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Gary D Lopaschuk - One of the best experts on this subject based on the ideXlab platform.
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rationale and benefits of Trimetazidine by acting on cardiac metabolism in heart failure
International Journal of Cardiology, 2016Co-Authors: Yuri Lopatin, Gary D Lopaschuk, Gabriele Fragasso, Giuseppe M C Rosano, Petar M Seferovic, Luis Henrique W Gowdak, Dragos Vinereanu, Magdy Abdel Hamid, P Jourdain, Piotr PonikowskiAbstract:Abstract Heart failure is a systemic and multiorgan syndrome with metabolic failure as a fundamental mechanism. As a consequence of its impaired metabolism, other processes are activated in the failing heart, further exacerbating the progression of heart failure. Recent evidence suggests that modulating cardiac energy metabolism by reducing fatty acid oxidation and/or increasing glucose oxidation represents a promising approach to the treatment of patients with heart failure. Clinical trials have demonstrated that the adjunct of Trimetazidine to the conventional medical therapy improves symptoms, cardiac function and prognosis in patients with heart failure without exerting negative hemodynamic effects. This review focuses on the rationale and clinical benefits of Trimetazidine by acting on cardiac metabolism in heart failure, and aims to draw attention to the readiness of this agent to be included in all the major guidelines dealing with heart failure.
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beneficial effects of Trimetazidine in ex vivo working ischemic hearts are due to a stimulation of glucose oxidation secondary to inhibition of long chain 3 ketoacyl coenzyme a thiolase
Circulation Research, 2003Co-Authors: Gary D Lopaschuk, Rick L Barr, Panakkezhum D Thomas, Jason R B DyckAbstract:High rates of fatty acid oxidation in the heart and subsequent inhibition of glucose oxidation contributes to the severity of myocardial ischemia. These adverse effects of fatty acids can be overcome by stimulating glucose oxidation, either directly or secondary to an inhibition of fatty acid oxidation. We recently demonstrated that Trimetazidine stimulates glucose oxidation in the heart secondary to inhibition of fatty acid oxidation. This inhibition of fatty acid oxidation was attributed to an inhibition of mitochondrial long-chain 3-ketoacyl CoA thiolase (LC 3-KAT), an enzyme of fatty acid beta-oxidation. However, the accompanying Research Commentary of MacInnes et al suggests that Trimetazidine does not inhibit cardiac LC 3-KAT. This discrepancy with our data can be attributed to the reversible competitive nature of Trimetazidine inhibition of LC 3-KAT. In the presence of 2.5 micromol/L 3-keto-hexadecanoyl CoA (KHCoA), Trimetazidine resulted in a 50% inhibition of LC-3-KAT activity. However, the inhibition of LC 3-KAT could be completely reversed by increasing substrate (3-keto-hexadecanoyl CoA, KHCoA) concentrations to 15 micromol/L even at high concentrations of Trimetazidine (100 micromol/L). The study of MacInnes et al was performed using concentrations of 3K-HCoA in excess of 16 micromol/L, a concentration that would completely overcome 100 micromol/L Trimetazidine inhibition of LC 3-KAT. Therefore, the lack of inhibition of LC 3-KAT by Trimetazidine in the MacInnes et al study can easily be explained by the high concentration of KHCoA substrate used in their experiments. In isolated working hearts perfused with high levels of fatty acids, we found that Trimetazidine (100 micromol/L) significantly improves functional recovery of hearts subjected to a 30-minute period of global no-flow ischemia. This occurred in the absence of changes in oxygen consumption resulting in an improved increase in cardiac efficiency. Combined with our previous studies, we conclude that Trimetazidine inhibition of LC 3-KAT decreases fatty acid oxidation and stimulates glucose oxidation, resulting in an improvement in cardiac function and efficiency after ischemia. The full text of this article is available online at http://www.circresaha.org.
