cardioКардиологияKardiologiia0022-90402412-5660Kardiomag10.18087/cardio.2451cardio-232Research ArticleОБЗОРЫREVIEWSВлияние хронической болезни почек на формирование диастолической дисфункции сердца у больных ХСН с сохраненной ФВEffect of chronic kidney disease on the formation of diastolic heart dysfunction in heart failure patients with preserved ejection fractionКузьминО. Б.KuzminO. B.noemail@neicon.ruЖежаВ. В.ZhezhaV. V.noemail@neicon.ruБелянинВ. В.BelyaninV. V.noemail@neicon.ruБучневаН. В.BuchnevaN. V.noemail@neicon.ruФГБОУ ВО «ОрГМУ» МЗ РФРоссияFederal State Budgetary Educational Institution of Higher Education, «Orenburg State Medical University» of the Ministry of Health of the Russian FederationRussian Federation201818112018584S3745Copyright © Kardiomag, 20182018KardiomagKardiomaghttps://cardio.elpub.ru/jour/about/submissions#copyrightNoticehttps://cardio.elpub.ru/jour/article/view/232

Хроническая болезнь почек встречается у большинства больных ХСН с сохраненной ФВ (ХСНсФВ) и является одним из основных ФР, ускоряющих развитие и прогрессирование диастолической дисфункции ЛЖ сердца. В обзоре представлены данные о влиянии хронической болезни почек на внутриклеточные сигнальные пути, нарушающие жесткость и диастолическое расслабление кардиомиоцитов в ответ на воспаление и эндотелиальную дисфункцию коронарных капилляров, избыточную активацию симпатической нервной системы и дисрегуляцию системы натрийуретических пептидов, непосредственно участвующих в формировании ХСНсФВ. Выяснение этих механизмов позволяет выявлять клеточные мишени для разработки новых подходов к лекарственной терапии пациентов с ХСНсФВ.

Chronic kidney disease is observed in most patients with CHF with preserved ejection fraction (HFpEF) and presents a major risk factor facilitating development and progression of LV diastolic dysfunction. The review focused on the effect of chronic kidney disease on intracellular signaling pathways affecting stiffness and diastolic relaxation of cardiomyocytes in response to inflammation and endothelial dysfunction of coronary capillaries, excessive sympathetic activation, and dysregulation of natriuretic peptides, which directly participate in the development of CHF. Elucidation of these mechanisms allows to identify new cell targets for new approaches to drug therapy for patients with HFpEF.

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