Methods: we investigated 60 patients men (age 64 ± 7,6 years) with COPD II-III stages (Global Initiative for Chronic Obstructive Lung Disease 2011) in remission period. The patients were without myocardial infarction, stroke, coronary artery disease. We used of a risk estimation system such as SCORE (Systematic Coronary Risk Estimation) to estimate total cardiovascular risk our patients. A calculated SCORE was 11.31±4 (high and very high risk). The patients were divided into 2 groups. One group (40 patients) received rosuvastatin 5-10 mg during one year. The other group was control (20 patients). The target level for low-density lipoprotein-cholesterol (LDC-?) was = 1,8 mmol/l. The basic therapy COPD did not change. The patients used the combination of anticholinergic agents (ipratropium bromide, tiotropium bromide) with beta-2-adrenomimetic fenoterol. High sensitivity C-reactive protein (hs-CRP), vascular cell adhesion molecule type 1 (VCAM-1) were estimated before and after the treatment period. We analyzed spirometry (severity of airflow limitation), quantity of exacerbations. The symptoms of COPD, health status were analyzed using the St. George’s Respiratory Questionnaire (SGRQ) before and after the rosuvastatin treatment.
Results: all patients reached target values LDC-?. Hs-CRP decreased from 4.5 [3,3; 8,77] mg/l to 3,2 [1,2; 4,1] mg/l (p<0,001). VCAM-1 – marker of endothelial dysfunction decreased from 1066,6 [870; 1381] ng/ml to 795,2 [(670; 1020] ng/ml (p<0,001). The symptoms activity of COPD decreased from 76,3 ± 23,1 to 60,8±11,3 (p<0,05). There was a 21% decrease of COPD exacerbations (p < 0,001). Forced expiratory volume in 1 second (FEV1) 5.2% increase was revealed (p=0,002). The control group did not have statistically significant dynamics in a year. Conclusions: rosuvastatin has anti-inflammatory and endothelial protective effects, improves lung function, and reduces the exacerbations number in patients with COPD. It is important because chronic systemic inflammation and endothelia dysfunction are basic mechanisms of vascular impairments and development of cardiovascular diseases in patients with COPD.