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beneficial effects of Trimetazidine in ex vivo working ischemic hearts are due to a stimulation of glucose oxidation secondary to inhibition of long chain 3 ketoacyl coenzyme a thiolase
Circulation Research, 2003Co-Authors: Gary D Lopaschuk, Rick L Barr, Panakkezhum D Thomas, Jason R B DyckAbstract:High rates of fatty acid oxidation in the heart and subsequent inhibition of glucose oxidation contributes to the severity of myocardial ischemia. These adverse effects of fatty acids can be overcome by stimulating glucose oxidation, either directly or secondary to an inhibition of fatty acid oxidation. We recently demonstrated that Trimetazidine stimulates glucose oxidation in the heart secondary to inhibition of fatty acid oxidation. This inhibition of fatty acid oxidation was attributed to an inhibition of mitochondrial long-chain 3-ketoacyl CoA thiolase (LC 3-KAT), an enzyme of fatty acid β-oxidation. However, the accompanying Research Commentary of MacInnes et al suggests that Trimetazidine does not inhibit cardiac LC 3-KAT. This discrepancy with our data can be attributed to the reversible competitive nature of Trimetazidine inhibition of LC 3-KAT. In the presence of 2.5 μmol/L 3-keto-hexadecanoyl CoA (KHCoA), Trimetazidine resulted in a 50% inhibition of LC-3-KAT activity. However, the inhibition of LC 3-KAT could be completely reversed by increasing substrate (3-keto-hexadecanoyl CoA, KHCoA) concentrations to 15 μmol/L even at high concentrations of Trimetazidine (100 μmol/L). The study of MacInnes et al was performed using concentrations of 3K-HCoA in excess of 16 μmol/L, a concentration that would completely overcome 100 μmol/L Trimetazidine inhibition of LC 3-KAT. Therefore, the lack of inhibition of LC 3-KAT by Trimetazidine in the MacInnes et al study can easily be explained by the high concentration of KHCoA substrate used in their experiments. In isolated working hearts perfused with high levels of fatty acids, we found that Trimetazidine (100 μmol/L) significantly improves functional recovery of hearts subjected to a 30-minute period of global no-flow ischemia. This occurred in the absence of changes in oxygen consumption resulting in an improved increase in cardiac efficiency. Combined with our previous studies, we conclude that Trimetazidine inhibition of LC 3-KAT decreases fatty acid oxidation and stimulates glucose oxidation, resulting in an improvement in cardiac function and efficiency after ischemia. The full text of this article is available online at http://www.circresaha.org.
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the antianginal drug Trimetazidine shifts cardiac energy metabolism from fatty acid oxidation to glucose oxidation by inhibiting mitochondrial long chain 3 ketoacyl coenzyme a thiolase
Circulation Research, 2000Co-Authors: Paul F Kantor, Arnaud Lucien, Raymond Kozak, Gary D LopaschukAbstract:Trimetazidine is a clinically effective antianginal agent that has no negative inotropic or vasodilator properties. Although it is thought to have direct cytoprotective actions on the myocardium, the mechanism(s) by which this occurs is as yet undefined. In this study, we determined what effects Trimetazidine has on both fatty acid and glucose metabolism in isolated working rat hearts and on the activities of various enzymes involved in fatty acid oxidation. Hearts were perfused with Krebs-Henseleit solution containing 100 microU/mL insulin, 3% albumin, 5 mmol/L glucose, and fatty acids of different chain lengths. Both glucose and fatty acids were appropriately radiolabeled with either (3)H or (14)C for measurement of glycolysis, glucose oxidation, and fatty acid oxidation. Trimetazidine had no effect on myocardial oxygen consumption or cardiac work under any aerobic perfusion condition used. In hearts perfused with 5 mmol/L glucose and 0.4 mmol/L palmitate, Trimetazidine decreased the rate of palmitate oxidation from 488+/-24 to 408+/-15 nmol x g dry weight(-1) x minute(-1) (P<0.05), whereas it increased rates of glucose oxidation from 1889+/-119 to 2378+/-166 nmol x g dry weight(-1) x minute(-1) (P<0.05). In hearts subjected to low-flow ischemia, Trimetazidine resulted in a 210% increase in glucose oxidation rates. In both aerobic and ischemic hearts, glycolytic rates were unaltered by Trimetazidine. The effects of Trimetazidine on glucose oxidation were accompanied by a 37% increase in the active form of pyruvate dehydrogenase, the rate-limiting enzyme for glucose oxidation. No effect of Trimetazidine was observed on glycolysis, glucose oxidation, fatty acid oxidation, or active pyruvate dehydrogenase when palmitate was substituted with 0.8 mmol/L octanoate or 1.6 mmol/L butyrate, suggesting that Trimetazidine directly inhibits long-chain fatty acid oxidation. This reduction in fatty acid oxidation was accompanied by a significant decrease in the activity of the long-chain isoform of the last enzyme involved in fatty acid beta-oxidation, 3-ketoacyl coenzyme A (CoA) thiolase activity (IC(50) of 75 nmol/L). In contrast, concentrations of Trimetazidine in excess of 10 and 100 micromol/L were needed to inhibit the medium- and short-chain forms of 3-ketoacyl CoA thiolase, respectively. Previous studies have shown that inhibition of fatty acid oxidation and stimulation of glucose oxidation can protect the ischemic heart. Therefore, our data suggest that the antianginal effects of Trimetazidine may occur because of an inhibition of long-chain 3-ketoacyl CoA thiolase activity, which results in a reduction in fatty acid oxidation and a stimulation of glucose oxidation.
