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

Doi, Masayuki; Nosaka, Kisato; Miyoshi, Toru; Iwamoto, Mutsumi; Kajiya, Masahito; Okawa, Keisuke; Nakayama, Rie; Takagi, Wataru; Takeda, Kazuki; Hirohata, Satoshi; Ito, Hiroshi

doi:10.1016/j.ijcard.2014.08.055

Cited by 47 publications

(26 citation statements)

References 38 publications

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“…There is accumulating evidence that blood EPA levels and the EPA/AA ratio predict the risk of cardiovascular events among the general population and patients with CAD [43]. It appears that EPA possesses a variety of biological actions including anti-inflammatory and anti-thrombotic effects, which may contribute to the prevention of cardiovascular events [22, 23, 44, 45]. Indeed, the present study also revealed improvements in inflammatory marker by using EPA and then improved endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Effects of 6-month eicosapentaenoic acid treatment on postprandial hyperglycemia, hyperlipidemia, insulin secretion ability, and concomitant endothelial dysfunction among newly-diagnosed impaired glucose metabolism patients with coronary artery disease. An open label, single blinded, prospective randomized controlled trial

Sawada

Tsubata

Hashimoto³

et al. 2016

Cardiovasc Diabetol

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BackgroundRecent experimental studies have revealed that n-3 fatty acids, such as eicosapentaenoic acid (EPA) regulate postprandial insulin secretion, and correct postprandial glucose and lipid abnormalities. However, the effects of 6-month EPA treatment on postprandial hyperglycemia and hyperlipidemia, insulin secretion, and concomitant endothelial dysfunction remain unknown in patients with impaired glucose metabolism (IGM) and coronary artery disease (CAD).Methods and resultsWe randomized 107 newly diagnosed IGM patients with CAD to receive either 1800 mg/day of EPA (EPA group, n = 53) or no EPA (n = 54). Cookie meal testing (carbohydrates: 75 g, fat: 28.5 g) and endothelial function testing using fasting-state flow-mediated dilatation (FMD) were performed before and after 6 months of treatment. The primary outcome of this study was changes in postprandial glycemic and triglyceridemic control and secondary outcomes were improvement of insulin secretion and endothelial dysfunction. After 6 months, the EPA group exhibited significant improvements in EPA/arachidonic acid, fasting triglyceride (TG), and high-density lipoprotein cholesterol (HDL-C). The EPA group also exhibited significant decreases in the incremental TG peak, area under the curve (AUC) for postprandial TG, incremental glucose peak, AUC for postprandial glucose, and improvements in glycometabolism categorization. No significant changes were observed for hemoglobin A1c and fasting plasma glucose levels. The EPA group exhibited a significant increase in AUC-immune reactive insulin/AUC-plasma glucose ratio (which indicates postprandial insulin secretory ability) and significant improvements in FMD. Multiple regression analysis revealed that decreases in the TG/HDL-C ratio and incremental TG peak were independent predictors of FMD improvement in the EPA group.ConclusionsEPA corrected postprandial hypertriglyceridemia, hyperglycemia and insulin secretion ability. This amelioration of several metabolic abnormalities was accompanied by recovery of concomitant endothelial dysfunction in newly diagnosed IGM patients with CAD.Clinical Trial Registration UMIN Registry number: UMIN000011265 (https://www.upload.umin.ac.jp/cgi-open-bin/ctr/ctr.cgi?function=brows&action=brows&type=summary&recptno=R000013200&language=E)Electronic supplementary materialThe online version of this article (doi:10.1186/s12933-016-0437-y) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Effects of 6-month eicosapentaenoic acid treatment on postprandial hyperglycemia, hyperlipidemia, insulin secretion ability, and concomitant endothelial dysfunction among newly-diagnosed impaired glucose metabolism patients with coronary artery disease. An open label, single blinded, prospective randomized controlled trial

Sawada

Tsubata

Hashimoto³

et al. 2016

Cardiovasc Diabetol

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“…Ventricular remodeling is an important pathophysiological process of heart failure developed through AMI, occurs throughout the entire course of the disease and is one of the major factors impacting the immediate and long-term prognosis of patients after AMI (17). While ventricular remodeling occurs via multiple mechanisms, it is widely recognized that inflammation is an important cause of ventricular remodeling after MI and constitutes the basic mechanism of chronic cardiac failure development (5). In the present study, gambogic acid significantly inhibited the activation of HW/BW as well as increases in LDH and cTnT levels in cardiac tissues of AMI model rats.…”

