Bruton’s tyrosine kinase inhibitors (BTKis) have altered the treatment landscape for chronic lymphocytic leukemia (CLL) by offering effective and well-tolerated therapeutic options. However, since the approval of ibrutinib, concern has risen regarding the risk of cardiovascular (CV) adverse events, including atrial fibrillation (AF), hypertension, and heart failure. Newer BTKis appear to have lower CV risks, but data are limited. It is important to understand the risks posed by BTKis and how those risks interact with individual patients, and we convened a panel of physicians with expertise in CLL and CV toxicities in oncology to develop evidence-based consensus recommendations for community hematologists and oncologists. Care providers should thoroughly assess a patient’s CV risk level before treatment initiation, including established CV diseases and risk factors, and perform investigations dependent on preexisting diseases and risk factors, including an electrocardiogram (ECG). For patients with high CV risk, BTKi treatment is often appropriate in consultation with a multidisciplinary team (MDT), and more selective BTKis, including acalabrutinib and zanubrutinib, are preferred. BTKi treatment should generally be avoided in patients with a history of heart failure. Ibrutinib should be avoided in patients with a history of ventricular arrhythmias, but the risk of newer drugs is not yet known. Finally, an MDT is crucial to help manage emerging toxicities with the goal of maintaining BTKi therapy, if possible. Optimizing heart failure, arrhythmia, and hypertension control will likely improve tolerance and maintenance of BTKi therapy. However, additional studies are needed to identify the most optimal strategy for these drugs.

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The aim of this study was to determine the concentration of galectin-3, PINP and PIIINP in patients with metabolic syndrome (MS) and atrial fibrillation (AF) with an assessment of the relationship with severity of left atrium fibrosis. A total of 480 subjects were included in the case-control study: MS patients (n = 337), 176 of whom had AF, 72 patients with AF without MS and 71 healthy subjects. Galectin-3, PINP and PIIINP blood concentrations and metabolic parameters were compared with the severity of left atrium fibrosis, measured by CARTO3. Galectin-3 in AF and MS patients is higher than in MS without AF and in healthy subjects (10.3 (4.8–15.4), 5.1 (4.3–8.8), 3.2 (2.4–4.2) ng/mL, p < 0.0001). Galectin-3 serum concentration in AF patients with MS is higher than in patients without MS: 10.3 (4.8–15.4), 6.8 (5.2–8.1) ng/mL, p = 0.0001. PINP and PIIINP concentration were higher in patients with AF and MS than in MS without AF: 3499.1 (2299.2–4567.3), 2130.9 (1425.3–2861.8) pg/mL, p < 0.0001, 94.9 (64.8–123.5), 57.6 (40.5–86.9) ng/mL, p < 0.0001. Galectin-3 correlates with PINP (r = 0.496, p < 0.001) and PIIINP concentration (r = 0.451, p < 0.0001). The correlation between galectin-3, PINP and the severity of left atrium fibrosis was found (r = 0.410, p < 0.001; r = 0.623, p < 0.001). Galectin-3 higher than 12.6 ng/mL increased the risk of AF more than five-fold. High galectin-3, PINP and PIIINP concentrations were associated with heart remodeling in MS patients and increased the risk of AF.

Aim. To determine the blood concentration of fibrosis biomarkers in patients with atrial fibrillation (AF) in combination with metabolic syndrome (MS) and to analyze the relationship with myocardial fibrosis.Material and methods. This cross-sectional case-control study included 547 patients aged 35 to 65 years: experimental group — patients with MS (n=373), of which 202 patients had AF; comparison group — AF patients without MS (n=110); healthy subjects without cardiovascular diseases and metabolic disorders (n=64). Patients with AF and MS who underwent electroanatomic mapping before pulmonary vein isolation (n=79) were assessed for left atrial (LA) fibrosis severity.Results. It was found that the blood concentration of circulating profibrogenic biomarkers in patients with AF and MS is higher than in patients with AF without MS: aldosterone (135,1 (80,7-224,1) and 90,1 (68,3-120,3) pg/ml, p<0,0001), galectin-3 (10,6 (4,8-15,4) and 5,8 (4,8-8,3) pg/ml, p=0,0001), GDF15 (938,3 (678,3-1352,1) and 671,0 (515,7-879,5) pg/ml, p=0,001), TGF-beta-1 (4421,1 (2513,5-7634,5) and 2630,5 (2020,7-3785,4) pg/ml, p=0,001), CTGF (167,8 (78,9-194,3) and 124,3 (74,4-181,9) pg/ml, p<0,0001), PIIINP (88,5 (58,6120,4) and 58,9 (40,7-86,1) ng/ml, p<0,0001), PINP (3421,4 (1808,1-4321,7) and 2996,1 (2283,8-3894,3) pg/ml, p<0,0001). Patients with paroxysmal AF have higher concentrations of TGF-beta1, CTGF and PINP than patients with persistent and permanent AF. In patients with persistent AF and MS, the concentrations of galectin-3, aldosterone, and PIIINP were higher than in patients with paroxysmal AF, while in patients with permanent AF, they were significantly lower. The plasma concentration of galectin-3 positively correlated with levels of PINP (p=0,465, p<0,0001), PIIINP (p=0,409, p<0,0001), GDF-15 (p=0,369, p<O,O001), CTGF (p=0,405, p<0,0001). According to multivariate regression, of all studied biomarkers, GDF-15 had a greater effect on PIIINP concentration (в=0,234, p=0,038), and galectin-3 — on PINP (в=0,248, p<0,021). Positive correlations of the severity of left atrial fibrosis with the concentration of galectin-3 (p=0,563, p<0,0001), PINP (p=0,620, p<0,0001), TGF-beta-1 (p=0,390, p<0,0001) and CTGF (p=0,551, p<0,0001). According to linear multivariate regression, the most significant effect on LA fibrosis severity among the studied biomarkers is exerted by galectin-3 (в=0,432, p<0,0001), PINP (в=0,343, p=0,001) and PIIINP (в=0,286, p=0,008).Conclusion. An increase in the blood concentration of profibrogenic biomarkers galectin-3, TGF-beta-1, CTGF, PIIINP, and PINP is associated with an increase in LA fibrosis severity and probably has a pathogenetic role in increasing the AF risk in patients with MS.