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the antianginal drug Trimetazidine shifts cardiac energy metabolism from fatty acid oxidation to glucose oxidation by inhibiting mitochondrial long chain 3 ketoacyl coenzyme a thiolase
Circulation Research, 2000Co-Authors: Paul F Kantor, Arnaud Lucien, Raymond Kozak, Gary D LopaschukAbstract:Abstract—Trimetazidine is a clinically effective antianginal agent that has no negative inotropic or vasodilator properties. Although it is thought to have direct cytoprotective actions on the myocardium, the mechanism(s) by which this occurs is as yet undefined. In this study, we determined what effects Trimetazidine has on both fatty acid and glucose metabolism in isolated working rat hearts and on the activities of various enzymes involved in fatty acid oxidation. Hearts were perfused with Krebs-Henseleit solution containing 100 μU/mL insulin, 3% albumin, 5 mmol/L glucose, and fatty acids of different chain lengths. Both glucose and fatty acids were appropriately radiolabeled with either 3H or 14C for measurement of glycolysis, glucose oxidation, and fatty acid oxidation. Trimetazidine had no effect on myocardial oxygen consumption or cardiac work under any aerobic perfusion condition used. In hearts perfused with 5 mmol/L glucose and 0.4 mmol/L palmitate, Trimetazidine decreased the rate of palmitate ...
Eric H Karran - One of the best experts on this subject based on the ideXlab platform.
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the antianginal agent Trimetazidine does not exert its functional benefit via inhibition of mitochondrial long chain 3 ketoacyl coenzyme a thiolase
Circulation Research, 2003Co-Authors: Alan Macinnes, David Fairman, Peter Binding, Jo Ann Rhodes, Michael J Wyatt, Anne Phelan, Peter S Haddock, Eric H KarranAbstract:Trimetazidine acts as an effective antianginal clinical agent by modulating cardiac energy metabolism. Recent published data support the hypothesis that Trimetazidine selectively inhibits long-chain 3-ketoacyl CoA thiolase (LC 3-KAT), thereby reducing fatty acid oxidation resulting in clinical benefit. The aim of this study was to assess whether Trimetazidine and ranolazine, which may also act as a metabolic modulator, are specific inhibitors of LC 3-KAT. We have demonstrated that Trimetazidine and ranolazine do not inhibit crude and purified rat heart or recombinant human LC 3-KAT by methods that both assess the ability of LC 3-KAT to turnover specific substrate, and LC 3-KAT activity as a functional component of intact cellular β-oxidation. Furthermore, we have demonstrated that Trimetazidine does not inhibit any component of β-oxidation in an isolated human cardiomyocyte cell line. Ranolazine, however, did demonstrate a partial inhibition of β-oxidation in a dose-dependent manner (12% at 100 μmol/L and 30% at 300 μmol/L). Both Trimetazidine (10 μmol/L) and ranolazine (20 μmol/L) improved the recovery of cardiac function after a period of no flow ischemia in the isolated working rat heart perfused with a buffer containing a relatively high concentration (1.2 mmol/L) of free fatty acid. In summary, both Trimetazidine and ranolazine were able to improve ischemic cardiac function but inhibition of LC 3-KAT is not part of their mechanism of action. The full text of this article is available online at http://www.circresaha.org.