Section: Discussionmentioning

confidence: 99%

“…Ischemia and anoxia of cardiac muscle tissues and the increase of wall strain may induce an inflammatory response (5). In the inflammatory process of AMI, interleukin (IL)-6 and tumor necrosis factor (TNF)-α have a major role.…”

Section: Introductionmentioning

confidence: 99%

Gambogic acid exerts cardioprotective effects in a rat model of acute myocardial infarction through inhibition of inflammation, iNOS and NF‑κB/p38 pathway

et al. 2017

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Abstract. Gamboge, the dried resin secreted by Garcinia maingayii (gambogic tree), was previously demonstrated to exert anti-inflammatory effects. The present study examined the effects of gambogic acid, the major active constituent of gamboge, on myocardial infarction (MI) and inflammation in a rat model and explored the possible underlying mechanisms. The results demonstrated that gambogic acid inhibited the ratio of heart weight to body weight and myocardial damage (via lactate dehydrogenase and cardiac troponin T) in rats with MI. Gambogic acid suppressed the activation of interleukin (IL)-6 and tumor necrosis factor-α, and increased IL-10 levels in MI rats. Furthermore, gambogic acid reduced inducible nitric oxide synthase (iNOS), matrix metalloproteinase (MMP)-2, MMP-9, intercellular adhesion molecule-1 (ICAM-1), nuclear factor (NF)-κB/p65 and phosphorylated p38 protein in ischemic myocardial tissue of MI rats. In conclusion, gambogic acid exerted anti-inflammatory effects in MI rats by targeting the iNOS, MMPs, ICAM-1, NF-κB and p38 pathways. Gambogic acid may protect against MI-induced inflammation in rats, which may be associated with the activation of the NF-κB/p38 pathway.

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“…15 Previous studies also demonstrated that early initiation of EPA after revascularization in patients with acute myocardial infarction reduced the acute inflammatory response. 16 The effect of EPA treatment on CAC, however, remains unknown. Furthermore, the effect of intervention with EPA supplementation on progression of CAC has not been studied.…”

Section: Study Protocolmentioning

confidence: 99%

Effect of Intensive and Standard Pitavastatin Treatment With or Without Eicosapentaenoic Acid on Progression of Coronary Artery Calcification Over 12 Months　― Prospective Multicenter Study ―

Miyoshi

Kohno

Asonuma³

et al. 2018

Circ J

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studies showing significant regression of CAC and contemporaneous data showing opposite results. 3-6 Several randomized controlled clinical trials have failed to show attenuation of progression of CAC despite a significant lowering of low-density lipoprotein cholesterol (LDL-C) by atorvastatin or pravastatin. 7-11 Pitavastatin has been reported to substantially reduce LDL-C, as have other statins. 12 A previous study showed a significant increase in T he prevalence of coronary artery calcification (CAC) is age and sex dependent, occurring in ≥90% of men and ≥67% of women aged >70 years. Background: The effect of lipid-lowering agents on progression of coronary artery calcification (CAC) remains unclear. We evaluated the effects of pitavastatin 2 mg/day (PIT2), pitavastatin 4 mg/day (PIT4), and PIT2 combined with eicosapentaenoic acid (PIT2+EPA) on CAC progression.

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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

Cited by 47 publications

References 38 publications

Gambogic acid exerts cardioprotective effects in a rat model of acute myocardial infarction through inhibition of inflammation, iNOS and NF‑κB/p38 pathway

Effect of Intensive and Standard Pitavastatin Treatment With or Without Eicosapentaenoic Acid on Progression of Coronary Artery Calcification Over 12 Months　― Prospective Multicenter Study ―

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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

Cited by 47 publications

References 38 publications

Gambogic acid exerts cardioprotective effects in a rat model of acute myocardial infarction through inhibition of inflammation, iNOS and NF‑κB/p38 pathway

Effect of Intensive and Standard Pitavastatin Treatment With or Without Eicosapentaenoic Acid on Progression of Coronary Artery Calcification Over 12 Months ― Prospective Multicenter Study ―

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Effect of Intensive and Standard Pitavastatin Treatment With or Without Eicosapentaenoic Acid on Progression of Coronary Artery Calcification Over 12 Months　― Prospective Multicenter Study ―