Impact of Trimetazidine on Incidence of Myocardial Injury and Contrast-Induced Nephropathy in Diabetic Patients With Renal Dysfunction Undergoing Elective Percutaneous Coronary Intervention

Shehata, Mohamed

doi:10.1016/j.amjcard.2014.04.052

Cited by 32 publications

(39 citation statements)

References 22 publications

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“…The beneficial effects of TMZ on mortality, hospitalization and left ventricular function in ischemic heart disease have been confirmed by clinical [24,25] and animal studies [13,14]; however, the underlying molecular mechanisms of cardioprotective effects of TMZ remain to be elucidated. Previous studies have shown that TMZ can optimize cardiac metabolism by reducing fatty acid oxidation through selective inhibition of mitochondrial 3-ketoacyl CoA thiolase, thus attenuating the adverse effects of free acid-associated oxidative stress [26] and improving mitochondrial metabolism and cardiac performance during ischemia [23].…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…Ряд экспериментальных и клинических исследований позволяют предполагать наличие у триметазидина нефро-протективного эффекта [78][79][80][81][82]. Например, при назначе-нии триметазидина МВ за 2 дня до проведения инвазив-ных коронарных процедур (коронарография и др.)…”

Section: на сегодняшний день обсуждаются плейотропные эффекты триметаunclassified

“…у пациентов с повышенным уровнем креатинина уменьша-ется частота нефропатии, вызванной введением рентген-контрастного вещества [79]. В другом исследовании при-менение триметазидина 70 мг в течение 3 дней перед плановой ЧКВ у пациентов с СД и почечной дисфункцией снижало риск развития контраст-индуцированной нефро-патии и повреждения миокарда по уровню сердечного тропонина I [80]. При использова нии триметазидина отмечено улучшение функции почек у пациентов с шоком [81].…”

Section: на сегодняшний день обсуждаются плейотропные эффекты триметаunclassified

Myocardial Cytoprotector Trimetazidine Mb-Preparat, Increases the Effectiveness of Treatment of Chronic Heart Failure and Coronary Heart Disease

Трухан¹,

Давыдов²,

Мазуров³

2017

Med. sov.

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“…Recently, it has TABLE 3 Prevention of contrast-induced acute kidney injury 53,[57][58][59][60][61]64,68,[72][73][74][90][91][92][93][94][95][96] The limitations of HD are somewhat overcome by continuous extracorporeal blood purification techniques such as continuous venovenous hemofiltration (CVVH). Marenzi et al 82 reported that CVVH had an advantage over saline hydration in the reduction of the rate of CI-AKI (5% vs 50% respectively, P <0.001), the need for repeated RRT (3% vs 25%), the rate of in-hospital complications, and the rates of in-hospital (2% vs 14%, P = 0.02) and 1-year mortality (10% vs. 30%, P = 0.01).…”

mentioning

confidence: 99%

Contrast-induced acute kidney injury: the dark side of cardiac catheterization

Wybraniec¹,

Mizia-Stec²,

Wiȩcek³

2015

Polish Archives of Internal Medicine

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POLSKIE ARCHIWUM MEDYCYNY WEWNĘTRZNEJ 2015; 125 (12) 938the diagnostic criteria applied, comorbidities, and the type of procedure (coronary angiography [CA]; percutaneous coronary intervention [PCI]). CI-AKI is a challenge mainly for well-developed countries, in which excessive amounts of CM are used on a daily basis. When using the definition of CI-AKI as an increase of serum creatinine concentrations (SCr) by more than 25% relative to baseline and/or by more than 0.5 mg/dl at 48 hours after PCI, the rate of CI-AKI ranged from 3.3% according to the Mayo Clinic PCI registry 6 to 13.1% as stated by Mehran et al. 7 In the largest registry by Gurm et al, 8 based on 68 573 procedures, the rate of CI-AKI was 2.5%, defined as an absolute elevation in SCr by more than 0.5 mg/dl. Still, when only clinically relevant CI-AKI requiring dialysis was considered, the incidence decreased to a range from 0.8% to 1.7%. 9 This review sought to summarize the contemporary knowledge on pathophysiology, risk factors, diagnostic markers, and management of CI-AKI, with a special interest in CI-AKI as a result of cardiac catheterization. Accordingly, the Medline and EmBase databases were queried to Introduction Contrast-induced acute kidney injury (CI-AKI), previously known as contrast--induced nephropathy (CIN), represents a specific form of acute renal function impairment triggered by the use of iodinated contrast media (CM). As CI-AKI remains the subtype of acute kidney injury (AKI), it is recommended to use common definitions of AKI, such as the 2012 KDIGO criteria, 1 RIFLE classification (Risk, Injury, Failure, Loss of Function, End-Stage Renal Disease), 2 AKI Network criteria, 3 or the definition by Harjai 4 (Supplementary material online, Table S1).The rapid development of invasive cardiology triggered a massive increase in CM exposure. Since the implementation of the first CM in the 1950s, CI-AKI has emerged as the third most common subtype of hospital-acquired renal failure (reaching 11% of all cases), after renal hypoperfusion (42%) and postoperative AKI.5 Nearly half of all cases of CI-AKI occur after invasive cardiac procedures owing to CM-related nephrotoxicity and frequently present hemodynamic instability. 5The exact rate of CI-AKI in the setting of a cardiology department varies depending on ABSTRACTThe rapidly growing number of percutaneous coronary interventions has led to a considerable improvement in the outcome of patients with acute coronary syndromes, yet concurrently exposing patients to enormous volumes of contrast media with the inherent risk of renal function impairment. The issue of contrast-induced acute kidney injury (CI-AKI) is not only associated with direct sequelae such as prolonged hospital stay, but also with increased risk of chronic kidney disease, recurrent acute coronary syndromes, cerebral ischemia, and increased mortality rate. The ubiquitous application of contrast media warrants active search for reliable risk factors, diagnostic markers, preventive measures, and therapeutic modalities th...

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Impact of Trimetazidine on Incidence of Myocardial Injury and Contrast-Induced Nephropathy in Diabetic Patients With Renal Dysfunction Undergoing Elective Percutaneous Coronary Intervention

Cited by 32 publications

References 22 publications

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

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

Myocardial Cytoprotector Trimetazidine Mb-Preparat, Increases the Effectiveness of Treatment of Chronic Heart Failure and Coronary Heart Disease

Contrast-induced acute kidney injury: the dark side of cardiac catheterization

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