Cardiac ArrhythmiasCardiac ArrhythmiasCardiac ArrhythmiasCardiac Arrhythmias2782-42842782-4233Eco-Vector10711210.17816/cardar107112ReviewsОбзорыReview ArticleEpicardial Adipose Tissue and Cardiac ArrhythmiasЭпикардиальная жировая ткань и аритмии сердцаhttps://orcid.org/0000-0003-1510-92046701465286O-8743-20177635-5330KanorskiiSergey G.КанорскийСергей Григорьевич
Russian Federation

Head of the Department of Therapy

заведующий кафедрой терапии

kanorskysg@mail.ruThe Kuban State Medical UniversityКубанский государственный медицинский университет Минздрава России1608202225092022225180405202207072022Copyright ©; 2022, Kanorskii S.G.Copyright ©; 2022, Канорский С.Г.Copyright ©; 2022, Kanorskii S.2022Kanorskii S.G.Канорский С.Г.Kanorskii S.https://creativecommons.org/licenses/by-nc-nd/4.0https://journals.eco-vector.com/cardar/article/view/107112

Obesity is associated with an increased risk of atrial and ventricular arrhythmias, including life-threatening ones. Epicardial adipose tissue (EAT) is located deep under the visceral pericardium (epicardium) and is therefore in direct contact with the underlying myocardium. In pathological conditions, EAT undergoes a phenotypic transition from a “neighbor” with protective properties to a substrate that secretes many substances that change the electrophysiology of cardiomyocytes by modulating ion currents that disrupt intercellular electrical connections and stimulate fibrosis. An excess of EAT can cause atrial and ventricular conduction disturbances, which are already evident with standard electrocardiography, predispose to the occurrence of the re-entry phenomenon and cardiac arrhythmias. Among the mechanisms of arrhythmogenesis under the influence of EAT, modulation of ion channels and gap junctions, fibrous remodeling and fatty infiltration are more often considered. However, most of these mechanisms have been studied in experimental studies and cannot easily be extrapolated to humans. There is convincing evidence of a direct relationship between EAT volume and the severity of atrial fibrillation, as well as the clinical benefit obtained from weight loss in patients with this arrhythmia. It is likely that the benefits of weight loss may extend to ventricular arrhythmias.

Ожирение связано с повышенным риском предсердных и желудочковых аритмий, в том числе угрожающих жизни. Эпикардиальная жировая ткань (ЭЖТ) локализуется глубоко под висцеральным перикардом (эпикардом) и, следовательно, находится в непосредственном контакте с нижележащим миокардом. При патологических состояниях ЭЖТ претерпевает фенотипический переход от «соседа» с защитными свойствами к субстрату, секретирующему множество веществ, которые изменяют электрофизиологию кардиомиоцитов путем модуляции ионных токов, нарушающих межклеточные электрические связи пациентов стимулирующих фиброз. Избыток ЭЖТ способен вызывать нарушения предсердной и желудочковой проводимости, которые очевидны уже при стандартной электрокардиографии, предрасполагать к возникновению феномена re-entry и аритмиям сердца. Среди механизмов аритмогенеза под влиянием ЭЖТ чаще рассматриваются модуляция ионных каналов и щелевых контактов, фиброзное ремоделирование и жировая инфильтрация. Однако большинство этих механизмов изучены в экспериментальных исследованиях и не могут быть легко экстраполированы на человека. Убедительно доказана прямая связь между объемом ЭЖТ и тяжестью течения фибрилляции предсердий, а также клиническая выгода, получаемая при снижении массы тела у пациентов с этой аритмией. Вполне вероятно, что польза от потери веса может распространяться и на желудочковые аритмии.

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