77.78%) than the no LVR (0.94%), P-value was <0.00. As regards gelactin-3, the median at baseline was significantly higher in the LVR group (21.8 ng/ml) than the no LVR group (9.6 ng/ml), P-value was <0.001 Table (8). The median percent change was significantly higher in the no LVR group (8.49%) than the LVR group (-31.4%). Conclusion: Gal-3 serum levels after pPCI were independently associated with LVR in patients with anterior STEMI and inversely related to LVEF after a STEMI. Therefore, this study opens the door for a hard question: could we use Gal-3 as part of a screening strategy to identify patients with anterior STEMI who are at higher risk of developing HF after STEMI.