Cardiovascular disease remains the leading cause of mortality accounting up to 40% of all deaths, but, currently, cancer is prominent cause of death globally. Anthracyclines are the cornerstone of chemotherapy in women with breast cancer. However, its clinical use is limited by their cardiotoxic effects that can trigger heart failure development. Vascular toxicity of chemotherapy may be linked with endothelial dysfunction because anthracycline damage of endothelial cells can lead to the development and progression of cardiomyopathy by decreasing the release and activity of endothelial factors and, ultimately, endothelial cell death. These processes suppress anti-inflammatory and vascular reparative functions and initiate the development of future cardiovascular events. Recent studies have shown that chemotherapy may induce toxicity in the vascular endothelium and is accompanied by systemic endothelial dysfunction in patients with diagnosed cardiovascular diseases. Because the initial endothelial cell insult is likely asymptomatic, there is often a long delay between the termination of doxorubicin therapy and the onset of vascular disorders. In this case, genetic susceptibility factor will help to identify susceptible patients in the future. The objectives of this study were to evaluate prognostic role of molecular (endothelin-1) and genetic factors (gene polymorphisms of endothelial nitric oxide (NO) synthase (NOS3, rs1799983), endothelin-1 receptor type A (EDNRA, C+70G, rs5335) and NADPH oxidase (C242T, rs4673) in development of endothelial dysfunction and anthracycline-induced cardiotoxicity in women without cardiovascular diseases.

OBJECTIVES: The objective of the study was to evaluate early and midterm outcomes after the frozen elephant trunk (FET) procedure with different proximal landing zones in patients with aortic dissection. METHODS: Forty-four patients with type A and type B aortic dissection that extended down to the abdominal aorta were enrolled in the study. All of the patients had the FET procedure. The patients were divided in 2 groups according to the level of the proximal landing zone: the zone 2 (Z2) group and zone 3 (Z3) group. Early and midterm outcomes including the false lumen (FL) thrombosis rate were monitored in both groups. RESULTS: The incidence of stroke, delirium and spinal cord ischaemia was 5.9% vs 3.7% (P = 0.533), 5.9% vs 7.4% (P = 0.903) and 5.9% vs 0 (P = 0.533) in the Z2 and Z3 groups, respectively. The 30-day mortality was 9.1% in both groups. The mean distal landing zone was T7.5 (T7; T9) in the Z2 group vs T9 (T8; T10) in the Z3 group (P = 0.668). The 2-year overall survival was 62.2% with no significant difference in the Z2 and Z3 groups (61.6% vs 64.2%; P = 0.940). There were no aortic-related deaths during the follow-up period. Freedom from reintervention at 24 months was 73% and was comparable between Z2 and Z3 (74.1% vs 91.7%; P = 0.123). The rate of early complete FL thrombosis was comparable in the Z2 and Z3 groups. By 24 months of observation in the Z3 group, the rate of complete FL thrombosis was significantly higher (60% vs 77%; P = 0.046). CONCLUSIONS: No statistically significant differences were observed between landing zones 2 and 3 during the FET procedure with regard to early outcomes. Proximalization of the FET was associated with a shorter FL thrombosis in the midterm follow-up period that affected the distal aortic reintervention rate.

Atherosclerosis, a systematic degenerative disease related to the buildup of plaques in human vessels, remains the major cause of morbidity in the field of cardiovascular health problems, which are the number one cause of death globally. Novel atheroprotective HDL-mimicking chemically modified carbon-coated iron nanoparticles (Fe@C NPs) were produced by gas-phase synthesis and modified with organic functional groups of a lipophilic nature. Modified and non-modified Fe@C NPs, immobilized with polycaprolactone on stainless steel, showed high cytocompatibility in human endothelial cell culture. Furthermore, after ex vivo treatment of native atherosclerotic plaques obtained during open carotid endarterectomy surgery, Fe@C NPs penetrated the inner structures and caused structural changes of atherosclerotic plaques, depending on the period of implantation in Wistar rats, serving as a natural bioreactor. The high biocompatibility of the Fe@C NPs shows great potential in the treatment of atherosclerosis disease as an active substance of stent coatings to prevent restenosis and the formation of atherosclerotic plaques.

(1) Background: The results of the international studies support the assumption that coronary microvascular dysfunction (CMD) occurs significantly more often than previously identified and is associated with adverse outcomes. However, there is a lack of the accurate comprehension of its pathophysiology. The objectives of this study were to evaluate the clinical and instrumental features of CMD and to assess its prognostic value during 12 months of follow-up period. (2) Methods: A total of 118 patients with non-obstructive coronary artery disease (CAD) and preserved LV ejection fraction (62 [59; 64]%) were enrolled in the study. Serum levels of biomarkers were analyzed by enzyme-linked immunoassay. CMD was defined as the reduced myocardial flow reserve (MFR) ≤ 2 obtained by dynamic CZT-SPECT. Two-dimensional transthoracic echocardiography with evaluation of LV diastolic dysfunction was performed baseline. (3) Results: Patients were divided into groups depending on the presence of CMD: CMD+ group (MFR ≤ 2; n = 45), and CMD− group (MFR > 2; n = 73). In CMD+ group, the severity of diastolic dysfunction, the levels of biomarkers of fibrosis and inflammation were higher than in CMD− group. Multivariate regression analysis showed that the presence of diastolic dysfunction (OR 3.27; 95% CI 2.26–5.64; p < 0.001), the hyperexpression of NT-proBNP ≥ 760.5 pg/mL (OR 1.67; 95% CI 1.12–4.15; p = 0.021) and soluble ST2 ≥ 31.4 ng/mL (OR 1.37; 95% 1.08–2.98; p = 0.015) were independent factors associated with CMD. Kaplan–Meier analysis showed that a rate of the adverse outcomes was significantly (p < 0.001) higher in patients with CMD (45.2%, n = 19) than in patients without it (8.6%, n = 6). (4) Conclusions: Our data suggest that the presence of CMD was associated with the severe diastolic dysfunction and hyperexpression of the biomarkers of fibrosis and inflammation. Patients with CMD had higher rate of the adverse outcomes than those without it.