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      Effect of Trimetazidine Dihydrochloride Therapy on Exercise Capacity in Patients With Nonobstructive Hypertrophic Cardiomyopathy : A Randomized Clinical Trial

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          Abstract

          Hypertrophic cardiomyopathy causes limiting symptoms in patients, mediated partly through inefficient myocardial energy use. There is conflicting evidence for therapy with inhibitors of myocardial fatty acid metabolism in patients with nonobstructive hypertrophic cardiomyopathy.

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          Assessment of patient outcome with the Minnesota Living with Heart Failure questionnaire: Reliability and validity during a randomized, double-blind, placebo-controlled trial of pimobendan

          Jay Cohn, Thomas S. Rector (1992)
          Article 0 comments Cited 96 times – based on 0 reviews     Review now
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            Hypertrophic cardiomyopathy due to sarcomeric gene mutations is characterized by impaired energy metabolism irrespective of the degree of hypertrophy.

            Jenifer G. Crilley, Ernest Boehm, Edward Blair … (2003)
            We investigated cardiac energetics in subjects with mutations in three different familial hypertrophic cardiomyopathy (HCM) disease genes, some of whom were nonpenetrant carriers without hypertrophy, using phosphorus-31 magnetic resonance spectroscopy. Familial hypertrophic cardiomyopathy is caused by mutations in sarcomeric protein genes. The mechanism by which these mutant proteins cause disease is uncertain. A defect of myocyte contractility had been proposed, but in vitro studies of force generation have subsequently shown opposing results in different classes of mutation. An alternative hypothesis of "energy compromise" resulting from inefficient utilization of adenosine triphosphate (ATP) has been suggested, but in vivo data in humans with genotyped HCM are lacking. The cardiac phosphocreatine (PCr) to ATP ratio was determined at rest in 31 patients harboring mutations in the genes for either beta-myosin heavy chain, cardiac troponin T, or myosin-binding protein C, and in 24 controls. Transthoracic echocardiography was used to measure left ventricular (LV) dimensions and maximal wall thickness. The PCr/ATP was reduced in the HCM subjects by 30% relative to controls (1.70 +/- 0.43 vs. 2.44 +/- 0.30; p < 0.001), and the reduction was of a similar magnitude in all three disease-gene groups. The PCr/ATP was equally reduced in subjects with (n = 24) and without (n = 7) LV hypertrophy. Our data provide evidence of a bioenergetic deficit in genotype-confirmed HCM, which is present to a similar degree in three disease-gene groups. The presence of energetic abnormalities, even in those without hypertrophy, supports a proposed link between altered cardiac energetics and development of the disease phenotype.
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              A randomized clinical trial of trimetazidine, a partial free fatty acid oxidation inhibitor, in patients with heart failure.

              Ottavio Alfieri, Alberto Margonato, Gabriele Fragasso … (2006)
              This study sought to assess whether the long-term addition of trimetazidine to conventional treatment could improve functional class, exercise tolerance, and left ventricular function in patients with heart failure (HF). Previous small studies have shown that trimetazidine may be beneficial in terms of left ventricular function preservation and control of symptoms in patients with post-ischemic HF. Fifty-five patients with HF were randomly allocated in an open-label fashion to either conventional therapy plus trimetazidine (20 mg three times daily) (28 patients) or conventional therapy alone (27 patients). Mean follow-up was 13 +/- 3 months. At study entry and at follow-up, all patients underwent exercise testing and two-dimensional echocardiography. Among the others, New York Heart Association (NYHA) functional class and ejection fraction (EF) were evaluated. In the trimetazidine group, NYHA functional class significantly improved compared with the conventional therapy group (p < 0.0001). Treatment with trimetazidine significantly decreased left ventricular end-systolic volume (from 98 +/- 36 ml to 81 +/- 27 ml, p = 0.04) and increased EF from 36 +/- 7% to 43 +/- 10% (p = 0.002). On the contrary, in the conventional therapy group, both left ventricular end-diastolic and -systolic volumes increased from 142 +/- 43 ml to 156 +/- 63 ml, p = 0.2, and from 86 +/- 34 ml to 104 +/- 52 ml, p = 0.1, respectively; accordingly, EF significantly decreased from 38 +/- 7% to 34 +/- 7% (p = 0.02). In conclusion, long-term trimetazidine improves functional class and left ventricular function in patients with HF. This benefit contrasts with the natural history of the disease, as shown by the decrease of EF in patients on standard HF therapy alone.
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                Author and article information

                Journal
                Title: JAMA Cardiology
                Abbreviated Title: JAMA Cardiol
                Publisher: American Medical Association (AMA)
                ISSN (Print): 2380-6583
                Publication date Created: March 01 2019
                Publication date (Print): March 01 2019
                Volume: 4
                Issue: 3
                Page: 230
                Affiliations
                [1 ]University College London Institute of Cardiovascular Science, London, United Kingdom
                [2 ]Queen Elizabeth University Hospital, Glasgow, United Kingdom
                [3 ]Department of Statistical Science, University College London, London, United Kingdom
                [4 ]Barts Heart Centre, St Bartholomew’s Hospital, Barts Health National Health Service Trust, West Smithfield, London, United Kingdom
                [5 ]Salisbury District Hospital, Salisbury, United Kingdom
                [6 ]University College London Institute of Neurology, London, United Kingdom
                [7 ]Royal Brompton Hospital, London, United Kingdom
                [8 ]St George’s Hospital, London, United Kingdom
                [9 ]University of East Anglia, Norwich Research Park, Norwich, United Kingdom
                Article
                DOI: 10.1001/jamacardio.2018.4847
                PMC ID: 6439550
                PubMed ID: 30725091
                SO-VID: 7425c1c0-fc7c-483d-8ea9-98c5c8f8bf05
                Copyright © © 2019
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