Coronary care unit CDK Cyclin-dependent kinase CHA 2 DS 2 -VASc Congestive heart failure, Hypertension, Age ≥ 75 years (2 points), Diabetes mellitus, Stroke (2 points)-Vascular disease, Age 65-74 years, Sex category (female) CIED Cardiac implantable electronic device CML Chronic myeloid leukaemia CMR Cardiac magnetic resonance COMPASS-CAT Prospective COmparison of Methods for thromboembolic risk assessment with clinical Perceptions and AwareneSS in real-life patients-Cancer Associated Thrombosis CPET Cardiopulmonary exercise testing CrCl Creatinine clearance CRF Cardiorespiratory fitness CRS Cytokine release syndrome CS Cancer survivors CT Computed tomography CTLA-4 Cytotoxic T lymphocyte-associated antigen-4 cTn Cardiac troponin CTRCD Cancer therapy-related cardiac dysfunction CTR-CVT Cancer therapy-related cardiovascular toxicity CV Cardiovascular CVD Cardiovascular disease CVRF Cardiovascular risk factorsData derived from a single randomized clinical trial or large non-randomized studies.Consensus of opinion of the experts and/or small studies, retrospective studies, registries.©ESC 2022 ESC Guidelines © ESC 2022This table refers to anthracycline equivalence dose using doxorubicin as a reference. Note that these isoequivalent doses are derived from paediatric CS. CS, cancer survivors; CV, cardiovascular.a Data for idarubicin are based upon an estimated anticancer efficacy ratio, not derived from cardiotoxicity data. The CV toxicity dose ratio provides the value that should be used to multiply the dose of the anthracycline of interest to convert to isoequivalent doses of doxorubicin; e.g. to convert 125 mg/m 2 of epirubicin to doxorubicin isoequivalent, multiply the dose by 0.8 (125 mg/m 2 × 0.8 = 100 mg/m 2 of doxorubicin).

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Despite evidence that essential hypertension (EH) is a state of increased oxidative stress, the data on oxidative protein modifications is lacking. Besides, the role of extracellular antioxidant enzymes in EH has not been systematically studied. Study was performed in 45 subjects with EH and 25 normotensive controls. Patients were divided into three groups according to the 2003 ESH/ESC guidelines (grade 1-3). Plasma protein reactive carbonyl derivatives (RCD) and SH-groups (as byproducts of oxidative protein damage) as well as antioxidant enzyme activities superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase were studied spectrophotometrically and correlated with blood pressure (BP). RCD levels were increased in EH patients compared to controls and correlated significantly with both systolic blood pressure (SBP) (r ¼ 0.495, Po0.01) and diastolic blood pressure (DBP) (r ¼ 0.534, Po0.01). Plasma SH-groups content was significantly lower in all patients with EH, with no correlation with BP. SOD and catalase activity in patients with grade 1 EH were similar to that of controls. Patients with grade 2 and 3 of EH had lower SOD and catalase activity. However, significant correlation with SBP and DBP was observed for catalase only (r ¼ À0.331; Po0.05 and r ¼ À0.365; Po0.05, respectively). EH patients exhibited higher plasma GPX activity compared to those in controls, and it correlated with SBP (r ¼ 0.328; Po0.05). The results presented show that increased oxidative protein damage is present in all grades of EH. In mild hypertension extracellular antioxidant enzyme activities are not decreased, suggesting they are probably not critical in early EH, but could be important in moderate to severe EH.