Цель. Изучить уровень галектина 3 и альдостерона в сыворотке крови у паци-ентов с метаболическим синдромом (МС) и с фибрилляцией предсердий (ФП) для определения их значимости. Материал и методы. Обследовано 100 пациентов с МС (IDF, 2005), из них 50 больных с ФП: 28 с пароксизмальной и 22 с персистирующей формами. Группу контроля составили 50 практически здоровых людей без сердечно-сосудис той патологии и метаболических нарушений. Уровень галектина 3 и альдостерона в сыворотке крови оценивался методом иммуноферментного анализа ELISA. Всем обследованным выполнены антропометрия, исследования липидного спек-тра и уровня гликемии натощак, трансторакальная эхокардиография. Результаты. Уровень галектина 3 в сыворотке крови у больных с МС в сочета-нии с ФП выше, чем у пациентов с МС без ФП и выше, чем у здоровых (0,72 [0,44;1,36], 0,44 [0,42;1,22] и 0,32 [0,28;0,42] нг/мл, соответственно; р<0,01). Уровень альдостерона в сыворотке крови в группе МС с ФП был также в 2 раза выше, чем у здоровых (202,2±82,4 и 98,4±51,2 пг/мл, р<0,001) и выше, чем в группе МС без ФП (202,2±82,4 и 148,3±73,3 пг/мл, р<0,001). У пациентов с персистирующей формой ФП установлен более высокий уровень галектина 3 и альдостерона в сравнении с больными с пароксизмальной формой. Уста-новлена положительная корреляция между уровнями альдостерона и галек-тина 3 в сыворотке крови (r=0,521, р<0,001). заключение. Маркеры фиброза миокарда галектин 3 и альдостерон в сыво-ротке крови у больных с фибрилляцией предсердий и метаболическим син-дромом выше, чем у пациентов с метаболическим синдромом без данной аритмии и выше, чем у здоровых. При персистирующей форме фибрилляции предсердий уровень галектина 3 и альдостерона выше, чем при пароксиз-мальной форме. Ионин В. А.* -ассистент кафедры факультетской терапии с курсом эндокри-нологии, кардиологии и функциональной диагностики, Соболева А. В. -к. м.н., ассистент кафедры терапии факультетской с курсом эндокринологии, кардиологии и функциональной диагностики, Листопад О. В. -ассистент кафедры терапии факультетской с курсом эндокринологии, кардиологии и функциональной диагностики, Нифонтов С. Е. -врач функциональной диаг-ностики и эхокардиографии клиники терапии факультетской с курсом эндо-кринологии, кардиологии и функциональной диагностики, Баженова Е. А. -к. м.н., ассистент кафедры терапии факультетской с курсом эндокринологии, кардиологии и функциональной диагностики, Васильева Е. Ю. -заведующая центральной клинико-диагностической лабораторией, ассистент кафедры клинической лабораторной диагностики и генетики, Баранова Е. И. -д. м.н., профессор кафедры терапии факультетской с курсом эндокринологии, кардио логии и функциональной диагностики, Шляхто Е. В. -академик РАН, заслуженный деятель науки РФ, Президент Российского кардиологического общества, заведующий кафедрой терапии факультетской с курсом эндокри-нологии, кардиологии и функциональной диагностики, директор ФГБУ. Aim. To study the levels of galectin 3 and aldostrone in blood serum of metabolic syndrome (MS) patients and atrial fibrillation (AF) for their...

Epicardial adipose tissue (EAT) has unique properties due to its special anatomical structure, thermoregulation, and metabolic activity. Dysregulated EAT provokes the synthesis of pro-inflammatory cytokines, disorders in the metabolism of fats and glucose, as well as contributes to fatty degeneration of the myocardium and heart failure development. EAT may serve as a risk factor and biomarker for cardiovascular diseases, and is also a potential therapeutic target. The purpose of this review was to highlight current research data on EAT, secreted adipokines, their effect on target tissue metabolism, and to systematize the relationship between EAT and cardiovascular diseases. In particular, its function, role in heart failure, atrial fibrillation, as well as the prognostic value of various microRNAs determined in EAT are highlighted.

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