Effect of rosuvastatin or its combination with omega-3 fatty acids on circulating CD34+ progenitor cells and on endothelial colony formation in patients with mixed dyslipidaemia

•Patients have lower number of progenitor cells and colonies compared with controls.•The numbers of cell parameters at baseline are inversely correlated with lipid levels.•Rosuvastatin or its combination with ω-3 PUFAs increases the cell parameters.•The increase in the number of cells is inversely associated with therapy-induced decrease in lipids.

Background and aimsHypercholesterolaemia is associated with a reduced number of circulating progenitor cells, a defect that is restored by statin therapy. We studied the effect of rosuvastatin monotherapy or its combination with omega-3 polyunsaturated fatty acids (ω-3 PUFAs) on progenitor cell number and function in patients with mixed dyslipidaemia.MethodsFifty patients with mixed dyslipidaemia and fifty-five normolipidaemic, apparently healthy, age- and sex-matched volunteers participated in the study. Patients were randomized to receive a daily dose of either 40 mg rosuvastatin (R group, n = 26) or 10 mg rosuvastatin plus 2 g of ω-3 PUFAs (R + O group, n = 24). The number of circulating CD34+ and CD34+/KDR+ progenitor cells as well as the number of colony-forming units-endothelial cells (CFU-ECs) at 10 days of culture were assessed at baseline and 3 months post-treatment.ResultsThe number of CD34+ and CD34+/KDR+ cells per 10,000 leukocytes as well as the number of CFU-ECs were significantly lower in both patient groups compared with healthy volunteers (all p = 0.03). A 3-month treatment with either R or R + O significantly increased circulating CD34+ and CD34+/KDR+ cells as well as the number of CFU-ECs compared with baseline (all p = 0.03). Importantly, the increase in the above parameters was inversely correlated with therapy-induced reduction in lipid parameters in both patient groups.ConclusionsPatients with mixed dyslipidaemia exhibit low numbers of circulating CD34+ and CD34+/KDR+ cells as well as CFU-ECs in culture, a defect restored by 3-month treatment with either high-rosuvastatin dose or a combination of low-rosuvastatin dose with ω-3 PUFAs. The pathophysiological meaning of our results regarding the increased cardiovascular risk in these patients remains to be established.