Non-classical and intermediate monocytes in patients following venous thromboembolism: Links with inflammation

Monocyte subsets are involved in atherosclerotic vascular disease and its thromboembolic complications. Moreover, the role of monocytes has been suggested in the pathogenesis of venous thromboembolism (VTE).

We hypothesized that pro-inflammatory non-classical and intermediate monocytes are increased in the first months following VTE.

We enrolled 70 patients aged 18-65 years (mean age 41.6 ±11.6) with the firstever provoked (n = 32; 45.7%) or unprovoked (n = 38; 54.28%) VTE episode, and 46 healthy controls. The exclusion criteria were: acute infection, cancer, autoimmune disorders, previous myocardial infarction (MI), or stroke. Monocyte subsets were assessed 12 (8.5-21.5) months after VTE using flow cytometry and were defined as classical (CD14++CD16-), intermediate (CD14++CD16+) and non-classical (CD14+CD16++).

Patients with VTE had higher intermediate and non-classical monocyte counts compared to the control group (16.8 ±9.3 vs 10.4 ±4.0 cells/μL, and 64.1 ±25.2 vs 44.1 ±19.2 cells/μL, respectively, both p < 0.001). Increased non-classical monocyte counts were observed in patients who experienced a VTE incident within 12 months prior to enrollment (71.5 ±27.4 vs 56.03 ±20.6 cells/μL; p = 0.01) and those with unprovoked VTE (70.2 ±4.1 vs 58.8 ±4.3 cells/μL; p = 0.06). There were no differences in monocyte subsets related to the current anticoagulation.

Our data has shown for the first time that VTE is associated with an increased number of nonclassical and intermediate monocytes, which may indicate the involvement of monocyte-related mechanisms in the pathophysiology of this disease.