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Loeffler's endocarditis remains is a very rare disease, develops due to eosinophilic inflammation predominantly of the endocardium with an outcome in fibrosis and massive thrombus formation and. He is generally characterized by an unfavorable prognosis. Clinical case of a 42-year-old patient with Loeffler endocarditis is presented. The development of the disease was preceded by a polyvalent allergy, mild dry eye syndrome and pansinusitis with a single eosinophilia of blood up to 16%. The reason for the hospitalization was the appearance of biventricular heart failure. During the previous year, the level of blood eosinophils remained normal, a threefold increase in the level of eosinophilic cationic protein was observed once. A 20-fold increase in the pANCA level, a 2.5-fold increase in the level of antibodies to DNA, an antibody to the nuclei of cardiomyocytes 1:160 were detected. The diagnosis was made on the basis of electrocardiography data (low QRS voltage, atrial hypertrophy), echocardiography, multispiral computed tomography and magnetic resonance imaging of the heart (thickening and delayed contrasting of the endocardium, massive thrombosis of the left ventricular apex with obliteration of its cavity, encapsulated fluid in the pericardium with compression of the right ventricle). Systolic dysfunction, severe signs of restriction and arrhythmias were absent. Trombectomy, tricuspid valve plasty, pericardial resection, suturing of an open oval window were performed. Signs of active inflammation with single eosinophils, vasculitis, perimuscular sclerosis, endocardial sclerosis were detected in morphological and immunohistochemical studies of endo-, myo-, pericardium. Viral genome was not found. The therapy with methylprednisolone 24 mg/day, azathioprine 75 mg/day was started. Six months after the operation, the symptoms of heart failure are completely absent, the thrombosis did not recur.

Цель – изучить эффективность плазмафереза (ПФ) в качестве основного вида патогенетического лечения или в сочетании с иммуносупрессивной терапией (ИСТ) у больных с дилатационной кардиомиопатией (ДКМП) иммунновоспалительного генеза в сопоставлении с группой сравнения. Материал и методы. В основную группу были включены 19 пациентов с синдромом ДКМП [18 мужчин, средний возраст – 45,3±11,5 года, конечно-диастолический размер левого желудочка (КДР ЛЖ) – 6,4±0,7 см, конечно-систолический объем(КСО ЛЖ) – 193,8±36,3 мл, фракция выброса (ФВ) – 34,6±6,9%, функциональный класс хронической сердечной недостаточности (ФК ХСН) II [II;III] по NYHA]. Критерием включения было повышение титров хотя бы 2 видов антикардиальных антител в 2 раза. Миокардит диагностирован с применением биопсии миокарда (n=13), МРТ (n=12), МСКТ (n=28), сцинтиграфии (n=15), коронарографии (n=13). Проведен курс дискретного ПФ (центрифуга Sorvall RC 3BP + Thermo Scientific, Германия). В группу сравнения вошли 19 пациентов с синдромом ДКМП (КДР ЛЖ 6,6±0,8 см, ФВ ЛЖ 32,6±7,3%, ФК ХСН III [II;III] по NYHA), которым ПФ не выполняли. Динамику оценивали в сроки 6 и 12 мес. Результаты. В основной группе отмечено достоверное снижение титров антикардиальных антител непосредственно после ПФ и при контрольных исследованиях (p3,7 см, обладающий 100% чувствительностью и специфичностью в предсказании хорошего ответа. В основной группе метилпреднизолон (МП) назначен 9 (47,4%) больным, в группе сравнения – 17 (89,5%), p3,7 см. У больных с синдромом ДКМП на фоне иммунного миокардита ПФ улучшает функциональные показатели сердца, толерантность к физическим нагрузкам и позволяет воздержаться от агрессивных режимов иммуносупрессии., The aim of the study is to investigate the clinical efficiency of therapeutic plasma exchange (TPE) in patients with inflammatory dilated cardiomyopathy (iDCM) due to immune-mediated myocarditis in comparison with control group without TPE. Material and methods. There were 19 iDCM patients in the treatment group (18 male, mean age 45.3±11.5 years, left ventricular end-diastolic diameter (LVEDD) 6.4±0.7 cm, left ventricular enddiastolic volume (LVEDV) 193.8±36.3 ml, left ventricular ejection fraction (LVEF) 34.6±6.9%, NYHA functional class II [II;III]) and 19 iDCM patients (12 male, mean age 46.3±12 years, LVEDD 6.6± 0.8 cm, LVEF 32.6±7.3%, NYHA functional class III [II;III]) who were followed without TPE. Treatment group patients underwent a single volume TPE filled with 0.9% sodium chloride (Sorvall RC 3BP+ Thermo scientific, Germany). All the patients had two or more fold increase of at least two anti-heart antibodies (AHA) level (to cardiac nuclear antigens, endothelial, cardiomyocytes, conduction and smooth muscle cells antigens) and underwent endomyocardial biopsy (EMB, n=13), cardiac CT (n=28), MRI (n=12), myocardial perfusion scan (n=15), and coronary angiography (n=13) to diagnose myocarditis. All the patients were treated either with immunosuppression drugs or without them. Echocardiographic parameters and AHA level detection were assessed at baseline and with two follow-up (FU) visits in about 6 and 12 month in both groups. We also evaluated a 6-minute walk test (6MWT) distance in the treatment group. Results. AHA level significantly decreased just after TPE and during the FU in the treatment group (p10% were classified as responders vs 6 (32%) responders in the control group. Responders in TPE group were characterized by initial lower LVEF (35 [25;37]% vs 40 [37;43]% in non-responders, p

After myocardial infarction (MI), activation of the immune system and inflammatory mechanisms, among others, can lead to ventricular remodeling and heart failure (HF). The interaction between these systemic alterations and corresponding changes in the heart has not been extensively examined in the setting of chronic ischemia. The main purpose of this study was to investigate alterations in cardiac gene and systemic cytokine profile in mice with post-ischemic HF. Plasma was tested for IgM and IgG anti-heart reactive repertoire and inflammatory cytokines. Heart samples were assayed for gene expression by analyzing hybridization to AECOM 32k mouse microarrays. Ischemic HF significantly increased the levels of total serum IgM (by 5.2-fold) and total IgG (by 3.6-fold) associated with a relatively high content of anti-heart specificity. A comparable increase was observed in the levels of circulating pro-inflammatory cytokines such as IL-1β (3.8X) and TNF-α (6.0X). IFN-γ was also increased by 3.1-fold in the MI group. However, IL-4 and IL-10 were not significantly different between the MI and sham-operated groups. Chemokines such as MCP-1 and IL-8 were 1.4- and 13-fold increased, respectively, in the plasma of infarcted mice. We identified 2079 well annotated unigenes that were significantly regulated by post-ischemic HF. Complement activation and immune response were among the most up-regulated processes. Interestingly, 21 of the 101 quantified unigenes involved in the inflammatory response were significantly up-regulated and none were down-regulated. These data indicate that post-ischemic heart remodeling is accompanied by immune-mediated mechanisms that act both systemically and locally.