Trimetazidine is an anti-ischemic agent with antioxidant activity. This study evaluated the effect of periprocedural administration of trimetazidine on the incidence of percutaneous coronary intervention (PCI)–induced myocardial injury and contrast-induced nephropathy (CIN) in diabetic patients with mild-to-moderate renal dysfunction. One hundred patients with a mean glomerular filtration rate of 48 ± 16 (ml/min/1.73 m 2 ) were prospectively enrolled, then randomly assigned to receive (50 patients; trimetazidine group) or not receive (50 patients; control group) periprocedural trimetazidine (70 mg/day) for 72 hours. The serum creatinine level was measured pre-PCI, 72 hours, and 10 days thereafter. An increase in the serum creatinine level by >0.5 mg/dl or 0.25% of the baseline value is considered as CIN. Cardiac troponin I levels were measured before and 6, 12, and 24 hours after PCI. Mean age of the study cohort was 59 ± 6 years (men 68%). The serum creatinine level in the control group increased significantly 3 days after PCI and decreased on the tenth day. However, it showed no significant change in the trimetazidine group. Incidence of CIN was 12% in the trimetazidine group and 28% in the control group (p <0.05). Cardiac troponin I levels were significantly reduced in the trimetazidine group (6 hours: 8 ± 0.3 vs 16 ± 0.2 pg/ml, 12 hours: 13 ± 0.9 vs 24 ± 0.8 pg/ml, 24 hours: 7 ± 0.7 vs 14 ± 0.3 pg/ml, p <0.001). In conclusion, trimetazidine intake before elective PCI in diabetic patients with mild-to-moderate renal dysfunction is associated with decreased incidence of CIN and myocardial injury.
Asymptomatic minor postprocedural myocardial necrosis does have an important prognostic signification after percutaneous coronary intervention (PCI). The magnitude of increase in the level of cardiac troponin I (cTnI) directly correlates with irreversible myocardial injury assessed by cardiovascular magnetic resonance imaging. This study sought to evaluate the impact of trimetazidine oral loading on the incidence of periprocedural myocardial damage, assessed by the frequency and level of cTnI release after PCI. Also, this study sought to evaluate the assumed role of the same drug as an antioxidant (decreasing oxygen free radicals) and anti-ischemic agent (decreasing renal medullary ischemia) in prevention of contrast-induced nephropathy (CIN) in the same clinical setting. This study targeted diabetic patients with mild-to-moderate chronic kidney disease (CKD).
Methods
One hundred consecutive diabetic patients, carrying the diagnosis of chronic stable angina and having mild or moderate CKD, were prospectively enrolled in this study. They were referred to the catheterization laboratory for planned PCI in the period from October 2011 to February 2013, owing to previous coronary angiography findings, obtained within 1 month before PCI. Mild-to-moderate CKD was defined by means of estimated glomerular filtration rate (eGFR) of 30 to <90 ml/min/1.73 m 2 . Exclusion criteria included severe CKD (eGFR <30 ml/min/1.73 m 2 ) ; end-stage renal disease (or patients on hemodialysis); acute myocardial infarction requiring emergency coronary intervention; cardiogenic shock; history of acute coronary syndrome; history of PCI or coronary artery bypass graft surgery; congenital heart disease or any myocardial disease apart from ischemia; limited life expectancy due to coexistent disease, for example, malignancy; positive preprocedural cTnI result; previous treatment with trimetazidine; and contraindications for aspirin, clopidogrel, or trimetazidine use (Parkinson disease and other motion disorders). After enrollment and before PCI, patients were randomly assigned in 1:1 fashion to either the trimetazidine group or the control group according to a computer-generated random series of numbers. Randomization was performed by block randomization (blocks of 10 patients). The trimetazidine group of patients received oral trimetazidine (35 mg twice daily) for 72 hours, starting 48 hours before PCI, in addition to periprocedural intravenous (IV) infusion of isotonic saline solution and oral N-acetylcysteine. The control group received IV infusion of isotonic saline solution and oral N-acetylcysteine only. Physicians participating in the PCI procedures were unaware of block randomization. All included patients were subjected to detailed history taking including drug intake, baseline 12-lead electrocardiography, and transthoracic echocardiography. Before inclusion, informed written consent was obtained from each patient, and the study protocol was reviewed and approved by our local institutional human research committee as it conforms to the ethical guidelines of the 1975 Declaration of Helsinki, as revised in 2008.
Assessment of regional and global left ventricular systolic functions was performed in all patients by transthoracic echocardiography using a General Electric Vivid 7 cardiac ultrasound machine (General Electric, Horten, Norway). Left ventricular ejection fraction (%) by the modified Simpson method, left ventricular internal dimensions using M-mode, and wall motion abnormalities were recorded. Regional wall motion was assessed according to the standard 17-segment model as recommended by the American Society of Echocardiography.
eGFR and serum creatinine values were recorded, immediately before PCI (baseline data) and 72 hours and 10 days after the procedure. eGFR was calculated using the Modification of Diet in Renal Disease (MDRD) equation :
eGFR MDRD ( mL ⋅ min − 1 ⋅ 1.73 m − 2 ) = 175 × ( s . creatinine ) − 1.154 × ( age ) − 0.203 × 0.742 ( if female ) × 1.212 ( if black )
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