Abstract
Objective: Galectin-3 (Gal-3) plays a big role in the development of cardiac fibrosis; however, its role in remodeling after acute myocardial infarction (AMI) has not received sufficient attention. Post-AMI measurements of global longitudinal strain (GLS) are beneficial in providing information about infarct area and remodeling. We aimed to determine the effect of N-acetylcysteine (NAC) on Gal-3 and GLS in AMI.
Design: This was a randomized, single-blind study with pre- and post-treatment evaluations performed from May 1 to August 31, 2018.
Setting: Dr. Moewardi Hospital, Indonesia
Patients: ST elevation myocardial infarction (STEMI) patients who received fibrinolytic therapy were randomly allocated to NAC and control groups.
Interventions: A total of 32 STEMI patients were administered fibrinolytic therapy (17 patients were administered standard therapy plus 600 mg NAC orally three times a day for 72 hours and 15 patients were administered standard therapy plus placebo as the control). Gal-3 samples were taken during admission and at 72 hours in both groups, while GLS measurement was only performed 72 hours after admission.
Measurements and results: Gal-3 levels in the NAC and control groups at admission were not significantly different; however, levels were significantly different after 72 hours (p=0.017). After comparing Gal-3 levels during admission and at 72 hours, the NAC group showed significant differences between Gal-3 levels at the time of admission and at 72 hours (p=0.0001); no difference was found in the control group. There were also significant intergroup differences in Gal-3 level changes (p=0.014). In the NAC group, a better and significantly different 72-h GLS value was obtained from that in the control group (p=0.023).
Conclusion: Supplementary therapy with NAC can reduce Gal-3 levels and GLS in AMI patients receiving fibrinolytic therapy.
Trisulo Wasyanto, Akhmad Jalaludinsyah, Ahmad Yasa
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- The effect of oral N-acetylcysteine on galectin-3 and global longitudinal strains in patients with acute myocardial infarction
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