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Targeting Inflammation with Galectin-3 and PIIINP Modulation Among ST-Segment Elevation Acute Coronary Syndrome
Saskia Dyah Handari1,2, Mohammad Saifur Rohman2, Djanggan Sargowo2
1Medical Faculty, Ciputra University, Surabaya 60271, East Java, Indonesia.
Insights
Colchicine effectively reduced cardiac fibrosis markers in patients with ST-elevation acute coronary syndrome undergoing delayed PCI. This anti-inflammatory drug shows promise for improving recovery and preventing cardiac remodeling after intervention.
Area of Science:
- Cardiology
- Pharmacology
- Biomarker Research
Background:
- ST-segment elevation acute coronary syndrome (STE-ACS) poses a significant global health burden.
- Cardiac remodeling and fibrosis impede recovery post-percutaneous coronary intervention (PCI).
- Colchicine's anti-inflammatory properties may modulate fibrotic markers like Galectin-3 and Procollagen III N-terminal Propeptide (PIIINP).
Purpose of the Study:
- To evaluate the efficacy of colchicine in modulating Galectin-3 and PIIINP levels in STE-ACS patients.
- To assess colchicine's impact on cardiac fibrosis biomarkers in patients undergoing early versus delayed PCI.
Main Methods:
- A multicenter, randomized, double-blind trial involving 164 STE-ACS patients.
- Patients received colchicine post-hospital admission.
- Biomarker analysis (Galectin-3, PIIINP) at 24 hours and five days using two-way ANOVA.
Main Results:
- In early PCI, Galectin-3 decreased significantly, suggesting primary PCI benefits beyond colchicine.
- In delayed PCI, Galectin-3 initially increased but did not significantly decrease by day five.
- PIIINP levels significantly reduced by day five in the delayed PCI group, indicating colchicine's antifibrotic effect.
Conclusions:
- Colchicine demonstrates significant antifibrotic efficacy in STE-ACS patients with delayed PCI.
- The drug effectively reduced PIIINP and modulated Galectin-3, suggesting a role in controlling cardiac fibrosis.
- Colchicine may represent a breakthrough therapy for improving outcomes in patients with delayed intervention.
Abstract:
Background/Objectives: ST-segment elevation acute coronary syndrome (STE-ACS) represents a significant global health challenge, with cardiac remodeling and fibrosis critically affecting recovery after percutaneous coronary intervention (PCI). Colchicine, known for its anti-inflammatory effects, may regulate key fibrotic markers such as Procollagen III N-terminal Propeptide (PIIINP) and Galectin-3. This study assesses colchicine's effect on these biomarkers in STE-ACS patients undergoing delayed PCI. Methods: In this multicenter, randomized, double-blind trial, we examined colchicine's impact on Galectin-3 and PIIINP in 164 STE-ACS patients undergoing early or delayed PCI. Patients received colchicine shortly after hospital admission. Biomarker changes were evaluated at 24 h and five days post-treatment using two-way ANOVA. Results: Clinical trials in the early PCI group revealed that Galectin-3 levels decreased significantly on day one (p < 0.01) and further on day five (p < 0.0001), indicating Primary PCI has benefits to inhibition of fibrosis beyond colchicine add-on treatment. But, in the delayed PCI group, Galectin-3 levels significantly increased on day one (p < 0.01), but the decrease observed by day five was not statistically significant. It is related that the benefits of colchicine treatment may exceed PCI implantation in preventing cardiac remodeling. In the delayed PCI group, PIIINP levels showed a significant reduction on day five (p < 0.0001). Conclusions: This Colchicine demonstrates novel efficacy in delayed PCI, with a significant increase in Galectin-3 and a sharp reduction in PIIINP, indicating its ability to control fibrosis. This positions colchicine as a breakthrough therapy for improving outcomes in STE-ACS patients with delayed intervention.
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