Photo Credit: wildpixel
The following is a summary of “Apelinergic System in the Left Ventricle Adverse Remodeling After Myocardial Infarction: A Preliminary Study,” published in the April 2025 issue of Vascular Health and Risk Management by Wyderka et al.
Researchers conducted a retrospective study to investigate the role of the apelinergic system in the development of adverse left ventricle (LV) remodeling in humans after an infarction.
They included 49 individuals with a first episode of ST-segment elevation myocardial infarction (STEMI) of the anterior wall who received invasive treatment. Echocardiographic assessments were performed during the initial hospital stay and again at the 1-year follow-up. Participants were then divided into 2 groups: those with adverse LV remodeling, defined as an increase in LV end-diastolic volume greater than 20% (n = 12), and those without adverse remodeling (n = 29). Levels of ELA, AP-17, AP-13, and the Apelin receptor (APJ) were measured at the 1-year follow-up.
The results showed that individuals with adverse LV remodeling had significantly higher plasma levels of AP-13 (85.63 [75.43–96.13] vs 65.43 [57.35–69.35], P= 0.001) and AP-17 (69.36 [42.61–77.04] vs 30.04 [25.97–41.95], P= 0.004). Univariable logistic regression indicated that elevated left ventricle end-diastolic volume (LVEDV), indexed LVEDV1, left ventricular end-systolic volume (LVESV), indexed LVESVi, increased wall motion score index (WMSI), SYNTAX score, and high-sensitivity C-reactive protein (hs-CRP) levels during initial hospitalization and elevated apelin-13 and apelin-17 levels at one year, were linked with adverse LV remodeling. In multivariable logistic regression, only AP-17 remained independently associated with adverse LV remodeling (P= 0.050).
Investigators concluded that the cholinergic system may have been involved in the development of post-infarction adverse LV remodeling.
Create Post
Twitter/X Preview
Logout