The occurrence of left ventricular (LV) remodeling after anterior ST-segment elevation myocardial infarction (STEMI) results in heart failure and death. Studies have found that calcium/calmodulin-dependent protein kinase II delta (CaMKIId) can be a key molecular mediator of LV modeling. This study aims to determine the effectiveness of NP202, an orally active inhibitor of CaMKIId, in preventing LV remodeling in patients with STEMI with early LV dysfunction.This double-blind, randomized, placebo-controlled clinical trial included a total of 147 patients with anterior STEMI and left ventricular ejection fraction (LVEF). Patients were randomly assigned to receive 1000 mg NP202 for three months or a corresponding placebo. The primary outcome of the study was a change in LV end-systolic volume index (LVESVi) on CMR, along with a change in LVEF, infarct size, and diastolic function.

The findings suggested that the baseline LVEF between the groups was similar. Patients who were randomized to NP202 have a higher LVESVi than those in the placebo group. No significant change in LVESVi from baseline to three months was observed in either of the groups.

The research concluded that three months of NP202 treatment after PCI in patients with STEMI and LVEF wasn’t associated with an improvement in LV remodeling when compared to placebo.