Relationship between changes in clinical blood analysis and vascular dysfunction in patients with obstructive sleep apnea and comorbid pathology

Aim. To study the relationship between changes in clinical blood test (CBT) and vascular dysfunction in patients with obstructive sleep apnea (OSA) and comorbid pathology.

Material and methods. A total of 152 patients were examined. The main group consisted of patients with OSA (n = 83), and the control group (n = 69) — without apnea. The subjects underwent anthropometry, polysomnography, transcranial Doppler, ultrasound examination of the brachial artery, and CBT examination.

Results. In patients with OSA, significantly higher values of 50% of the CBT indices, systemic immune inflammation index (SII), leukocyte shift index (LSI), and neutrophil-to-lymphocyte ratio (NLR) were found than in the control group. The timeaveraged maximum blood flow velocity (TAMV) in patients of the main group before the tests was significantly lower only on the right (0.55 (0.43; 0.62) m/s, p = 0.004) compared to the control group (0.59 (0.51; 0.72) m/s) and remained lower after the tests. The cerebrovascular reactivity index values during the hypercapnic test in patients with apnea were within 0.90–1.00 and significantly lower after the 1st and 5th minutes on both sides and the 10th minute on the left than in the control. Endothelial dysfunction was detected in 66.30% of patients in the main group when assessing endothelium-dependent dilation (p = 0.000) and in 50.60% with endothelium-independent dilation of the brachial artery (p = 0.000) compared to the control group (26.10% and 17.40%, respectively).

Conclusion. For patients with OSA, the most significant changes in the CBT are the “red blood” indices, as well as LSI, NLR and SII. An increase in these blood parameters in patients with apnea may indicate the development of systemic inflammation and oxidative stress. The revealed decrease in TAMV, resistance index, impaired adaptation of cerebral circulation against the background of intermittent hypoxemia, endothelial dysfunction may be etiopathogenetic factors in the development of chronic cerebral ischemia in patients with OSA.

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