Metabolic pharmacotherapy in the treatment of patients with coronary heart disease and cardiac arrhythmias | Ukrainian Medical Journal

The aim is to determine the additional possibilities of metabolic therapy with ethylmethylhydroxypyridine succinate in patients with coronary artery disease and heart rhythm disturbances. Object and research methods. The study included 30 patients with coronary heart disease and atrial and ventricular arrhythmias. Ethylmethylhydroxypyridine succinate (Mexicor, «Lekhim») was used at a dose of 400 mg intravenously drip for 10 days in addition to antiarrhythmic and standard therapy for coronary artery disease. All patients underwent: electrocardiography, echocardiography, Holter monitoring, a treadmill test, a flow-dependent vasodilation test, the subpopulation composition of blood monocytes and lymphocytes, the content of malondialdehyde and carboxyhemoglobin were studied. Results. The administration of ethylmethylhydroxypyridine succinate in patients with coronary artery disease and cardiac arrhythmias was accompanied by a significant decrease in the number of episodes of myocardial ischemia and their total duration, determined using Holter monitoring, as well as an increase in exercise tolerance by 27%. An additional positive trend was established to reduce the amount of supraventricular extrasystole (1.8 times compared with the outcome), paroxysms of atrial fibrillation (6.3 times), ventricular and paired ventricular extrasystole. There was an increase in the growth of endothelium-dependent brachial artery vasodilation in response to reactive hyperemia, which was combined with an increase in the number of CD31 cells due to the antioxidant effect of ethyl methyl hydroxypyridine succinate. Conclusions. The use of ethylmethylhydroxypyridine succinate in patients with arrhythmias during coronary heart disease in addition to standard therapy has improved the metabolic state of the myocardium, reduced the severity of free radical and inflammatory processes, restored the functional state of the endothelium, thereby increasing the viability and functional activity of the myocardium, which may underlie the antiarrhythmic action of the drug.

Published: 20.12.2019

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Dyck J.R.B., Cheng J.-F., Stanley W.C. et al. (2004) Malonyl coenzyme A decarboxylase inhibition protects the ischemic heart by inhibiting fatty acid oxidation and stimulating glucose oxidation. Circ. Res., 94: e78–e85. doi: 10.1161/01.RES.0000129255.19569.81
Eelen G., Zeeuw P., Treps L. et al. (2018) Endothelial cell methabolism.Physiol. Rev., 91(1): 5–58. doi: 10.1152/physrev.00001.2017
Labarthe F., Khairallah M., Bouchard B. et al. (2005) Fatty acid oxidation and its impact on response of spontaneously hypertensive rat hearts to an adrenergic stress: benefits of a medium-chain fatty acid. Am. J. Physiol. Heart Circ.Physiol., 28: H1425–H1436. doi: 10.1152/aipheart.00942.2005
Lewandowski E.D. (2000) Metabolic mechanisms associated with antianginal therapy. Circ. Res., 86: 487–489. doi: org/10.1161\01.RES.86.5.487.
Stanley W.C. (2004) Metabolic changes in ischemia and myocardial infarction. Heart Metabolism, 23: 39–43. doi:10.1097/FJC.0000000000000054
Tamaki N., Morita K., Kyge Y. et al. (2000) The role of fatty acids in cardiac imaging. J. Nuclear Med., 41: 1525–1534. doi:10.1007/s12350-010-9305