Oct, 2014
Early eicosapentaenoic acid treatment after percutaneous coronary intervention reduces acute inflammatory responses and ventricular arrhythmias in patients with acute myocardial infarction: A randomized, controlled study
INTERNATIONAL JOURNAL OF CARDIOLOGY
- Volume
- 176
- Number
- 3
- First page
- 577
- Last page
- 582
- Language
- English
- Publishing type
- Research paper (scientific journal)
- DOI
- 10.1016/j.ijcard.2014.08.055
- Publisher
- ELSEVIER IRELAND LTD
Objective: We examined whether early loading of eicosapenlaenoic acid (EPA) reduces clinical adverse events by 1 month, accompanied by a decrease in C-reactive protein (CRP) values in patients with acute myocardial infarction (MI).
Background: Acute MI triggers an inflammatory reaction, which plays an important role in myocardial injury. EPA could attenuate the inflammatory response.
Methods: This prospective, open-label, blinded endpoint, randomized trial consisted of 115 patients with acute MI. They were randomly assigned to the EPA group (57 patients) and the control group (58 patients). After percutaneous coronary intervention (PCI), 1800 mg/day of EPA was initiated within 24 h.The primary endpoint was composite events, including cardiac death, stroke, re-infarction, ventricular arrhythmias, and paroxysmal atrial fibrillation within 1 month.
Results: Administration of EPA significantly reduced the primary endpoint within 1 month (10.5 vs 29.3%, p = 0.01), especially the incidence of ventricular arrhythmias (7.0 vs 20.6%, p = 0.03). Peak CRP values after PCI in the EPA group were significantly lower than those in the control group (median [interquartile range], 8.2 [5.6-10.21 mg/dl vs 9.7 [7.6-13.91 mg/dl p < 0.01). Logistic regression analysis showed that EPA use was an independent factor related to ventricular arrhythmia until 1 month, with an odds ratio of 0.29 (95% confidence interval, 0.09 to 0.96, p = 0.04).
Conclusions: Early EPA treatment after PCI in the acute stage of MI reduces the incidence of ventricular arrhythmias, and lowers CRP values. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
Background: Acute MI triggers an inflammatory reaction, which plays an important role in myocardial injury. EPA could attenuate the inflammatory response.
Methods: This prospective, open-label, blinded endpoint, randomized trial consisted of 115 patients with acute MI. They were randomly assigned to the EPA group (57 patients) and the control group (58 patients). After percutaneous coronary intervention (PCI), 1800 mg/day of EPA was initiated within 24 h.The primary endpoint was composite events, including cardiac death, stroke, re-infarction, ventricular arrhythmias, and paroxysmal atrial fibrillation within 1 month.
Results: Administration of EPA significantly reduced the primary endpoint within 1 month (10.5 vs 29.3%, p = 0.01), especially the incidence of ventricular arrhythmias (7.0 vs 20.6%, p = 0.03). Peak CRP values after PCI in the EPA group were significantly lower than those in the control group (median [interquartile range], 8.2 [5.6-10.21 mg/dl vs 9.7 [7.6-13.91 mg/dl p < 0.01). Logistic regression analysis showed that EPA use was an independent factor related to ventricular arrhythmia until 1 month, with an odds ratio of 0.29 (95% confidence interval, 0.09 to 0.96, p = 0.04).
Conclusions: Early EPA treatment after PCI in the acute stage of MI reduces the incidence of ventricular arrhythmias, and lowers CRP values. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
- Link information
-
- DOI
- https://doi.org/10.1016/j.ijcard.2014.08.055
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/25305703
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000343893300028&DestApp=WOS_CPL
- Scopus
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84908179513&origin=inward
- Scopus Citedby
- https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=84908179513&origin=inward
- ID information
-
- DOI : 10.1016/j.ijcard.2014.08.055
- ISSN : 0167-5273
- eISSN : 1874-1754
- Pubmed ID : 25305703
- SCOPUS ID : 84908179513
- Web of Science ID : WOS:000343893300028