To access this material please log in or register

Register Authorize

Role of cytoprotective therapy at myocardial revascularization

Kanaeva T. V., Nemchenko E. V., Bazylev V. V.

Keywords: coronary artery bypass, coronary heart disease, treatment, preductal, myocardial revascularization, cytoprotein therapy

DOI: 10.18087/rhj.2012.5.1703

Relevance. According to modern point of views, ischemic and reperfusion myocardial changes develop as a result of cardiomyocyte metabolic disorder. One of drugs of metabolic action is myocardial cytoprotector trimethazidine (Preductal MB, Servier, France). Mechanism of trimethazidine action is connected with suppression of fat acid metabolism, which allows carrying out more sound aerobic glucose disposal. Objective. Estimate efficiency of trimethazidine in CHD patients who underwent to coronary artery bypass surgery (CABS), in protection of the myocardium from ischemic and reperfusion damages. Materials and methods. 40 male patients, aged 50–65, with stable exertional angina FC II–III, were included in the study. Patients were randomized in two groups. Group 1 included 20 patients who, besides a standard therapy, took trimethazidine 1 tablet bid for 2 weeks prior to CABS. Group 2 included 20 patients who took only the standard therapy. In all patients before operation, blood levels of creatine phosphokinase MB, troponin Т, myoglobin, lactate were defined. Further, troponin Т level was defined in 2, 12–14 and 48 hours after the beginning of reperfusion; myoglobin – in 4–6, 14–16 and 48 hours and CPK MB in 12 and 24 hours. Arterial blood lactate levels tested in 2, 12–14 and 48 hours after the beginning of reperfusion. Results. Statistically significant differences in the levels of some tested cardiomarkers in Groups 1 and 2 were revealed. Troponin T levels in 2 and 48 hours after the beginning of reperfusion, and myoglobin in 4–6 hours after the beginning of reperfusion were significantly lower in the group of patients received trimethazidine before the operation. The analysis of necessity for the administration of inotropic drugs during operation and in the early postoperative period and EF dynamics after operation in comparison with presurgical level revealed no significant differences between the groups. Conclusion. Addition trimethazidine to the standard therapy of CHD patient before CABS reduces degree of reperfusion myocardial damages.
  1. Weintraub WS, Spertus JA, Kolm P et al. Effect of PCI on qua­lity of life in patients with stable coronary disease. N Engl J Med. 2008;359 (7):677–687.
  2. Taegtmeyer H, King LM, Jones BE. Energy substrate metabolism, myocardial ischemia, and targets for pharmacotherapy. Am J Cardiol. 1998;82 (5A): 54K-60K.
  3. Lopaschuk GD. Optimizing cardiac energy metabolism: how can fatty acid and carbohydrate metabolism be manipulated? Coron Artery Dis. 2001;12 (Suppl 1):S8–11.
  4. Lopaschuk GD. Treating ischemic heart disease by pharmacologically improving cardiac energy metabolism. Am J Cardiol 1998;82 (5A): 14K-17K.
  5. Fabiani JN, Ponzio O, Emerit I et al. Cardioprotective effect of trimetazidine during coronary artery graft surgery. J Cardiovasc Surg (Torino). 1992;33 (4):486–491.
  6. Vedrinne JM, Vedrinne C, Bompard D et al. Myocardial protection during coronary artery bypass graft surgery: a randomized, double-blind, placebo-controlled study with trimetazidine. Anesth Analg. 1996;82 (4):712–718.
  7. Tunerir B, Colak O, Alatas O et al. Measurement of troponin T to detect cardioprotective effect of trimetazidine during coronary artery bypass grafting. Ann Thorac Surg. 1999;68 (6):2173–2176.
  8. Kantor PF, Lucien A, Kozak R, Lopaschuk GD. The antianginal drug trimetazidine shifts cardiac energy metabolism from fatty acid oxidation to glucose oxidation by inhibiting mitochondrial long-chain 3‑ketoacyl coenzyme A thiolase. Circ Res. 2000;86 (5):580–588.
  9. Mody FV, Singh BN, Mohiuddin IH et al. Trimetazidine-induced enhancement of myocardial glucose utilization in normal and ische­mic myocardial tissue: an evaluation by positron emission tomography. Am J Cardiol 1998;82 (5A): 42K-49K.
  10. Spedding M, Tillement JP, Morin D, Le Ridant A. Medicines interacting with mitochondria: anti-ischemic effects of trimetazidine. Therapie. 1999;54 (5):627–635.
  11. Терекова Н. А., Яворский А. Г., Белоус А. Е. и др. Защита миокарда от ишемических и реперфузионных повреждений при реконструктивных операциях на сердце. Анестезиология и реаниматология. 1995;2:8–15.
  12. Birnbaum J, Kloner RA. Therapy for myocardial stunning. In: New Paradigms of Coronary Artery Disease. Eds. G. Heusch, R. Schulz. – Springer. 1996;103–105.
  13. Elsässer A, Schlepper M, Zimmermann R et al. The extracellular matrix in hibernating myocardium – a significant factor causing structural defects and cardiac dysfunction. Mol Cell Biochem. 1998;186 (1-2):147–158.
Kanaeva T. V., Nemchenko E. V., Bazylev V. V. Role of cytoprotective therapy at myocardial revascularization. Russian Heart Journal. 2012;11(5):303-308.

To access this material please log in or register

Register Authorize
Ru En