The death was ascertained in 6 patients of subgroup A, 14 patients of subgroup B, 11 patients of subgroup C and 18 patients of subgroup D. According to the results of autopsy material, the morphology of the right ventricle myocardium, segmental bronchi, small circulation vessels, liver and diaphragm was studied in patients with CLL For comparison, data from autopsy material of the same organs of 30 practically healthy people who died from life-incompatible injuries (main control subgroup; control) and patients with COPD and HLS without an associated lympho-proliferative disease (additional control subgroups) were used: 10 people with COPD without signs CPH (control subgroup a to ) 23 persons with COPD symptoms and compensate CPH in step (subgroup B control to ), 30 people with COPD and signs of HPS in the decompensation stage (control subgroup C to ). Patients of the control subgroups by age and sex matched the patients with CLL.

A morphological study of segmental bronchi in patients with CLL deaths with COPD events identified four forms of chronic obstructive bronchitis: 1) catarrhal chronic bronchitis (CBC) was detected in 6 cases (20%) – in group A in 4 cases, in subgroup B in 2 cases; 2) catarrhal sclerosing chronic bronchitis (CACS) was detected in 12 cases (38%) – in subgroup A in 2 cases, in subgroup B in 6 cases, in subgroup C in 4 cases; 3) sclerosing chronic bronchitis (CHB) was detected in 10 cases (32%) – in subgroup B in 6 cases and in subgroup C in 4 cases; 4) granulating chronic bronchitis (HCB) – diagnosed in 3 cases (10%) in subgroup C. Summing up the morphological and morphometric studies of segmental bronchi in patients with COPD associated with CLL and COPD without concomitant hemoblastosis, it can be concluded that there are no significant morphological differences between these two cohorts of patients. An exception is the presence in patients with CLL with progressive, tumor and splenic forms of lymphoid infiltration disease. radios of the bronchi and the presence of clusters of lymphocytes in the vessels. In addition, in patients with CLL, due to the pathogenesis of the disease, the number of neutrophilic granulocytes in the cellular bronchial infiltrate is reduced. These changes can largely explain the protracted dynamics of COPD in patients with CLL. Lymphoid infiltration impairs the drainage function of the bronchi. Leukemia stasis and blood clots in the vessels of the bronchial wall lead to impaired microcirculation and blood supply to the wall of the bronchi. Disorders of microhemocirculation contribute to a severe, prolonged and recurrent course of COPD. A decrease in the number of neutrophils in the cellular infiltrate leads to a decrease in local immunity and contributes to a more protracted dynamics of the main COPD syndromes.

Indicators of the wall thickness of the pancreas, the width of the pancreas and the perimeter of the TSC in subgroups A and D were within normal limits. In subgroups B and C, their progressive increase was observed with a significant difference from control (P <0.001). In subgroup B, these changes are associated with concentric hypertrophy of the pancreatic wall and in subgroup C with dystrophic processes, which result in thinning of the wall and dilation of the pancreatic cavity with the development of relative tricuspid insufficiency. The LA circumference progressively increased from subgroup A to subgroups B and C, reaching a maximum in patients with decompensated CPH. The indicator of the circumference of the aircraft in the subgroup D with confidence <0.05 was different from the control. A significant increase in pancreatic mass was diagnosed in subgroups A, B, C, and D relative to the control (P <0.001). Ventricular index (LM) in all subgroups was significantly different from control. The absolute mass of the pancreas was significantly different from the control in all subgroups of the study. In subgroups A, B and D, microscopic examination of the pancreatic myocardium revealed fibromuscular hyperplasia and hypertrophic-hyperplastic processes, especially expressed in the stage of compensated CPHD. Atrophic and sclerotic processes prevailed in the stage of decompensation of the HPS. Significant differences in the above indicators among the patients of the respective main and additional control subgroups (COPD and HPS with CLL and COPD and HPS without concomitant hemoblastosis) were not found. but. At the same time, during the histological study of the myocardium of the pancreas in patients with CLL, additional control subgroups not characteristic of the patients were revealed : moderately severe lymphoid infiltration of the myocardium and accumulations of lymphocytes in the lumen of the coronary vessels. Lymphoid infiltration in the myocardium in CLL was significantly less pronounced than in the lungs, and was never detected in a macroscopic study .