Additional Use of Trimetazidine in Patients With Chronic Heart Failure

Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital of Fudan University, Shanghai, China.
Journal of the American College of Cardiology (Impact Factor: 16.5). 03/2012; 59(10):913-22. DOI: 10.1016/j.jacc.2011.11.027
Source: PubMed


The aim of this meta-analysis was to evaluate the effects of additional trimetazidine (TMZ) treatment on patients with chronic heart failure (CHF).
Conflicting results currently exist on the clinical use of TMZ in CHF patients.
PubMed, MEDLINE, EMBASE, and EBM Reviews databases were searched through November 2010 for randomized controlled trials (RCTs) assessing TMZ treatment in CHF patients. Data concerning the study design, patient characteristics, and outcomes were extracted. Risk ratio (RR) and weighted mean differences (WMD) were calculated using fixed or random effects models.
Sixteen RCTs involving 884 CHF patients were included. Hospitalization for cardiac causes (RR: 0.43, p = 0.03), but not all-cause mortality (RR: 0.47, p = 0.27), was reduced by TMZ treatment. Moreover, TMZ therapy was associated not only with the increase of left ventricular ejection fraction (WMD: 6.46%, p < 0.0001) and total exercise time (WMD: 63.75 seconds, p < 0.0001), but also with the decrease of New York Heart Association functional class (WMD: -0.57, p = 0.0003), left ventricular end-systolic diameter (WMD: -6.67 mm, p < 0.0001), left ventricular end-diastolic diameter (WMD: -6.05 mm, p < 0.0001), and B-type natriuretic peptide (WMD: -203.40 pg/ml, p = 0.0002).
Additional use of TMZ in CHF patients may decrease hospitalization for cardiac causes, improve clinical symptoms and cardiac function, and simultaneously ameliorate left ventricular remodeling.

18 Reads
  • Source
    • "One year later, Zhang et al. [54] presented another meta-analysis on the use of trimetazidine in CHF patients. This time, 16 randomized studies were evaluated, with 884 patients in the study group. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Trimetazidine is a cytoprotective drug whose cardiovascular effectiveness, especially in patients with stable ischemic heart disease, has been the source of much controversy in recent years; some have gone so far as to treat the medication as a ‘placebo drug’ whose new side effects, such as Parkinsonian symptoms, outweigh its benefits. This article is an attempt to present the recent key studies, including meta-analyses, on the use of trimetazidine in chronic heart failure, also in patients with diabetes mellitus and arrhythmia, as well as in peripheral artery disease. This paper also includes the most recent European Society of Cardiology guidelines, including those of 2013, on the use of trimetazidine in cardiovascular disease.
    Drugs 06/2014; 74(9). DOI:10.1007/s40265-014-0233-5 · 4.34 Impact Factor
  • Source
    • "These trials investigated clinical symptoms, cardiac function, quality of life, hospitalization, mortality and cardiovascular events, comparing TMZ with placebo. In addition, two meta-analyses of RCTs have also been performed to assess the therapeutic effects of TMZ in CHF patients [7], [8]. However, some conclusions drawn from these two meta-analyses are not consistent. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Whether additional benefit can be achieved with the use of trimetazidine (TMZ) in patients with chronic heart failure (CHF) remains controversial. We therefore performed a meta-analysis of randomized controlled trials (RCTs) to evaluate the effects of TMZ treatment in CHF patients. We searched PubMed, EMBASE, and Cochrane databases through October 2013 and included 19 RCTs involving 994 CHF patients who underwent TMZ or placebo treatment. Risk ratio (RR) and weighted mean differences (WMD) were calculated using fixed or random effects models. TMZ therapy was associated with considerable improvement in left ventricular ejection fraction (WMD: 7.29%, 95% CI: 6.49 to 8.09, p<0.01) and New York Heart Association classification (WMD: -0.55, 95% CI: -0.81 to -0.28, p<0.01). Moreover, treatment with TMZ also resulted in significant decrease in left ventricular end-systolic volume (WMD: -17.09 ml, 95% CI: -20.15 to -14.04, p<0.01), left ventricular end-diastolic volume (WMD: -11.24 ml, 95% CI: -14.06 to -8.42, p<0.01), hospitalization for cardiac causes (RR: 0.43, 95% CI: 0.21 to 0.91, p = 0.03), B-type natriuretic peptide (BNP; WMD: -157.08 pg/ml, 95% CI: -176.55 to -137.62, p<0.01) and C-reactive protein (CRP; WMD: -1.86 mg/l, 95% CI: -2.81 to -0.90, p<0.01). However, there were no significant differences in exercise duration and all-cause mortality between patients treated with TMZ and placebo. TMZ treatment in CHF patients may improve clinical symptoms and cardiac function, reduce hospitalization for cardiac causes, and decrease serum levels of BNP and CRP.
    PLoS ONE 05/2014; 9(5):e94660. DOI:10.1371/journal.pone.0094660 · 3.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The heart is an omnivore organ that requires constant energy production to match its functional demands. In the adult heart, adenosine-5'-triphosphate (ATP) production occurs mainly through mitochondrial fatty acid and glucose oxidation. The heart must constantly adapt its energy production in response to changes in substrate supply and work demands across diverse physiologic and pathophysiologic conditions. The cardiac myocyte maintains a high level of mitochondrial ATP production through a complex transcriptional regulatory network that is orchestrated by the members of the peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family. There is increasing evidence that during the development of cardiac hypertrophy and in the failing heart, the activity of this network, including PGC-1, is altered. This review summarizes our current understanding of the perturbations in the gene regulatory pathways that occur during the development of heart failure. An appreciation of the role this regulatory circuitry serves in the regulation of cardiac energy metabolism may unveil novel therapeutic targets aimed at the metabolic disturbances that presage heart failure. This article is part of a Special Issue entitled:Cardiomyocyte Biology: Cardiac Pathways of Differentiation, Metabolism and Contraction.
    Biochimica et Biophysica Acta 08/2012; 1833(4). DOI:10.1016/j.bbamcr.2012.08.015 · 4.66 Impact Factor
Show more


18 Reads
Available from