In the study of the functional ability of right heart diseases in patients of subgroup A, there was a decrease in E TK (P <0.05) and a significant increase in A TK (P <0.001), respectively, the ratio E / A TK (P <0.001) decreased. Other hemodynamic parameters were not significantly different from the control data. Compared with subgroup A KONT , the A value of TK was significantly increased and the ratio E / A decreased (P <0.001), which is explained by an increase in heart rate at the late stages of tumor progression in CLL, due to anemia and intoxication .
In subgroup B, there was an increase in BWW of the pancreas (P <0.001), CSR pancreas (P <0.001), a decrease in PV of the pancreas (P <0.01). Compared with the control, E TK was significantly reduced (P <0.05), A TK increased (P <0.001). Revealed a decrease in E / A TC (P <0.001). Compared with subgroup B KONT , there were significant differences in the indices A TC and E / A (P <0.001) .
In patients with decompensated CPHC on the background of CLL (subgroup C), the diffuse reflectance and CSR of the pancreas were significantly increased (P <0.001); EF significantly decreased the prostate (P <0.001), IAs pancreas (P <0.01), SR pancreas (P <0.05). Patients in subgroup C showed a significant decrease in E TK (P <0.01), an increase in A TK (P <0.001) and a decrease in the E / A ratio (P <0.001). Significant differences of A TK and E / A compared with subgroup C KONT were noted. Due to significant dilatation of the pancreas, the SR pancreas was reduced .
In patients with HPS, the main role in the violation of hemodynamics of the ICC belongs to prolonged pulmonary hypertension, leading to morphological changes in the ICC vessels and in the right ventricular myocardium.
In subgroup D, an increase in the CRD of the pancreas (P <0.05), an increase in KDO (P <0.05) and CSR (P <0.05) of the pancreas were diagnosed. An increase in the SI of the pancreas was noted (P <0.001) due to an increase in the heart rate; an increase in A TK (P <0.05), a decrease in E TK (P <0.05) and, accordingly, a decrease in the ratio E / A (P <0.001). In this group, a violation of pulmonary hemodynamics, systolic and diastolic functions of the pancreas is a consequence of hemoblastosis ( myocardial dystrophy, lymphoid infiltration of the myocardium, etc.), and not bronchopulmonary pathology. Ane mia, intoxication, lymphoid infiltration of the myocardium in patients with CLL, in the later stages of tumor progression, promote different vitiyu not adequate circulation . Myocardial dystrophy caused many violations of pulmonary hemodynamics in subgroup D, including an increase in pressure in the aircraft system.
In the study of the contractile ability of the left ludochka in patients with COPD associated with CLL of subgroup A, an increase in A MK was diagnosed (0.5 ± 0.03 m / s; P <0.01), and a decrease in the E / A LV ratio (1 , 2 ± 0.05 m / s; P <0.001), not typical for patients of subgroup A KONT . This is due to the initial increase in A MK in patients with CLL, due to an increase in heart rate. The remaining indices of the ultrasound study of the left ventricle corresponded to those of healthy individuals and subgroup A KONT . Patients diagnosed in the sub-group of reliable, as compared to control increasing A MK (0.53 ± 0.03 m / s; P <0.001) and, accordingly, a decrease in the E / A ratio (1.0 ± 0.05; P <0.001). No significant difference was found in other indicators of the LV contractile function from those of the control and subgroup B KONT . In the study of the systolic function of the left ventricle in patients of subgroup C, a decrease in the contractile ability of the LV was recorded . Compared with the control, the differential diffuse reflectance and LV CSR were increased (143 ± 5.8. P <0.05 and 60.5 ± 3.0, P <0.01 ml; respectively), EF decreased (61 ± 2, 7%; P <0.01). There was a decrease compared with the control of LV LV (35.6 ± 1.6; P <0.05), LV SI (2.8 ± 0.05 l / ml / m 2 ; P <0.05). Significant differences of these indicators with those in subgroup C CONT is not revealed. In subgroup C, a significant increase was diagnosed compared with the control and subgroup C KONT , A MK (0.55 ± 0.02 m / s; P, respectively, <0.001 and <0.01), which is explained by an increase in heart rate in these patients, and respectively, a decrease in E / A (P <0.001). Thus, LV diastolic dysfunction in patients with COPD associated with CLL has been observed even in patients with normal pulmonary artery pressure. But dilatation of the left ventricle and
The development of its contractile ability develops only into the stage of decompensated HPS. Patients of subgroup D have diastolic and systolic LV dysfunctions (increase in BWW – 140 ± 5.0 ml, P <0.05; CSR – 55 ± 5.0 ml, P <0.05; And MC – 0.58 ± 0.03, P <0.001, a decrease in E MK – 0.53 ± 0.02; E / A – 0.93 ± 0.5, P <0.001) and an increase in SI LV – 3.6 ± 0.25 l / ml / m 2 , P <0.05 (due to increased heart rate).
