microcirculationРегионарное кровообращение и микроциркуляцияRegional blood circulation and microcirculation1682-66552712-9756Academician I.P. Pavlov First St. Petersburg State Medical University10.24884/1682-6655-2019-18-3-9-15microcirculation-436Research ArticleОБЗОРЫREVIEWSГибернация миокарда: молекулярные механизмы, клиническая значимость и методы диагностикиMyocardial hibernation: molecular mechanisms, clinical significance and diagnostic methodsГалагудзаМ. М.GalagudzaM. M.

д-р мед. наук, профессор, член-корреспондент РАН, директор Института экспериментальной медицины

Doctor of Medical Sciences, Professor, RAS Corresponding Member, Director of the Institute of Experimental Medicine

galagudza@almazovcentre.ruСонинД. Л.SoninD. L.

канд. мед. наук, заведующий НИО микроциркуляции и метаболизма миокарда Института экспериментальной медицины

Candidate of Medical Sciences, Head of the Department of Microcirculation and Myocardial Metabolism, Institute of Experimental Medicine

sonin_dl@almazovcentre.ruАлександровИ. В.AleksandrovI. V.

младший научный сотрудник НИО микроциркуляции и метаболизма миокарда Института экспериментальной медицины

Junior Researcher at the Department of Microcirculation and Myocardial Metabolism, Institute of Experimental Medicine

aleksandrov_iv@almazovcentre.ruФедеральное государственное бюджетное учреждение «Национальный медицинский исследовательский центр имени В. А. Алмазова» Министерства здравоохранения Российской ФедерацииРоссияAlmazov National Medical Research CentreRussian Federation201906102019183915Copyright © Галагудза М.М., Сонин Д.Л., Александров И.В., 20192019Галагудза М.М., Сонин Д.Л., Александров И.В.Galagudza M.M., Sonin D.L., Aleksandrov I.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.microcirc.ru/jour/article/view/436

Гибернация миокарда – стойкое угнетение сократимости жизнеспособного миокарда левого желудочка, возникающее вследствие его гипоперфузии. Важнейшим проявлением гибернации является сохранение жизнеспособности миокарда на тканевом уровне. В основе этого явления лежат три основных механизма: 1) метаболическая адаптация миокарда, проявляющаяся усиленным захватом глюкозы; 2) активация генетической программы выживания кардиомиоцитов; 3) программируемая клеточная гибель, т. е. аутофагия и апоптоз кардиомиоцитов. Методы диагностики жизнеспособного миокарда включают стресс-эхокардиографию с добутамином, однофотонную эмиссионную компьютерную томографию миокарда, позитронно-эмиссионную томографию, магнитно-резонансную томографию и электромеханическое картирование. В клиническом аспекте наличие и объем жизнеспособного миокарда учитываются при решении вопроса о реваскуляризации у пациентов с одно- и двухсосудистым поражением коронарных артерий без вовлечения передней нисходящей артерии, а также у больных со значительным снижением глобальной сократительной функции миокарда, когда оперативное вмешательство может привести к увеличению фракции выброса левого желудочка.

Myocardial hibernation is a persistent inhibition of contractility of the viable myocardium of the left ventricle, resulting from its hypoperfusion. The most important manifestation of hibernation is the preservation of the viability of the myocardial tissue. This phenomenon is based on three main mechanisms: 1) myocardial metabolic adaptation, manifested by enhanced glucose uptake; 2) activation of the cardiomyocyte death gene program; 3) programmed cell death, i. e. autophagy and apoptosis of cardiomyocytes. Methods for diagnosing viable myocardium include dobutamine stress echocardiography, single photon emission computed tomography of the myocardium, positron emission tomography, magnetic resonance imaging and electromechanical mapping. In the clinical aspect, the presence and volume of viable myocardium are taken into account when addressing the issue of revascularization in patients with one- and two-vessel coronary artery disease without involvement of the anterior descending artery, as well as in patients with a significant decrease in the global myocardial contractile function, when surgery can lead to an increase in the left ventricular ejection fraction.

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The authors declare that there are no conflicts of interest present.