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the antianginal agent Trimetazidine does not exert its functional benefit via inhibition of mitochondrial long chain 3 ketoacyl coenzyme a thiolase
Circulation Research, 2003Co-Authors: Alan Macinnes, David Fairman, Peter Binding, Jo Ann Rhodes, Michael J Wyatt, Anne Phelan, Peter Haddock, Eric H KarranAbstract:Trimetazidine acts as an effective antianginal clinical agent by modulating cardiac energy metabolism. Recent published data support the hypothesis that Trimetazidine selectively inhibits long-chain 3-ketoacyl CoA thiolase (LC 3-KAT), thereby reducing fatty acid oxidation resulting in clinical benefit. The aim of this study was to assess whether Trimetazidine and ranolazine, which may also act as a metabolic modulator, are specific inhibitors of LC 3-KAT. We have demonstrated that Trimetazidine and ranolazine do not inhibit crude and purified rat heart or recombinant human LC 3-KAT by methods that both assess the ability of LC 3-KAT to turnover specific substrate, and LC 3-KAT activity as a functional component of intact cellular beta-oxidation. Furthermore, we have demonstrated that Trimetazidine does not inhibit any component of beta-oxidation in an isolated human cardiomyocyte cell line. Ranolazine, however, did demonstrate a partial inhibition of beta-oxidation in a dose-dependent manner (12% at 100 micromol/L and 30% at 300 micromol/L). Both Trimetazidine (10 micromol/L) and ranolazine (20 micromol/L) improved the recovery of cardiac function after a period of no flow ischemia in the isolated working rat heart perfused with a buffer containing a relatively high concentration (1.2 mmol/L) of free fatty acid. In summary, both Trimetazidine and ranolazine were able to improve ischemic cardiac function but inhibition of LC 3-KAT is not part of their mechanism of action. The full text of this article is available online at http://www.circresaha.org.
Jason R B Dyck - One of the best experts on this subject based on the ideXlab platform.
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beneficial effects of Trimetazidine in ex vivo working ischemic hearts are due to a stimulation of glucose oxidation secondary to inhibition of long chain 3 ketoacyl coenzyme a thiolase
Circulation Research, 2003Co-Authors: Gary D Lopaschuk, Rick L Barr, Panakkezhum D Thomas, Jason R B DyckAbstract:High rates of fatty acid oxidation in the heart and subsequent inhibition of glucose oxidation contributes to the severity of myocardial ischemia. These adverse effects of fatty acids can be overcome by stimulating glucose oxidation, either directly or secondary to an inhibition of fatty acid oxidation. We recently demonstrated that Trimetazidine stimulates glucose oxidation in the heart secondary to inhibition of fatty acid oxidation. This inhibition of fatty acid oxidation was attributed to an inhibition of mitochondrial long-chain 3-ketoacyl CoA thiolase (LC 3-KAT), an enzyme of fatty acid β-oxidation. However, the accompanying Research Commentary of MacInnes et al suggests that Trimetazidine does not inhibit cardiac LC 3-KAT. This discrepancy with our data can be attributed to the reversible competitive nature of Trimetazidine inhibition of LC 3-KAT. In the presence of 2.5 μmol/L 3-keto-hexadecanoyl CoA (KHCoA), Trimetazidine resulted in a 50% inhibition of LC-3-KAT activity. However, the inhibition of LC 3-KAT could be completely reversed by increasing substrate (3-keto-hexadecanoyl CoA, KHCoA) concentrations to 15 μmol/L even at high concentrations of Trimetazidine (100 μmol/L). The study of MacInnes et al was performed using concentrations of 3K-HCoA in excess of 16 μmol/L, a concentration that would completely overcome 100 μmol/L Trimetazidine inhibition of LC 3-KAT. Therefore, the lack of inhibition of LC 3-KAT by Trimetazidine in the MacInnes et al study can easily be explained by the high concentration of KHCoA substrate used in their experiments. In isolated working hearts perfused with high levels of fatty acids, we found that Trimetazidine (100 μmol/L) significantly improves functional recovery of hearts subjected to a 30-minute period of global no-flow ischemia. This occurred in the absence of changes in oxygen consumption resulting in an improved increase in cardiac efficiency. Combined with our previous studies, we conclude that Trimetazidine inhibition of LC 3-KAT decreases fatty acid oxidation and stimulates glucose oxidation, resulting in an improvement in cardiac function and efficiency after ischemia. The full text of this article is available online at http://www.circresaha.org.