During ultrasound examination of the diaphragm in patients of subgroup A, the thickness of the diaphragm did not change significantly. The position, shape, echogenicity of the diaphragm did not differ from those in the control group. There was a significant decrease in the excursion of the diaphragmatic muscle with calm and forced breathing. Significant differences in the indices of TD, EDS and EDF in subgroups A and A KONT were not found. However, in subgroup A KONT , in contrast to subgroup A, the EMF did not significantly differ from the same in control. A more pronounced violation of EDS in CLL can be explained by an enlarged liver and spleen in patients with a tumor form of hemoblastosis included in this group, which contributed to the violation of the excursion of the diaphragm .
In patients with subgroup C, an increase in the thickness of the diaphragm was registered (P <0.001). The dome of the diaphragm was flattened, the echo structure became non-uniform. The mobility of the diaphragmatic muscle decreased not only with forced but also with quiet breathing. Significant differences in the indices of TD, EDS and EDF in subgroups B and B KONT were not found .
In patients with subgroup C, the dome of the diaphragm, during the ultrasound study, was fuzzy, slightly wavy, the echo structure was diffusely uneven, with foci of inclusions. The thickness of the diaphragm muscle was 5.5 ± 0.3 mm (P> 0.05). A decrease in the thickness of the diaphragm, as compared with subgroup B (P <0.001), is associated with dystrophic changes in this muscle. In this subgroup, the mobility of the diaphragm was significantly reduced. Her excursion decreased with calm and forced breathing. It should be noted that TD, EDS, and EDF differed significantly from those of subgroup B, which indicates a progressive diaphragm dysfunction. Significant differences in these indicators in subgroups C and C KONT were not found.
The results of the study allowed us to trace the development of changes in the functional state of the diaphragm in patients with CLL and COPD at different stages of the formation of the CID. An increase in the thickness of the diaphragm in patients with compensated HPS, a decrease in its thickness during decompensation of the HPS, and a decrease in the mobility of the diaphragm during calm and forced respiration indicate a progressive impairment of the functional state of the diaphragm as the COPD and HPS develop. Among patients with CLL, with the presence of concomitant COPD, the greatest changes in the functional capacity of the diaphragm were observed in patients with decompensated COP.
In subgroup D, the thickness of the diaphragm did not change, but its excursion during calm and forced breathing was significantly reduced . Violation of the excursion of the diaphragm in these patients is explained by its compression by significantly enlarged liver and spleen and leukemic damage ( lymphoid infiltration, leukostasis in vessels). It must be borne in mind that in subgroup D included a large number of patients with a significant increase in the liver and spleen.
Thus, it can be concluded that in patients with COPD without PH, the functional state of the diaphragm depends on impaired bronchial patency. In compensated drugs, the functional capacity of the diaphragm is impaired due to severe bronchial obstruction, arterial hypoxemia, pulmonary hypertension, and systolic and diastolic function of the pancreas. In patients with decompensated CPH, a significant decrease in the contractile ability of the pancreas joins the above. In patients with CLL, without concomitant COPD, with the presence of LH, the leading role in the disruption of the functional state of the diaphragm belongs to its compression significantly increased by the liver and spleen, and specific leukemic lesion.
Treatment of HPS in the stages of compensation and decompensation was carried out in accordance with modern guidelines .
SrDLA was measured prior to the initiation of appropriate therapy and after its termination. It was possible to achieve a decrease in SrDLA in patients with subgroups B (22.0 ± 2.6); C (27.7 ± 4.0); D (17.6 ± 1.1) mm. Hg Art. However, when conducting a statistical study, this decrease was not significant (P> 0.05).
After treatment in patients of subgroup A (COPD without LH), a significant decrease in the CSR of the pancreas compared to the baseline was observed – to 43.6 ± 2.5 ml (P <0.05), an increase in pancreas to 0.57 ± 0, 03 m / s (Р <0.05) and Е / А ratios – up to 1.03 ± 0.03 (Р <0.01).
In subgroup B (compensated for CPV), after treatment, there was a significant decrease compared to baseline in BWW of the pancreas (123.6 ± 2.0 ml; P <0.05), CSR pancreas (56.3 ± 2.2 ml; P < 0.05), an increase in the E / A ratio (1.18 ± 0.08; P <0.01).
In patients with subgroup C (decompensated pulmonary heart), after therapy, there was a decrease compared with baseline BWW of the pancreas and CSR pancreas,respectively, to 130.0 ± 4.1 ml (P <0.05) and 70.4 ± 4.1 ml (P <0.05). An increase in EF of the pancreas to 49.9 ± 2.9% (P <0.05), UI PZH to 39.2 ± 1.6 ml / m 2 (P <0.05), SI PZH to 3.1 ± 0.1 l / min / m 2 (P <0.01). On the part of the diastolic function of the pancreas, a significant increase in the pancreas E to 0.56 ± 0.04 m / s (P <0.05) was established; the E / A ratio to 0.9 ± 0.05 (P <0.01) However, these indicators after treatment were not normalized.
After treatment in patients of subgroup D (CLL with LH, but without concomitant COPD), an increase in the E / A ratio was observed to 1.34 ± 0.05 (P <0.05). The remaining hemodynamic parameters of the ICC before treatment did not significantly differ from the norm and remained practically unchanged after treatment.