Trimetazidine in the Prevention of Tissue Ischemic Conditions

Kallistratos, Manolis S.; Poulimenos, Leonidas; Giannitsi, S.; Tsinivizov, Pavlos; Manolis, Athanasios

doi:10.1177/0003319718780551

Cited by 24 publications

(19 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Various methods for preventing CIN have been investigated in recent years [6,7]. Trimetazidine (TMZ), a type of myocardial metabolic and anti-ischemic agent, is widely used in patients with coronary disease due to its protective action against free radical damage and ischemia/reperfusion injury [8]. Oxygen-free radical release leading to medullary ischemic injury is a major pathophysiology of CIN.…”

Section: Electronic Supplementary Materialsmentioning

confidence: 99%

The effect of trimetazidine on preventing contrast-induced nephropathy after cardiac catheterization

Lian

Zhan

et al. 2019

Int Urol Nephrol

View full text Add to dashboard Cite

Purpose Trimetazidine has been shown to prevent the risk of contrast-induced nephropathy (CIN) in patients with renal dysfunction undergoing percutaneous coronary intervention (PCI). However, the effect of trimetazidine on CIN in unselected patients is unknown. We aimed to evaluate the effect of trimetazidine on preventing CIN in unselected patients treated with PCI. Methods 2154 consecutive patients were enrolled and divided into the trimetazidine (n = 529) and non-trimetazidine group (n = 1625). Patients in the trimetazidine group received trimetazidine 20 mg thrice daily starting at least 24 h before the procedure and continuing until discharge. The primary outcome was CIN. Results CIN was observed in 197 (9.2%) patients. The incidence of CIN was similar between two groups (9.1% vs. 9.2%, P = 0.947). After adjusting for other potential risk factors, trimetazidine did not significantly reduce the risk of CIN (OR = 0.70, 95% CI 0.46-1.08, P = 0.104). The results remained similar when using the alternate definitions of CIN and different subgroup analysis based on diabetes or chronic kidney disease. In additional, no significant difference between two groups was found with respect to in-hospital major adverse clinical events (1.89% vs. 1.66%, P > 0.05). Conclusions Trimetazidine did not exert significant renal protective effect on preventing CIN and in hosptial major adverse clinical events in unselected patients undergoing PCI.

show abstract

Section: Electronic Supplementary Materialsmentioning

confidence: 99%

The effect of trimetazidine on preventing contrast-induced nephropathy after cardiac catheterization

Lian

Zhan

et al. 2019

Int Urol Nephrol

View full text Add to dashboard Cite

show abstract

“…Trimetazidine (TMZ) is a metabolic anti-ischemic agent that can shift the energy substrate metabolism and enhance glucose metabolism ( Kallistratos et al, 2019 ). Clinically, TMZ is administered as treatment for angina pectoris and heart failure ( Shu et al, 2020 ; Amoedo et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Function and Mechanism of Trimetazidine in Myocardial Infarction-Induced Myocardial Energy Metabolism Disorder Through the SIRT1–AMPK Pathway

et al. 2021

View full text Add to dashboard Cite

Myocardial energy metabolism (MEM) is an important factor of myocardial injury. Trimetazidine (TMZ) provides protection against myocardial ischemia/reperfusion injury. The current study set out to evaluate the effect and mechanism of TMZ on MEM disorder induced by myocardial infarction (MI). Firstly, a MI mouse model was established by coronary artery ligation, which was then treated with different concentrations of TMZ (5, 10, and 20 mg kg–1 day–1). The results suggested that TMZ reduced the heart/weight ratio in a concentration-dependent manner. TMZ also reduced the levels of Bax and cleaved caspase-3 and promoted Bcl-2 expression. In addition, TMZ augmented adenosine triphosphate (ATP) production and superoxide dismutase (SOD) activity induced by MI and decreased the levels of lipid peroxide (LPO), free fatty acids (FFA), and nitric oxide (NO) in a concentration-dependent manner (all P < 0.05). Furthermore, an H2O2-induced cell injury model was established and treated with different concentrations of TMZ (1, 5, and 10 μM). The results showed that SIRT1 overexpression promoted ATP production and reactive oxygen species (ROS) activity and reduced the levels of LPO, FFA, and NO in H9C2 cardiomyocytes treated with H2O2 and TMZ. Silencing SIRT1 suppressed ATP production and ROS activity and increased the levels of LPO, FFA, and NO (all P < 0.05). TMZ activated the SIRT1–AMPK pathway by increasing SIRT1 expression and AMPK phosphorylation. In conclusion, TMZ inhibited MI-induced myocardial apoptosis and MEM disorder by activating the SIRT1–AMPK pathway.

show abstract

“…By selectively inhibiting the activity of enzyme 3-ketoacyl coenzyme A thiolase (3KAT) in the β-oxidation pathway, TMZ enhances glucose metabolism of cardiomyocytes and maintains energy production with less oxygen consumption [ 11 ]. Due to its significant anti-ischaemic properties [ 12 ], TMZ has become a standard treatment for ischaemic cardiomyopathy (ICM) [ 13 ] as monotherapy or adjunct therapy since 1978 [ 14 , 15 ]. Nowadays, TMZ is prescribed as a long-term treatment of angina pectoris in more than 90 countries around the world [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Trimetazidine ameliorates hindlimb ischaemic damage in type 2 diabetic mice

Yang

et al. 2021

Annals of Medicine

View full text Add to dashboard Cite

Background: Ischaemia caused by lower extremity artery stenosis is the main cause of peripheral artery disease (PAD) in patients with diabetes. Trimetazidine (TMZ) has traditionally been used as an anti-ischaemic drug for coronary artery disease. The effect of TMZ on PAD in a diabetic animal model and the underlying molecular mechanisms remain unclear. Methods: The db/db mice were challenged with femoral artery ligation (FAL), followed by TMZ treatment for 2 weeks. Scores on hindlimb ischaemia and function were evaluated. Histological and capillary density analyses of gastrocnemius were performed. The expression of vascular endothelial growth factor (VEGF) and myogenic regulators was also confirmed by Western blotting. We also detected serum intercellular adhesion molecule 1 (ICAM-1) level through ELISA. Results: Diabetic mice exhibited limb ulceration and motor dysfunction after FAL while TMZtreated db/db mice exhibited milder ischaemic impairment. Furthermore, decreased capillary density in the gastrocnemius muscles of ischaemic hindlimb and reduced expressions of VEGF, myogenic markers, and serum ICAM-1 could be partially reversed by TMZ treatment. Conclusion: TMZ may alleviate hindlimb ischaemic damage in db/db mice, at least partly, through enhancing angiogenesis and promoting myogenesis in ischaemia region. KEY MESSAGESTMZ intervention could alleviate hindlimb ischaemic damage in db/db mice. TMZ intervention could enhance angiogenesis and stimulate myogenesis in ischaemia region.

show abstract

Trimetazidine in the Prevention of Tissue Ischemic Conditions

Cited by 24 publications

References 44 publications

The effect of trimetazidine on preventing contrast-induced nephropathy after cardiac catheterization

The effect of trimetazidine on preventing contrast-induced nephropathy after cardiac catheterization

Function and Mechanism of Trimetazidine in Myocardial Infarction-Induced Myocardial Energy Metabolism Disorder Through the SIRT1–AMPK Pathway

Trimetazidine ameliorates hindlimb ischaemic damage in type 2 diabetic mice

Contact Info

Product

Resources

About