Effects of trimetazidine in patients with acute myocardial infarction: data from the Korean Acute Myocardial Infarction Registry

Kim, Jeong Su; Kim, Chang Hoon; Chun, Kook Jin; Kim, June Hong; Park, Yong Hyun; Kim, Jun; Choi, Jin Hee; Lee, Sang Hyun; Kim, Eun Jung; Yu, D.G.; Ahn, Eun Young; Jeong, Myung Ho

doi:10.1007/s00392-013-0611-0

Cited by 25 publications

(26 citation statements)

References 24 publications

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“…TMZ, an antianginal drug, protects ischemic cardiomyocytes by restoring their ability to produce energy, and has been widely used to treat various cardiovascular diseases such as coronary heart disease and heart failure [24,25]. In basic medical science, TMZ has been demonstrated to have pleiotropic effects.…”

Section: Discussionmentioning

confidence: 99%

Trimetazidine Protects Umbilical Cord Mesenchymal Stem Cells Against Hypoxia and Serum Deprivation Induced Apoptosis by Activation of Akt

Gong

Fan

Wang

et al. 2014

Cell Physiol Biochem

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Background: Mesenchymal stem cell (MSC) transplantation is a promising therapy for cardiac repair. However, the efficacy is limited by the poor viability of MSCs in the infarcted heart. Recent findings have implicated that trimetazidine (TMZ) enhanced the survival of the stem cells under various conditions. However, as the stem cells in these studies were animal-derived, little information is available about the effects of TMZ on human MSCs. Herein, we propose that TMZ may protect human MSCs against apoptosis induced by Hypoxia/Serum deprivation (H/SD). Methods: Human umbilical cord MSCs (UC-MSCs) from Wharton's jelly were pretreated with 10µM TMZ of H/SD with or without the Akt inhibitor LY294002. The morphological changes were assessed using Hoechst 33342. Apoptosis was evaluated via Annexin V/PI staining; and apoptosis-related proteins were detected using Western-blot. Protein chip technology was used to screen for differences between the cell supernatants. Results: TMZ had a significant protective effect against H/SD-induced apoptosis, accompanied by an increase in Bcl-2 and p-Akt. The TMZ-mediated anti-apoptotic effect on MSCs could be attenuated by treatment with LY294002. Moreover, protein chip assays showed that TMZ treatment increased the paracrine functions of MSCs. Conclusion: Trimetazidine protects human UC-MSCs from H/SD-induced apoptosis via the Akt pathway and may therefore be a potentially useful therapeutic adjunct for transplanting MSCs into damaged heart after myocardial infarction.

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Section: Discussionmentioning

confidence: 99%

Trimetazidine Protects Umbilical Cord Mesenchymal Stem Cells Against Hypoxia and Serum Deprivation Induced Apoptosis by Activation of Akt

Gong

Fan

Wang

et al. 2014

Cell Physiol Biochem

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“…Clinical trials have shown that TMZ exerts cardioprotective effects in the setting of myocardial ischemia, including acute myocardial infarction [8,9]. It was reported that daily use of TMZ (20 mg, three times a day) for 5 ± 2 days before coronary angiography and a loading dose of 60 mg 30 min before percutaneous coronary intervention (PCI) could significantly reduce the frequency of angina pectoris attacks and myocardial damage during PCI, and improve left ventricular function during follow-up after PCI [10].…”

Section: Introductionmentioning

confidence: 99%

Trimetazidine Pretreatment Inhibits Myocardial Apoptosis and Improves Cardiac Function in a Swine Model of Coronary Microembolization

Liu

et al. 2015

Cardiology

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Objective: Trimetazidine (TMZ) is a well-known anti-ischemic agent; however, its efficacy and mechanism of cardioprotection on coronary microembolization (CME) are largely unknown. The present study was undertaken to determine whether TMZ pretreatment could attenuate myocardial apoptosis and improve cardiac function in a swine model of CME. Methods: Fifteen swine were randomly and equally divided into a sham-operated (control) group, CME group and CME plus TMZ (TMZ) group. CME was induced by injecting inert plastic microspheres (42 μm in diameter) into the left anterior descending artery. For the control group, the same dose of normal saline was substituted for the microspheres, and the TMZ group was pretreated with TMZ 30 min before microsphere injection. Cardiac function was assessed by echocardiography, myocardial apoptosis was detected by TUNEL staining, and the expression levels of cleaved caspase-9/3 were measured by Western blot 12 h after operation. Results: Compared to the control group, cardiac function in the CME group was significantly decreased (p < 0.05); however, TMZ pretreatment showed significantly improved cardiac function as compared to the CME group (p < 0.05). The myocardial apoptotic rate and the expression levels of cleaved caspase-9/3 increased remarkably in CME group as compared with the control group (p < 0.001). Again, TMZ pretreatment significantly reduced the apoptotic rate and also the expression levels of cleaved caspase-9/3 (p < 0.001). Conclusion: The present study demonstrated that TMZ pretreatment could significantly inhibit CME-induced myocardial apoptosis and improve cardiac function, and that the cardioprotective effect appeared to be mediated by the blockade of the mitochondrial apoptotic pathway. These results emphasize the importance of TMZ pretreatment in the therapy of CME-induced myocardial injury.