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beneficial effects of Trimetazidine in ex vivo working ischemic hearts are due to a stimulation of glucose oxidation secondary to inhibition of long chain 3 ketoacyl coenzyme a thiolase
Circulation Research, 2003Co-Authors: Gary D Lopaschuk, Rick L Barr, Panakkezhum D Thomas, Jason R B DyckAbstract:High rates of fatty acid oxidation in the heart and subsequent inhibition of glucose oxidation contributes to the severity of myocardial ischemia. These adverse effects of fatty acids can be overcome by stimulating glucose oxidation, either directly or secondary to an inhibition of fatty acid oxidation. We recently demonstrated that Trimetazidine stimulates glucose oxidation in the heart secondary to inhibition of fatty acid oxidation. This inhibition of fatty acid oxidation was attributed to an inhibition of mitochondrial long-chain 3-ketoacyl CoA thiolase (LC 3-KAT), an enzyme of fatty acid beta-oxidation. However, the accompanying Research Commentary of MacInnes et al suggests that Trimetazidine does not inhibit cardiac LC 3-KAT. This discrepancy with our data can be attributed to the reversible competitive nature of Trimetazidine inhibition of LC 3-KAT. In the presence of 2.5 micromol/L 3-keto-hexadecanoyl CoA (KHCoA), Trimetazidine resulted in a 50% inhibition of LC-3-KAT activity. However, the inhibition of LC 3-KAT could be completely reversed by increasing substrate (3-keto-hexadecanoyl CoA, KHCoA) concentrations to 15 micromol/L even at high concentrations of Trimetazidine (100 micromol/L). The study of MacInnes et al was performed using concentrations of 3K-HCoA in excess of 16 micromol/L, a concentration that would completely overcome 100 micromol/L Trimetazidine inhibition of LC 3-KAT. Therefore, the lack of inhibition of LC 3-KAT by Trimetazidine in the MacInnes et al study can easily be explained by the high concentration of KHCoA substrate used in their experiments. In isolated working hearts perfused with high levels of fatty acids, we found that Trimetazidine (100 micromol/L) significantly improves functional recovery of hearts subjected to a 30-minute period of global no-flow ischemia. This occurred in the absence of changes in oxygen consumption resulting in an improved increase in cardiac efficiency. Combined with our previous studies, we conclude that Trimetazidine inhibition of LC 3-KAT decreases fatty acid oxidation and stimulates glucose oxidation, resulting in an improvement in cardiac function and efficiency after ischemia. The full text of this article is available online at http://www.circresaha.org.
Alan Macinnes - One of the best experts on this subject based on the ideXlab platform.
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the antianginal agent Trimetazidine does not exert its functional benefit via inhibition of mitochondrial long chain 3 ketoacyl coenzyme a thiolase
Circulation Research, 2003Co-Authors: Alan Macinnes, David Fairman, Peter Binding, Jo Ann Rhodes, Michael J Wyatt, Anne Phelan, Peter S Haddock, Eric H KarranAbstract:Trimetazidine acts as an effective antianginal clinical agent by modulating cardiac energy metabolism. Recent published data support the hypothesis that Trimetazidine selectively inhibits long-chain 3-ketoacyl CoA thiolase (LC 3-KAT), thereby reducing fatty acid oxidation resulting in clinical benefit. The aim of this study was to assess whether Trimetazidine and ranolazine, which may also act as a metabolic modulator, are specific inhibitors of LC 3-KAT. We have demonstrated that Trimetazidine and ranolazine do not inhibit crude and purified rat heart or recombinant human LC 3-KAT by methods that both assess the ability of LC 3-KAT to turnover specific substrate, and LC 3-KAT activity as a functional component of intact cellular β-oxidation. Furthermore, we have demonstrated that Trimetazidine does not inhibit any component of β-oxidation in an isolated human cardiomyocyte cell line. Ranolazine, however, did demonstrate a partial inhibition of β-oxidation in a dose-dependent manner (12% at 100 μmol/L and 30% at 300 μmol/L). Both Trimetazidine (10 μmol/L) and ranolazine (20 μmol/L) improved the recovery of cardiac function after a period of no flow ischemia in the isolated working rat heart perfused with a buffer containing a relatively high concentration (1.2 mmol/L) of free fatty acid. In summary, both Trimetazidine and ranolazine were able to improve ischemic cardiac function but inhibition of LC 3-KAT is not part of their mechanism of action. The full text of this article is available online at http://www.circresaha.org.
