Abstract
Introduction: Immune response plays a significant role in heart repair and regeneration after myocardial infarction and/or ischemia-reperfusion injury (MI/RI). Prolonged inflammation response contributes to adverse cardiac remodeling and reduction in pump function. In stable angina pectoris and patients with high-risk for heart disease, Beta 1.3 1.6 D Glucan has demonstrated reduced inflammation parameters including IL-6, TNF-α and CRP. Hypothesis: Beta 1.3 1.6 D Glucan modulates inflammation responses related to myocardial infarction or MI/RI, therefore preventing adverse heart remodeling measured by Left Ventricle Mass Index (LVMI) and Left Ventricle Ejection Fraction (LVEF). Method: In May - August 2018 a randomized double-blind placebo-controlled trial was conducted comprising of 50 STEMI/NSTEMI patients at the Saiful Anwar General Hospital, Malang, Indonesia. Next to standard therapy, 25 patients received Beta 1.3 1.6 D Glucan, 540 mg/day for 90 days, while the other 25 patients received placebo. Results: During the study duration, 5 patients dropped out. The mean value of pre-test LVMI for all patients is 114.07 ± 59.61 g/m 2 . After 90 days, there was a significant difference (p=0.012) in LVMI between the Beta 1.3 1.6 D Glucan and placebo group. The Beta 1.3 1.6 D Glucan group had a LVMI reduction of 4.55 ± 14.46 g/m 2 compared to the placebo group with an increase of 11.48 ± 23.94 g/m 2 in LVMI. The mean value of pre-test LVEF for all patients is 57.2 ± 11.39%. Post-test results demonstrated a significant difference (p=0.042) between both groups, with an increase in LVEF of 2.3 ± 9.77% for Beta 1.3 1.6 D Glucan group and a decrease in LVEF of 2.08 ± 3.35% for placebo group. Conclusion: Beta 1.3 1.6 D Glucan as an adjuvant therapy may have a beneficial effect to repair the vascular, heart tissues and function in myocardial infarction patients.
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