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“…From an initial set of 156 nonduplicate records, a total of 7 clinical studies were finally included in the meta-analysis [13,14,15,16,17,18,19]. The characteristics of these included studies are detailed in table 1, and the results of the modified Newcastle-Ottawa assessment scale quality assessment of these included studies are detailed in table 2.…”

Section: Resultsmentioning

confidence: 99%

“…The retrospective analysis by Kim et al [13] of acute MI patients revealed that adjunctive trimetazidine therapy reduced the all-cause mortality risk by 59% and that of total MACE by 76% over a 12-month follow-up period. Moreover, the prospective study of Shehata [19] on diabetic acute MI patients revealed that adjunctive trimetazidine therapy was associated with reduced myocardial damage, earlier reperfusion, amelioration of left ventricular ejection fraction, and lower total MACE.…”

Section: Discussionmentioning

confidence: 99%

Efficacy and Safety of Adjunctive Trimetazidine Therapy for Acute Myocardial Infarction: A Systematic Review and Meta-Analysis

Li¹,

Wang²,

Hu³

et al. 2016

Cardiology

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Background: Several lines of evidence support the clinical use of trimetazidine as an adjunctive therapy in cardioischemic patients. Therefore, we assessed here the efficacy and safety of adjunctive trimetazidine therapy in acute myocardial infarction (MI) patients by a systematic review and meta-analysis of the current literature. Methods: PubMed, the Cochrane Library, and the China National Knowledge Infrastructure databases were searched for clinical studies comparing adjunctive trimetazidine therapy against placebo in adult acute MI patients. Several clinical outcomes [early/short-term all-cause mortality, long-term all-cause mortality, total major adverse cardiac events (MACE), recurrent nonfatal MI, in-hospital adverse events, target vessel revascularization (TVR), and coronary artery bypass graft (CABG)] were analyzed by the intention-to-treat principle. Odds ratios (OR) and their 95% confidence intervals (CI) were derived from the number of outcome events in each study arm to estimate the association between adjuvant trimetazidine administration and the various clinical outcomes. A random-effects model was applied for all meta-analyses. Results: We found that adjunctive trimetazidine therapy showed a significant effect upon total MACE (OR = 0.33, 95% CI = 0.15-0.74; p = 0.007) but showed no significant effect upon early/short-term all-cause mortality, long-term all-cause mortality, recurrent nonfatal MI, in-hospital adverse events, TVR, or CABG (p > 0.05). Conclusions: This is the first meta-analysis to report that adjunctive trimetazidine therapy has a beneficial effect upon total MACE in acute MI patients. Clinical investigators should consider further trials on adjunctive trimetazidine therapy in order to better define its risks and benefits in acute MI patients.

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Effects of trimetazidine in patients with acute myocardial infarction: data from the Korean Acute Myocardial Infarction Registry

Abstract: Trimetazidine appeared to improve clinical outcomes in AMI patients by significantly reducing all-cause mortality and MACE over 12 months.

Cited by 25 publications

References 24 publications

Trimetazidine Protects Umbilical Cord Mesenchymal Stem Cells Against Hypoxia and Serum Deprivation Induced Apoptosis by Activation of Akt

Trimetazidine Protects Umbilical Cord Mesenchymal Stem Cells Against Hypoxia and Serum Deprivation Induced Apoptosis by Activation of Akt

Trimetazidine Pretreatment Inhibits Myocardial Apoptosis and Improves Cardiac Function in a Swine Model of Coronary Microembolization

Efficacy and Safety of Adjunctive Trimetazidine Therapy for Acute Myocardial Infarction: A Systematic Review and Meta-Analysis

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