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the antianginal agent Trimetazidine does not exert its functional benefit via inhibition of mitochondrial long chain 3 ketoacyl coenzyme a thiolase
Circulation Research, 2003Co-Authors: Alan Macinnes, David Fairman, Peter Binding, Jo Ann Rhodes, Michael J Wyatt, Anne Phelan, Peter Haddock, Eric H KarranAbstract:Trimetazidine acts as an effective antianginal clinical agent by modulating cardiac energy metabolism. Recent published data support the hypothesis that Trimetazidine selectively inhibits long-chain 3-ketoacyl CoA thiolase (LC 3-KAT), thereby reducing fatty acid oxidation resulting in clinical benefit. The aim of this study was to assess whether Trimetazidine and ranolazine, which may also act as a metabolic modulator, are specific inhibitors of LC 3-KAT. We have demonstrated that Trimetazidine and ranolazine do not inhibit crude and purified rat heart or recombinant human LC 3-KAT by methods that both assess the ability of LC 3-KAT to turnover specific substrate, and LC 3-KAT activity as a functional component of intact cellular beta-oxidation. Furthermore, we have demonstrated that Trimetazidine does not inhibit any component of beta-oxidation in an isolated human cardiomyocyte cell line. Ranolazine, however, did demonstrate a partial inhibition of beta-oxidation in a dose-dependent manner (12% at 100 micromol/L and 30% at 300 micromol/L). Both Trimetazidine (10 micromol/L) and ranolazine (20 micromol/L) improved the recovery of cardiac function after a period of no flow ischemia in the isolated working rat heart perfused with a buffer containing a relatively high concentration (1.2 mmol/L) of free fatty acid. In summary, both Trimetazidine and ranolazine were able to improve ischemic cardiac function but inhibition of LC 3-KAT is not part of their mechanism of action. The full text of this article is available online at http://www.circresaha.org.
Agnieszka Gajdowska - One of the best experts on this subject based on the ideXlab platform.
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original paper protective effect on visual functions of long term use of Trimetazidine in treatment of primary open angle glaucoma and degenerative myopia
Archives of Medical Science, 2007Co-Authors: Michal S Nowak, Katarzyna Wybor, Roman Goś, Alicja Zemanmiecznik, Arleta Waszczykowska, Miroslaw Pastuszka, Anna Klysik, Agnieszka GajdowskaAbstract:Introduction: The purpose of the study was to evaluate selected visual parameters in the group of patients undergoing long-term treatment with Trimetazidine as an adjuvant therapy for primary open angle glaucoma and degenerative myopia. Material and methods: Thirty patients, including 20 patients with advanced primary open angle glaucoma (40 eyes) and 10 patients with severe degenerative myopia (20 eyes), were treated with Trimetazidine 20 mg twice a day. We excluded from the study patients with: systemic hypertension and/or diabetes, cataract, history of chronic and recurrent severe inflammatory eye disease and smokers. Patients with primary open angle glaucoma were taking various ocular hypotensive drops topically. Ophthalmic examination has been performed before administration of Trimetazidine and then every month. Visual acuity, contrast sensitivity test (Pelli-Robson test), glare test, color vision (Farnsworth-Munsell test) and visual field were recorded. Follow-up period was 6 months. For statistical analysis paired Student’s t- test (p<0.05) was used. Results: The contrast sensitivity and visual acuity improved in all patients and the results were statistically significant. Glare tests, colour vision and visual fields did not reveal any statistically significant changes. Conclusions: The results of the study demonstrate that long term use of Trimetazidine improved contrast sensitivity and visual acuity. The drug was well tolerated and might be considered as the adjunctive therapy in patients with primary open angle glaucoma and degenerative myopia.
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Original paperProtective effect on visual functions of long-term use of Trimetazidine in treatment of primary open angle glaucoma and degenerative myopia
Termedia Publishing House, 2007Co-Authors: Michal S Nowak, Katarzyna Wybor, Roman Goś, Arleta Waszczykowska, Miroslaw Pastuszka, Alicja Zeman-miecznik, Anna Kłysik, Agnieszka GajdowskaAbstract:Introduction: The purpose of the study was to evaluate selected visual parameters in the group of patients undergoing long-term treatment with Trimetazidine as an adjuvant therapy for primary open angle glaucoma and degenerative myopia.Material and methods: Thirty patients, including 20 patients with advanced primary open angle glaucoma (40 eyes) and 10 patients with severe degenerative myopia (20 eyes), were treated with Trimetazidine 20 mg twice a day. We excluded from the study patients with: systemic hypertension and/or diabetes, cataract, history of chronic and recurrent severe inflammatory eye disease and smokers. Patients with primary open angle glaucoma were taking various ocular hypotensive drops topically. Ophthalmic examination has been performed before administration of Trimetazidine and then every month. Visual acuity, contrast sensitivity test (Pelli-Robson test), glare test, color vision (Farnsworth-Munsell test) and visual field were recorded. Follow-up period was 6 months. For statistical analysis paired Student’s t- test (p
