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Chemotherapy and targeted therapy have significantly improved the prognosis of oncohaematological patients. Antineoplastic treatment can cause adverse cardiovascular effects known as cardiotoxicity, which requires modification, interruption or withdrawal of life-saving drugs. The onset of cardiotoxicity may depend on the class, dose, route, and duration of anticancer drug administration and individual risk factors. Standard chemotherapy exerts its toxic effect mainly by inducing oxidative stress and genomic instability. At the same time, new targeted molecules work by interfering with signalling pathways that are important for tumour cells and cardiomyocytes. For example, Bruton tyrosine kinase (BTK) inhibitors interfere with phosphatidylinositol-3-kinase isoforms involved in cardiac hypertrophy, contractility, and regulation of various proteins. Off-target effects of BTK inhibitors are associated with an increased incidence of atrial fibrillation. This review summarises current knowledge about the cardiotoxic effects of targeted therapies used in haematology. Fig. 2, Tab. 3, Ref. 44, on-line full text (Free, PDF) www.cardiology.sk [ABSTRACT FROM AUTHOR]

Ixazomib is approved for use in combination with lenalidomide and dexamethasone (IRd) for patients with multiple myeloma (MM) who received at least one previous therapy. Registration study "TOURMALINE MM-1" was published in 2016. Nevertheless, clinical trials are significantly different from real-world use. From June 2016 to December 2018, IRd was available for Slovak patients with relapsed/refractory MM through a Named Patient Program. The aim of this study was to evaluate the efficacy and safety of ixazomib. We analyzed in this cohort study outcomes of 106 MM patients treated with IRd at 2 academic centers. The median age at diagnosis was 63 years (44–78). The median number of prior lines was 2 (1–7). The majority had high international staging system (ISS) score: 18, 29, and 59 were in the ISS I, ISS II, and ISS III groups, respectively. Treatment continued until progression, unacceptable toxicity, or death. The median follow-up for the entire cohort was 29 (0–49) months. The overall response rate was 74.5% (complete remission, 7.5%; partial remission, 67%). The median overall survival was not reached. Median progression-free survival (PFS) was 43 months (95% CI 35.6–50.4). The Kaplan–Meier method was used to generate survival curves, and we compared the influence of different factors on PFS. The most common hematological adverse events of any grade were neutropenia (90.4%), anemia (55.6%), and thrombocytopenia (43.4%). Our real-world data support the use of IRd as a highly effective and well-tolerated oral treatment protocol for relapsed myeloma. [ABSTRACT FROM AUTHOR]

Background: Most results on the treatment of chronic myeloid leukaemia (CML) with imatinib were obtained from clinical trials that may differ from the routine practice. We report the results of treatment of consecutive patients with CML at ten major centres during 2000–2008. Patients and methods: Data reporting was retrospective in 2000–2004 and prospective from 2005 on. A total of 661 patients [301 womenand 360 men; median age 51 (range, 15–83)] with Ph + CML were registered. The median follow-up was 46.1 months (0–122.2). Results: Most patients were treated with first- (379; 57.3%) or second-line (193; 29.2%) imatinib; some of the patients underwent allogeneic hematopoietic stem cell transplantation (AHSCT) (83; 12.6%), but 6.1% were treated with other modalities [40 patients; median age 66 (range, 32–83)]. The probability of overall survival (OS) at 5 years, according to Kaplan and Meier, was 88.9%, 77.5% and68.7% for chronic-phase patients treated with first-line imatinib, second-line imatinib and first-line AHSCT, respectively, but only 25.2% for patients receiving other modalities. The OS was dependent on the disease phase and Sokal, Hasford and European group for blood and marrow transplantation (EBMT) risk scores (P < 0.001; each). Only 46.2% of deaths in patients treated with other modalities were attributable to CML. Elderly patients over 65 years achieved similar response rates and progression-free survival to the younger ones. There was a trend for inferior results of AHSCT performed after the failure of imatinib (P = 0.075), probably as a result of differences in EBMT risk scores (P < 0.001). Conclusions: The ability to achieve results comparable to those of previous clinical studies in our CML cohort was influenced by centralised care. Decisions not to initiate imatinib or to delay AHSCT may have a negative impact on OS,but comorbidities may limit the treatment potential of imatinib in the elderly. [ABSTRACT FROM AUTHOR]