The Effect of Rosuvastatin on a murine model of deep vein thrombosis

Introduction

Rosuvastatin reduces C-reactive protein and cardiovascular mortality. After deep vein thrombosis (DVT), elevated inflammatory markers persist. We hypothesize that statins may reduce the inflammation that may be associated with the development of post thrombotic syndrome (PTS).

Materials and methods

Wildtype CD1 mice were fed either regular chow or 1 mg/kg rosuvastatin diets for 1 week prior to surgically induced DVT. Thrombus weights, plasma inflammatory markers, and histology were examined on postoperative days 3 and 7.

Results

Thrombus weights were equivalent in the rosuvastatin treated mice compared to control mice on day 3 (1.25 mg/g±0.61 vs 1.46 mg/g±0.61, p = 0.23) and day 7 (1.07 mg/g ± 0.39 vs 1.04 mg/g±0.32, p = 0.43). On day 3, rosuvastatin treated mice demonstrated decreased levels of monocyte chemoattractant protein-1(MCP-1) (8.20 pg/mL ± 4.07 vs 17.37 pg/mL ±3.26, p = 0.04) and tumor necrosis factor-α (TNF-α) (2.42 pg/mL ±0.42 vs 4.74 pg/mL ± 0.91, p = 0.02) in comparison to the control mice. On day 7, rosuvastatin treated mice demonstrated increased levels of interferon-γ (IFN-γ) (4.22 pg/mL ±5.02 vs 0.49 pg/mL ±0.01, p = 0.04) in comparison to the control mice. There was a significant increase in collagen deposition seen both in the thrombus (2.00 ± 0.63 vs 0.75 ± 0.46, p = 0.002) and vein wall (2.33 ± 0.82 vs 1.13 ± 0.35 p = 0.008) on day 7 in the rosuvastatin treated animals compared to the control animals.

Conclusions

After DVT, rosuvastatin did not accelerate thrombus resolution nor did it affect thrombus formation. However, rosuvastatin decreases MCP-1 and TNF-α during thrombus formation and increases IFN-γ in early thrombus resolution. Additionally, rosuvastatin may promote positive remodeling within the thrombus but increases vein wall fibrosis.