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Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
Attenuation of ischemia-reperfusion injury by intracoronary chelating agent administration
Donghoon Han1, Si-Hyuck Kang2, Chang-Hwan Yoon3
1Department of Internal Medicine, Cardiovascular Center, Hallym University Kangnam Sacred Heart Hospital, Seoul, Korea.
Insights
Intracoronary ethylenediaminetetraacetic acid (EDTA) reduced heart damage and improved function after reperfusion injury in a swine model. This study suggests EDTA may be a promising adjunctive therapy for ST-segment elevation myocardial infarction.
Area of Science:
- Cardiology
- Cardiovascular Research
- Regenerative Medicine
Background:
- Ischemia-reperfusion (IR) injury exacerbates myocardial damage, limiting the benefits of reperfusion therapy for acute myocardial infarction.
- Effective strategies to mitigate IR injury are crucial for improving outcomes in myocardial infarction patients.
Purpose of the Study:
- To evaluate the efficacy of intracoronary ethylenediaminetetraacetic acid (EDTA) as an adjunctive treatment to reduce IR injury in a swine model.
- To assess the impact of EDTA on infarct size, mitochondrial integrity, and cardiac remodeling post-myocardial infarction.
Main Methods:
- A swine model of myocardial infarction was created by occluding the left anterior descending artery for 1 hour.
- Ethylenediaminetetraacetic acid (EDTA) or saline was infused intracoronary during reperfusion.
- Infarct size was measured by tetrazolium chloride assay, myocardial edema by echocardiography, mitochondrial damage by electron microscopy, and left ventricular remodeling/function by echocardiography at 4 weeks.
Main Results:
- EDTA treatment significantly reduced infarct size and increased myocardial salvage compared to the control group.
- Electron microscopy revealed significantly less mitochondrial loss in cardiomyocytes of the EDTA group.
- Four-week echocardiography showed reduced left ventricular remodeling and improved ejection fraction in the EDTA-treated swine.
Conclusions:
- Intracoronary EDTA administration effectively reduced infarct size, mitochondrial damage, and adverse post-infarct cardiac remodeling in a swine model.
- These findings support further clinical investigation of EDTA as a therapeutic agent for ST-segment elevation myocardial infarction.
Abstract:
Ischemia-reperfusion (IR) injury accelerates myocardial injury sustained during the myocardial ischemic period and thus abrogates the benefit of reperfusion therapy in patients with acute myocardial infarction. We investigated the efficacy of intracoronary ethylenediaminetetraacetic acid (EDTA) administration as an adjunctive treatment to coronary intervention to reduce IR injury in a swine model. We occluded the left anterior descending artery for 1 h. From the time of reperfusion, we infused 50 mL of EDTA-based chelating agent via the coronary artery in the EDTA group and normal saline in the control group. IR injury was identified by myocardial edema on echocardiography. Tetrazolium chloride assay revealed that the infarct size was significantly lower in the EDTA group than in the control group, and the salvage percentage was higher. Electron microscopy demonstrated that the mitochondrial loss in the cardiomyocytes of the infarcted area was significantly lower in the EDTA group than in the control group. Echocardiography after 4 weeks showed that the remodeling of the left ventricle was significantly less in the EDTA group than in the control group: end-diastolic dimension 38.8 ± 3.3 mm vs. 43.9 ± 3.7 mm (n = 10, p = 0.0089). Left ventricular ejection fraction was higher in the EDTA group (45.3 ± 10.3 vs. 34.4 ± 11.8, n = 10, respectively, p = 0.031). In a swine model, intracoronary administration of an EDTA chelating agent reduced infarct size, mitochondrial damage, and post-infarct remodeling. This result warrants further clinical study evaluating the efficacy of the EDTA chelating agent in patients with ST-segment elevation myocardial infarction.
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