Radiotherapy is an integral part of the cancer treatment, including with mediastinum, breast cancer. In this case, cardiovascular complications of the treatment are quite common. The long-term prognosis can be determined not only by the effectiveness of radiotherapy, but also by cardiovascular risks. A feature of cardiotoxicity of radiation therapy is the high probability of its occurrence in the delayed period of 3–30 years after treatment. The article highlights the results of published epidemiological studies of cardiotoxicity of radiotherapy, as well as the available screening algorithms for cardiovascular complications in patients who underwent radiotherapy. Own clinical observation of the early debut of coronary artery disease after combined chemoradiotherapy of diffuse large B-cell non-Hodgkin lymphoma is presented.

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Objective: The aim of the study was to evaluate the 24-h profile of peripheral and central blood pressure (BP) in hypertensive patients with type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) according to the presence of proteinuria. Design and method: The study included 90 patients with HTN, T2DM and CKD with eGFR 30-<60 ml/min/1.73 m2 and urine albumin–creatinine ratio (UACR) <300 mg/g (66% females, median age 60 years, median duration of DM–7.5 years, median duration of HTN 18 years). All received antihypertensive therapy and antidiabetic drugs (insulin in 58%). The analysis was performed according to CKD phenotype: proteinuric (UACR 30-<300 mg/g) and non-proteinuric (UACR < 30 mg/g). Office BP was measured with a validated oscillometric device. Clinical central BP and 24-hour ABPM of brachial and central aortic BP were performed with BPLab Vasotens. All results are presented as median values. p < 0.05 was considered significant. Results: Office brachial BP was 156/83 mmHg, aortic – 139/90 mmHg, median UACR was 26.5 mg/g. Proteinuric phenotype was found in 78% and compared to non-proteinuric phenotype was characterized by higher rate of dyslipidemia (85% vs 45%, p = 0.0004), more frequent history of coronary artery disease (53% vs 10%, p = 0.001), longer duration of HTN and DM (19.5 vs 7.5 years and 8 vs 3 years respectively, p < 0.01), lower HDL-C (1.2 vs 1.9, p = 0.02) and higher office brachial DBP (83 vs 80 mmHg, p = 0.04) and central SBP (147 vs 137 mmHg, p = 0.007). Proteinuric phenotype compared to non-proteinuric was associated with worse 24-h profile of central SBP (daytime 147 vs 138 mmHg, p = 0.008; night-time 143 vs 130 mmHg, p = 0.04). HTN phenotypes according to diurnal index for proteinuric and non-proteinuric CKD were as follows: dippers 0 vs 10%, non-dippers 6 vs 5%, night-peakers 82 vs 70% over-dippers 12 vs 15% (all differences were non-significant). Presence of proteinuric phenotype positively correlated with daytime and night-time aortic SBP (r = 0.28 and 0.21 respectively, p < 0.05). Conclusions: Proteinuric phenotype of CKD in patients with HTN and T2DM is associated with worse 24-h profile of central BP. The publication was prepared with the of the RUDN University Program 5-100

Background and Aims 24-h blood pressure (BP) may be superior to office BP in the prediction of cardiovascular mortality and also central aortic BP may better predict outcomes than brachial one. Hypertensive patients with type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) have higher risk and poorer BP control than patients with normal glycemic state and renal function. 24-h profile of central BP and arterial stiffness according to CKD phenotypes are not well described in this population. The aim of the study was to evaluate the associations of kidney function and proteinuria with 24-h central BP and parameters of arterial stiffness in hypertensive patients with T2DM and CKD. Method 90 patients with hypertension (HTN), T2DM and CKD (eGFR 30-60 ml/min/1.73 m2 and morning spot urine albumin–creatinine ratio (UACR) &lt;300 mg/g) were included. 66% of them were females, median age was 60 years, 69% were smokers, 53% obese, 77% with dyslipidemia. Median duration of T2DM and HTN was 7.5 years and 18 years, respectively. All received antihypertensive drugs (77% – combinations of 2 or 3 drugs) and glucose lowering therapy (insulin in 58%). The analysis was performed according to CKD phenotype: proteinuric (UACR 30-300 mg/g) and non-proteinuric (UACR &lt;30 mg/g) and according to CKD stage assessed by GFR (G3a and G3b, KDIGO (2012)). Office brachial BP was measured with a validated oscillometric device. Office aortic BP and arterial stiffness were assessed with applanation tonometry (SphygmoCor AtCor). 24-hour ABPM of brachial and aortic BP was performed with BPLab Vasotens. All results are presented as median values. P&lt;0.05 was considered significant. Results Median brachial BP was 156/83 mmHg, aortic BP 139/90 mmHg. Median eGFR was 53 ml/min/1.73 m2, UACR – 62.2 mg/g. Phenotypes of CKD were as follows: proteinuric in 78% (GFR 50 ml/min/1.73 m2, UACR 62 mg/g) and non-proteinuric in 22 % (GFR 54 ml/min/1.73 m2, med UACR 5 mg/g, p&lt;0.01 for trend compared non-proteinuric). Patients with proteinuric phenotype compared to non-proteinuric were characterized by higher rate of dyslipidemia (85% vs 45%, p&lt;0.001), longer duration of HTN and DM (19.5 vs 7.5 years and 8 vs 3 years, respectively, p &lt;0.01 for trend) and lower HDL-C (1.2 vs 1.9, p=0.02). Both groups had similar office brachial SBP (156 vs 157 mmHg; p=0.48), but patients with proteinuric phenotype had higher office central SBP (147 vs 137 mmHg, p=0.007) and worse 24-h profile of central SBP (daytime 147 vs 138 mmHg, p=0.008; night-time 143 vs 130 mmHg, p=0.04). Proteinuric phenotype significantly correlated with office aortic SBP (r=0.28; p=0.01) and daytime and night-time aortic SBP (r=0.28 and 0.21 respectively, p &lt;0.05 for trend). The eGFR phenotypes were as follows: G3a in 82.2% (GFR 54 ml/min/1.73 m2, UACR 20 mg/g) and G3b in 17.8% (GFR 38 ml/min/1.73 m2, med UACR 46 mg/g, p&lt;0.01 for trend compared to G3a). Patients with worse kidney function had longer duration of HTN and DM (16 vs 11 years and 10 vs 6 years, respectively, p &lt;0.01 for trend), higher median brachial and aortic BP levels (158/90 vs 146/82 mmHg and 150/95 vs 138/80 mmHg, respectively, p&lt;0.01 for trend), worse 24-h profile of central SBP (daytime 148 vs 138 mmHg, p=0.008; night-time 146 vs 130 mmHg, p=0.006), higher central pulse pressure (56 vs 49 mmHg, p=0.007), augmentation index (33 vs 14%, p=0.007). Conclusion Hypertensive patients with T2DM and CKD G3b and proteinuria were characterized by worse 24-profile of central BP and higher arterial stiffness.

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