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Deep vein thrombosis and pulmonary artery thromboembolism are the most commonly occurring cardio-vascular complications of oncological diseases, which may develop at any stage of the oncological process. These life-threatening complications take the leading positions within the structure of mortality among cancer patients, giving place only to the oncology disease itself. It is important to note that the patients with cancer-associated thromboses are the most difficult group of patients, in which the development of thromboses and thromboembolisms may not only delay the vitally important treatment of the main disease, but also to completely cease the treatment due to the lack of possibility for its adequate performing. This is an important social and economic task, taking into consideration the costs for the healthcare system required to treat the disease itself and its concomitant complications. Thus, there is a criticality factor of not only the treatment itself, but also of the prevention of oncology-associated thromboses and thromboembolisms. Currently, due to the wide spreading of the said complications, the therapy and the prevention of them undergo significant changes. The traditionally used warfarin is being switched to low molecular weight heparin. At the present moment, oral anticoagulants are used more and more often. The analysis of special scientific literature has allowed for evaluating the novel principles of treatment in cases of oncology-associated thromboses and thromboembolisms depending on the location of the process, on its stage, on the severity of the patient status, as well as to define the risk factors of oncology-associated thromboses, the practicability and possible methods of its prevention in various groups of patients.

Advances in the diagnostics and treatment of cancer have led to improved survival of patients and decreased mortality. Cardiovascular complications (CVC) however, are among the most frequent side effects of anticancer treatment, which can have an adverse effect on the prognosis. This may be the result of cardiotoxicity, which involves direct effects of the radiation therapy and /or chemotherapy on the heart function and structure. Heart failure with cancer therapy was associated with a 3.5-fold increase in the risk of mortality compared with idiopathic cardiomyopathy. The cardiotoxicity risk assessment is often difficult, due to the different susceptibility of patients to drugs and their combinations, and coadministration of radiation therapy. Therefore, the likelihood of development and the time of occurrence of cardiotoxicity may vary and not always depend on the initial risk. Strategies for managing such patients are in most cases based on the expert opinion. This article provides recommendations for the prevention and therapy of cardiotoxicity, set out in the consensus of the European Society of Cardiology 2016.

Background: Increased arterial stiffness (AS), intima-media thickness (IMT), and the presence of atherosclerotic plaques (PP) have been considered as important aspects of vascular aging. It is well documented that the cardiovascular system is an important target organ for growth hormone (GH) and insulin-like growth factor (IGF)-1 in humans, and GH /IGF-1 deficiency significantly increases the risk for cardiovascular diseases (CVD). The telomere length of peripheral blood leukocytes (LTL) is a biomarker of cellular senescence and that has been proposed as an independent predictor of (CVD). The aim of this study is to determine the role of GH/IGF-1, LTL and their interaction cardiovascular risk factors (CVRF) in the vascular aging.Methods: The study group included 303 ambulatory participants free of known CVD (104 males and 199 females) with a mean age of 51.8 ± 13.3 years. All subjects had one or more CVRF [age, smoking, arterial hypertension, obesity, dyslipidemia, fasting hyperglycemia, insulin resistance—HOMA (homeostatic model assessment) >2.5, or high glycated hemoglobin]. The study sample was divided into the two groups according to age as “younger” (m ≤ 45 years, f ≤ 55 years) and “older” (m > 45 years, f > 55 years). IMT and PP were determined by ultrasonography, AS was determined by measuring the carotid-femoral pulse wave velocity (c-f PWV) using the SphygmoCor system (AtCor Medical). LTL was determined by PCR. Serum IGF-1 and GH concentrations we measured by immunochemiluminescence analysis.Results: Multiple linear regression analysis with adjustment for CVRF indicated that HOMA, GH, IGF-1, and LTL had an independent relationship with all the arterial wall parameters investigated in the younger group. In the model with c-f PWV as a dependent variable, p < 0.001 for HOMA, p = 0.03 for GH, and p = 0.004 for LTL. In the model with IMT as a dependent variable, p = 0.0001 for HOMA, p = 0.044 for GH, and p = 0.004 for IGF-1. In the model with the number of plaques as a dependent variable, p = 0.0001 for HOMA, and p = 0.045 for IGF-1. In the older group, there were no independent significant associations between GH/IGF-1, LTL, HOMA, and arterial wall characteristics.Conclusions: GH/IGF-1, IR, HOMA, and LTL were the important parameters of arterial aging in younger healthy participants.

With advancing age the left ventricle (LV) undergoes structural and functional changes, thereby creating the substrate for the development of diseases. One possible mechanism of the ageing heart is a cellular senescence. Leukocyte telomere length (LTL) is a marker of replicative ageing. The purpose of this study was to evaluate the structure and function of the LV in people of different ages free of cardiovascular diseases (CVD) and regular drug medication and to assess their relationship with LTL. We hypothesized that age-related changes in LV myocardium are associated with telomere length.The study population consisted of 150 healthy, non-obese volunteers aged 28 to 78 years without history of CVD, significant deviations by 12-lead electrocardiogram and negative exercise test (treadmill stress test). All the participants underwent standardized transthoracic echocardiography using an available system (iE33; Philips). The LTL was measured by real-time quantitative polymerase chain reaction. We determined the relative ratio of telomere repeat copy number (T) to single-copy gene copy number (S).In the older people there was a higher wall thickness than in the younger (1.03 ± 0.09 vs. 0.88 ± 0.10, p